PSYCHOSOMATIC

DISORDERS IN
DENTISTRY

INTRODUCTION:
Psychosomatic disorder, also called Psycho physiologic Disorder, condition in which
psychological stresses adversely affect physiological (somatic) functioning to the point of
distress. It is a condition of dysfunction or structural damage in bodily organs through
inappropriate activation of the involuntary nervous system and the glands of internal
secretion. Thus, the psychosomatic symptom emerges as a physiological concomitant of an
emotional state. In a state of rage, for example, the angry persons blood pressure is likely to
be elevated and his pulse and respiratory rate to be increased. When the anger passes, the
heightened physiologic processes usually subside. If the person has a persistent inhibited
aggression (chronic rage), however, which he is unable to express overtly, the emotional state
remains unchanged, though unexpressed in the overt behaviour, and the physiological
symptoms associated with the angry state persist. With time, such a person becomes aware of
the physiological dysfunction. Very often he develops concern over the resulting physical
signs and symptoms, but he denies or is unaware of the emotions that have evoked the
symptoms.
According to Harry J Johnson, human body has been designed to resist an infinite
number of changes and attacks brought about by its environment. The secret of god health
lies in successful adjustment to changing stresses on the body . A healthy person will have a
healthy mind. Mind and body are like two sides of a coin. If one of the two is affected in any
way, then the other will also be affected. Body and mind are one and hence influence each
other. The relation between mind and body depends in fact upon the relation between central
nervous system and the rest of the body or between emotional, intellectual fields and physical
organs or yet, between subconscious unconscious mind and the body. All of us are born with
endless aims and when these critical aims are not fulfilled we become in a state of pain. The
automatic mechanism of repression then shuts off perception of pain as well as the original
aim. This state of being is experienced as tension and neurosis. A faulty neurosis can result in
a psychosis. According to Martin Luther, heavy thoughts bring on physical maladies; when
the soul is oppressed so is the body. A rational approach to understanding and treating these
conditions can only come when there is a readiness to examine both physiological and
psychological components at the same time
The term Psychosomatic is derived from Greek words psyche and soma. Psyche
means soul or mind. Soma refers to physical organism of the body. Term psychosomatic
refers to influence of psychological processes on the biological processes.

HISTORICAL HIGHLIGHTS:
The notion that the mind affects organic processes and that what happens in the body
is more or less intensely connected to thinking and emotional patterns, had been frequently
described throughout history. Hippocrates (460-377 BC), the father of clinical medicine,
explained about four bodily fluids (humors) that, when out of balance, led to various physical
maladies. The humoral imbalances thought to cause illness, also, in his view, produce
characteristic and chronic emotional states. Although Hippocrates may have had the details
wrong, he provided prescient guidance regarding possible connection between emotion and
health. (14) The system "psyche soul/soma body" has been an essential philosophical theme
for at least the last 2500 years. In ancient Greece, Anaxgoras (500-428 BC) established a
distinction between the two.In the 1600's Rene Descartes proposed that the soul's main
function is related to thinking/intellectual ability and that all other functions are part of the
physical realm

(15).

Descartes called the organic component the res extensa (extended matter),

opposed to the res cogitans (thinking matter), his designation for the soul. From then on the
perception of the body as predominantly a mechanic system became preponderant in western
culture.
This concept had been documented in Indian history, in Ayurveda. The renowned
Indian sage and scholar Patanjah has emphasized on 'yoga' as a way to healthy mind, strong
body, and spirituality, which enables an individual to attain self-actualization. The mind body
concept also features in the western literature with regard to the development of
psychosomatic medicine. The relationship of a sound mind to the maintenance of healthy
body has been recognized throughout most of recorded history. The ancient Romans and
Greeks discussed the importance of the patient's mental attitude and temperament in
treatment of physical disease.
In the medieval Islamic world the Persian psychologist-physicians Ahmed ibn Sahl alBalkhi and Haly Abbas developed an early understanding of illness that was due to the
interaction

of

the

mind

and

the

body.

They

realized

how

patient's physiology and psychology can have an effect on one another. They found
correlations between patients who were physically and mentally healthy and between those
who were physically and mentally ill. Platos dictum is unequivocal: Any defect of psyche
or soma is the occasion of the greatest discord and disproportion in the order.

It was not until the second half of the last century, that the need to recover an
integrated view of human life led to the inclusion and conceptualization, in modern thought,
of the important role played by emotions and affective bonds in health and disease
(16).

Heinroth in 1818, coined the term psychosomatic.

The basic concept in psychosomatic medicine was first introduced by Sigmond Freud

who used the term conversion hysteria in describing the re-action in which emotional
conflicts are converted into bodily or somatic symptoms. When an emotion cannot be
normally or consciously expressed the individual may resolve this frustration by overt
aggressive acts and gain relief in this manner. However if the individual has built up tension,
which he does not relive, then tension may be subconsciously expressed as somatic symptom
through conversion. Since the oral tissues are of high psychological potential, oral symptoms
are common psychosomatic manifestation. Freud pursued a deep interest in psychosomatic
illnesses following his correspondence with Georg Groddeck who was, at the time,
researching the possibility of treating physical disorders through psychological processes.(2)
In 1892 Dr. Sigmund Freud collaborated with Dr. Josef Breuer in a study of hysterical
symptoms, later redefined as "conversion disorders". The techniques and theories of
psychoanalysis originated as answers to the problems presented by hysterical patients. Freud
stated his belief that the hysterical symptoms represented an abnormal form of discharge.
When a person experiences a significant event, Freud proposes that a discharge of feeling is
the habitual reaction. When such discharge is avoided as the event takes place, hysterical
symptoms may develop. This crucial realisation of a relationship between psychic illness and
emotional energy was thus found . The concepts of Ego, Id and Superego were used by Freud
to describe the structure of the psyche. The central nervous system and the concept of Freud's
'ego' are interdependent. According to Nunnely

(17)

, in the instance where the ego encounters

deeper primitive body mechanisms is where the ego meets the other Freudian concept, the
'id'. The conscious (ego) meets the unconscious (id).Wilhelm Reich, an enthusiast of Freud's
first theories on psychoanalysis, expanded the latter's investigation of anxiety and, among
other early contributions, described how it appears to be a psychic counterpart to a vasomotor
neurosis (an outdated concept that refers to changes in the circulatory system due to
involuntary nervous system dysfunction). The development of this theory into a full
psychosomatic understanding required many more years and further research after which
emerged the basis for related psychotherapic approaches that include emotional treatment
associated with bodywork techniques.

The concept of psychological medicine, was included in the first edition of

diagnostic and statistical Manual of mental disorder(DSM-1) in 1952 as psychosomatic
disorders and in DSM-II, published in 1968, as psycho physiological autonomic and visceral
disorder. In 1980s DSM-III has renamed it has a psychological factor affecting the physical
conditions. Franz Alexander led the movement looking for the dynamic interrelation
between mind and body.(1)
Since the 1970s, due to the work of Thure von Uexkll and his colleagues
in Germany, biosemiotic theory had been used as a theoretical basis for psychosomatic
medicine. Particularly, the umwelt concept and the theory of organism by Jakob von
Uexkll has been found useful as an approach to describe psychosomatic phenomena.
The term 'psychosomatic' is used to refer to a variety of concepts from diseases to
biopsychosocial research to consultation liaison work. The word 'psychosomatic' is frequently
used to depict illnesses in a pejorative way. A psychosomatic disorder is a disease which
involves both mind and body. Also called psychophysiologic disorder. Psychosomatic
diseases are bodily (somatic) disorders, thought to be initiated or aggravated by physiological
disorders that persist for over 2 years.To an extent, most diseases are 'psychosomatic' involving both mind and body.
There is a mental aspect to every physical disease. How we react to and cope with
disease varies greatly from person to person. There can be physical effects from mental
illness. The oral mucosa is highly reactive to psychological influences. In some cases oral
disease may be direct expression of emotions or conflicts, while in other instances lesions of
the mouth may be indirect result of emotional problem. Mouth is directly or symbolically
related to major human instincts and passions. The mouth represents the organ for expression
of certain instinctual craving and is changed with the psychological potential. Oral changes
with psychosomatic etiology are still an unexplored subgroup of psychosomatic diseases
which have long been known in medicine. Many of them, which are believed to be of
psychosomatic character, still do not have sufficient explanation of their etiology, or it is
considered to be multi causal. There are a number of disorders affecting the oral and Para oral
structures, which have a definitive psychosomatic cause.

DEFINITION & TERMINOLOGIES:

Psychology:

It is that specialty of science, which studies the working of normal mind, the
perceptions, sense organs, the personality formation, learning, anger, stress etc. Sperling calls
it the science of individual behavior and experience.
Psychiatry:
It is that branch of medical sciences which diagnoses and treats the diseases of mind,
and also tries to elucidate the disorders which are in the twilight zone of mind and body i.e
the psychosomatic disorders. Sperling defines it as the study and the treatment of mental and
emotional disorders.
Psychosomatic disorders:
DSM-II, 1968 defined psychosomatic disorders as psychosomatic symptoms that are
caused by emotional factors and involves a single organ system, usually under autonomic
nervous innervations. The psychological changes involved are those that normally
accompany certain emotional states, but in these disorders the changes are more intense and
sustained. The individual may not be aware of his emotional states.
Stress:
It is an undesirable or health threatening response of the body, which is brought on by
deleterious external influences (stressors).
Anxiety:
It is an unpleasant emotional state characterized by fearfulness and unwanted and
distressing physical symptom. It is a normal and appropriate response to stress but becomes
pathological when it is disproportion to the severity of the stress, continues after the stressor
has gone, or occurs in the absence of any external stressor.
Depression:
It is more severe, yet unwarranted response to stress. Its description varies from a
feeling of normal unhappiness, through persistent and pervasive ways of feeling and thinking
to psychosis. Most depressions have triggering life events, especially in a first episode. Many
patients present initially with physical symptoms (somatization), and some may show
multiple symptoms of depression in the apparent absence of low mood ("masked"
depression).
Core features Pervasive low mood
Loss of interest and enjoyment

 Reduced energy, diminished activity

Other features Poor concentration and attention
Poor self-esteem and self confidence
Ideas of guilt and unworthiness
Bleak, pessimistic views of the future
Ideas or acts of self harm or suicide
Disturbed sleep
Diminished appetite
Stress, anxiety & depression can be screened and measured by instruments such as
questionnaire, which are acceptable to patients, have adequate sensitivity and specificity in
their ability to identify such disorders, and are sensitive to change.
Neurosis:
A disorder due to unresolved emotional conflicts, anxiety being its chief
characteristic. A neurosis is usually less severe than a psychosis with minimal loss of contact
with reality; nevertheless, thinking and judgement may be impaired. A neurotic illness is an
attempt to resolve unconscious emotional conflicts which handicaps the effectiveness of the
person.
Compulsion:
An insistent, repetitive, intrusive and unwanted urge to perform an act which is often
contrary to the person's conscious wishes or standards. It may be a defensive substitute for
hidden and more unacceptable ideas and wishes. Failure to perform the compulsive act results
in overt anxiety.
Somatization:
Somatization is a form of deep seated neurosis and has been defined as "a tendency to
experience and communicate somatic distress and symptoms unaccounted for by pathological
findings, to attribute them to physical illness and to seek medical help for them".
Depressive neurosis:
This often follows a mental trauma such as bereavement. A patient suffering in this
way does not usually show the biological features of depression, well at loss of appetite and
disturbance of normal sleep or sexual function. This form of depressive illness shows a
frequent admixture of phobic, hysterical or obsessional features, depending on the personality
of the patient.
Dysmorphobia:

A belief in personal ugliness. This is not a phobia, but can vary from an overvalued
idea to a delusion and should be renamed morphodysphoria.
Hypochondriacal neurosis:
Here there is persistent concern with health. The patient is preoccupied with his
bodily symptoms and signs, has a phobia of disease, is convinced of its presence and,
furthermore, responds poorly to reassurance. However, transient hypochondriasis is a
common reaction to stressful events, e.g. clinical students may develop brain tumours,
Hodgkin's disease or AIDS prior to examinations.
Neurasthenia:
This is characterized by lassitude, fatiguability, headaches and disturbance in sleep.

RELATIONSHIP BETWEEN 'PSYCHE' & 'SOMA' (3)

Two trends are developing explaining this concept. One suggests that specific
emotions, conflicts and personality constellations led to specific cell and tissue damage.
(Specific hypothesis) Second theorized that generalized stress created the preconditions for a
number of not necessarily predetermined diseases. (Nonspecific hypothesis) (3)
1) Specific Hypothesis:
If a specific stimulus, emotional conflict, or stress occurred, it expressed itself in a
specific response or illness in a genetically predetermined organ. After stress is suppressed
through the ANS, however, the sympathetic responses may remain alert for heightened
aggression or flight or parasympathetic nervous system responses may be altered for
increased vegetative activity. Such prolonged alertness and tension can produce physiological
disorders and eventually pathology of organs or viscera. Eg; Peptic ulcer.
2) Nonspecific Hyphothesis:
According to this hypothesis, four varieties of reactions takes place due to stress.
a) Healthy normal: On which alertness is followed by an action of defense;
b) The neurotic: In which alert signal of anxiety is too great, the defense fails.
c) The psychotic: On which alarm may be misperceived or even ignored
d) The psychosomatic: In which defense by the psyche becomes ineffective, and the alertness
is translated into somatic symptoms, causing changes in body tissues.

STRESS
Stress, the term coined by Hans Selye who observed that many highly diverse ways of
perturbing the organism resulted in common physiological responses. Stress refers both to a

subject and a predicate, an event and the consequence of that event. Adrenocortical system is
the the crusial responder to the stress full stimulation.
Stress may be defined as the psychophysiological response of the organism to a
perceived challenge or threat (Breivik et al 1996). Stress has been associated with conditions
including cardiovascular disease, gastrointestinal disorders, malignancy, autoimmune disease,
neurodermatitis and infectious disease.'Stress is not what happens to someone, but how
someone reacts to what happens' (Breivik etal 1996)(3)
General Adaptation Syndrome:
Selye's General Adapatation Syndrome (GAS) was based on the observation that
stress significantly influences endocrine function through the hypothalamus and anterior
pituitary gland, leading to enlargement and increased function of the adrenal cortex.(4)
Stress biomarkers:
Stress biomarkers are as follows: the first is the nervous system markers, such as
catecholamines; adrenaline, noradrenaline, and dopamine in the blood, urine, and saliva. The
second

is

the

endocrine

system

markers,

such

as

corticoids

(Cortisol,

17-

hydroxycorticosteroid and aldosterone) in the blood, urine and saliva, and ACTH in the
blood. The third is the immune system markers, such as the number of total lymphocytes and
lymphocyte subsets such as T cells, B cells and natural killer (NK) cells, the activity of NK
cells, mitogen reactivity, immunoglobulin (IgA, IgM, IgG, and IgE), and cytokines such as
interleukin (IL)-1, IL-2, BL-6, interferon (IFN) and tumor necrosis factor (TNF). In addition,
these biomarkers can change to other forms of stress, depending on the kind and duration of
the initial stress. The body reaction to stress is defined as anything (real, symbolic or
imagined) that threatens an individuals survival is to put into responses that seek to diminish
the impact of the stressor. Stress causes cultivation of physiological responses that seek to
react to the stressors, bring about an adaptive response, and restore homeostasis.
The psychological or physical response to stress in humans.(5)
Stress
Psychological factors affecting medical conditions

Acting out.
Avoiding Socializing
Healthy ventilation
Hobby, sports etc

Alexithymia, Overadaptation
Disease prone, Personality
Psychological,
dysfunction
Endocrine response
to stress;
Physical
dysfunction, psychosomatic disease

Anxiety disorders,

depression
CRF is secreted from the hypothalamus into the hypophysial-pituitary portal system.

CRF acts at the anterior pituitary to trigger release of adrenocorticotrophic hormone (ACTH),
Once ACTH is released, it acts at the adrenal stimulate the synthesis and release of
glucocorticoids. Glucocorticoids themselves have myriad effects within the body, but their
actions can be summarized in by short term as promoting energy utilization, increasing
cardiovascular activity (in service of the "flight-or-fight response), and inhibiting functions
such as growth, reproduction, and immunity".
This hypothalamo-pituitary-adrenal axis is subject to tight negative feedback control
by its own end products (ACTH and Cortisol) at multiple levels including the anterior
pituitary, the hypothalamus, and suprahypothalamic brain regions such as the hippocampus. It
is now known that the hypothalamo-pituitary-adrenal axis is also influenced by multiple
extrinsic systems, which should not be surprising given the coordinated nature of the stress
response: For example, in addition to CRF, numerous secretagogues exist that can by pass
CRF release and act directly to initiate the glucocorticoid cascade. Examples of such
secretagogues include catecholamines, vasopressin, and oxytocin. Interestingly, different
stressors (e.g., cold stress versus hypotension) trigger different patterns of secretagogue
release, again demonstrating
that the notion of a uniform stress response to a generic Stressor is an oversimplification.(5)
A relevant feature of the hypothalamo-pituitary-adrenal axis response to stress is that it varies
depending on whether the organism (most of these data come from rats) is exposed to the
stressor on a single occasion, more than once, or over a prolonged period of time.
Interestingly, it has not been possible yet to rely on a model that can predict whether
sensitization (an enhanced response to the same stress over time) or desensitization (a
reduced response to the same stress over time) will occur for a given stressor. Nonetheless,
the fact that the stress response can change dramatically depending on the frequency and
duration of exposure highlights the necessity of specifying these elements when trying to
understand the role of stress in clinical psychiatric illness

Stress
Activate hypothalamus
Release CRF. (Corticotropin-releasing factor)
Hypophysial pituitary portal system -ve feed back
Anterior pituitary
ACTH release
Adrenal cortex
Glucocorticoids

Glucocorticoids:
Promote:

Energy use, increased vascularity,

Reduce:

Immunity, growth, reproduction.

Experimental evidences:
Decreased number of eosinophils and lymphocytes in blood begins after few minutes of
injection of cortisol.
Reduced output of both T cells and antibodies.
Large doses: causes atrophy of the lymphoid tissues.
Immune Response to Stress

Part of the stress response consists of the inhibition of immune functioning by

glucocorticoids, However, this inhibition may reflect a compensatory action of the
hypothalamo-pituitary-adrenal axis to mitigate other physiological effects of stress. Stress can
cause immune activation through a variety of pathways. CRF itself can stimulate
norepinephrine release via CRF receptors located on the locus coeruleus, which activates the
sympathetic nervous system, both centrally and peripherally and increases epinephrine
release from the adrenal medulla. In addition, there are direct links of norepinephrine neurons
that synapse upon immune target cells, Thus, in the face of stressors there is also a profound
immune activation, includiling the release of humoral immune factors (cytokines) such as
interlukin-I (IL-1) and IL-6. These cytokines can themselves cause further release of CRF,
which in turn serves to increase glucocorticoid effects and thereby self-limit the immune
activation(6). Life stresses such as divorce, school examinations, and caring for Sick relative
have been shown in numerous studies to have a deleterious effect on antiviral immunity (e.g,
as manifest in increased herpes simplex virus recurrence rates as reduced cellular immunity)
in human. In one well-controlled study volunteer subjects who had been exposed to high
levels of stress in the preceding year were at greater risk than low stressed subjects for
developing clinical colds following the intranasal administration of respiratory viruses by
droplet. Acute stress has been shown in most studies to increase the activity of natural killer
cells, which are involved in the early nonspecific cellular mediated response to infection. In
contrast, the effects of chronic stress on natural killer cell activity are less clearly defined.
The tentative consensus about the effects of stress on immune function is that whereas small
amounts of stress may enhance immune function. Excessive stress seems to impair it. The
functional health significance of these stress- related alterations in immunity remains to be
determined.
NEUROTRANSMITTER RESPONSE TO STRESS(7)
Stressors of many kinds activate noradrenergic systems in the brain (most notably in
the locus coeruleus) and cause the release of catecholamines from the autonomic nervous
system. Prior exposure to chronic stress results in enhanced synthesis of brain
norepinephrine, apparently through the induction of tyrosine hydroxylase, the rate limiting
step in catecholamine synthesis. Although an animal exposed chronically to a given stressor
may develop tolerance (both behaviorally and in terms of noradrenergic activation) to it over,
time, this same animal may exhibit an enhanced response to a novel stressor. In other words,
chronic stress may dampen the autonomic nervous system response to that particular stress

but leave the animal more sensitive to the effects of ensuing stressors. Stressors also activate
serotonergic systems in the brain as evidenced by increased serotonin turnover. Recent
evidence suggests that although glucocorticoids tend to enhance overall 5HT functioning,
there may be differences in glucocorticoid regulation of serotonin-receptor subtypes that may
have implications for serotonergic functioning in depression and related illnesses. For
example, glucocorticoids may increase serotonin( 5-HT) type 2 (5-HT2)-mediated actions of
5-HT, possibly contributing to the intensification of actions of the central nervous system of
these receptor types that have, been implicated in the pathophysiology of major depressive
disorder, stress also has the effect of increasing dopaminergic neurotransmission in
mesoprefrontal pathway.(7)
Since the late 1980s it has become clear that amino acid and peptidergic
neurotransmitters are also intricately involved in the stress response. Studies have shown that
corticotropin-releasing factor (CRF) (as a neurotransmitter, not just as hormonal regulater of
hypothalamic-pituitary-adrenal axis functioning), glutamatethrough N-methyl-o- aspartate
(NMDA) receptors and Gamma aminobutyric acid (GABA)-all play important roles the
generation of the stress response or in modulation of other Stress-responsive systems such as
dopaminergic and noradrenergic brain circuitry. As these interactions come to be better
understood, it is likely that they will enhance the knowledge base of how stress responses are
cordinated and individualized for specific stressors.
Stressors
Catecholamines- release from ANS. (Adr, NA, DA)
Effects general organ system
Adr,NA
Reticular activating system
Maintains extreme degree of wakefulness
Prevents adequate sleep
Progressive bodily fatigue and mental dissociation.

Transmission of psychosomatic effects through ANS

Hyperactivity of Sympathetic & Para sympathetic NS.

Heart rate, Arterial pressure , Metabolic rate

Peristalsis Diarrhoea, Hyper acidity of stomach

Cortisol secretion has a protective role, inducing a number of biological reactions

(gluconeogenesis, mobilization of free fatty acids, and reduction of protein synthesis) which
lead to an increase in energy supplies. Moreover, cortisol secretion controls glucocorticoids
action and their effects on immunocellular defensive mechanisms, as described by studies
underlining the immunosuppressive action of cortisol to prevent toxic effects of primary
defensive mechanism activated as a response to stress. Thus, a decrease in cortisol
availability in traumatized or chronically stressed individuals may determine an increased
vulnerability to bodily disorders, promoting a disinhibition of immune disorders,
inflammation, chronic pain syndromes and allergies.
THROUGH ANTERIOR PITUITARY STRESS
ACTH
Anterior pituitary
Adrenal glands
ACTH
Hyperacidity
Seratonin & Encephalin system suppression
Depression

The relationship between stress and the neuro-endocrine-immune systems.(8)

Sensory stressors stimulate the hypothalamus, which in turn stimulates the cerebral
cortex and associated areas, and the limbic system, a center of emotion, is thus stimulated.
The limbic system and thalamus activate the hypothalamus, which is the center of the
autonomic nervous and endocrine systems. Thereafter, these systems affect the immune
system, which produces several cytokines. The internal organs are influenced by these three
systems. Conversely, these hormones, cytokines and metabolic materials also affect the
central nervous system. As shown here, when functioning normally, the response of these
three systems to stress results in the maintenance of homeostasis of the organs.(9)
Classification of Psychosomatic Disorders
According to International Classification of Diseases (ICD-10; WHO-1993),
psychosomatic disorders can be broadly classified depending on whether or not there is tissue
damage.
A) Under the category "Psychological malfunction arising from mental factors", it describes
varieties of physical symptoms or types of Psychological malfunctioning of mental origin,
not involving the tissue damage, and usually mediated through the autonomic nervous system
(ANS). Includes in this category are respiratory disturbances, such as hyperventilation and
psychogenic cough; cardiovascular disturbances such as cardiac neurosis; skin disorders such
as pruritis.
B) If there is tissue damage, and psychological factors are associated with a disease process,
the following definition is used: Mental disturbances or psychic factors of any type may be
thought to have played a major part in the etiology of certain physical conditions usually
involving tissue damage. Included under this designation are psychogenic conditions, such as
asthma, dermatitis, eczema, gastric ulcer, mucous colitis, ulcerative colitis, urticaria.(11)
According to ZEGARELLI.E.V, KUTSCHER.A.H and HYMAN.G.A (1978) (12)
1) Psychoneurotic disorders
2) Psycho physiologic disorders
3) Personality disorder
4) Psychotic disorder

1) Psychoneurotic disorder:
Basic characterstic is subject of feeling anxiety
Types of neurosis phobic
Obsessive compulsive
Depression
Conversion
2) Psycho physiologic disorders: distress renders individual of physiologic dysfunction and
eventually tissue damage, rather than neurotic defences or psychic withdrawal.
3) Personality disorder: individual utilizes the pattern of action or behavior rather than
mental, somatic or emotional symptoms.
4) Psychotic disorder: characterized by personality disintegration with failure in the ability to
perceive, evaluate, and test real.
PSYCHOSOMATIC ORAL MEDICINE
A wide spectrum of psychiatric disorders may affect the orofacial region, where
unfortunately they often remain unrecognized because of the common and limited nature of
their presenting features. These include pain, disturbances in jaw movement, burning
sensation or altered salivation or ulceration.(13)
The association of emotional and mental suffering with the mouth may be interpreted
in a number of ways, based on our understanding of the anatomical, physiological and
developmental aspects of oral function. Not only do the lips, tongue and oral mucosa have
exceptionally rich sensory innervations but also the muscles of emotional expression gain
their principal insertions around the mouth. In infancy the mouth plays a vital role in
exploration, feeding and establishing the affectional bond with the mother. (13)
Freud postulated that not only do the oral stage of development determine important
personality traits, but that problems at this stage lead to predisposition to certain depression in
later life (13)
On the other hand learning theorist see the role of mouth during development as providing a
highly specialized and delicate field, which may acquire at critical periods in the course of
growth, such as childhood, adolescence and adult life, a special capacity for the experience of
pleasurable function or emotional pain. Certainly all observers agree that tasting, eating,
speaking give the oral region a special significance in every patients thinking and feeling. (13)

This creates a latent complex situation for the dental surgeon, making his role in treating tne
mouth and teeth a difficult one. Not only he has to prevent or control an anticipated painful
experience, but he may also be interfering with other aspects of the emotional well being of
his patient. (13)
It is important to understand what psychosomatic diseases is not figment of the
patient's imagination. The emotions can disturb a wide variety of hormonal, vascular and
muscular functional, all of which may produce peripheral changes varying from pain and
xerostomia and frank ulcerations.
In some situations the causal relationship may be complex, for instance, in
postpueperal or menopausal depressions, where alteration in sex hormones and amine
metabolism may precipitate both the emotional disturbances, usually called the affective
disorders, and also produce peripheral symptoms such as burning mouth tongue, facial pain
and pruritis.
I) Classification of Oral Psychosomatic Disorders
Acoording to McCarthy PL and Shklar G (l980) (9)
1) Oral psychosomatic disease
Lichen planus
Apthous stomatitis
Glossitis and stomatitis areata migrans
2) Oral diseases in which psychologic factors may play some etiologic role
Erythema multiforme
Mucous membrane pemphigoid
Chronic periodontal diseases
3) Oral infections in which emotional stress serves as a predisposing factor
Recurrent herpes labialis
Necrotizing gingivitis
4) Oral diseases induced by neurotic habits
Leukoplakia
Biting of oral mucosa (self mutilation)
Physical/mechanical irritation
Dental / periodontal disease produced by bruxism
5) Neurotic oral symptoms
Glossodynia (Glossopyrosis)

Dysgeusia
Mucosal pain
II. Classification of Oral Psychosomatic Disorders (10)
Bailoor and Nagesh. (2001)
1. Pain related disorders
a) Myofacial pain dysfunction syndrome
b) Atypical facial pain
2. Disorders related to altered oral sensation
a) Burning mouth syndrome
b) Idiopathic xerostomia
c) Idiopathic dysguesia
3. Miscellanous
a) Oral lichen planus
b) Recurrent apthous ulcers
c) Psoriasis
d) Erythema multiforme
e) Cancerophobia
f) ANUG
g) Anorexia nervosa
h) Bruxism
III. Classification according to presentation of symptoms (9,10,13)
A. PAIN
1. Facial Arthromyalgia
a) TMJ dysfunction syndrome
b) Myofacial pain dysfunction syndrome
c) Costens syndrome
d) Recurrent subluxations
e) Persistent trismus
2. Atypical facial pain
a) Atypical facial neuralgia
b) Idiopathic facial pain
3. Tension headache

4. Atypical odontalgia
a) Idiopathic periodontalgia
b) Phantom tooth pain
5. Intractable pain
6. Psychotic pain (delusional pain)
7. Myalgic encephalomyelitis
a) Post viral fatigue syndrome
b) Royal free syndrome
c) Icelandic disease
d) Epidemic neurasthenia
B, Oral Dysaesthesia: (Disturbances of oral sensation)
. Burning mouth syndrome
. Glossopyrosis
. Glossodynia
. Denture intolerance
. Dysgeusia, hypoguesia
. Ptylism
. Xerostomia
.The phantom bite syndrome
C. Hysterical or Conversion Disorders
D. Somatopsychic Problems
1. Dysmorphophobia ( morphodyshoria)
2. Cancerophobia
3. Hypochondriasis
4. Monosymptomatic hypochondrial psychosis
5. Mental retardation or Handicap.
6. Manchausens Syndrome.
E. Oral psychosomatic diseases
1. Aphthous ulcers
2. Factitious ulceration- stomatitis artefacta
3. Lichen planus
4. Geographic tongue
5. Erythema multiforme
6. Mucous memberane pemphigoid

7. Periodontal diseases
a. Acute necrotizing ulcerative gingivitis
b. Atypical gingivostomatitis
c. Excoriative gingivitis (gingivitis artefacta)
d. Thegosis and somatization (parafunctional occlusal traumatism)
e. General adaptation syndrome
8. Herpis Labialis
9. Bruxism
F. Anorexia Nervosa and Bulimia, Eating Disorders
G. Litigation, Compensation and the Post Traumatic Stress Disorder

INDIVIDUAL DISEASES

PAIN
MYOFACIAL PAIN DYSFUNCTION SYNDROME
Synonyms:

Tempormandibular joint dysfunction syndrome

Masticatory myalgia syndrome

Myofacialpain dysfunction syndrome

Facial arthromyalgia

Myofacial pain

Trigger point myalgia

Myofacial trigger point myalgia

Primary myofacial and muscle pain dysfunction is the most common cause of pain and
discomfort of all temopormandibular disorders and originates from the muscle of head and
neck, recognition of primary muscle pain is important for successful treatment of patients
with acute and chronic pain.(24,26)

History
Laszlo Schwartz in 1956 introduced the temporomandibular pain dysfunction
syndrome. Late in the decade the myofacial pain dysfunction (MPD) syndrome was named.
Significant advances in neurophysiology were made by Thailander, Kawamura Storey and
Lupton. Also important advances in occlusal therapy were being made with notable
contributions by Ramjford and Krogh-Poulsen.(26)

Pathophysiology:
The jaw muscles have been suggested as chain of events. The jaw muscles have been
included in such a general hypothesis by many authors, and in 1969 Laskin building on the
contributions of many others, proposed a "vicious circle" model of myofascial pain in the
orofacial region. It was suggested that factors such as emotional changes produced

hyperactivity in the jaw muscles leading to fatigue and pain and injury in the muscles and
joints.(27).Whatever etiologic factors are involved it appears that the development of trigger
point may be progressive process with a stage of neurovascular dysfunction, muscle
hyperactivity and irritability that is sustained by numerous perpetuating factors, followed by
stage of organic dystrophic changes in muscle bands with trigger points.(28)
Etiologic factors like macrotrauma, microtrauma may disturb normal or weakened
muscle through muscle injury through whiplash, excess jaw opening or sustained muscle
contraction like bruxism, muscle tension, postural habits. These traumas release free calcium
within muscle through disruption of sarcoplasmic reticulum with ATP, stimulate actin and
myosin interaction and local contractile and metabolic activity resulting in increases in
noxious by products.(29)
Substances like serotonin, histamine, kinins and prostaglandins sensitize and fire
group III & IV muscle nociceptors and a reverbatory neural circuit is established between
nociceptors, CNS and motor units. These afferent inputs converge with other visceral and
somatic inputs in cells like those of lamina I or V of dorsal horn on way to cortex resulting in
perception of local and referred pain. These inputs may be facilititated or inhibited by
multiple peripherally or centrally initiated alterations in neural input to various this central
biasing mechanism of brain stem through various treatment modalities like cold, heat,
analgesic medications, massage, trigger point injections and transcutaneous electrical
stimulation. The cycle may be perpetuated by protective splinting of painful muscle through
distorted muscle posture and avoiding painful stretching of muscle. The reverbatory circuit
will be supported by any other perpetuating factors that produce further sustained neural
activity, continued bruxism, poor postural habits or inputs from pathological viscera or
dysfunctional joints.(29)
With sustained contractile activity local blood flow decreases resulting in low oxygen
tension, depleted ATP reserves, decreased calcium pumping. Free calcium Continues to
interact with ATP to trigger contractile activity, especially if actin and myosin are overlapping
within shortened muscle, Sustained increases in local noxious by products of oxidative
metabolism then contribute to beginning of organic musculodystrophic stage with
sensitization of nociceptors with interstitial connective tissue at trigger points and their
further disruption of calcium pump. Functional,postural and behavioral disturbances may
further perpetuate the problem if normal muscle length is not restored and pain continues. If
the process continues the muscle band initially tries to respond with hypertrophy but later
breaks down to granular

ground substance eventually resulting in localized fibrosis.(29)

Etiology:
Masticatory muscle dysfunction may occur for the following reasons:
A poor accommodation due to malocclusion.
Destructive habits such as clenching or grinding.
Protective response to other conditions, such as TMJ synovitis, disc derangement or cervical
muscle imbalance.
Trauma
Systemic diseases such as polymyositis or polymyalgia rheumatica.(30)
The major etiologic factor of acute muscle disorders is muscle hypersensitivity.
Although this may begin with protective activity surrounding an occlusal condition or an
unusual jaw position or movement, many of these symptoms relate to parafunctional activity.
Therefore both occlusal condition and level of emotional stress play an important in such
disorders. Pain produced by myospasms can actually self perpetuate myospasms. This is
accomplished by cyclic effect of pain on emotional stress. It is significant since once
myospasms are present the pain cycle can continue even after original cause of myospasms
has been resolved. This cyclic effect was first described in 1942 and later was related to
masticatory muscles by Schwartz.The term widely used to describe the cyclic effect of
muscle activity is the myofacial pain dysfunction syndrome. The syndrome represents one of
several conditions that fit into the category of acute muscle disorders.(31)
Since myalgia predominates in this disorder, it is common for persons to report pain
affecting their functional activity. The ordinary complaint of inability to eat or even to speak
comfortably. Functional activity is rarely responsible for the symptoms related to muscle
disorders. These activities merely bring persons symptoms to level of awareness. It is the
subconscious parafunctional activity that underlies most of these symptoms. Once the pain is
present however functional activity that elicits pain can further contribute to the disorder by
the cyclic effect of pain as well as by inducing muscle splinting which potentiates the muscle
hyperactivity.(31). Muscle fatigue is caused by chronic oral habits as grinding or clenching of
teeth. These habits are believed to be an involuntary tension relieving mechanism involving
emotional as well as mechanical factors as etiological agents, thus this explanation of the
syndrome had been termed the "Psycho-physiologic Theory" by Laskin and his associates.(25)
In a study conducted by Greene and his associates on 277 patients it was found that
80% had a history of psycho physiologic diseases such as GIT ulcers, migraine headache or

dermatitis. It was found that these patients had significant higher urinary excretion levels of
17-OH steroids and catecholamines, which have been linked to stress phenomenon.
(26)

.Patients with a night time habit of clenching or grinding the teeth (bruxism) may awake

with joint pain, which abates during the day. In people who clench or grind during working
hours the symptoms tend to worsen towards evening and sometimes have a psychogenic
basis.(32)
Different etiological factors that have been implicated include muscle over activity
( such as bruxism and clenching), disruption of the temporomandibular joint, and
psychological stress (such as anxiety and stressful life events ).(32). Precipitating factors may
include wide mouth opening, local trauma, nail biting, and emotional upset. However, there is
rarely one specific etiology, and a combination of factors is often contributory. Occlusal
factors do not in general seem to be important.(32)

Clinical Features: (34)

Bell has described general characteristics of muscle pain as being of deep somatic category,
having the following characteristics.
1) The pain is usually of dull and deep quality
2) The pain is of diffuse nature.
3) The incidence and severity of pain vary with the stimulus
4) Associated restriction in movement may be present.
There are four cardinal signs and symptoms of the syndrome(36)
a) Pain
b) Muscle tenderness
c) Clicking or popping in TMJ
d) Limitation of jaw motion, unilaterally or bilaterally, sometimes with deviation on opening.
The two typical negative disease characteristics:
A) An absence of clinical, roentgengraphic or biochemical evidence of organic changes in
joints itself.
B) Lack of tenderness in joint when it is palpated through the external auditory meatus.

Recurrent clicking in the temporomandibular joint at any point of jaw movement, and
there may be crepitus especially with lateral movements.

Periods of limitation of jaw movement, with variable jaw deviation or locking but
rarely severe trismus.

Pain in the joint and surrounding muscles, which may be tender to palpation.(34)

Associated symptoms:
One reason why myofacial pain of head and neck is misdiagnosed is because
additional signs and symptoms are occasionally reported with more severe cases and
coincidental Pathologic conditions are often associated with myofacial trigger points.
Additional symptoms may include scratchy sensations, tingling, numbness, hyperesthesia,
teeth sensitivity, excess lacrimation, increased salivation, nausea and vomiting. Additional
signs such as excessive sweating, skin flushing, muscle twitching, and swelling have been
seen.(29).Numerous otologic symptoms such as ear pain, tinnitus, diminished hearing,
dizziness, vertigo and fullness in ear have been reported despite negative examinations of ear.
These signs and symptoms may appear to mimic many other conditions including migraine,
headache, neuralgias of head and neck, temporal arteritis, causalgia, arthritis, sinusitis, tooth
pathology and other common pain
producing conditions of head and neck.(29)
Contributing factors: (29)
As with many chronic pain conditions one will also see concomitant social,
behavioral and psychological disturbances that may proceed of follow development of pain.
Patients report psychological symptoms such as frustrations, anxiety, depression,
hypochondriasis and anger if in acute cases become chronic through inadequate treatment.
Maladaptive behaviors such as pain verbalization, poor sleep, dietary habits, lack of exercise,
poor posture, clenching, bruxism can be seen when pain becomes prolonged.
Parafunctionl oral habits such as bruxism and clenching can be generated as form of
tension release as well as learned behavioral response. As stress increases there is increase in
contraction of masticatory muscles cause trigger points and pain. Higher than normal urinary
levels of 17-hydrooxysteroid commonly associated with high number of stressful events were
also found in group of myofacial patients compared to controls. Because trigger points
usually develop in adults, others suggested they might result from progressive stress placed
on certain muscles as we age. Poor muscle health caused by lack of exercise. Poor muscle
use, posture can predispose to development of trigger points.

Clinical characteristics of elevator spasm

When elevator muscles are in spasm the patient reports pain with biting or chewing as
well with wide opening. Biting on separator between the posterior teeth does not change this
pain. Some restrictions of mandibular opening may be present, but it is of extra capsular
origin.(31)

Clinical characteristics of inferior lateral pterygoid spasms: (31)

Myospasms of inferior lateral pterygoid can also be identified by pain during
contraction or stretching. When the mandible protrudes against resistance the inferior lateral
pterygoid is contracting and pain indicates spasms of this muscle. When the teeth are
clenched in centric occlusion, inferior lateral pterygoid is stretching and can produce pain it is
spasm. When a separator is placed between the posterior teeth, stretching of the inferior
lateral pterygoid is reduced and therefore the pain is also reduced.(31)
Spasm of the inferior lateral pterygoid rarely causes any resistance of mandibular
movement it can however cause an acute malocclusion. Usually this is noticed as the absence
of posterior tooth contacts on the ipsilateral side with premature contact of the anterior teeth
on the contra lateral side and is due to shortening of the inferior lateral pterygoid, which
shifts the jaw downwards, forwards and inwards of the affected side.

Clinical characteristics of superior lateral pterygoid spasms.(31)

Pain originating from myospasms of superior lateral pterygoid is increased by
clenching with and without a separator. It is not increased when the mouth is opened or when
the mandible protrudes against resistance. Since the superior lateral pterygoid is attached to
the articular disc, spasms of this muscle can influence disc function. If disc attachments are
elongated and disc morphology is altered, spasms on the superior lateral pterygoid can create
disc interference disorders. The symptoms often disappear as the spasms resolve

Clinical characterstics of elevator and superior and lateral pterygoid

spasms: (31)
When all three muscles groups are in spasm, a combination of previously mentioned
symptoms results. Pain is present in all muscle groups. The pain noticed during clenching is
only partially reduced by biting on separator. Restriction of mandibular movement is
extracapsular and normally occurs only with opening movements. Other movements may be
inhibited by pain. Acute malocclusion may result with disc interferences caused by both
increased passive interarticular pressure and shortening of superior lateral pterygoid. There
are secondary effects of myospasms. When myospasms occurs the resting or passive
interarticular pressure of joint is increased by tension in elevators muscles. The increased

passive interarticular pressure then predisposes the joint to disc condyle interferences during
movement. Healthy joints may not be affected greatly by this increase but subclinical or
slight disc displacements can become evident at this time. An increase in the passive
interarticular pressure accompanied by continued function can convert these subclinical joint
disorders into clinical problems. Prolonged myospasms therefore actually create discinterference disorders.(31).Another secondary effect of myospasms is acute malocclusion.
Spasms of lateral pterygoid or elevator muscles can alter the resting position of mandible and
result in an apparent change in occlusion. Usually the patient will report this symptom but
only with major changes can it be observed clinically.(31)

Examination of trigger points:

When patients with temporomandibular disorder, or TMD, describe their pain
practitioners may assume the pain's source is the same as its site. Unfortunately, the pain
could be referred from a distant location, as is commonly seen with a heart attack. During a
heart attack, the site of the pain may be in the left arm or shoulder, while the pains source is
the heart.(34).Treatment for the pain must be directed toward the source, not the site where it is
felt. Referred pain is prevalent in the head and neck region and frequently causes confusion
for both the practitioner and patient. For example, it has been demonstrated that an oftenoverlooked source for temporal headaches is referred pain from trigger points in the upper
trapezius muscle. If the pain's source is not identified, the practitioner may make the wrong
diagnosis and recommend inappropriate treatment.(34).As early as the 1930s, investigators
attempted to identify referred pain patterns by injecting hypertonic saline into a variety of
skeletal muscles and observing the location of both primary and referred pain sites .(34).Trigger
points are localized, firm, hyperirritable nodules that patients often describe as "knots" within
their muscles. In the head and neck region, trigger points are small (usually between 2 and 10
millimeters in diameter), while they are larger in the shoulder region (usually 10 to 20 mm in
diameter). Trigger points are very discernible, localized, firm nodules that are tender to
palpation and, if sufficiently sensitized, can be the referred pain source .(34).Trigger points are
known to become aggravated from muscle use, poor sleep, psychological tension and
emotional stress, and their severity can fluctuate as the contributing factors change. It appears
that trigger points are caused by a cluster of microscopic neuromuscular dysfunctions,
scattered throughout the nodule, at a skeletal muscle fiber's motor endplate. Trigger points

cannot be identified by laboratory or imaging test, they cannot be studied electro

physiologically, and they do not have a uniformly distributed histological change throughout,
which leads some investigators to question their existence. The easiest and most common
way to identify trigger points is through manual palpation. They often are identified by
rolling a finger over the muscle and feeling for firm, hyperirritable nodules within the muscle.
When a sufficiently irritable trigger point is the referred pain source, moderate sustained
pressure applied to the trigger point usually is able to reproduce a patient's referred pain .
(34)

.Hong and colleagues applied pressure over trigger points until their fingernails blanched

(estimated to be 3-4 kilograms per square centimeter). They were able to reproduce the
patient's referred pain complaint more than 80 percent of the time.
Sustained pressure against the trigger point to produce the referred pain is for few seconds,
but occasionally it may take up to 10 seconds or longer. The reliability and validity of
identifying trigger points within the masticatory musculature has not been established in
patients with TMD. In one controlled study of trigger points that generated referred pain
when needled, researchers found that only 62 percent generated referred pain when palpated.
The natural fluctuation of trigger point irritability also may cause an inconsistent ability to
generate referred pain over time.(34).It has been demonstrated to apply pressure directly to the
trigger point to generate the patient's referred pain. Palpating over a muscle band that
contains a trigger point or an adjacent band within the same muscle often is all that is needed
to reproduce the patient's referred pain; however, it does require greater palpating pressure.
Locating a trigger point sometimes is difficult, especially when there is no firm structure
behind the muscle to support it when the muscle is palpated. It also has been found that
palpating nodules of spot tenderness is a highly reliable method for generating the patient's
referred pain. Masticatory and cervical muscles are not the only structures that can refer pain
to the orofacial region. It has been demonstrated that other structures including the TMJ,
sinuses and teeth also can produce referred orofacial pain.(34)

Treatment
Once a secure diagnosis is being made of MPS, patient education and problem
management can proceed. A through evaluation of disorders includes locating the muscles
involved as well as recognizing all direct contributing factors any psychological, behavioral
and social consequences.(29) .Treating the muscle includes reducing the trigger point or muscle
contraction through repetitive action on it with a form of counter stimulation coupled with
muscle stretching and postural rehabilitation .(29).Initially, Weinberg divided TMD treatment

into three general categories: palliative therapy, causative therapy, and adjunctive therapy.
Other authors have suggested a fourth category, known as definitive therapy.

Palliative therapy:
Palliative therapy is used to reduce pain and improve mandibular function. This
therapy includes procedures such as temporary intraoral appliances, medications,home
remedies (For example, ice, moist heat, exercises, and a soft diet), and even voluntary
disengagement of the teeth.

Temporary Appliances:
The temporary use of intraoral appliances can help to reduce pain and establish an
accurate diagnosis. With this type of therapy, an appliance is used to decrease symptoms, not
to place the mandible in a new or therapeutic position. For example, if a patient suffers from
articular disc displacement in one or both joints and if the pain symptoms are caused by
muscle pain, an appropriate form of palliative therapy would involve a flat or superior
repositioning appliance that does not alter the mandibular position.(35)
Intraoral Appliances: (36)
Intraoral appliances (splints, orthodontics appliances, bite guards, night guards, or
bruxing guards) are used in TMD treatment, and their use is considered to be a reversible part
of initial therapy. Most common purposes advocated for appliance therapy are to provide
joint stabilization, protect the teeth, redistribute forces, relax elevator muscles, and decrease
bruxism. To avoid the possibility of occlusal change, the appliance should not be worn
continuously (ie, 24 hours per day) over prolonged periods. Many patients continue to wear
stabilization splints during sleep with periodic monitoring. Full-coverage appliance therapy
during sleep is a common practice to reduce the effects of bruxing and if not usually
associated with occlusal change, splints that reposition the mandible anteriorly have been
used effectively in treating disk displacements, but they increase the risk of permanently
altering the occlusion and should be used with caution.

Pharmcotherapy
Metaxalone

Muscle relaxant

Reduces

muscle 400-800mg every 6

hyperactivity

hours

Chlorzoxazone

Muscle relaxant

Reduces muscle

500mg every 6 hours

Rofecoxib

COX-2 inhibitor

hyperactivity
Reduces

25-50mg per day

inflammation and

Celecoxib

COX-2 inhibitor

pain
Reduces

100-200mg per day

inflammation and
Valdecoxib

COX-2 inhibitor

pain
Reduces

10 mg per day

inflammation and
Nortriptyline
Amitriptyline

Antidepressant

pain
Improves quality of

Antidepressant

sleep
Improves quality of 10-25 mg at bedtime

10-25 mg at bedtime

sleep

Counter stimulation of muscle:

There are two considerations in reducing muscular pain.
1) Repetitive action on trigger point with a mode of counter stimulation.
2) Muscle rehabilitation through active and passive stretching and postural exercises to
restore the muscle to normal length, posture and range of motion(29
)

.Many of the methods for providing counter stimulation appear to reduce trigger

points. Massage, acupuncture and ultrasound provide noninvasive mechanical disruption of

trigger points. Moist heat, ice packs, fluorimethane, ethyl chloride and diathermy change skin
and muscle temperature as form of counter stimulation. TENS, electroacupuncture and direct
current stimulation provide electric currents to stimulate the muscles and trigger points.
Acupuncture (dry needling), cryoprobe therapy, trigger point injection of LA, corticosteroids
cause direct mechanical disruption with needling to reduce trigger points. Three common
methods of counter stimulation are spray and stretch, trigger point injections and
acupuncture. Other modalities such as ultrasound or direct electrical stimulation may be
particularly useful for muscle contracture.(29)

Spray and stretch

This technique was first developed and described by Janet Travell and can be used as
an effective, noninvasive technique for providing counter stimulation to reduce mild
to moderate pain.(29,31).Ethyl chloride spray can reduce musculoskeletal pain and myospasms
and is very effective at reducing or eliminating myofascial trigger points when used in
conjunction with moist heat. These tiny areas of hypercontraction within muscles produce
pain and limit motion when active. Applying ethyl chloride in fine, parallel sweeps over the

skin of the muscle followed by the application of moist heat .(31).Spray and stretch therapy is
performed by cooling the skin with fluoromethane (a refrigerant spray) and then gently
stretching the involved muscle. The cooling is done to allow the stretching to take place
without the pain leading to a reactive contraction or strain. Patients who respond to this
therapy can use a variation at home by first warming the muscle, then briefly icing it, and
then gently stretching the jaw passively.(36).It is applied in one direction from trigger points
towards reference zone in slow, even sweeps over adjacent parallel areas at a rate of about 10
cm/second.(29).The vapocoolant spray provides abrupt of cutaneous stimulation that
temporarily reduces pain perception in the area. It must be applied from distance of 18 inches .
(31).

Failure to reduce trigger points with Spray and stretch may be due to:

1) Inability to secure full length of muscle due to bone or joint abnormalities, muscle
contracture or patient avoiding voluntary relaxation.
2) Incorrect spray technique.
3) Failure to reduce perpetuating factors.I9

Pressure and Massage:

In some instances massage or manipulation of trigger point can cause it to be
manipulated. Care must be taken not to produce pain. It has suggested that increased pressure
applied to trigger point can also relieve pain. Pressure is increased to about 20 pounds and is
maintained to 30 to 60 seconds. If this technique produces pain, it must be stopped since the
pain can reinforce cyclic muscle pain.(31)

Trigger Point Therapy:

Trigger point therapy has used two modalities: the cooling of skin over the involved
muscle and stretching and the direct injection of local anesthetic into the muscle.
Intramuscularly trigger point injections have been performed by injecting local anesthetic,
saline, or sterile water or by dry needling without depositing a drug or solution. The choice of
solution for injection exists because of the lack of established benefits of any one method.
Injection of sterile water is associated with greater injection pain than injection of saline and
should thus probably be avoided.
In a study in which MPD patients were treated with injection of lidocaine or with dry
needling, both groups reported decreased pain immediately after injection, but the group that
received dry needling experienced greater soreness 48 hours after the procedure .(36).Procaine
diluted to 0.5% with saline has been recommended because of its low toxicity to the muscle,
but lidocaine (2% without vasoconstrictor) is also used, with a standard dental syringe. There

are no tested protocols for trigger point injection therapy, but the injections are often given to
a muscle group in a series of weekly treatments for 3 to 5 weeks; this may be continued with
modification of the intervals between injections, depending on the response. If there is no
response to the initial series of injections, this treatment should be abandoned .(31,36).Needling
has been shown to increase range of motion and exercise tolerance, which subsequently
increases muscle circulation. Since critical factor in needling is mechanical disruption of
trigger point by needle and not injection of anesthetic, precision in needling of exact trigger
point and the intensity of pain during needling appear to be major factors in trigger point
inactivation. Trigger point injections with LA are generally more comfortably than dry
needling or injecting other substances, although acupuncture may be helpful for patients with
multiple chronic muscle trigger points. The LA must be used in concentration less than that
required for neve block. This can remarkably lengthen the relative refractory period of
peripheral nerves and
limit the maximum frequency of impulse conduction.(29)
Contraindications to use trigger point injections include:
1) Severe acute cases of muscle injury, trauma or pain.
2) Allergies to LA
3) Patients with active bleeding disorders, diathesis or anticoagulants
4) Patients with cellulites of the area.(29)

Moist Heat and Ice: (31)

Moist heat (for inflammation) and ice (for swelling) are simple yet effective forms of
palliative therapy. Because the effectiveness of these modalities is transitory, prolonged
problems also may require the use of anti-inflammatory medications. Moist heat opens the
capillary beds to promote increased blood flow; in addition, it is excellent as a muscle
conditioner prior to exercise or physical therapy. However, moist heat should be withheld for
approximately 72 hours after an acute injury, while ice is quite effective for reducing muscle
swelling and pain, especially in acute situations.

Exercises: (31)
Home exercises are an excellent method for treating a patient's symptoms, getting the
patient and family members actively involved in the patient's therapy. Fast, active,aerobic
exercises should be avoided; passive stretching that is, keeping the muscle fibers relaxed
while slowly stretching the muscle, preventing it from tightening via the stretch reflex in

conjunction with moist heat (followed by the application of ice) is beneficial for decreasing
muscle and joint pain and for improving ranges of motion.

Adjunctive therpy:
Adjunctive therapy consists of treatment modalities that augment and assist definitive
or causative types of treatment for TMD.

Physiotherapy:
Physiotherapy is a combination of physical therapy; massage therapy, and electro
modalities. These techniques are very effective at providing palliative relief of pain when
Physiotherapy has been shown to be better than placebo, but no differences between various
physical therapies have been shown. Both passive and active treatments are commonly
included as part of therapy. Posture therapy has been recommended to avoid forward head
positions that are thought to adversely affect mandibular posture and masticatorys muscle (31)
Electrotherapy:
Electrotherapy is another category of adjunctive therapy that can be administered in
the dental office. Modalities include electrogalvanic stimulation, ultrasound, low-level laser,
and infrared, all of which are useful for decreasing swelling and pain by opening the
capillaries in the area and increasing circulation. Each of these types of electrotherapy
accomplishes.(31)
Electro galvanic stimulation:
Electro galvanic stimulation utilizes negative polarity over the painful, swollen area.
This negative charge produces an alkaline effect within the tissues, denaturing proteins and
producing vasodilatation of the capillaries; this in turn permits the outward flow of metabolite
and tissue fluids. High voltage electro galvanic stimulation rhythmically pulsates the muscle
to levels of fatigue, causing muscle relaxation.(31)

Ultrasound:
Ultrasound is a mechanical vibration that produces heat and vasodilatation by
increasing the tissue temperature, thus increasing metabolic activity. It produces deep heat to
the area of trigger point, causing local muscle relaxation.(31).This mechanical vibration also
decreases pain by activating large myelinated peripheral neurons that attenuate pain or
nociception stimulation at the spinal cord and trigeminal (pons) levels. The effects of
ultrasound may be enhanced when used in conjunction with massage and exercise .(31)
.Ultrasound therapy relies on high-frequency oscillations that are produced and converted to

heat as they are transmitted through tissue; it is a method of producing deep heat more
effectively than the patient could achieve by using surface warming.(36)

Iontophoresis:
Iontophoresis is the process in which ions in solution are driven through intact skin by
using a direct current between two electrodes. It is a safe and effective method of
electrotherapy that uses ultrasonic energy to drive a medication deep into the tissues. This is
especially useful for directing anti-inflammatory medications into the TMJ. The current is so
low that the patient perceives little or no.21

Low-Level Laser:
Dentists have utilized laser therapy in various applications for years. Low level laser
treatment is beneficial for reducing the pain of TMD by causing endorphin release.Laser
therapy induces nitric oxide synthesis, which causes the endothelial linings of capillaries to
dilate, improving circulation in the area. Laser therapy also may return injured tissues to a
more optimum energy level improving Circulation and decreasing pain and swelling as a
result.

Infrared:
Like most forms of electrotherapy, infrared produces vasodilatation of the capillary
beds by initiating the synthesis of nitric oxide, improving circulation and decreasing swelling
as a result. This small neurotransmitter improves circulation by opening the endothelial
linings of capillaries.(31)

Capsaicin:
Capsaicin is a topical analgesic that has been approved for pain relief. It releases
substance P and pain related neuropeptides to reduce pain perception and inflammation and
must be applied multiple times every day for at least 14 days before analgesic effects are
noted. Side effects include local burning and warming and reddening of the skin; these side
effects diminish with time and eventually disappear.(31)
Botulinum Toxin:
Botulinum toxin has been advocated for treating chronic myofascial trigger points and
headache pain. This type of therapy presents three problems. First, treatments last only 9-12
months at most and require multiple toxin injections. Second, this type of therapy is aimed at
symptoms in most cases, rather than at the cause of the trigger points's perpetuation. Third, a
session of these injections can be costly and uncomfortable for the patient .(31).Hypnosis,
biofeedback, acupuncture, nutritional counseling, supplements and vitamin usage, and

alternative types of therapy all are reasonable and often-recommended types of adjunctive
therapy.(31)

Transcutaneous electrical nerve stimulation: (TENS)

It is often used to start physical therapy, reduce pain, and allow the patient to perform
jaw exercises that promote recovery. TENS uses a low voltage biphasic current of varied
frequency and is designed for sensory counter stimulation for the control of pain. It is thought
to increase the action of the modulation that occurs in pain processing at the dorsal horn of
the spinal cord and (in the case of the face) the trigeminal nucleus of the brainstem .
(36)

.Acupuncture (dry needling) and percutaneous electrical nerve stimulation ( electro

acupuncture or PENS) Recent studies have suggested that part of effect of accumulation and
electro acupuncture is achieved by stimulation and release of endogenous analgesic peptides.
Other studies have suggested that the needle effect on inactivating trigger points is another
mechanism that helps explain the wide ranging effects of acupuncture. With this phenomena
the immediate reduction of tenderness occurs with any needling of precise trigger point and is
helpful in managing severe cases of MPS with multiple trigger points in multiple muscles.(29)
The use of electro acupuncture or PENS with needling of trigger points in these cases
will not only implement the local needle effect to reduce pain and restore normal muscle
analgesic system to provide more generalized effects of analgesia.Acupuncture needling
coupled with proper muscle rehabilitation, reduction of perpetuating factors and other
contributing factors are effective means of treating MPS. Local point therapy includes
needling pons to inactivate them. Distal point therapy includes needling points on opposite
end of involved meridians with low frequency (1 to 5 hertz) electrical stimulation to stimulate
endogenous opiate system.(29)

Recurrent subluxation and persistent trismus

Recurrent subluxation:
Recurrent subluxation of the mandibular joint in the absence of any connective tissue
pathology or brain damage, i.e. spasticity, can be considered to be one of two extreme ends of
the facial arthromyalgia spectrum, the other being persistent trismus. These patients
spontaneously and frequently dislocate their jaw, invariably seeking assistance to reduce it.
Occasionally, there may be an associated hallucinatory element. One such patient complained
she went blind on dislocation and her sight was restored after manual reduction.
The response to a phenothiazine drug and continued reassurance is excellent in
patients who retain insight as to the nature of their problem. However, those with a hysterical

or manchausen-like personality are impossible to control in the long term.Despite claims in

the surgical literature, procedures such as eminectomy, Dautrey's operation and less-specific
surgical interference are of no permanent value. Although often irresistible, the surgery
merely

Persistent trismus:
This also may be an isolated manifestation of a psychotic disturbance and the history
is important in establishing the diagnosis. However, one must exclude intraarticular
pathology of the temporomandibular joint such as adhesions, degenerative or post traumatic
osteoarthrosis, as well as sources of 'silent' reflex irritation such as a nasopharyngeal
carcinoma. A more common cause of Short-term hospitalization for medical management and
psychiatric supervision is often essential, extra-articular ankylosis is contracture formation in
the

medial

pterygoid

following

an

inferior

dental-injection-induced

haematoma.

Paradoxically, phenothiazines may produce to extrapyramidal facial dyskinesia which

presents as a tetanus-like fades. Withdrawal ofthe drug in these cases leads to rapid resolution
of the trismus. The more severe drug induced tardive dyskenesia may not remit. Parkinson's
disease can also present with a similar focal facial dyskinesia which is not immediately
recognized, and excess
levodopa therapy will do the same. With psychogenic trismus, opening can be achieved with
intravenous sedation or general anaesthetic. However, prolonged trismus will give rise to
elevator muscle atrophy and a fibrous extra-articular ankylosis of the mandible, which can
only be confirmed under a general anaesthetic with complete muscle relaxation. If this is
severe, bilateral temporalis and masseteric myotomies or coronoidectomies may be necessary
in order to stretch the mouth open.Psychiatric care is, however, the treatment of choice for
underlying emotional disturbance (31)

ATYPICAL FACIAL PAIN

Synonyms
Atypical facial neuralgia
Atypical facial pain
Psychogenic facial pain

History: (37)
Although the term was introduced by Frazier and Russell (1924) and used by Ruth
Moulton (1966) to describe what was thought to be an hysterical conversion syndrome, many
patients appear to be suffering from depression ( Lascelles, 1966).(37)It has since been renamed

persistent idiopathic facial pain (PIFP). PIFP refers to pain along the territory of the
trigeminal nerve that does not fit the classic presentation of other cranial neuralgias.
The International Headache Society defines PIFP as follows (Headache Classification
Subcommittee of the International Headache Society, 2004)
Pain

is in the face.

Pain

is present daily and persists for all or most of the day.

Pain

is confined at onset to a limited area on one side of the face, deep ache, and poorly

localized.
In

addition, the pain is not associated with sensory loss or other physical signs, with no

abnormalities in laboratory or imaging studies.

Etiology:
Bailoor DN and Nillofer s analyzed 21 cases of female and 7 males and strong relationship
was noted between the atypical facial pain and depression and life stressors. The females
invariably showed higher intensities of the varied symptoms. Most responded to
antidepressants and multiple counseling sessions. Psychiatrist was invited to department of
Oral Medicine and Radiology to evaluate certain severe cases that were reluctant to go to the
psychiatry department due to social phobia.(38)
PIFP usually does not have a specific cause; however, injury of the trigeminal nerve
proximally or distally may lead to this disorder. Demyelination, either central or peripheral,
may initiate PIFP symptoms and infectious etiologies should also be considered.

Classification of atypical facial pain(37,40)

I. Bilateral
II. Unilateral
1. Nerve injury
2. Nerve compression or irritation
3. Vascular
4. Unknown
The most important discrimination is between unilateral and bilateral atypical facial pain,

28 .

Bilateral atypical facial or intraoral pain is a plague for the dentist, physicians and their
patients. It occurs almost exclusively in middle-aged women who are depressed and agitated.
The pain is described as constant and burning, it usually is not triggered and cutaneous
stimulation is only discernible not painful. There is rarely any sensory loss. Although is
described with great vehemence, the pain does not interrupt eating or talking. It is not

paroxysmal. There are no associated autonomic abnormalities that can be detected clinically.
Unilateral atypical facial pain also contains different pain syndromes. Patients complain of
constant burning pain restricted to one side of the face. Sometimes there is a component of
shock like stabbing pain superimposed upon the constant background pain.

Clinical features:
Atypical facial pain is more common in women than in men. Although any area of
face can be involved the most commonly affected area is maxillary region. Atypical pain is
characterized by continuous, daily pain that is described as dull and aching. The pain is really
deep and diffuse and does not interfere with sleep. The pain may be bilateral with wide extra
facial distribution and is not provoked by jaw movements and rarely relieved by analgesics.(37)
At onset the pain may be confined to a limited area on one side of the face, while later
it may spread to involve a larger area. The pain is refractory to a variety of treatments.
Frequently, patients present with a history of multiple consultations, multiple ineffective
treatments, and surgical explorations and treatments that may have perplexed the condition.
At onset the pain may be confined to limited area on one side of face, while later it
spread to involve larger area. Psychological stress like anxiety and depression is prevalent
among patients with atypical facial pain. A small subset of patients develops typical features
of trigeminal neuralgia, which is described as dull, constant pain that precedes development
of trigeminal neuralgia by days or years.
The following criteria are recommended before the dental practitioner can brand a
patients pain as atypical pain.
All tests and clinical examinations should reveal lack of detectable pathology in the dental
and oral region, a minimum dental radiograph, orthopantomography; biopsy and complete
blood investigations report should be attempted, together with neurologist opinion.
A definitive hypochondriac patient who keeps detailed notes about his illness from last
many years is a more likely candidate.
A patient who changes his pain location and character every time he reports back. When
pain does not follow anatomic pathway, crosses midline and traverses across body planes it is
likely to be atypical facial pain.(38)
Once diagnose the patient should be counseled and depression and anxiety inventory
may be administered to determine the psychological status and minor tranquilizers and
antidepressants may be prescribed after consulting with on oral medicine expert. If
unmanageable then psychiatrist should be called in. Atypical facial pain often occurs in

molars and Premolar regions. Thermal and mechanical tests for affected area are equivocal.
Menopausal females, geriatric patients and sometimes younger spinsters would combine this
atypical facial pain with others forms of hypochondriac like fits of fainting, weakness,
nervousness.(38)
Time course and prognosis:
Atypical facial pain usually occurs in young or middle aged adults. The symptoms
amazingly constant over time. Medical therapy is rarely effective, denervating operations
usually make the patients pain syndrome more severe. Over many years the patient seems to
manifest less florid pain behavior, but the somatic preoccupation, passive lifestyle and
depression are long term characteristics of these patients.(40)

Treatment:
Once diagnosed atypical facial pain is an ideal disorder to be treated in hospital with
help of psychiatric social worker, psychiatric and dental surgeon. Counseling, short term
antidepressant medication and or minor tranquilizer normally provide good prognosis. At
present even a computed tomography scan is considered a basic test in order to rule out any
pathology lying in deep cranial areas.(38)
Pharmacotherapy: (40)
It is important to recognize that atypical facial pain is central pain state, characterized
by absence of pathology in painful area. Medications suppress nociception, the pain due to
tissue damage, do not have much value in alleviate tic pain have any value in management of
pain due to tissue damage such as abscessed tooth. Medications used to treat PIFP include
antidepressants, anticonvulsants, substance P depletion agents, topical anesthetics, N -methylD-aspartate (NMDA) antagonists, and opiate medications. Of these classes of medications,
anticonvulsants and antidepressants appear to be the most effective. The neuropathic
component of pain responds well to anticonvulsants and antidepressants.
Narcotic may be of short term value during a crisis, but they are rarely adequate in
long term management of Atypical facial pain. Many vitamins, tranquilizers and
antidepressants have been claimed to be of value all that is shred of evidence of their efficacy.
Spontaneous remissions are certainly responsible for some of these claims. 29 It is prudent to
avoid performing ablative surgical procedures on patients with atypical facial pain. Those
operations that involve additional denervation, such as nerve avulsions, gangliolysis and
rhizotomy usually fail to relieve the existing pain and results in additional complains about
pain and numbness. Some neurosurgeons have reported that patients with unilateral atypical

facial pain have a lesion (blood vessel, rarely tumor) that is compressing the trigeminal nerve
distal to the juxtapontine site of lesion responsible for the tic douloureux. Others have
disputed these findings.(40)
Some success in patients with unilateral atypical facial pain have been reported
following chronic stimulation of the gasserian ganglion as reported by Meyerson and
Hakansson (1980) and Lazorthes (1987). A stimulating electrode can be introduced either
percutaneously or via temporal craniotomy and connected to stimulus generator implanted on
the chest wall. It is not clear how to select patients for this operation; about two-thirds seem
to have good long-term results. Trigeminal tractomy or nucleotomy have also been used with
variable results in a small number of patients.(40)

TENSION HEADACHE
Tension headaches are the most common type of headaches among adults. They are
commonly referred to as stress headaches. Tension headache is a steady non-pulsatile bandlike ache which may be acute or chronic. The pain radiates to the forehead, temples, back of
the head and neck. It may be uni or bilateral and may involve the temporal, occipital or
parietal regions or a combination of all these areas.The continuous character may be
interrupted by pounding exacerbations associated with nausea and vomiting and photophobia.
This presentation is often misdiagnosed as migraine.(39)
The acute form is very common and affects both sexes equally; however, with the
chronic form, four times as many women present for diagnosis and treatment. The condition
is associated with stress, anxiety and depression. The exclusion of Hypertension and
Intracranial lesions are of course essential in making such a diagnosis. Until recently it has
been assumed that the pain occurred as a result of muscular contraction. However, Philips
(1978) questioned the traditional assumption that these headaches are caused by sustained
contraction of the skeletal muscles of the shoulders, neck and head. She found considerable
overlap between electromyographic records during headache and nonheadache periods and
suggested that other changes besides muscular spasm affected the presence or absence of
head pain (Philips and
Hunter, 1981). These could be vascular or central nervous system disturbances. Simple
analgesics are used for acute cases, but recurrent chronic cases can be controlled with
tricyclic antidepressants. In some patients supportive psychotherapy and cognitive therapy
can be effective.(41)
The commonly observed relationship of FAM and AFP with head pains has led to the

belief that malocclusion is not only responsible for FAM, but also migraine (Higson, 1986).
However, there is no good evidence for this hypothesis. Furthermore, although 38% of FAM
patients have THs, there is no significant association of FAM with migraine.

ATYPICAL ODONTALGIA
(Idiopathic periodontalgia, phantom tooth pain)
Odontalgia is usually due to infective or traumatic inflammation of the pulp or
periodontal membrane, but patients may present with identical symptoms without any
discernible cause (Harris, 1974; Rees and Harris, 1979). The pain is severe and throbbing in
character and the teeth are hypersensitive to any stimulus. It is often widespread and bilateral
but occasionally may be precisely localized.
Some cases have been precipitated by a dental procedure such as the fitting of a
bridge or an extraction, but they are invariably made worse by any further active treatment.
An important differential diagnosis is the 'split tooth. Here a vertical crack in a vital tooth
may be detected with a fibre-optic light or at the base of a cavity. Unfortunately, bruxism in
patients with long standing atypical odontalgia may give rise to a split tooth which, despite
treatment or extraction, does not relieve pain, one is therefore confronted by a patient with a
history of pain accelerated by unnecessary pulp extirpations and extractions and whose
remaining teeth, even when sound and vital are tender to percussion. The problem appears to
be an idiopathic state of hyperalgesia of Pulp and/or periodontal pain receptors. A carefully
taken history will reveal significant emotional problems in many patients, and the condition
may arise after a period of depression especially where drug therapy has ceased or as part of
the so-called 'post-viral fatigue Syndrome, others may not manifest the features of a primary
psychiatric disorder and, as in some cases of AFP, attempts to force one on them do not
produce any therapeutic advantage.(42)
Occasionally, hypotensive drug therapy may precipitate the condition, suggesting a
disturbance in catecholamine metabolism may be an important aetiological factor. These
patients are best considered to have a variant of AFP and should be treated in the same
manner. The temptation to devitalize or extract teeth must be strenuously resisted. The
condition has been considered to be deafferentation neuralgia (causalgia) rising when a dental
extraction or pulp extirpation produces either an amputation neuroma or a central
degenerative change in the trigeminal nucleus (Marbach, 1986). This is an attractive
explanation, except that many cases arise without a history of extraction or pulp extirpation,
and with pain that may migrate across the mid line atypical odontalgias are not consistently

abolished with a dental local analgesic block as is deafferentation neuralgia. Attempts to

curette or excise microscopic neuromas
invariably have little effect beyond 1-2 weeks. However, repeated root canal therapy and
local surgery could well produce a causalgia which complicates both the aetiology and
clinical features.

The management is that of AFP, using tricyclic antidepressants and

phenothiazines. However, some patients with acute overwhelming pain experience relief
lasting 4-6 days following a stellate ganglion block. This can be repeated until the condition
is brought under control.(37)
Data based on 120 patients tend to support earlier findings that indicate that primarily
women (81%) between the ages of 23 and 60 have this condition. Pain is generally localized
in the teeth but may involve several areas of the oral cavity. On the basis of this larger sample
size, the relationship between atypical odontalgia and migraine does not appear to be as
strong as initially reported. Psychologic disturbance also may play a less significant role than
initially thought. Follow-up data on 28 patients suggest that many patients will continue to
experience episodes of pain.Antidepressant medication still appears to be the treatment of
choice for this
condition.(37)

INTRACTABLE PAIN
Although this is an apparently arbitrary classification, there is a residue of patients in
the previous groups whose symptoms either persist indefinitely or recur sufficiently often for
them to be considered separately.(37) The study of what Pilowsky and Spence (1976) have
called abnormal illness behaviour sheds some light on why patients suffer from long-standing
and intractable symptoms. They suggest that with many conditions, 'patients' form a very
small group compared to the individuals in the general population who may be shown to
suffer similar symptoms. This need to attend a doctor or dental surgeon has been described as
the taking up of the "sick role' and the process leading up to it has been called by Mechanic
(l972) illness behaviour'. As already stated, physical symptoms may be the end result of many
kinds of distress due to social and cultural pressures, life events involving real or symbolic
losses, marital discord, etc. The illness is presented by the patient for the doctor's diagnosis,
which endorses the sick role for the individual, his family and for society. The usual pattern
once such an illness has been diagnosed is for the symptoms to respond to explanation,
reassurance and other appropriate treatment. When the patient does not respond then this may
be described as 'abnormal illness behaviour. One advantage of pilowskys approach is that it

seeks to avoid pejorative labelling, such as calling the patient a malingerer, hypochondriacal
or hysterical. It also involves the recognition of the full range of complex factors which lead
to the patient presenting with facial pain, emphasising the importance of taking a
comprehensive history which goes into the patient's background, and seeks to understand this
lack of normal response (Marbach and Lipton, 1978). Such an understanding may lead to
appropriate conservative treatment, i.e. nonsurgical management of the intractable patient,
with attention being paid to previously untreated factors.(37)
Curiously enough, patients with refractory pain are often relatively uncomplaining
and appear to be satisfied with continued consultations (if sufficiently long and supportive) in
which the same unchanging symptoms are discussed and treatment is prescribed. However,
Sternbach (1974) describes these refractory cases as 'playing pain games' where the patient
derives some form of benefit from the persistent pain and has suggested that these benefits
include financial compensation, narcotic analgesics or even the satisfaction of baffling the
clinician. Some of such patients could be classified as suffering from hysteria, which is best
considered to be a state where the illness represents an unconscious means of attracting
emotional support or evading responsibility. The pain or dysesthesia is thus a peripheral
symptom of an underlying psychopathological conflict and for this reason is called a
conversion symptom. The only clues to the diagnosis are the length of suffering, and a
previous history of questionable surgical procedures, especially when associated with
personal or family crises. Vigorous attempts to deprive some of these patients of their
symptoms may even precipitate a crisis, such as dramatic syncopal attacks, urinary retention,
whole-body analgesia or ataxia, all without detectable neurological cause and which remit as
suddenly as they arise. Lefer (1966) and delaney (1976) have both noted the precipitation of
frank psychotic states in such patients following vigorous 'anti-pain treatment. (43)
The concept of untreatable non-malignant pain is difficult to accept, especially by
surgeons. Despite this, any temptation to operate should be resisted, especially as most
proedures not only result in irreversible damage but also appear to contribute to the
intractability (Gerschmann et al., 1976). For pain 'crises', a regimen of simple analgesics
supplemented with an antidepressant drug appears to be an effective means of management,
if the patient will tolerate continued medication, and the clinician continued complaints of
pain.(43)

BURNING MOUTH SYNDROME

Synonyms stomatopyrosis, glossopyrosis, stomatodynia, glossodynia, sore mouth, sore

tongue, and oral dysesthesia.
In this syndrome pain represents the main symptom within a variety of chronic oral
complaints.The term burning mouth syndrome (BMS) refers to a chronic oral burning pain,
diagnosed in the absence of any visible mucosal abnormality or other organic disease. Herein
lays the challenge in the initial recognition of the condition by clinicians. The second
challenge is that psychogenic factors are a probable cause in the majority of cases. The
primary symptom complaint of this condition is sometimes referred to as stomatodynia. This
leading symptom of oral mucosal pain is often accompanied by subjective complaints of
dysgeusia and xerostomia, with or without the presence of salivary hypofunction.(44)
Burning Mouth Syndrome (BMS) is a chronic pain syndrome that mainly affects
middle-aged/old women with hormonal changes or psychological disorders. This condition is
probably of multifactorial origin, often idiopathic, and its etiopathogenesis remains largely
obscure.(45)
Definition:
Despite the fact that a voluminous amount has been published in this field, a
universally accepted definition of this syndrome is still lacking.
International Association for the Study of Pain (IASP) has identified BMS as a
"distinctive nosological entity" characterized by "unremitting oral burning or similar pain in
the absence of detectable oral mucosa changes" (46)
Burning mouth syndrome (BMS) is characterized by pain or burning sensation
affecting an apparently healthy oral mucosa and that cannot be attributed to other disorders
such as candidiasis or irritation caused by dentures. According to Bergdahl and Bergdahl,

,Syndrome affects 3.7% of the general population, and is more common in women (5.5%) particularly after menopause - than in men (1.6%).
Despite the large body of knowledge, some issues on BMS are still debated, and they
present a challenge for both researchers and clinicians. What generates a major dilemma is
that BMS is defined by symptoms that can potentially arise from numerous different
local/systemic pathologies, some of which can be clearly identified and managed, and others
that elude diagnosis and, thus, hamper management.
Very recently, several authors have focused their efforts on establishing whether BMS
should be considered as a distinct "syndrome", or if it mostly represents a "symptom
disruption" for a large number of conditions arising from a wide array of pathologies

(hormonal changes, nutritional deficiency, etc.).

(45)

They have proposed the lack of

local/systemic factors as inclusion criteria for a "true BMS", and assumed that all the other
types of "unremitting oral burning" correlated to different pathologies may be one symptom
within the clinical spectrum of such a group of pathologies.(45)
Epidemiology
BMS is a disorder typically observed in middle-aged and elderly subjects with an age
range from 38 to 78 years

(44).

Occurrence below the age of 30 is rare and the female-to-male

ratio is about 7:1.(45)Adequate numbers of studies reporting appropriate epidemiological

samplings of BMS patients are still lacking. Thus, BMS prevalence appears to be widely
inaccurately estimated. At first, there was an over-diagnosis of BMS patients in the
investigated populations. Previous studies, in fact, reported various and extremely large
ranges of BMS prevalence, from 0.7% to 4.6% or more. This variability was likely due to the
various criteria used for BMS diagnosis. For instance, when BMS was identified only on the
basis of a prolonged burning sensation of the oral mucosa, a prevalence of 14.8% was
estimated

(46)

. However, when diagnosis was arrived at by the use of more correct criteria

BMS prevalence fell to 0.7%.

(45)

at present, this syndrome is more widespread than is

estimated around the world. The use of an appropriate and consistent classification system
based on a universally accepted definition of BMS and strict diagnostic criteria is mandatory,
if the prevalence of this syndrome is to be accurately estimated.
Classification
I) Based on neuropathic basis of disease two clinical forms of BMS are identified (46)
1)"Primary BMS", or essential/idiopathic BMS for which organic local/systemic causes
cannot be identified.
2) "Secondary BMS", resulting from local/systemic pathological conditions and thus
potentially sensitive to etiology-directed therapy.
According to this criteria, "idiopathic" BMS as well as the "secondary" form may represent
two distinctive subgroups of the same "pathological entity" (46).
II) Based on sign and symptom: 37 BMS has been divided into three types
Type- I: it is characterized by daily pain where symptoms are absent upon awakening but
gradually increase in severity as the day progress, unrelated psychiatric conditions. Its
prevalence is 35% of total BMS.
Type-II: it is characterized by constant pain in day & night. These patients are very anxious.
Its prevalence is 55% of total BMS.

Type-III: it is characterized by intermittent pain, with pain free intervals. It occurs in nonusual sites such as floor of the mouth and the posterior oropharynx. Pain is related to the type
of food taken as well as allergens. Its prevalence is 10% of total BMS 47

Clinical findings

Association

Type- I

Daily pain, not present on

awakening, worsens as the day
progresses.

Non psychiatric

Type- II

Constant pain

Psychiatric, chronic anxiety

TypeIII

intermittent pain in usual sites

such
as floor of the mouth

Allergic contact stomatitis due to

preserving agents and additives

III ) Classification
It has been noted that specific chronic pain conditions, such as BMS, "atypical facial
pain"

and

"atypical

odontalgia",

some

"masticatory

muscle

disorders",

and

"temporomandibular joint disorders" show common clinical features, such as similar pain
patterns in the absence of clear etiologic evidence, and they are equally difficult to manage.
As a result, it has been proposed that all these chronic pain disorders should be included in a
1) Unified concept of idiopathic orofacial pain: According to this concept, the pain or
burning of the oral mucosa caused by a known pathological process should be considered
only as one symptom of this pathology.
2)"True BMS" (or "stomatodynia") is pain that cannot be attributed to any local or
systemic causes.
The inclusion of stomatodynia (BMS) in the above new classification is very cogent,
but it would assume that little is known about the mechanisms capable of generating oral
mucosal burning or pain-like symptoms. Thus, if all BMS patients are grouped into this
proposed orofacial pain category, effective therapies for managing the local or systemic
etiological factors underlying this syndrome might be lost. The clinical features of BMS
underscore that the same specific symptomatic pattern (pain, dysgeusia, and/or xerostomia) in
the absence of mucosal lesions exists in BMS patients with identified etiologies as well as in
idiopathic cases. Thus, the above proposed BMS classification is likely to result in the

exclusion of many patients, since recent pivotal studies, utilizing sophisticated diagnostic
techniques, have drown attention to the neuropathic background in BMS 47.

Etiopathogenesis:
The etiopathogenesis of BMS is still unclear, and the issue has generated considerable
controversy in the literature. The most debated aspect is whether BMS should be definitively
considered either as a "distinctive no sological entity" or as a "symptom disruption" which
has its origin in different pathologies. The crux of the problem is that BMS may represent a
complex of multiple diseases with overlapping symptoms. Consequently, dealing with a
syndrome which is poorly defined by symptom(s) without regard to etiology actually causes
more problems relative to diagnosis and management.49,50
The action of or interaction among one or more either unknown (x, y?) or well
identified
(local, systemic, and/or maybe psychogenic) precipitation factors (a) might determine an
either reversible or irreversible neuropathic damage/disorder (b)such as peripheral nerve
damages, dopaminergic system disorders, and/or other neurological alterations. These
disorders could result in BMS symptoms (c). The etiologic role of psychological distress is
still pending. However, long periods of chronic pain may also result in psychogenic disorders
(d), which can intensify BMS symptoms.49,50

PATHOPHYSIOLOGY: 50
The pathophysiology of primary BMS is unclear and has generated controversy
overthe years. The etiopathogenesis seems to be complex and in a large number of
patientsprobably involves interactions among local, systemic, and/or psychogenic
factors.Particular emphasis has been placed on the concurrent symptoms of dry mouth
andtaste alterations. Elements regarding pathophysiology have been discussed at 4 levelsthat
may be interacting: 47
(1) Local environmental factors,
(2) Peripheral nervous system,
(3) The central nervous system,
(4) Psychosocial issues.

Local factors 47

Parafunctional activities: Parafunctional activities (tongue thrusting, grinding andclenching)

resulting in Excess of occlusal or denture wear, lip sucking, lip pressureand mouth breathing
were also noted in patients. BMS patients with parafunctionalhabits such as clenching may be
associated with anxiety.
Galvanic currents: Have been implicated in oral burning there is no objectiveclinical
method to confirm galvanic currents in or between metallic restorations.
Dry Mouth:
It was theorized that BMS is related to decreased salivary gland function, but most studies
have shown no clear-cut association between BMS and decreased salivary flow rates.
Studies have demonstrated alterations in various salivary components, such as mucin,IgA,
phosphates, pH and electrical resistance. The relationship of these changes in salivary
composition to burning mouth syndrome is unknown, but the changes may result from altered
sympathetic output related to stress, or from alterations in interactions between the cranial
nerves serving taste and pain sensation.

Taste Function:
Changes in taste have been reported in over 60% of patients with BMS, and BMS patients
have been shown to have different thresholds of taste perception than matched controls.
Dysgeusia (particularly an abnormally bitter taste) has been reported by 60% of BMS
patients. This association has led to a concept that BMS may be a defect in sensory peripheral
neural mechanisms.
The role of taste in burning mouth syndrome is not straightforward, although recent
studies by one set of investigators demonstrated possible relationship between taste activity
and the disorder. There is an increased prevalence of so-called supertasters" (persons with
enhanced

abilities to detect taste) among patients with burning mouth syndrome.

Supertasters would be more likely to be affected by burning pain syndrome because of their
higher density of taste buds, each of which is surrounded by a basketlike collection of the
pain neurons of the trigeminal nerve. This model would also explain the lack of effect of
hormone replacement therapy once neural damage has already occurred.
Other investigations have found that the ability to detect bitter taste decreases at the
time of menopause. This reduction in bitter taste at the chorda tympani branch of the facial

nerve results in intensification of taste sensations from the area innervated by the
glossopharyngeal nerve and the production of taste phantoms. It has been suggested that
damage to taste might also be associated with loss of central inhibition of trigeminal-nerve
afferent pain fibers, which can lead to oral burning symptoms. Peripheral neural injury or
dysfunction due to oral, facial or systemic trauma might be source of oral burning. Selective
damage to chorda tympani has been implicated following a mandibular block. Injury to
chorda tympani bring about changes in taste

51.

Mucosal diseases, fungal infections, bacterial

infections, allergies, rough teeth, broken restorations, local factors and temporomandibular
dysfunction are thought to cause BMS. Despite reports suggesting a significant relationship
between burning mouth syndrome and mucosal ulcerative or erosive lesions, periodontitis
and geographic tongue, most studies have reported no significant changes in intraoral soft or
hard issues. Allergic reactions have also been suspected, but there is no evidence to support
the hypothesis that BMS is the result of allergic reactions to food, oral hygiene products, or
dental materials. A contact allergy can affect the oral mucosa are present in cases of contact
allergy and absent in BMS patients.49

II) Systemic factors.

Although burning mouth syndrome has not been linked to any specific medical
condition, association with wide variety of concurrent health conditions and chronic pain
conditions, including headaches and pain in other location, have been documented. Patients
with burning mouth syndrome often have high blood glucose levels but no Consistent or
causal relationship has been documented.50
A. Nutritional deficiencies: (Vtamins Bl. B2 and B6, zinc, etc.) are other findings that are
not consistently supported by the literature.
B. Diabetes: Diabetes predisposes patients to dry mouth and candidiasis which may be
responsible for oral burning in 2 to 10% of cases.
C. Gastric regurgitation: It is also thought to be factor responsible for oral burning.
D. Psychological Dysfunction:
BMS has been associated with psychological disorders in many studies. Depression is
frequently associated with BMS, and in some studies, close to one-third of BMS patients
have significant depression scores although, as with any chronic pain disorder, it is unclear if
depression is the cause or the effect of the symptoms. It is likely that some cases of BMS

have a strong psychological component, but other factors, such as chronic low-grade trauma
resulting from Para functional oral habits (e.g., rubbing the tongue across the teeth or
pressing it on the palate), are also likely to play a role.
Personality and mood changes (especially anxiety and depression) have been
consistently demonstrated in patients with burning mouth syndrome and have been used to
suggest that the disorder is a psychogenic problem. However, psychologic dysfunction is
common in patients with chronic pain and may be the result of the pain rather than its cause.
Similarly, the usefulness of tricyclic antidepressants and some benzodiazepines mat be more
closely related to their analgesic and anticonvulsant properties, and to the possible effect of
benzodiazepines on taste-pain pathways.49
E. ACE inhibitors:
Oral burning due to ACE inhibitors decreases with several weeks after reducing,
changing or discontinuing the ACE inhibitors. As there is no definite etiology for BMS all
probable systemic causes need to be ruled out with proper medical consults and appropriate
laboratory tests. Complete blood count ( CBC) with differential serum iron, B12/B1, B2.B6,
folic acid, ferritin and fasting blood sugar levels are few recommended laboratory tests.
F. Hormonal Changes:
The increased incidence of BMS in women after menopause has led investigators to
suspect an association with hormonal changes, but there is little evidence that women with
BMS have more hormonal abnormalities than matched controls who do not have BMS.
Studies of estrogen replacement therapy used to treat BMS have yielded mixed results, and
few investigators recommend hormone replacement as a primary therapy for BMS in patients
who do not require it for other reasons. This variable response is related to presence or
absence of estrogen receptors in oral mucosa. It is suggested that there is reduction in number
of taste buds in postmenopausal women with loss of inhibition of trigeminal nerve, through
facial nerve carrying taste to anterior tongue. Approximately 90 percent of the women in
studies of the syndrome have been postmenopausal, with the greatest frequency of onset
reported from three years before to 12 years after menopause.

Clinical Manifestations:
Women experience symptoms of BMS seven times more frequently than men.when
questioned, 10 to 15% of postmenopausal women are found to have a history of oral burning

sensations, and these symptoms are most prevalent 3 to 12 years after menopause. The tongue
is the most common site of involvement, but the lips and palate are also requently involved.
The burning can be intermittent or constant, but eating, drinking, or placing candy or chewing
gum in the mouth characteristically relieves the symptoms. This contrasts with the increased
oral burning noted during eating that occurs in patients with lesions or neuralgias affecting
the oral mucosa. Patients presenting with BMS are often apprehensive and admit to being
generally
anxious or 'high-strung." They may also have symptoms that suggest depression, such as
decreased appetite, insomnia, and a loss of interest in daily activities.

Pain Characteristics:
In more than one half of patients with burning mouth syndrome, the onset of pain is
Spontaneous, with no identifiable precipitating factor. Approximately one third of Patients
relate time of onset to a dental procedure, recent illness or medication course (including
antibiotic therapy). Regardless of the nature of pain onset, once the oral burning starts, it
often persists for many years. In many patients with the syndrome, pain is absent during the
night but occurs at a 'mild to moderate level by middle to late morning. The burning may
progressively increase throughout the day, reaching its greatest intensity by late afternoon and
into early evening. Patients often report that the pain interferes with their ability to fall asleep.
Perhaps because of sleep disturbances, constant pain, or both, patients with Oral burning pain
often have mood changes, including irritability, anxiety and depression. Earlier studies
frequently minimized the pain of burning mouth syndrome, but more recent studies have
reported that the pain ranges from moderate to severe and is similar in intensity to toothache
pain. Little information is available on the natural course of burning mouth syndrome.
Spontaneous partial recovery within six to seven years after onset has been reported in up to
two thirds of patients, with recovery often preceded by a change from constant to episodic
burning. No clinical factors predicting recovery have been noted. Most studies have found
that oral burning is frequently accompanied by other symptoms, Including dry mouth and
altered taste. Alterations in taste occur in as many as two thirds of patients and often include
complaints of persistent tastes (bitter, metallic, or both) or (changes in the intensity of taste
perception. Dysgeusia tastes accompanying oral burning are often reduced by stimulation
with food. In contrast, application of a topical anesthetic may increase oral burning while
decreasing dysgeusia tastes.

Other causes of burning symptoms of the oral mucosa must be eliminated by

examination and laboratory studies before the diagnosis of BMS can be made. Patients with
unilateral Symptoms should have a thorough evaluation of the trigeminal and other cranial
nerves to eliminate a neurologic source of pain. A careful clinical examination for oral lesions
resulting from candidiasis, lichen planus, or other mucosal diseases should be performed.
Patients complaining of a combination of xerostomia and burning should be evaluated for the
possibility of a salivary gland disorder, particularly if the mucosa appears to be dry and the
patient has difficulty swallowing dry foods without sipping liquids. When indicated,
laboratory tests should be carried out to detect undiagnosed diabetic neuropathy, anemia, or
deficiencies of iron, folate, or vitamin B12. Primary burning mouth syndrome is idiopathic,
clinical exam and the results of laboratory testing and diagnostic imaging fail to detect any
evidence of pathology.

Treatment
Medical disorders, the patient should be reassured of the benign nature of the
symptoms. Counseling the patient in regard to the nature of BMS is helpful in management,
particularly because many patients will have had multiple clinical evaluations without an
explanation for the symptoms. Counseling and reassurance may be adequate management for
individuals with mild burning sensations, but patients with symptoms that are more severe
often require drug therapy. The drug therapies that have been found to be the most helpful are
low doses of TCAs, such as amitriptyline and doxepin, or clonazepam (a Benzodiazepines
derivative). It should be stressed to the patient that these drugs are being used not to manage
psychiatric illness, but for their Well-documented analgesic effect. Clinicians prescribing
these drugs should be familiar with potential serious and annoying side effects. Burning of
the tongue that result from Para-functional oral habits may be relieved with the use of a splint
covering the teeth and/or the palate.51

Medical Management of Burning Mouth Syndrome50

Medications

Drugs

Dose

Prescription

Tricyclic
Antidepressa
nt

Amitriptylin
e
Nortriptyline

10to150
mg/day

10 mg at bedtime; increase dosage by 10 mg

every 4 to
7 days until oral burning is relieved or side
effects
occur.

Benzodiazep
ines

Clonazepam

0.25 to 2
mg/day

0.25 mg at bedtime; increase dosage by 0.25

mg every 4
to 7 days.

Chlordiazep
oxide

10 to 30
mg/day

Anticonvuls
ants

Gabapentin

300
to1,600
mg/day

5 mg at bedtime; increase dosage by 5 mg

every 4 to 7
days until oral burning is relieved or side
effects occur;
as dosage increases, medication is taken in
three divided
doses
100 mg at bedtime; increase dosage by 100 mg
every 4 to 7 days until oral burning is relieved.

Capsaicin52

Hot pepper
and water

Variable

Rinse mouth with 1 teaspoon of a 1:2 dilution

(or
higher) of hot pepper and water; increase
strength of
capsaicin as tolerated to a maximum of 1:1
dilution

Local anesthetic solutions have been used to eliminate or decrease the burning
Sensation, although the intensity of the burning did not change in most cases; solutions
studied in recent years include viscous lidocaine, topical benzocaine, and benzamine
hydrochloride. Other topical agents, such as capsaicin, have been reported as treatment
alternatives but controlled trials are absent. Local antifungal therapy is indicated when
Candida is identified as the probable causative agent. Desensitizing appliances are useful in
limiting tissue irritation associated with parafunction. When an allergy to a specific material
has been identified for example, when localized erythema is associated with acrylic
temporary restorations or denture base material removal of the material removing the material
can resolve symptomatology.
The pharmacologic approach to symptom management involves using sedatives, anxiolytics,
antidepressants, local anesthetic solutions, and other psychoactive substances. Some success
has been achieved using tricyclic antidepressants and serotonin selective reuptake inhibitors
(SSRIs) in doses 8-10 times smaller than the effective antidepressant dose.53
DYSGEUSIA AND HYPOGEUSIA
Synonym:

 Phantom taste
Distorted taste
Dysgeusia is defined as persistent abnormal taste.It is much less common than simple
deficiencies in smell (Hyposmia, Anosmia) and taste (hypogeusia, ageusia) perception.
Dysgeusia is less tolerated than hypogeusia or Hyposmia explaining why it accounts for more
than a third of patients in chemosensory centers. Most cases of dysgeusia are produced by or
associated with underlying systemic disorders or by radiation therapy to head and neck
region. Trauma, tumors or inflammation of the peripheral nerves of the gustatory system
usually produce transient hypogeusia rather than dysgeusia. In contrast relatively common
upper respiratory infections produce a temporary and mild dysgeusia. And neoplasms
predominantly produce dysgeusia. Taste hallucinations are common during migraine
headaches. Bell's palsy or herpes Zoster of the geniculate ganglion. The perception of a
particular taste depends on its concentration in a liquid environment; hence persons with
severe dry mouth may suffer from hypogeusia and dysgeusia. More than 200 drugs are
known to produce taste disturbance.40% of persons with clinical depression complain of
dysgeusia.

54

The local intraoral causes of dysgeusia are periodontal or dental abscess, oral

candidiasis, routine gingivitis or periodontitis. The latter may produce a salty taste because of
high sodium chloride content of oozing crevicular fluid.
Pharmaceutical agents, which may be associated with altered taste.
Anticoagulants, Antihistamines, Antihypertensives, Diuretics, Antimicrobial agents
Anti parkinsonian agents, Antipsychotic or anticonvulsants, Antirheumatic, Antithyroid
Hypoglycemic, Sympathomimetic, Vasodialators
Local and systemic factors associated with altered taste sensations (dysgeusia) or
diminished taste sensation (hypogeusia).
Local factors:
1. Oral candidiasis
2. Oral trichomoniasis
3. Desquamtive gingivitis
4. Oral galvanism
5. Periodontitis and gingivitis
6. Chlorhexidine rinse
7. Oral lichen planus

8. Xerostomia
Systemic factors: 54
1) Vitamin A deficiency
2) Vitamin B12 deficiency
3) Zinc and iron deficiency
4) Nutritional overdose (zinc, vitamin A, pyrodoxine)
5) Food sensitivity or allergy
6) Sjogrens syndrome
7) Chorda tympani nerve damage
8) Anorexia, cachexia, bulima
9) Severe vomiting during pregnancy
10) Liver dysfunction
11) Crohns disease
12) Cystic fibrosis
13) Familial dysautonomia
14) Addisions disease
15) Turners syndrome
16) Alcoholism
17) Medication
18) Psychosis or depression
19) Pesticide ingestion
20) Lead, copper, mercury poisoning
21) Temporal artertitis
22) Brain stem ischemia or infarction
23) Migranous headaches
24) Temporal lobe CNS tumors
25) Nerve trauma, gustatory nerves
26) Upper respiratory tract infection
27) Chronic gastritis or regurgitation
28) Bells palsy
29) Radiation therapy to head and neck.
Clinical features:

Dysgeusia is discerned promptly and distressingly by affected individuals. The

clinical must be certain that the patient's alteration is intact, a taste disorder rather than an
olfactoryone because of 75% of flavor information is derived from smell. Abnormal taste
function should be verified through normal taste testing by using standard tasteants that are
representative of each of the four primary taste qualities (eg, sweet, sour, salty, bitter) in a
non-odourous solutions. Electric and chemical analysis of taste bud may be frequently
required.55 Affected patients may describe their altered tastes as one of the primary ones, but
many describe the new taste as metallic, foul or rancid. The latter two are more likely to be
associated with aberrant odour perception (parosmia) than with dysgeusia. The altered taste
may require a stimulus such as certain foods or liquids, in which case the taste is said to be
distorted. If no stimulus is required the dysgeusia is classified as phantom taste. Patient
complains of an array of oral sensory abnormalities that are difficult to Explain in terms of
recognized oral sensory modalities and that no objective findings to confirm them (eg,
complain of lumpy gritty or paticulate saliva, roughness of lining of mouth, idiopathic
dysgeusia, areas of numbness or swelling that cannot be identified by changes in pinprick or
tactile sensitivity or by inspection of the oral cavity).
Depressive symptoms frequently can be noted during interview of these patients and
treatment of depression not uncommonly reduces the severity or eliminates these complaints.
Like patients with atypical facial pain these patients must also receive adequate follow up
examinations to detect changes in symptoms of any signs of a physical lesion that may
explain the apparently bizarre symptoms. These symptoms have been also been noted to
appear as depressive equivalents in some patients described in the literature.
Evaluation of dysgeusia: 56
In general the evaluation of the patient with other chronic oral sensory problems (e g,
dysgeusia, burning, dryness) follows same pattern as that described for orofacial pain.
Additional information that should be collected in the evaluation of patients with dysgeusia is
described below.
1) General medical history: Drug history, Radiation to head and neck leading to xerostomia
2) Physical examination: Careful evaluation of cranial nerve function
3) Taste testing
A variety of technique that differs in their degree of sophistication are available for
taste testing. The midline of tongue and V shaped row of valate separate the tongue into four
quadrants, the anterior 2/3rd bear fungiform papillae with gustatory receptors via the right

and left lingual branches of 5th cranial nerve to the chorda tympani and facial nerve. The
posterior to quadrants include the right and left valates and the pharyngeal surface of tongue,
innervated by gustatory fibers of the lingual branches of right and left glossopharyngeal and
vagus nerves. Testing of these 4 quadrants thus allows separation of abnormalities of right
and left and 5th versus 9th nerve function. To achieve this tongue must be dried or rinsed
between each application until the patient gives his response. Cards on which the 4 taste
qualities and the comment " no taste" and "plain water are painted allow the patient to
respond while keeping his tongue extended. Some techniques make use of crystals of four
tasteants and rely on lingual salivary secretions or small drop of water applied to the quadrant
under test to dissolve the molecules and make them available to the lingual chemoreceptors.57

4) Oral examination
Careful examination for caries and periodontal pockets in which food and plaque may
be retained as exogenous sources of malodor and bad taste. This should be accomplished by
search for cryptic tonsils, postnasal discharge, rhinitis and sinusitis with retention of nasal
secretion. The dorsum of tongue and the seating surface of dentures should be inspected for
retained food particles and heavy bacterial coatings and the oral mucosa for evidence of
candidiasis, the dorsum of the tongue should be checked for the normal compliment of
fungiform, valate and foliate papillae and the absence of extensive mucosal lesions such as
lichen planus, leukoplakia and glossitis.
The side of tongue, floor of mouth and mylohyoid area should be examined for evidence of
damage to the lingual nerve, and the pharyngeal surface of tongue inspected for masses that
may affect the lingual branch of cranial nerve 9.58
5) Laboratory test
Laboratory tests may indicate the Presence of problems sometimes associated with
dysgeusia include 2 hour post prandial blood glucose estimations and the glucose tolerance,
serum triglycerides and lipoprotein electrophoresis, blood urea nitrogen, thyroid function
studies and possibly 24 hour urinary excretion of zinc and serum zinc evels.59
Treatment and prognosis
If an underlying disease or process is identified and treated successfully the taste
function should return to normal. For idiopathic cases there is no effective pharmacological

or surgical therapy. Dysgeusia in particular tends to depression, anxiety or nutritional

deficiencies from altered eating habits. Fortunately 2/3rd of dysgeusia patients experience
spontaneous resolution (average duration of 10 months).

Denture intolerance.
Discomfort or pain in the absence of any mucosal or bony lesion is a comparable
problem. The diagnosis can be made on the many sets of dentures carried by the patient.
Allergy to methyl methacrylate monomer, especially where there are high levels of free
monomer in the denture, have been found to be the cause in only a quarter of 22 cases studied
by Ali et al. (1986). These patients were relieved by further heat curing of the prosthesis or
the provision of nylon-based dentures. The correction of faults in stability, fit or occlusion
only helped in one case. Most studies of this condition appear to reveal a high percentage of
patients with psychogenic or idiopathic denture intolerance. Sessle and Grushka (1986) have
also shown that these patients have an unexplained abnormality on a range of sensory testing.
A full history and appropriate investigations should eliminate any deficiencies of serum iron,
vitamins BI2, B1, B2 and B6 and folate. A localized diabetic neuropathy can be excluded by
blood and urine glucose estimations. Candidiasis, unless clinically obvious, does not appear
to be a causative factor. But it is probably worthwhile carrying out acrylic patch tests where
there is mucosal inflammation. This leaves the bulk of these patients to be classifieds either
psychogenic or idiopathic. Both should be treated with antidepressant or phenothiazine drug
therapy. The calcium channel blocker nifedipine 10-20 mg three times daily can be helpful in
some cases, although its specific value has not been tented.

THE PHANTOM BITE SYNDROME

Phantom bite syndrome is characterized by an uncomfortable sensation mainly
affecting corrected dentition in which no abnormality is clinically detectable. Despite
repeated failures of dental surgery, sufferers persist in seeking bite correction from a
succession of dentists. Although not uncommon this problem was probably first described by
Marbach (1978). These patients complain of continuous discomfort because their teeth do not
meet correctly. The etiology-pathogenesis of phantom bite is unknown but some consider the
syndrome to be a psychosomatic disorder. They are often intensively involved with, and
superficially knowledgeable about, 'details of dental anatomy, physiology and restorative
dentistry. At consultation they frequently present numerous radiographs of the teeth, casts,
splints, old crowns and pictures of themselves when perfect. A careful history will reveal a

long succession of attempted treatment plans by a variety of dentists who have not been
successful. The spouse may be involved in the delusion (a folie a deux). Dentists must be
cautious in trying to provide any treatment for these patients. The same applies to removable
prostheses and one wonders if, in such cases, the presentation may even be an emotional
response to the traumatic loss of the patient's natural dentition. This pathological narcissism is
comparable to other phantom syndromes where a limb or a breast has been removed.
Psychogenic orofacial problems even appear to follow mutilating surgery elsewhere in the
body. Like some cases of oral dysaesthesia this condition has the characteristic features of a
monosymptomatic hypochondriacal psychosis. It is possible that the problem is a disturbance
in kinesthesia (position sense), particularly as this can be produced experimentally when
vibration is applied to muscle tendons. (Goodwin et al, 1972). Prolonged dental treatment,
especially occlusal equilibration and the replacement of natural tooth contour may have a
similar effect, particularly in obsessional individuals. Continued attempts to 'equilibrate' the
occlusion do not help. If there is no clinical evidence of an iatrogenic grossly deranged
occlusion the condition should be considered to be an obsessional or psychotic problem. If
this is not recognized, the patient will eventually be rendered cuspless then edentulous,
incapable of tolerating dentures and invariably acquiring other intractable syndromes. These
patients usually refuse to see psychiatrists and are not amenable to psychotherapy. Small
doses of phenothiazines, e.g. trifluoperazine (Stelazine) 2 mg three times daily or
flupenthixol 0.5-1.0 mg three times daily, are sometimes helpful, but it is difficult to persuade
the patients to take the tablets. Without medication the disorder is often intractable and the
patients litigenous. Dentists to be cautious when planning treatment. Anything but minimal
intervention is almost bound to fail and the patient will reject the dentist and move on to
further help.Cotreatment by psychiatrist and dentist can be successful.60

XEROSTOMIA
Xerostomia is a new Latin word xerostomia: xero-meaning dry + Greek stomos
means mouth. Xerostomia, or dry mouth, is the abnormal reduction of saliva and can be a
symptom of certain diseases or be an adverse effect of certain medications. Xerostomia is the
subjective complaint of oral dryness, and is medically classified as a symptom. The term
Xerostomia can be used for: aptyalism, asialism, dry mouth . Xerostomia (dry mouth) is an
uncomfortable and potentially harmful oral symptom which is usually caused by a decrease
in the secretion rate of saliva (salivary gland hypofunction). It is more prevalent in the elderly
population, primarily due to their increased use of drugs and their susceptibility to disease. 52

Hyposalivation is the objective reduction in salivary secretion, as the consequence of reduced

salivary gland function. The average person produces at least 500 mL of saliva over a 24hour period. Salivary flow rates vary considerably during any one 24-hour period depending
on the demand or the current physiologic status of the patient. The unstimulated/resting flow
rate is 0.3 mL/ min, whereas the flow rate during sleep is 0.1 mL/min; during eating or
chewing, it increases to 4.0 to 5.0 mL/min. In human beings, saliva is always hypotonic to
plasma, with sodium and chloride ion concentrations being less than those of plasma. The
greater the secretory flow rate, the higher the tonicity of the saliva. Salivary gland secretion is
mainly under autonomic nervous control, but various hormones may also modulate salivary
composition. Secretion appears to be dependent on several modulatory influences that act
either through a cyclic adenosine monophosphatedependent or a calcium-dependent
pathway.61,62 Generally, these conditions are closely related to each other a reduced salivary
flow is the most frequent cause of xerostomia, and it is generally accepted that hyposalivation
causes the symptom of oral dryness when salivary secretion rate is reduced by at least 50%.
Nevertheless, in certain cases these entities do not seem to be interrelated, since some patients
complaining of dry mouth do not show any objective evidence of a reduced salivary flow and,
in turn, some patients with proven salivary gland "hypofunction do not report symptoms of
xerostomia. The variability of normal salivary secretion rate in the population is very large.
Ideally, reduction in salivary secretion should be established on an individual basis when
compared to the normal secretion of every single patient in the past.63
Scientific evidence supports the following observations:
1- Saliva plays a significant role in the maintenance of oral and general health.
2- A variety of medical conditions and medications alter salivary secretion and composition.
3- Xerostomia and salivary gland hypofunction are common clinical findings.
4- Aging per se has no significant clinical impact on salivary secretion.
5- The most common cause of salivary gland hypofunction in the elderly population
medication use.
6- Xerostomia and salivary gland hypofunction are not always present simultaneously.
7- Dental caries and oral fungal infections are the most common complications associated
with salivary gland hypofunction.
8- Xerostomia and salivary gland hypofunction affect the quality of life. Sreebny LM et al,
Clinical signs associated with xerostomia and salivary gland hypofunction55
loss of glistening of the oral mucosa
dryness of the oral mucous membrane

 oral mucosa appears thin and pale

fissuring and lobulation, dorsum of tongue
angular cheilosis / chelitis
Candidiasis, especially on the tongue and palate
Denture-related stomatitis,
Dental caries: increase in prevalence
Thicker, more stringy whole saliva,
Difficulty with 'milking' saliva from the ducts of the major salivary glands
Swelling of the salivary glands
Sreebny LM et al (1992)55 reported Symptoms associated with xerostomia
Oral:
Saliva: decrease in amount, foamy viscous, ropy,(increase in 'spinnbarkeit)
Lips: dry, cracked, fissured (cheilosis)
Tongue: burning (glossopyrosis), pain (glossodynia)
Cheeks: dry
Salivary glands: swelling, pain
Thirst: frequent ingestion of fluids, especially while eating
Mastication: difficulty with eating dry foods; difficulty with the use of a denture
Swallowing: difficulty with (dysphagia)
Speech: difficulty with (dysphonia)
Taste: difficulty with (dysgeusia)
Systemic:
Throat: dryness, hoarseness, persistent dry cough, pharyngitis and laryngitis
Nose: dryness, frequent crust formation, decrease in olfactory acuity
Eyes: dryness, burning, itching, gritty sensation, feeling that the lids stick together,
blurred vision, sensitivity to light
Skin: dryness, butterfly rash, vasculitis
Joints: arthritis, pain, swelling, stiffness
G I tract: constipation, reflux esophagitis, heartburn and constipation.
Vagina: dryness, burning, itching, history of fungal infections, dyspareuma
General symptoms: fatigue, weakness, generalised aching, weight loss, depression
Principal causes of long-standing xerostomia: 61
1. Iatrogenic
Drugs, Local radiation, Chemotherapy

 Chronic graft-versus-host disease

2. Diseases of the salivary glands
Sjogren's syndrome, Sarcoidosis, HIV disease
Hepatitis C virus infection, Primary biliary cirrhosis
Cystic fibrosis, Diabetes mellitus, Others
3. Rare causes
Amyloidosis, Hemochromatosis, Wegener s disease, Salivary gland agenesis (with or
without ectodermal dysplasia), Triple a syndrome Others
4. Psychological disorders; depression
5. ageing: contributory factor; probably does not cause xerostomia per se.
6. Decreased mastication.

Mahvash Navazesh (2003) 65 described how to determine if patients have dry

mouth.
CHIEF COMPLAINT: Does patient complain of dry mouth?

Yes
DRY MOUTH QUESTIONNAIRE

1. Does the amount of saliva in your mouth seem to be too little, too
much, or you don't notice it?
2. Does your mouth feel dry when eating a meal?
3. Do you have difficulties swallowing any foods?
4. Do you sip liquids to aid in swallowing dry food?

Yes
Medical history and review of system: does patient have any known risk factors?

Yes
Clinical evaluations;
Does patient manifest any of the following conditions?

MAJOR SALIVARY
GLAND
enlarged?
Tender?
No saliva on
palpation?
No saliva pool?
Saliva contaminated
with pus or blood?

LIPS:
Dry?
Chapped?
Fissured?
Erythematous?

MUCOSA/TONGUE
Dry?
Erythematous?
Lobulated?
Fissured?

DENTITION

Extensive restorative
experience?
Rampant caries?
Caries involving
incisal
cervical or root
surface?

CONSIDER FURTHER DIAGNOSTIC WORKUP:

Sialometric evaluation
Serologic evaluation
Microbial analysis
Histologic evaluation Imaging
Nutritional councellng
Medical consultation
Psychological evaluation

Summary of oral care in patients with xerostomia: 66

Oral hygiene: plaque control, oral hygiene instruction, dietary advice, chlorhexidine
mouthwash fluoride mouthwash daily (0.05%) to minimize the risk of caries.
Dentures: Should fit well. Implant-retained. Provide instructions on denture hygiene.
Antifungals: Nystatin pastilles, amphotericin lozenges, miconazole gel
Topical saliva substitutes: Sugar-free gum and candies; oral moisturizers
Systemic therapies: Pilocarpine, cevimeline, and others
Some topical therapies for xerostomia58
Sugar-free gum, candies, and liquids
Lubricating gels, mouthwashes, lozenges, and toothpaste, Salivary stimulant
pastilles
Mucin spray, Humidifiers. Saliva substitute placed in intraoral device

SOMATOPSYCHIC PROBLEMS 13, 4

Dyamorphophobia (morphodyashoria)

Dysmorphophobia is the belief in a cosmetic defect in a person of normal appearance. The

complaint may range from mild unattractiveness to ugliness and, Frequently the patient seeks
treatment to correct the supposed deformity. Not surprsingly, the face and its components (the
teeth, nose, mouth, ears, eyes and chin) make up a large percentage of structures for which
patients seek and undergo cosmetic surgery. These patients often have bizarre complaints
about their profile or their smile. The disorder is in fact not a phobia at all but an obsession,
or a delusion, hence the more appropriate term of morphodysphoria. Primary
dysmorphophobia is a neurotic or psychotic characteristic, diagnosed in the absence of any
other psychiatric illness. The distinction between an overvalued idea and a delusion
determines whether the case is neurotic or psychotic. Primary cases can be considered to be a
form of monosymptomatic hypochondriacal neurosis or psychosis. Although with time the
disturbance seems to spread beyond the concern for a localized cosmetic change. However,
some cases arise secondary to depression, anxiety or schizophrenia. Dissatisfaction with
ethnic features 'ethnic dysphoria' is used to describe patients who desire a change from an
oriental or Negro to a Caucasian appearance. Frequently, the complaint is first vocalized in
early adolescence and the patients may report being teased at school about their appearance.
Sexual or gender dysphoria is an obsessional need to change gender. This complex problem
may present the maxillofacial surgeon with the task of reducing the masculine features of a
male transsexual. Such cases should only be treated in collaboration with a unit specializing
in the appropriate psychiatric, hormonal and surgical sexual realignment. Morselli (1886),
who first described dysmorphophobia, emphasized that a patient could be perfectly healthy,
perhaps emotionally rather sensitive, and then suddenly develop the complaint and become
completely preoccupied by it Patients tend to be socially isolated, sensitive, introverted
individuals with no sexual experience. Environmental stresses such as employment problems,
difficulties in personal relationships, or acute events such as bereavements, are liable to
concentrate attention on facial appearance. A morbid affective state such as depression may
also make the patient more likely to express dissatisfaction. Although dysmorphophobia is a
rare symptom in isolation, necessary psychiatric evaluation of patients requesting cosmetic
surgery is not always possible. Few psychiatrists understand the nature and scope of cosmetic
surgery and many patients refuse to see psychiatrists. The Problem is whether to do what the
patient wants, what the patient needs or nothing. The outcome of surgery is usually
unsatisfactory, except where some recognizable deformity has been carefully corrected But
with no or minimal deformity and inappropriate concern the progress is poor. Psychiatric
management is very difficult because of poor drug compliance and a tendency to 'surgeon

shopping. The relationship between surgeon and patient is a vital factor in achieving good
results and a psychiatrist should be included in management. It is essential to have several
meetings preoperatively so that mutual trust can be established. Detailed discussion about
possible surgery and a close follow up after surgery are all necessary if the patient is to be
satisfied. Repeat surgery is invariably unsuccessful

ORAL PSYCHOSOMATIC DISEASES

Lichen planus
Aphthous stomatitis
Glossitis .and stomatitis areata migrans
A substantial body of evidence supports the concept that emotional stress is a major etiologic
factor in these three diseases. In lichen planus and glossitis areata, 26 the lesions often appear
after an episode of intense emotional stress that is obvious to both the patient and the
clinician who is recording the patient's recent history. The disease then undergoes remissions
and exacerbations that often relate to the patient's emotional status.

ORAL LICHEN PLANUS

Synonym: lichen Ruber Planus.
Introduction
Lichen planus is a mucocutaneous disease of unknown etiology. The term lichen
refers to a kind of plant found growing on trees which is formed by mutualistic combination
of algae and fungus. The term lichen rubber planus is used even today as a synonym for the
lichen planus in European literature. This disease was first described in 1869 by Erasmus
Wilson as lichen planus an eruption of pimples remarkable for their color, their figure, their
structure and their habits of isolated and aggregated development, their local and chronic
character and for melasmic stains which they leave behind them when they disappear.59
Lichen planus is a relatively common disorder, estimated to affect 0.5% to 2.0% of the
general population. It is a chronic, inflammatory disease that affects mucosal and cutaneous
tissues. Oral lichen planus (OLP) occurs more frequently than the cutaneous form and tends
to be more persistent and more resistant to treatment Oral lichen planus is a chronic disease
that can persist in some patients for a long time. In contrast to cutaneous lichen planus, the
oral form may persist for up to 25 years. Oral lesions may coexist with lesions of the genital
mucous membranes or with lesions of cutaneous lichen planus. It affects woman more often
than men in a ratio 2:3. Oral lichen planus is a disease of adulthood and children are rarely

affected. Audry was first to point out that the oral lesion could occur in the absence of dermal
lesion. Lieberthal D first described the oral manifestation of lichen planus in American
literature. In 1895wickham described the physical findings that are named after him. Darier
in 1909 described the histological features of lichen planus. Poor V in1905 first described the
occurrence of vesicular or bullous lesions in oral lichen planus and described them as
subepithelial bullae with exudation from the surrounding blood vessels. 69

Epidemiology:
Singh OP & kanwar AJ did an analytical study of 441 patients with lichen planus in
India and found the occurrence to be 7.6% of conditions seen at their institution. The sex ratio
was 3: 2 between males and females. Most patients having the disease were in the 3 rd decade
of life. Axell T et al in 1976 conducted an epidemiological survey in a general population of
30,118 persons in Sweden. The prevalence of about oral lesions were recorded among which
lichen planus was 1.85%.79 The prevalence of OLP in the general population ranges between
0.5% in a selected Japanese population, 1.9% in the Swedish population and 2.6% in the
Indian
population. It is a relatively uncommon mucosal disorder in Malaysia, affecting 0.38%of the
population. 79
Lichen planus is a common mucocutaneous disease affecting 1% to 2% of general
population. Forty percent of lesions occur on both oral and cutaneous surfaces. 35% occur on
skin alone and 25% on mucosa alone. Oral lichen planus occurs in men and women usually
between the ages of 30 and 70 years. The prevalence of lichen planus in Indians is between
0.1% to 1%. Spontaneous remissions of skin lichen planus after 1 year occurs in about 70%
of patients.The reticular form has best prognosis. The reported mean duration of OLP is 5
years, but erosive form can persist for upto 15 to 20 years.

Etiology and Pathogenesis: 80.

Although the etiology has not been fully elucidated, an immunologically induced
degeneration of the basal cell layer of the oral mucosa has been suggested. In the past,
speculatioin about the etiology covered a wide range of possibilities including trauma,
specific bacteria, syphilis, parasites, viruses, mycotics, allergies, toxicity, and neurogenic,
hereditary and psychosomatic disorders. Basal cells are the prime target of destruction in oral
lichen planus. The mechanism of basal cell damage is related to a cell mediated immune
process involving Langerhans cells, T lymphocytes and macrophages. Langerhans cells and

macrophages in the epithelium are the antigen producers that provide the antigenic
information for T lymphocytes.69
Histochemical studies have identified a T-cell origin with CD4 and CD8 subsets in
oral lichen planus. There are fewer CD4 helper/inducer cells than CD8 cells, and the CD8
cells are those that are associated with the basal layer. The CD4 cells act as helper cells and
the destroyer CD8 cytotoxic T-cells damage the basal layer. After a proliferation phase, T8
lymphocytes become cytotoxic for basal keratinocytes.
The role of Langerhans cells is to contact and recognize the antigen and then to
process and present appropriate antigenic fragments (epitopes), together with class II major
histocompatibility complex to CD4 cells after the T lymphocytes have been attracted by
interleukin-1. Interleukin-1 is the lymphokine of the Langerhans cells and macrophages and
stimulates the T lymphocytes to produce interleukin-2, which cause T cell proliferation.
Activated lymphocytes are cytotoxic for basal cells and they secrete gamma-interferon, which
induces keratinocytes to express the class II histocompatibility antigens HLA-DR and
increases their rate of differentiation. This results in thickening of the surface, which is seen
clinically as a white lesion. Langerhans cells and macrophages transfer the antigenic
information when there is a mutual expression of HLA-DR antigen.69
During this mutual excretion between keratinocytes and lymphocytes normally
express HLA-DR antigens, lymphocytes may make contact with epithilial cells and take the
inappropriate epithelial antigenic information by HLA-DR linkage. Self antigens may
therefore be recognized as foreign and cause an autoimmune response. Regazi in (2008)71
reported that although the cause of lichen planus is unknown, it is generally considered to be
an immunologically mediated process that microscopically resembles a hypersensitivity
reaction. It is characterized by an intense T-cell infiltrate (CD4 and especially CD8 cells)
localized to the epitheliumconnective tissue interface. Other immune regulating cells
(macrophages, factor XIIIa positive. dendrocytes, Langerhans cells) are seen in increased
numbers in lichen planus tissue. The disease mechanism appears to involve several steps that
could be described as follows:

an initiating factor/event,

focal release of regulatory cytokines,

up-regulation of vascular adhesion molecules,

Recruitment and retention of T lymphocytes, and cytotoxicity of basal

keratinocytes mediated by the T lymphocytes.

The factor that initiates lichen planus is unknown. It is apparent, however, that
recruitment and retention of lymphocytes is a requisite process. From what is known of
leukocyte kinetics in tissue, attraction of lymphocytes to a particular site would require
cytokine-mediated up-regulation of adhesion molecules on endothelial cells and concomitant

expression of receptor molecules by circulating lymphocytes. In oral lichen planus there is in

fact increased expression of several vascular adhesion molecules (known by acronyms
ELAM-1, ICAM-1, VCAM-1) and infiltrating lymphocytes that express reciprocal receptors
(known as L - selectin, LFA-1, and VLA4), supporting the hypothesis that there is activation
of a lymphocyte homing mechanism in lichen planus. Some of the cytokines that are believed
to be responsible for the up-regulated adhesion molecules are tumor necrosis factor (TNF-),
interleukin-1, and interferon-. The source of these cytokines is thought to be from resident
macrophages, factor XIIIa-positive dendrocytes, Langerhans cells, and the lymphocytes
themselves. The overlying keratinocytes in lichen planus have a significant role in disease
pathogenesis. They may be another source of chemoattractive and proinflammatory cytokines
mentioned earlier, and more important, they appear to be the immunologic target of the
recruited lymphocytes. This latter role seems to be enhanced through keratinocyte expression
of the adhesion molecule ICAM-1, which would be attractive to lymphocytes with
corresponding receptor molecules ( LFA-1). This could set up a favorable relationship
between T cells and keratinocytes for cytotoxicity. The T cells appear to mediate basal cell
death through the triggering of apoptosis. Diabetes mellitus and hypertension have been
described when associated with oral lichen planus as "Grinspan's syndrome". In addition, it
can be seen in severa members of one family, but this does not suggest that oral lichen planus
is a hereditary disease.69
Clinical variants of oral lichen planus: 36
A) Keratotic
_ Reticular
_ Papular
_ Annular
_ Linear
_ Floral
_ Plaque like
B) Erosive/ulcerative
C) Erymematous/Atropic
D) Bullous
Oral lichen planus:
Lichen planus has wide range of clinical appearance with 3 distinct clinical
presentations most often seen are reticular, erosive and plaque. Lichen planus affects

primarily middle-aged adults, and the prevalence is greater among women. Symptoms vary
mucosal sensitivity to continuous debiliting pain. Lesions usually persist for many years with
periods of exacerbations and quiescence. During periods of exacerbations there is increased
erythemas or ulceration with increased pain ands sensitivity. Exacerbations are seen during
periods of anxiety and stress.
The lesions shows white striations, which are slightly, elevated fine whitish lines
called wickhams striae (Honiton lace), which is characteristic of lichen planus with central
umbilicated areas. They usually affect buccal mucosa, ventral and lateral borders of tongue
and also gingival and floor of mouth.4 On gingival lesions frequently present as fiery red
erythema affecting the entire width of attached gingival called Desquamative Gingivitis"
which was once thought to be due postmenopausal changes in women. It is associated with
intense sensitivity of gums to hot or spicy for or brushing the teeth with intense burning
sensation to pain which persists for more than 3 month interfering with oral hygiene
maintenance.36
Reticular OLP: 25, 36, 69
The reticular form is the most common type of OLP. It presents as interlacing white
keratotic lines (known as Wickham's striae) with an erythematous border. The striae are
typically located bilaterally on the buccal mucosa, mucobuccal fold, gingiva and, less
commonly, the tongue, palate and lips. They are asymptomatic and patients become aware of
their presence when it is
noticed by dentist Patient may complain of slight roughness or dryness on affected surface 36
Plaque-Like Form: 25, 36, 69
These plaque-like lesions can range in presentation from smooth, flat areas to
irregular, elevated areas. They may be smaller and vary in sizes ranging from 0.5 to 2mm.
which clinically resembles leukoplakia but which has a multifocal distribution. The presence
of wickham striae at the periphery can help it from differentiate from leukoplakia. This
variant is commonly found on the dorsum of the tongue and on the buccal commisures, which
are more prevalent in smokers. They are usually asymptomatic.
Papular form:
Manifest as small white raised areas of 1 to 2mm in size commonly on buccal mucosa
and dorsum of tongue.

Erosive OLP:
Erosive OLP is the second most common type. It presents as a mix of erythematous
and ulcerated areas surrounded by finely radiating keratotic striae. When erosive OLP
involves the attached gingival tissue, it is called desquamative gingivitis. The lesions of
erosive OLP migrate over time and tend to be multifocal. Patients with this form of OLP
often present with symptoms ranging from episodic pain to severe discomfort that can
interfere with normal masticatory function. Atrophic (erosive OLP) appears as mixture of
intensely erythematous mucosa with large irregular shaped ulcerations with yellowish white
pseudomembranous. The
junction of red and normal mucosa exhibits faint fine white striae. This form can cause
significant discomfort Atrophic lesion on long standing into erosive form.
Bullous Form:
It is rare form of lichen planus, which is characterized by large bullae ranging in size
from 4mm to 2cm. This bullae like phemphigus vulgaris rupture immediately leaving
ulceration on bed of Inflamed mucosa. Intraoral bullae are present on the buccal mucosa and
the lateral borders of the tongue.
Ulcerative form:
Frank ulcers with in areas of whiteness. They are consequences of bullous form.
Patient complains of soreness, which gets severe with spicy food or acidic foods.
General aspects of lichen planus79
Lichen planus affects primarily middle-aged adults, and the prevalence is greater
among women. Children are only rarely affected. Patients with OLP may have coincident
skin lesions that appear as small, angular, flat topped papules and plaques, which are
violaceous. The classic skin lesions of the cutaneous form of lichen planus can be described
as purplish, polygonal, planar, pruritic papules and plaques with a central umbilication. They
may discrete and gradually coalesce into large plaques each covered with fine glistening
scale. Papules are sharply demarcated from surrounding skin. Early in onset of disease appear
red soon take on reddish purple or violaceous hue. These skin lesions commonly involve the
flexor surfaces of the legs and arms, especially the wrists, forearms, inner aspect of thighs,
trunks especially in sacral areas.in chronic cases hypertrophy plaques can be seen over shin

areas, which are bilaterally symmetrical associated with intense pruritis. The nail beds may
also be affected, with resultant ridging, thinning and subungual

hyperkeratosis. Scalp

involvement, if untreated, can lead to scarring and permanent hair loss.Since 30% to 50% of
patients with oral lesions also have cutaneous lesions, the presence of these characteristic
cutaneous lesions can aid in the diagnosis of OLP.
Malignant transformation of lichen planus:
It is generally accepted that malignant transformation in presence of OLP is more
likely seen in atrophic, erosive and ulcerative which has postulated that the lesions predispose
mucosa to damage from carcinogenic agents. The mucosa gets more sensitive to exogenous
mutagens in tobacco, alcohol, betel nut quid, and Candida albicans. Chronic inflammatory
response in OLP may increase likelihood of cancer forming gene mutations. The latter
hypothesis is supported that links chemical mediators of T cell tumourigenesis. Studies
showed that macrophages- migration inhibitory factor (MIF) released from T cells and
macrophages suppress transcriptional activity o f P53 tumor suppressor protein. Normal P53
function is central to prevention of many cancers. Hence blocking p53 function by MIF may
underlie the increased risk of oral cancer in OLP 69
Role of Candida albicans in Lichen Planus:
Candida albicans, which is natural inhabitants of oral mucosa, which often develops
secondarily to long-term topical steroid therapy. It can be another extrinsic factor involved in
development of malignancy. It has been hypothesized that they catalyze the formation of
known carcinogens N- nitrosobenzyl methylamine. Other debates revolved around the use of
immunomodulating agents in treatment of lichen planus as causative factor in development of
malignancies as they depress local cell mediated immunity. Epithelial dysplasia (lichenoid
dysplasia) that progressed subsequently to squamous cell carcinoma in about 0.2% of OLP
patients.
Histopathologic Features:
The classic histopathologic features of OLP include hyperkeratois with short pointed
saw tooth rete ridges, thickening of spinous cell layer which give rise to the clinically
apparent Wickham's striae. Liquefaction of the basal cell layer accompanied by apoptosis of
the keratinocytes, a dense band-like lymphocytic infiltrate at the interface between the
epithelium and the connective tissue. Colloid bodies (Civatte bodies), which represent

degenerating keratinocytes, are often visible in the lower half of the surface epithelium,
scattered with in the epithelium and superficial connective tissue. They are epithelial cells
with eosinophilic cytoplasm with pyknotic nucleus. These bodies represent apoptotic
keratinocytes. In erosive lichen planus there is thinning and ulceration of epithelium with
complete loss of rete ridges formation and dense T cell infiltrate extending well into middle
and upper levels of epithelium is lost revealing underlying connective tissue. Plaque likes
form histological similar to striae of reticular form with out intermittent areas of epithelial
atrophy. Ortho and Parakeratosis are seen in combination with acanthosis. Basement
membrane is thickened with band of T cells that is less dense than in reticular form.71
Immunofluorescent studies:
Direct Immunofluorescent of OLP lesional tissue usually demonstrates ragged band of
fibrinogen along the basement membrane zone. Occasionally specimens demonstrate IgM
staining cytoid bodies in dermal papilla or Peribasilar areas. When present in large numbers
or clusters these cytoid bodies are highly suggestive of lichen planus. Direct
immunofluorescence studies show that these bodies stain for immunoglobulins IgA, IgG, and
IgM.72
Immunohistochemical studies:
Immunohistochemical staining using the antibody to the S-100 protein indicates an
increase in langerhans cells in mid layers of the epithelium. The immunofluorescence pattern
is not specific or diagnostic, as similar patterns are seen in lupus erythematosus and erythema
multiforme.72
Clinical Significance of OLP:
OLP is one of the most common mucosal conditions affecting the oral cavity.
Therefore, dentists in clinical practice will regularly encounter patients with this condition.
Because patients with the atrophic and erosive forms of OLP typically experience significant
discomfort, knowledge of the treatment protocols available is important. The similarity of
OLP to several other vesiculo-ulcerative conditions, some of which can lead to significant
morbidity, makes accurate diagnosis essential. For example OLP and Graft versus host
disease (OVHD) can have similar histologic and clinical presentations. GVHD is a serious
condition that occurs in bone marrow transplant patients when transplanted marrow cells
react against host tissues. The extent of oral involvement is highly predictive of the severity

and prognosis of GVHD. Erosive OLP and lichenoid drug reactions can be indistinguishable
both histological and clinically.73
Medications associated with mucosal lichenoid reactions 73, 74
Drug class
1) Antimaiarials
Hydrochloroquine, Quinidine, Quinine
2) Nonsteroidal anti-inflammatory drugs
Indomethacin, Naproxen, Phenylbutazone
3) Diuretics
Furosemide, Hydrochlorothiazide,
4) Antihypertensives
Angiotensin-converting enzyme inhibitor: Captopril, Enalapril
Beta-blocker: Propranolol
5) Antibiotics
Penicillin, Sulfonamides, Tetracyclines
6) Antifungals
Ketoconazole
7) Heavy metals
Bismuth, Chromium, Mercury, Nickel
9) Miscellaneous
Allopurinol, Carbamazepine, Lithium, Lorazepam, Methyldopa, Oral contraceptives
It is also necessary to distinguish isolated erosive or reticular lesions from lichenoid
reactions to dental amalgam. Lichenoid reactions to amalgam do not migrate, they occur on
mucosal tissue in direct contact with the restoration, and they resolve once the amalgam
restoration is removed. Some studies indicate an increased risk of squamous cell carcinoma in
patients with OLP lesions. This increased risk appears most common with the erosive and
atrophic forms and in cases of lesions of the lateral border of the tongue. Risk of developing
squamous cell carcinoma in patients with OLP is approximately 10 times higher than that in
the unaffected general population. Other published reports have noted a possible association
between OLP and hepatitis C, sclerosing cholangitis, and primary biliary cirrhosis.
Differential Diagnosis:

The diagnosis of OLP can be rendered more confidently when characteristic

cutaneous lesions are present except for the pathognomonic appearance of reticular OLP
(white striae occurring bilaterally on the buccal mucosa), in most cases histopathologic
evaluation of lesional tissue is required to obtain a definitive diagnosis. Even classic cases of
lichen planus may be worthy of biopsy so as to establish baseline histopathologic features.

The differential diagnosis of erosive OLP includes

Squamous cell carcinoma,
Discoid lupus erythematosus,
Chronic candidiasis,
Benign mucous membrane pemphigoid,
Pemphigus vulgaris,
Chronic cheek chewing,
Lichenoid Reaction to dental amalgam or drugs,
Graft-versus-host disease (GVHD),
Hypersensitivity mucositis and erythema multiforme.
The plaque form of reticular OLP can resemble oral leukoplakia.
Treatment
There is currently no cure for OLP. Excellent oral hygiene is believed to reduce the
severity of the symptoms, but it can be difficult for patients to achieve high levels of hygiene
during periods of active disease. Treatment is aimed primarily at reducing e length and
severity of symptomatic outbreaks. Asymptomatic reticular and plaque forms of OLP do not
require pharmacological intervention. Before initiating treatment, the diagnosis must be
confirmed histological. It is important to rule out candidiasis.Since many treatment
modalities can aggravate an existing candidal infection. About 2% patients develop squamous
cell carcinoma.76
Corticosteroids:
The most widely accepted treatment for lesions of OLP involves topical or systemic
corticosteroids to modulate the patient s immune response.
Topical corticosteroids: 77

They are the mainstay in treating mild to moderately symptomatic lesions. Options
(presented in terms of decreasing potency) include 0.05% clobetasol propionate gel, 0.1% or
0.05% betamethasone valerate gel, 0.05% fluocinonide gel, 0.05% clobetasol butyrate
ointment or cream, and 0.1% triamcinolone acetonide ointment. Lozada (1980) flucinonide
0.5% (fluorinated corticosteroids) have been introduced in treatment of various
vesiculoeosive lesions. It has been proven to be standard, firstline therapies in treatment of
OLP (Plemons et al, 1990). 0.05% clobetasol ranks as one of the most potent topical steroid,
which is used in an orabase paste three times daily. Patients are instructed to apply a thin
layer of the prescribed topical corticosteroid up to 3 times a day, after meals and at bedtime.
The gel or ointment can be applied directly or can be mixed with equal parts Orabase
adhesive paste, to facilitate
adhesion to the gingival tissues.68 Gingival lesions of OLP are often resistant to mouth rinses
and topical applications of steroids. So occlusive splints can be used to improve the contact
time of topical agent to gingival. 0.05% clobetasol orabase with l lakh IU of nystatin be given
to prevent fungal infections.78
The choice of delivery vehicle depends on clinician and patient preference. In general,
oral application is best accomplished with a gel preparation if available. In patients with
widespread symptomatic lesions, in whom direct mucosal application of topical medication
would be too uncomfortable, options include 1.0 mg/mL aqueous triamcinolone acetonide or
0.1 mg/mL dexamethasone elixir. Patients should be instructed to gargle with 5 mL of the
solution for 2 minutes after meals and at night. After rinsing, the solution should be
expectorated, and nothing should be taken by mouth for one hour. Alternative delivery
methods include the use of cloth strips and custom trays to serve as reservoirs for the
corticosteroid. The advantage of topical steroid application is that side effects are fewer than
with systemic administration. Adverse effects include candidiasis, thinning of the oral mucosa
and discomfort on application. Topical formulations of the more potent corticosteroids can
cause adrenal suppression. If used in large amounts for prolonged periods or with occlusive
dressings. The lowest-potency steroid that proves effective should be used.Topical
betamethasone disodium phosphate caused adrenal suppression in eight out of 10 patients
(Lehner and Lyne, 1969) Betamethasone valerate aerosol in the form of Valisone could also
be harmful or even fatal when applied to the oral mucosa (Beckman, 1981) Despite the
encouraging results obtained with topical steroids, but still they do not alleviate pain or heal
ulceration in all patients. Undoubtedly the frequency of application makes compliance
difficult since optimal results are not achieved unless patients apply for 5 to 10 times daily

(Silverman et al, 1991).The elderly who comprise a major portion of patients may find it
difficult to apply medication to all locations of oral cavity. Compounding the problem of
achieving contact between medication and affected areas is difficulty of adherence to moist
mucous membranes that are dislodged easily.81
Intralesional injection: 77
Topical corticosteroids are of limited value for some cases of oral lichen planus. In
such cases, it may be appropriate to use topical corticosteroids in combination with
intralesional preparations. They are used for recalcitrant or extensive lesions involve the
subcutaneous injection of 0.2-0.4 mL of an l0mg/mL solution of triamcinolone acetonide.
However, intralesional corticosteroids have some contraindications, including atrophy of
tissueand secondary candidiasis after frequent injections. It may not be possible to it
sufficient quantities into gingival lesions.
Systemic steroid therapy should be reserved for patients in whom OLP lesions are
recalcitrant to topical steroid management because the dosage ranges for corticosteroids are
wide and patient responses variable, numerous dosing options have been proposed. Dosages
should be individualized according to the severity of the lesions and the patient's weight and
should be modified on the basis of the patient's response to treatment. It must be given in a
dose of 1 mg/kg/day. Prednisone should be taken as a single morning dose to reduce the
potential for insomnia and should be taken with food to avoid nausea and peptic ulceration.
Significant response should be observed within one to 2 weeks. When systemic
corticosteroids are prescribed for periods of longer than 2 weeks, the dosage of steroid must
be gradually tapered to avoid precipitating an adrenal crisis. Tapering can be accomplished by
decreasing the daily dose of prednisone by 5 mg per week. The potential side effects of shortterm systemic steroid therapy are numerous. They include insomnia, diarrhea, disturbances of
the central nervous system including psychotic episodes, sodium and fluid retention, muscle
weakness, and decreased resistance to infection, hypertension, hyperglycemia and adrenal
suppression. Steroid use is contraindicated in patients who are breast-feeding. Steroids should
be used with
caution in patients with herpetic infections, glaucoma, pregnancy, HIV infection,
tuberculosis, diabetes mellitus and hypertension.
Other Approaches:

Twice-daily topical application of compounded 0.1% tacrolimus ointment was

recently reported to be effective in controlling symptoms as well as clearing lesions of OLP.
Tacrolimus is a macrolide immunosuppressant with a mechanism of action similar to that of
cyclosporine, but is 10 to 100 times more potent and is better able to penetrate the mucosal
surface. It is an immunomodulator, which inhibits the T cell activation and proliferation. It is
associated with carcinogenicity, mutagenecity and infertility.81
Retinoids: 81, 82
Retinoids were first used for the treatment of asymptomatic, white, reticulated oral
lichen planus by Gunther. Vitamin A was applied locally to the lesions with good results. The
systemic use of vitamin A is limited because of its toxicity and sideeffects including skin
dryness and hair loss. Schuppli reported that etretinate, which is a vitamin A analogue, was
more effective in the treatment of oral lichen planus. Topical retinoids are usually favored
over their systemic counterparts because the latter may be associated with adverse effects
such as liver dysfunction and teratogenicity.
Cyclosporin: The topical use of cyclosporine seems to be beneficial in treating recalcitrant
cases of OLP. Cyclosporin is an immunosuppressant and reduces the production of
Lymphokines. Damage to the basement membrane in oral lichen planus is the result of the
production of lymphokines such as interferon gamma by activated T lymphocytes. It inhibits
the proliferation and function of T lymphocytes. This molecule induces the expression of
intracellular adhesion molecule 1 and HLA antigen on surface of keratinocytes. This
interaction is thought to lead to destruction of basement membrane. (Farthing and Cruchley,
1989). Its main adverse reaction is renal dysfunction as a result of prolonged use, so patients
taking cyclosporin need to be monitored closely. The primary side-effect of cyclosporin
therapy was reported to be transient sensations of burning on the mucosal surface of the
lesion, Cyclosporin is expensive go its use in the treatment of oral lichen planus could be
limited by cost.82
Griseofulvin: Griseofulvin has been advocated for the treatment of erosive-ulcerative lesions
when steroid treatment is contraindicated or when the lesions are resistant to steroids.
Aufdermorte et al. supported its use, but Bagan et al. reported that they saw no improvement
in the appearance of lesions from the use of griseofulvin.78

Phenytoin: It is used in refractory cases of OLP. Phenytoin is an anticonvulsant medication

that has been shown to promote wound healing and modulate immunologic functions.81
Azathioprine:
It is used in refractory cases of OLP. It is a potent immunosuppressive agent with
well-known adverse effects like bone marrow suppression. Additionally long term use of mis
medication may increase the risk of internal malignancies.
Ultraviolet light:
One of the more common treatments for cutaneous lichen planus as well as other
dermatoses involves photochemotherapy with psoralens and long wave ultraviolet-A (PUVA).
Jansen et al (1987) modified a unit intended for light cured dental composite fillings to
administer UV-A in oral cavity. Patients ingested psoralens, a photosensitizer prior to
irradiation at intervals of 2 to 3 days. All eight patients with refractory and symptomatic
atrophic and erosive oral lichen planus responded to therapy. At a 6-month follow up, five out
of eight patients had complete or marked resolution of their disease.Patients exposed to
PUVA are known to have increased
risk of developing squamous cell carcinomas (Forman et al, 1989). The efficacy of mouth
PUVA and UVA in treatment of OLP supports the role of immune system in its pathogenesis,
but this treatment should be considered experimental. Other treatment modalities are use of
dapsone, levamisole, and thalidomide.

Surgical Management of Oral Lichen planus:

77

Cryosurgery and carbon dioxide laser

ablation have been suggested for the surgical treatment of oral lichen planus. It is an
alternative to scalpel surgery where re-epithelization occurs by 4 to 6 weeks. The post
surgical period is minimal pain and healing occurs without contractions. However, excision
should not be a primary method of treatment as it is an inflammatory Condition that can
recur. In addition, surgical management is not suitable for the erosive and atrophic types
because the surface epithelium is eroded. Surgical treatment is more applicable to the plaque
like lesions, because the affected surface epithelium can be removed easily. However, it is
likely that surgery has a
limited application in the management of oral lichen planus since tissue is destroyed and
lesion cannot be completely examined histologically.

Eliminating exacerbating factors: 77

Oral habits:
Lichen planus is known to be associated with "kobners phenomena", damage or
trauma to clinically normal skin in patients with lichen planus results in development of new
lesions. These phenomena may explain the frequency of lichen planus erosions on buccal
mucosa and tongue, which are prone to trauma. Local irritants need to be removed. Cigarette
smoking may act as an irritant as well. Prevalence of OLP is higher in individuals who chew
tobacco or betel (Pindborg et al, 1972: Daftary et al 1980).
Plaque:
It certainly could induce lesions through kobners phenomena, especially with gingival
lichen planus. Care must be taken with aggressive periodontal treatment and surgery that may
result in worsening of lichen planus, presumably by kobners phenomena.
Stress: In 1869 Erasmus Wilson noted that many of his patients experienced emotional stress
(Wilson, 1869). Since then various conflicting reports have been published in regarding the
link between psychogenic factors and OLP.78
Diet:
With widespread oral ulcerations, eating is often compromised due to pain and
discomfort Poor and delayed wound healing can result from an inadequate nutritional status,
especially in elderly patients. Correction of low levels of vitamin Bl and B6 resulted in
clinical and subjective improvement in majority of treated patients (Jolly and Nobile, 1977).81
Restorative materials:
There are reports that contact mucositis to mercury and other restorative dental
materials may be significant in etiology of OLP. Frykholm et al, in 1969 suggested contact
mucositis to copper in dental alloys as a cause of OLP. Electro galvanic effects of metals have
been implicated as well (Banoczy et al, 1979: Holland, 1980). Even gold restorations have
been suggested although never substantiated (Conklin and Blasber, 1987). Composite
restorations may cause lichenoid reactions (Land, 1988).
Candida:

When treating OLP the role of Candida always should be evaluated carefully. Krogh
et al (1987) showed that Candida albicans was the dominating species isolated from OLP,
although Saccharomyces cerevisiae and C. pintolopesii also were found. The higher rate of
Candida may indicate possible impairment in cellular immunity in patients with oral lichen
planus. The benefit of antifungal therapy in treatment of OLP has been accepted by most
authors. Systemic ketoconazole 200mg for 2 to 3 weeks at the initiation iff therapy will
augment the effects of most therapies employed. Topical antifungal therapy with equally
good results. (Silverman et al, 1991).82

APHTHOUS ULCERS
Synonyms:

Recurrent Apthous Stomatitis

Cancer sores

Periadenitis mucosa necrotica recurrence

Mikulicz ulcer

suttons disease

Recurrent apthous stomatitis (RAS, aphthe, canker sores) is typified by recurrent ulceration
of the oral mucosa. Whereas patients with RAS have no other clinical abnormalities, people
with bachets disease may also develop wide spectrum of genital, ocular, cutaneous,
neurological and vascular problems. 80 Aphthous ulcers are a common and painful disease of
the oral mucosa affecting 20% of the general population. A higher prevalence has been found
in the higher socioeconomic groups, in females, and among individuals with 'stress', such as
students at the time of examinations. The aphthous lesion appears as a white or yellow oval
"oral ulcer with an inflamed red border affecting non-keratinized mucosa.80
Epidemiology:
The onset of RAS seems to peak between the ages of 10 and 19 years before becoming less
frequent with advancing age and does not seem to depend on geography, age, gender or race.
RAS is seen worldwide and may affect up to 25% of the population but may be three times
more common in US whites than in African Americans.
It is being classified into 4 types: 36
Apthous minor
Apthous major (Suttons disease, periadentits mucosa necrotica recurrens)
Herpetiform ulcers

 Recurrent ulcers associated behcets syndrome

Aetiology and pathogenesis: 80
The cause of RAS is still unknown. The histopathological Changes in the preulcerative stage
include infiltration of the epithelium by mononuclear (lymphocytic) cells. Oedema develops,
followed by keratinocyte vacuolisation and localized vasculitis causing localised swelling
that ulcerates and is infiltrated by neutrophils, lymphocytes, and plasma cells before there is
healing and regeneration of the epithelium. There is a cell-mediated immune response that
involves T-cells with generation of tumour necrosis factor alpha (TNF-a) from these and
other leucocytes
(macrophages and mast cells). TNF-a is a major inflammatory cytokine that has a
chemotactic effect on neutrophils so driving acute inflammation and expression of major
histocompatibility (MHC) complexes. This results in the targeting of epithelial cells for attack
by cytotoxic (CD8+) T-cells. Other cytokines that may be implicated include interleukin-2,
IL-10 or interleukins IL-1 beta and IL-6.gamma delta T lymphocytes may have a role in
antibody dependent cell-mediated cytototoxic reaction towards the epithelium of the oral
mucosa.83
Role of heat shock protein:
It has been suggested that immunologically driven reactions to heat shock proteins are
important, as patients with RAS have cross-reactivity between a streptococcal heat shock
protein and the oral mucosa, considerably raised levels of serum antibodies to heat shock
protein, and have increased lymphoproliferative responses to a heat shock protein-derived
peptide. RAS may therefore represent a T-cell mediated response to antigens of Streptococcus
sanguis that cross-reacts with mitochondrial heat shock protein and causes damageto the oral
mucosa 80.
Role of genetics:
A genetic predisposin has been suggested as at least 40% of patients with RAS have a
familial history.The patients may develop ulcers earlier and more severely. RAS may be
associated with HLA-B51, and other genes close by such as those that control heat shock
proteins or cytokines may be implicated.83
Role of immunity:

It is likely that several immunologically mediated mechanisms are involved in the

pathogenesis of RAS. It may be that an unopposed or excessive production of IL-l beta or IL6 is pivotal to its development, a notion that may explain why ulceration worsens after local
injury, or cessation of smoking tobacco or both.
Predisposing etiologic factors:
Precipitating factors can act on genetic predisposition to cause simple aphthous lesions. Most
patients appear to be otherwise well, but a minority has etiologic factors that can be identified
by the history.
These factors may include the following: toothpastes containing sodium-laurylsulfate,
trauma, stress, cessation of smoking, hormonal state, and food hypersensitivity. Patients
affected by RAS usually are nonsmokers. Some patients reveal an onset of RAS after
smoking cessation and disappearance on reinitiation of smoking. This is likely to be due to
the positive effect of nicotine on keratinization of oral mucosa. Food allergy such as that for
chocolate, cheese, wheat flour, tomatoes, peanuts and strawberries might beresponsible for
the onset of oral ulcers.80
Systemic:
Aphthous-like ulceration occurs in Behcet disease, MAGIC syndrome, cyclic neutropenia,
PFAPAsyndrome, Sweet syndrome (acute febrile neutrophilic dermatitis) and various
nutritional deficiencies with or without underlying gastrointestinal disorders and some
immunodeficiencies both primary, and secondary, including infection with human
immunodeficiency virus (HIV).80
Psychologic Stress:
Stress and psychologic imbalance have been associated with RAS. In women appearance of
RAS may coincide with menses
Etiologic factors associated with recurrent Apthous Stomatitis:
local

Trauma , Smoking

Microbial

Bacterial: streptococcal. Viral: varicella zoster, cytomegalo virus

Systemic

Behcets disease, Mouth and genital ulcers with inflamed cartilage

Crohns disease, ulcerative colitis, HIV infection, Marshall
syndrome, stress,
psychological imbalance, menstrual cycles

Nutritional

Gluten sensitivity enteropathy

Iron, folic acid, zinc deficiency. Vitamin Bl, B2, B6, B12 deficiency

Genetic

Ethnicity, HLA haplo types

Allergic

Local T cell cytotoxicity, Abnormal CD4.CD8 ratio, dysregulated

cytokine
levels, microbe induced hypersensitivity, food sensitivity
Antioxidants, NSAIDs, Beta blockers

Others

Syndromes associated with apthous ulcer: 80

Behcet disease
Aphthous-like ulceration is a cardinal feature but may be more severe, and is more likely to
comprise major or herpetiform ulcers, or both. Patients also have recurrent genital ulceration,
cutaneous disease (usually papulopustular lesions or erythema nodosum), ocular disease and
a range of gastrointestinal, neurological, renal, joint and haematological abnormalities.
Principal clinical features of Behcet disease
System
Gastrointestinal
Urogenital
Dermatological
Ocular
Musculoskeletal
Neural
Vascular system

Features
RAS, Ileo-caecal ulceration
Scrotal or penile ulcers, or both, Vulval or vaginal ulcers, or both
Perianal ulcers, Epididymo-orchitis
Papules, Pustules, Erythema nodosum, Ulcers, Cutaneous pathergy
response
Anterior or posterior uveitis, Retinal vasculitis
Arthralgias, Arthritis, Fatigue
Headaches, Dural sinus thrombosis
Parenchymal inflammatory lesions, Meningo-encephalitis
Superficial thrombosis, Deep venous thrombosis
Arterial occlusion or aneurysms, or both

MAGIC syndrome: 80
A possible variant of Behcet disease, comprising major aphthae and generalized inflamed
cartilage. In 1985, Firestein et al, described 5 patients with relapsing polychondritis and
Behet's disease (BD) and proposed the term "MAGIC" syndrome as an acronym for "Mouth
and Genital ulcers with Inflamed Cartilage". Associated with chondritis and oral aphthous
ulcers, as well as ocular inflammation (mainly anterior uveitis or scleritis/episcleritis). Most
patients also presented with genital ulcers and arthritis. In one case, aortic aneurysm, in

another aortic insufficiency, meningoencephalitis, antiphospholipid syndrome and HIV

positive.

Sweet syndrome:
Acute neutrophilic dermatosis, first described in 1964 by Robert Douglas Sweet, has been
termed Sweet's syndrome. Patients have ulceration similar to RAS, but with sudden onset of
fever, leucocytosis and well-demarcated cutaneous, plum-coloured skin papules or plaques.
There is an associated malignancy (such as acute myeloid leukaemia) in half of patients.
Classic Sweet's syndrome occurs in middle-aged women after a nonspecific infection of the
respiratory or gastrointestinal tract. Raised erythematous plaques with pseudoblistering and
occasionally pustules occur on the face, neck, chest, and extremities, accompanied by fever
and general malaise.
PFAPA syndrome:
Comprises periodic fever, aphthae, pharyngitis, and cervical adenitis. Although rare, it tends
to occur in young children. Although throat cultures may be negative about two thirds of
children improve after tonsillectomy,
Immunopathogenesis: 80
The pathogenesis of PFAPA syndrome is still poorly understood. The immunobiological
mechanisms underlying formation of oral ulcers are thought to be similar to those occurring
in RAS. Different cytokines can contribute to the pathogenesis of oral lesions in RAS such as
IL-2, IL-6 and IL-10. Elevated levels of IL-2 and TNF-a, and lower levels of IL-10, have
been reported in lesional mucosa of patients with RAS. IL-10 usually stimulates epithelial
proliferation in a healing process; therefore, its low levels in patients with RAS may delay
epithelization and prolong the duration of the ulcers. A markedly increased Plasma level of
IL-2 has been recorded in the active stage of RAS. Also, natural killer (NK) cells activated by
IL-2 may play a role in disease pathogenesis. An increased activity of these cells has been
noted in active lesions, diminishing during periods of remission. In 1987, Marshall et al,
described a new periodic fever that was initially indicated as Marshalls syndrome and
subsequently given the acronym FAPA (fever, aphthous stomatitis, pharyngitis and cervical
adenitis). This was later changed to PFAPA (periodic fever, aphthous stomatitis, pharyngitis

and cervical adenitis) syndrome to emphasize the presence of periodic fever, which is
considered a main characteristic of the illness.80
Cyclic neutropenia:
Cyclic reduction in circulating levels of neutrophils about every 21 days. Patients develop
recurrent oral ulceration, fever, cutaneous abscesses, upper respiratory tract infections and
lymphadenopathy. Other oral complications include severe gingivitis and aggressive
periodontitis. Treated with recombinant granulocyte colony stimulating factor (rG-CSF).
HIV disease:
Oral ulcerations associated with HIV infection include recurrent aphthous ulcers (RAU).
Whereas RAU prevalence is not increased, lesion severity is: among a group of HIV+
patients, 66% had the more severe herpetiform or major RAU. This increased severity
suggests that HIV disease-related changes in the immune system may exacerbate RAU. HIV
disease-related immune system changes are characterized by reversed CD4:CD8, lowered
CD4 cell counts and an inverse correlation between CD4 cell counts and per cent activated
gamma delta lymphocytes. In patients with active HIV disease/AIDS, serum TNF alpha
levels are increased.
Thalidomide, which inhibits TNF alpha production, is effective treatment for RAU. Some
RAU patients have vitamin B12 or folate deficiencies, levels of which are commonly low in
HIV+/AIDS patients. However, in a case control study of HIV+ patients, vitamin B12- or
folate-deficiencies were not found to be significant risk factors for RAU.83
Nutritional Deficiencies:
Deficiencies of haematinics - iron, folic acid, or vitamin B12
Wray D, Ferguson MM, et al conducted a study on 130 patients with recurrent aphthous
stomatitis for deficiencies of vitamin B12, folic acid, and iron. In 23 patients (17.7%) such
deficiencies were found; five were deficient in vitamin B12, seven in folic acid, and 15 in
iron. Four had more than one deficiency. The 23 deficient patients with recurrent aphthae
were treated with specific replacement therapy. Of the 23 patients on replacement therapy 15
showed complete remission of ulceration and eight definite improvement. Most patients with
proved vitamin B12 or folic acid deficiency improved rapidly on replacement therapy; those
with iron deficiency showed a less dramatic response. They suggest that the high incidence of
deficiencies found in this series and the good response to replacement therapy shows the need

for haematological screening of such patients.

85

Aphthous-like ulceration can also be a

feature of bowel disease, both of Crohn disease. Intraoral involvement in Crohn's disease is
observed in only approximately 9% of cases; oral inflammation precedes intestinal symptoms
of CD in about 60% of these patients. As oral lesions are sometimes treated without a definite
diagnosis,
Plauth M, Jenss H, Meyle J et al evaluated 75 cases for morphology and site of oral and
intestinal manifestations of CD, clinical manifestation, and treatment. Oral CD was the
presenting symptom in 43 of 72 (60%). Edema (62 lesions), ulcers (57 lesions), and polypoid
papulous hyperplastic mucosa (45 lesions) were the most common type of lesions. They
conclude that oral CD exhibits a characteristic morphologic appearance, as often as not
preceding intestinal symptoms in adolescents and young adults.
Ulcerative colitis and gluten-sensitive enteropathy: 85
Pyostomatitis vegetans (PV) is a rare condition characterized by pustules that affect the oral
mucosa. It is a highly specific marker for inflammatory bowel disease and its correct
recognition may lead to the diagnosis of ulcerative colitis or Crohns disease. PV
pathogenesis is as yet unknown. It is characterized by erythematous, thickened oral mucosa
with multiple pustules and superficial erosions.
Clinical manifestations
RAS comprises recurrent bouts of one or several rounded, shallow, painful ulcers at intervals
of a few months to a few days in people who are otherwise well. RAS patients usually
experience prodromal burning that last from 2 to 48hrs before ulcer appears. The ulcers are
round with symmetrical, shallow with well-defined erythematous margins covered by
yellowish gray fibrinous pseudomembrane. They are painful when secondarily infected which
interferes with the eating process, which is associated with burning when spicy foods are
taken.
Like viral ulcers RAS ulcers not do have tissue tags as seen in irregular ulcers such as
erythema multiforme, phemphigus and phemphigoid. They are very commonly seen of nonkeratinized mucosa, which lasts for 10-14 days with out scar formation.
Minor aphthae:
Minor aphthae (also called Mikulicz's aphthae or mild aphthous ulcers) account for 75 to 85
percent of all cases of RAS. Minor aphthae can involve every non-keratinized mucosa of the

oral cavity (usually the labial and buccal mucosa, the floor of the mouth and the ventral or
lateral surface of the tongue), are smaller than 8-10 mm and tend to heal within 10 to 14 days
without scarring. Minor aphthae heal more slowly man do other oral wounds; an intensive
lymphocytic infiltrate may play a role in this.36
Major Aphthae.
Major Aphthae (sometimes referred to as periadenitis mucosa necrotica recurrens or Sutton's
disease) tends to involve mucosa overlying minor salivary glands. Approximately 10 to 15
percent of RAS cases are major. Usually appearing after puberty, they are round or ovoid
with clearly defined margins. The prodromal symptoms are more intesne than those of minor
aphthae, and the ulcers usually are deeper and larger and last significantly longer than do
minor aphthae. They have a raised irregular border and exceed 1 centimeter in diameter, are
painful and tend to appear on the lips, soft palate and throat, they can last for weeks for
months and often leave a scar after healing. Fever, dysphasia and malaise sometimes can
occur early in the disease process.
Herpetiform ulcers:
Constituting only 5 to 10 percent of all RAS cases, herpetiform ulcers are rare. Multiple (5 to
100) 1 to 3 mm crops of small, rounded, painful ulcers resembling ulcers of herpes simplex
are seen anywhere on the mucosa. They tend to fuse and produce much larger ulcers lasting
10 to 14 days. These ulcers tend to appear in women and generally have a later age onset than
the other types of RAS. Most patients have only one to three ulcers, and some have
recurrences only two to four times each year (simple aphthosis). Others may have almost
continuous disease activity with new lesions developing as older lesions heal, or may have
ulcers associated with systemic diseases (complex aphthosis).
Classification
Currently classification of aphthous lesions is based on severity and they are associated with
systemic factors.
Simple aphthosis: is described when ulcer recurrences are few and not associated with
systemic factors and occurs only 24 times each year.
Complex aphthosis is a disorder in which patients develop recurrent oral and genital
aphthous ulcers or when there is a continuous disease activity with new lesions developing as
older lesions heal, or when ulcers are associate with systemic diseases.

Diagnosis of RAS: The diagnosis of RAS is based on history and clinical findings. There is
no specific diagnostic test, but there is a need to exclude other possible causes of recurrent
oral ulceration, such as Behcet disease, PFAPA syndrome, and possible infection by HIV. A
medical history should be taken to rule out other ulcerative disorders and conditions such as
Crohns disease, celiac disease, neutropenia, HIV infection and Behcets syndrome. A
complete blood cell count, hematinic estimation and test for antiendomysial antibodies are
indicated to rule out immune disturbances, vitamin and iron deficiencies, and malabsorption
(such as in celiac disease).80

Cause
Unknown

Infections

Examples
Aphthae
Periodic fever,
aphthae, pharyngitis,
and adenitis
TNFreceptor
associated periodic
syndrome
Recurrent infection
with herpesvirus

HIV infection
Clinical presentation
and HIV testing
Rheumatic
diseases

Behets syndrome

Suggestive Findings
A history of recurrent round
or ovoid mouth ulcers since
childhood
A history of recurrent mouth
ulcers since childhood;
recurrent fever, pharyngitis,
lymphadenitis

Basis of Diagnosis
Clinical presentation
and the exclusion of
systemic illnesses
Clinical
presentation and the
exclusion of other
systemic illnesses

A history of recurrent
localized
ulcers, sometimes aphthouslike,
usually on the palate or
tongue,
generally at the same site in
each
episode, often appearing
after
oral trauma; may be
evidence of
immunocompromised state
Intraoral infections
(candidiasis, hairy
leukoplakia) or neoplasms
(Kaposis sarcoma,
lymphoma); other
Aphthous-like ulcers
occurring on genital or other
mucosae; skin pustules,
erythema nodosum, or other
lesion suveitis; joint
involvement;

Clinical
presentation and
virologic studies

Clinical evidence of
or risk factors for
HIV infection
Clinical
presentation and
serologic testing to
rule
out
other
conditions

Reactive arthritis
(Reiters syndrome)

Sweets syndrome

Cutaneous
diseases

Erythema
multiforme

Hematologic
diseases

Cyclic
neutropenia
Leukemias

Gastrointesti
nal diseases

Glutensensitive

central nervous system

manifestations.
Urethritis; colitis;
keratoderma
blennorrhagicum;
conjunctivitis,
balanitis; joint and other
involvement; usually found
in
men
Red plaques on skin; fever;
aphthous-like ulcers on
genital or other mucosae;
often associated with other
conditions (e.g.,
inflammatory bowel disease,
leukemia)
Lesions on mucosae other
than oral or on skin or eyes;
lip swelling
Recurrent fevers; associated
intraoral and other recurrent
infections; onset in
childhood or adolescence
Infections; anemia;
petechiae or purpura
Dental defects;
malabsorption;
bloating; diarrhea; weight
loss

enteropathy

Inflammatory
bowel disease
(ulcerative colitis,
Crohns disease)
Drugs

NSAIDS,Beta
-blocker

Labial or facial swelling;

bloody diarrhea; weight
loss; occasionally, joint
manifestations;
hepatobiliary disease
Rash

Serologic testing to
rule out other
conditions

Serologic testing to
rule out other
conditions

Clinical
presentation and
biopsy of
perilesional tissue
Clinical
presentation and
complete blood
count
Complete blood
count
Clinical
presentation
presence of
antigliadin and
transglutaminase
antibodies; biopsy
of small intestine
Clinical
presentation and
colonoscopy or
biopsy of ulcer
tissue
History and
response to drug
withdrawal

Histologic findings
The preulcerative lesions demonstrate sub-epithelial; inflammatory mononuclear cells with
abundant mast cells, connective tissue edema and lining of the margins with neutrophills.

Damage to the epithelium usually begins in basal layer and progresses through the superficial
layers, leading eventually to ulceration and surface exudates. The presence of extravasated
erythrocytes around the ulcer margin, sub-epithelial extra vascular neutrophils, numerous
macrophages loaded with phagolysosomes and nonspecific binding of stratum spinosum cells
to thyroglobulin and complements may be result of vascular leakage and passive diffusion of
serum. These findings suggest that pathogenesis RAS may be mediated by immune complex
vasculitis.
Immunohistochemical
Studies of RAS biopsy tissues have demonstrated numerous inflammatory cells with variable
ratios of CD4: CD8 cells depending on ulcer duration. CD4 cells were numerous during Preulccrative and healing phase while CD8 cells tended to be more during ulcerative phase.
MANAGEMENT
Since the etiology of RAS remains unknown, and the cyclic nature of the disease makes it
difficult to conduct well-designed prospective double-blind controlled clinical studies, there
is no definitive treatment. Treatment is symptomatic, the goal being to decrease symptoms,
reduce ulcer number and size, increase disease-free periods.
The best treatment is that which will control ulcers for the longest period with minimal
adverse side effects. The treatment approach should be determined by disease severity(pain),
the patients medical history, the frequency of flare-ups and the patients ability to tolerate the
medication.In all patients with RAS, it is important to rule out predisposing factors and treat
any such factors, where possible, before introducing more specific therapy To help determine
management strategies, it is useful to classify RAS in three clinical presentations: type A,
type B and type C.86
Type A. RAS episodes lasting for only a few days, occurring only a few times a year, are
classified as type A. In this scenario, pain is tolerable. The clinician should try to identify
what precipitates the ulcers, what the patient uses to treat them, and how effective that
treatment is. If it is effective and safe, the health care provider, or HCP, should encourage the
patient to
continue it. If a precipitating factor(s) is identified, the HCP should try eliminating it first.
Type B. Painful RAS each month, lasting between three and 10 days, is type B. In this
scenario, the patient may have changed diet and oral hygiene habits because of the pain.

Type C. Painful, chronic courses of RAS in which by the time one ulcer heals another
develops.86

Treatment
Topical agents are preferred as they lack serious side-effects but, in severe aphthae, systemic
immunomodulation may be necessary. In mild cases with two or three small lesions, use of a
protective emollient such Orabase is all that is necessary. Pain relief of minor lesions can be
obtained with use of topical anesthetic agent or topical diclofenac, an NSAID frequently used
topically
Topical preparation: 80
The proper treatment of RAS depends on frequency, size and number of ulcers Patients who
experience occasional episodes of minor apthous ulcers experience significant relief with
appropriate topical therapy containing 2% viscous lidocaine gel. Other topical agents include
Diclofenac, amlexanox paste that has been also shown to decrease the healing time of minor
apthae.
Corticosteroids:
Topical corticosteroids are the mainstay of RAS treatment in most countries but there are few
well-controlled studies The corticosteroids vary in their degree of potency and may be given
as mouth rinses, ointments, creams or in adhesive vehicles. Several different topical
corticosteroids may reduce symptoms and hasten healing of RAS Corticostriods regimens
include dexamethasone 0.05 mg/ 5 mL (rinse and spit three times per day) or a high-potency
topical corticosteroid such as clobetasol 0.05% in Orabase or fluocinonide 0.05 % in Orabase
(1:1) if the ulcer(s) recur on the same site, used three times daily. If corticosteroids are used,
patients should be monitored for yeast super infection. The effectiveness of the topical steroid
is partially based upon good instruction and patient compliance regarding proper use.
Other anti-inflammatory agents
Benzydamine: Benzydamine hydrochloride mouthwash is the only over the counter topical
agent to have been assessed formally that may provide transient relief of painful symptoms,
but doesnot aid healing. Matthews RW, Scully CM et al (1987) eighteen patients with minor
recurrent aphthous stomatitis were given alcoholic benzydamine hydrochloride, aqueous
chlorhexidine, or a benzydamine-free placebo mouthwash in random order. Each patient used
each preparation for a 3-month period. Statistical analysis of the results showed no significant
differences between any of the treatments tested. Eight patients stated a personal preference

for benzydamine because of the transient local anesthetic effect of benzydamine, which gave
pain relief.87
Amlexanox:
Amlexanox is anti-allergic and anti-inflammatory and is of some benefit in the treatment of
RAS, but its exact mode of action is unknown. It has been available in the USA (approved by
the FDA) and Canada and may become available in the UK. The results of several trials
suggest that it may be of benefit in the treatment of RAS. Amlexanox 5% paste applied to
ulcers 24 times daily may considerably reduce their size and pain, and speed up healing.80
Antimicrobials;
Antimicrobials may be used for their anti-inflammatory and analgesic effects rather than their
antimicrobial functions.
Chlorhexidine: RCTs have established that chlorhexidine can reduce the duration of RAS
and increase the number of ulcer-free days. Addy M, Hunter L et al (1987) conducted a
double-blind placebo-controlled crossover study of a 0.2% chlorhexidine gluconate
mouthwash used 3 times daily on plaque, staining and candidal carriage in a group of
recurrent aphthous ulcer suffers who maintained normal oral hygiene measures. At the end of
2 - 6week treatment periods, chlorhexidine has significant adjunctive effects on plaque
inhibition in recurrent aphthous ulcer.88
Triclosan:
Triclosan, an antibacterial agent introduced in toothpastes and mouthrinses, has recently been
shown to have anti-inflammatory and analgesic properties. Skaare AB, Herlofson BB,
Barkvoll P et al (1996) 122 double-blind cross-over study was to examine the effect of
triclosan on the incidence of recurrent aphthous ulceration (RAU) when administered in
mouthrinses. The study included 30 patients with a history of multiple recurrent aphthous.
The results showed that the patients experienced a significant decrease in the number of oral
ulcers. It concluded that triclosan has the potential to reduce the number of aphthous ulcers
presumably due to its anti-inflammatory properties.
Tetracyclines:
Placebo-controlled studies of tetracyclines (such as Aureomycin, chlortetracycline and
tetracycline) suggest that these may also reduce healing times, or reduce the associated pain
of RAS, or both, but should be avoided in children and pregnant or lactating mothers. In the

UK, doxycycline 100 mg in 10 mls water used for 23 minutes, 4 times daily for 3 days as a
mouthwash in the British National Formulary. Gorsky D, Epstein D et al assessed
minocycline and tetracycline oral rinses in patients with frequent episodes of RAS in a
clinical randomized crossover trial. 17 patients with high frequency recurrent minor RAS
were randomly allocated to a crossover topical therapy with 0.2 percent minocycline or 0.25
percent tetracycline aqueous solution mouthwash. Minocycline mouthwashes as compared to
topical tetracycline rinses resulted in significantly improved pain control, by reducing the
severity and duration of pain.89
Other agents:
Topical non-corticosteroid based agents thought to be of benefit in RAS include sodium
cromoglycate, azelastine, alpha-2-interferon, ciclosporin, deglycirrhizinated liquorice, 5
aminosalicylic acid (5-ASA), prostaglandin E2 (PGE2), granulocyte macrophage colonystimulating factor, sucralfate, aspirin, and diclofenac in hyaluronidase, irsogladine maleate,
Eupatorium laevigatum, and oxolin.
Sodium Cromoglycate:
Dolby, Walker et al (1975) In a random double blind trial on 24 patients with recurrent
aphthous ulcers (RAU), cromoglycic acid tablets significantly reduced the pain experienced
when compared with placebo but did not reduce the number of days with oral ulceration
present. It is concluded that the cromoglycate compounds may have a valuable part to play in
the symptomatic relief of RAU.90
Interferon Alfa: Hamuryudan V, Yurdakul S et al (1990) evaluated the effect of topical
recombinant interferon alfa 2c hydrogel (IFN alpha 2C) in the aphthous lesions of the mouth
in Behcet's syndrome was assessed in twenty patients in a twelve-week open trial. IFN alpha
2C applied to the mouth for four weeks significantly reduced the number of aphthae in the
post-treatment phase compared to the pretreatment and treatment phases. No side effects were
recorded. Topical IFN alpha 2C seems to be effective in the treatment of the aphthae in
Behcet's
syndrome.91
Deglycyrrhizinated Liquorice (Dgl) Mouth Wash:
Das SK, Gulati AK, Singh V Peta (1989) evaluated 20 patients with aphthous ulcers and were
advised deglycyrrhizinated liquorice (DGL) mouth wash, followed for two weeks. Fifteen

patients experienced 50-75% improvement within one day followed by complete healing of
the ulcers by third day.92.
5-aminosalicylic acid (5-ASA):
Collier PM, Neill SM, Copeman P Wet al (1992) conductd a double-blind placebo controlled
trial on 5% 5-aminosalicylic acid (5-ASA) cream for the treatment of oral aphthous ulcers in
22 subjects. The cream or a placebo (11 patients each) was applied to the ulcers three times
daily for up to 14 days. Daily discomfort was reduced by half and less pain was experienced
by the treated group. Treatment with 5-ASA shortened healing time and reduced the difficulty
in eating. No significant side-effects were reported. They believe 5-ASA cream to be an
effective treatment for aphthous ulcers.93.
Topical Prostaglandin E2 (Pge2):
Taylor LJ, Walker DM, et al (1993): Thirty-five patients suffering from minor recurrent
aphthous ulceration (RAU) entered a single-phase double-blind clinical trial of treatment with
topical prostaglandin E2 (PGE2). The PGE2 was applied as a gel at a dose of 0.3 mg twice
daily for 10 days. The vehicle alone acted as control. Patients using the active PGE2 gel
experienced significantly fewer new lesions than those on placebo over the 10-day trial
period. There were no significant differences between the PGE2 and placebo gels in terms of
speed of healing or pain relief of established aphthous ulcers. Prostaglandin E2 may,
therefore, have useful prophylactic activity in RAU.94.
Granulocyte macrophage colony-Stimulating Factor:
Bacanli, O Yerebakan Dicle et al: Seven patients with Behet's Disease were given topical GCSF for OU (4 120 g/day, for 5 days) and/or GU (4 30 g/day, for 5 days) and followedup for 3 months after treatment. No concurrent disease-specific or immunosuppressive topical
or systemic drugs were given during the study period. G-CSF treatment decreased the healing
time and.95
Sucralfate:
Sucralfate, which acts by locally binding with the proteins at the base of an ulcer to provide a
protective covering, has been suggested as a treatment for aphthous ulcers.
3% Diclofenac in 2.5% Hyaluronidase:
Saxen MA, Ambrosius WT, et al: conducted a randomized, double-blind, single dose study on
60 healthy adults with aphthous ulcers in three treatment groups--3% diclofenac in 2.5%

hyaluronan, 2.5% hyaluronan, 3% viscous lidocaine. They conclude that a dose of 3%

diclofenac in 2.5% hyaluronan is an effective and novel treatment for this common, painful
ulcer.96
Eupatorium laevigatum Lam:
Eupatorium laevigatum Lam is a plant common to the central region of Brazil, where it is a
widely used remedy for lesions such as buccal aphthae. Paulo Filho, W Ribeiro et al (1990)
97

conducted two part study: For the first part of this two-part study, a phytotherapeutic

preparation from E. laevigatum extracts was formulated into an orabase paste appropriate for
use on the buccal mucosa. The study evaluated the toxicologic safety of this paste in 20
healthy volunteers. The second part of the study was a randomized, double-blind comparison
of efficacy with triamcinolone 0.1% orabase in 60 patients. The healthy volunteers tolerated
the phytotherapeutic paste well, and no adverse effects could be attributed to its use. In the
clinical comparison, after 5 days of treatment, 40% of the patients who used the paste and
26.7% of those who used triamcinolone obtained complete cure of the ulcers. Pain was
alleviated in 70% of the phytotherapeutic group and in 33.3% of the triamcinolone group.
Irsogladine maleate:
Irsogladine maleate, which reinforces gap junctional intercellular communication in vitro,
was effective for the treatment of transient and relapsing aphthous stomatitis, as well as
symptomatic and drug-induced aphthous stomatitis.
Mouthwashes:
Aqueous preparation of 0.1 to 0.2% triamcilone, 0.3% hydrocortisone and dexamethasone
elixir 0.5/5ml can also be used about 3 to 4 times a day as mouthwashes. 98 Intralesional
steroids can be used to treat large indolent major RAS lesions. The individual lesions may be
injected with triamcinilone acetonide or covered with 0.05% clobetasol proprionate gel or
0.05% halobetasol proprionate ointment.98
Systemic therapy
Patients with particularly frequent or severe RAS may require systemic immunosuppressive
treatment.

Corticosteroids:
Prednisolone or azathioprine, or both, can improve healing of severe RAS, but longterm use
should be avoided as adverse effects will usually outweigh clinical benefit.
Anti-TNF- agents
Pentoxifylline:
Chandrasekhar J, Liem AA et al (1999) 132: A 6-week open trial and a patient survey
regarding pain were conducted on Twenty-four patients. A 4-week period of treatment with
oxypentifylline (400 mg administered orally 3 times daily) was given. The encouraging
results of this study support the suggestion that the use of oxypentifylline be considered in
refractory cases of recurrent oral aphthous ulcers.
Thalidomide:
Thalidomide is the most reliably effective agent available for the management of RAS. It
produces remission in almost half of patients and several case studies, confirm that
thalidomide (50100 mg daily) is of clinical benefit. However, the adverse effects seriously
limit its application to short-term use, and in women who will not get pregnant.
Adalimumab:
Adalimumab is an anti-TNF-alfa monoclonal antibody that has been used to treat severe,
recalcitrant, RAS, but in view of the risk of serious adverse effects, it should be used with
extreme caution.
Colchicine:
Colchicine maybe of some clinical benefit in the management of RAS (1.5 mg/day) but at
least 20% of patients can have painful gastrointestinal symptoms or diarrhoea, and long-term
use can cause infertility in young men.
Levamisole:
Levamisole was once described as an effective treatment for RAS, but five RCTs reported no
significant benefit (150 mg daily for 3 days), and four suggested that, while it might reduce
the duration, number, size, and frequency of ulceration, the adverse effects (nausea,
hyperosmia, dysguesia and agranulocytosis) discouraged its use.

Other immunomodulatory agents

Dapsone, transfer factor, gammaglobulin therapy and cimetidine, have been suggested to be
beneficial, bu more detailed studies are needed to confirm these preliminary observations.
Other agents
Silver nitrate cautery
Alidaee MR, Taheri A, et al (2005) 133 in a randomized, patient-blinded, placebocontrolled
study, 97 patients with painful minor oral aphthous ulceration were randomized to receive
silver nitrate cautery or placebo. In the treatment group, the ulcer was gently painted with a
silver nitrate stick until it turned white. In the placebo group, the ulcer was gently painted
with a placebo stick. The results showed that one application of silver nitrate can decrease the
severity of pain in aphthous ulceration without significantly shortening or prolonging healing
time.
MUCOUS MEMBRANE PEMPHIGOID
Synonym:
Cicatricial pemphigoid
Benign mucous membrane phemphigoid
MMP is a chronic, subepithelial autoimmune disease that results in mucosal blistering,
ulceration and subsequent scarring. The condition belongs to group of mucocutaneous
autoimmune blistering disorder often called sub epithelial bullous dermatoses (SEBDs).
These disorders result in blistering of skin or oral mucosa and include bullous pemphigoid
(BP), MMP. Linear IgA disease (LAD), Chronic Bullous Dermatosis of Childhood (CBDC)
and Epidermolysis Bullosa Acquisita (EBA). MMP is a chronic, subepithelial autoimmune
disease that results in mucosal blistering, ulceration and subsequent scarring.99
Definition: Mucous membrane pemphigoid (MMP) as defined as 'group of putative
autoimmune, chronic inflammatory, subepithelial blistering diseases predominantly affecting
mucous membranes, with or without clinically observable scarring.3 Antibodies are produced
against certain target antigens found in the basement membrane, resulting in the epithelium
being detached from the underlying lamina propria.

Historical review
Mucous membrane pemphigoid was apparently first described by wichmanns in the late 18th
century. He described a female patient who had ocular and oral involvement as well as skin
lesions. The duration of disorder was 3 years and the entire oral cavity was denuded of
epidermis.3 Thost in 1896 and in subsequent papers distinguished between "acute pemphigus
of mucous membrane" usually seen in pemphigus vulguris, folacious and vegetans and a
"chronic pemphigus of the mucous membrane".
Epidemiology
The true incidence of MMP is unclear. Data in dermatology literature suggests that MMP is
approximately seven times less common than BP. Ocular phemphigoid may occur in 1 of
every

15,000

to

40,000

individuals

seen

by

ophthalmologist.

Retrospective

immunofluorescent studies oral mucosal diseases that MMP occurs upto 3 times more
frequently than phemphigus.100 MMP is an autoimmune condition predominantly affecting
women, with mean age at onset of 50 years. Children's are rarely affected.
Clinical features
Oral lesions:
It primarily affects the mucous membranes, including the eyes, mouth and pharyngeal
mucosal of patients over the age of 50. It occurs in more than 90% of patients with MMP.
Whereas oral involvement may be present in upto 50% of those with BP. Oral manifestation
are variable and often include desquamative gingivitis. The disease typically presents in
patients between 55 and 70 years of age, although childhood cases have been reported. The
female to male ratio is approximately 2:1.82 Oral lesions are the most common presentation
and can be found in 85% to 90% of patients. Virtually all sites in the oral cavity can be
involved, including gingivae,
buccal mucosa, palate, and, less commonly, alveolar ridges, tongue, and lips. A subgroup of
patients presents with desquamative gingivitis (DG) as the sole manifestation, although other
patients present with involvement of parts of the oral mucosa without DG, and in a third
group all of the oral mucosa can be involved. Most patients are symptomatic often
complaining of oral pain caused by mucosal ulceration and desquamation. Patients with
gingival involvement frequently have poor oral hygiene because of inability to clean the
dentition effectively secondary to mucosal pain. 101 Thus patients may often present with
bleeding gums. Patients may describe inability to eat certain types of foods for fear of

exacerbating the symptoms. Occasionally patients may complain of halitosis, from lack of
maintaining good oral hygiene. Other scaling and root planning or peeling of the gingival
tissue with simple prophylaxis.
Ocular lesions:
The conjunctiva appears to be the second most frequent site of involvement and in a clinical
subgroup is often the only site affected. Conjunctival biopsy specimens from patients
presenting with oral disease show basement membrane zone deposition in more than 50% of
patients, this strongly suggests that routine ophthalmological examination should be part of
the clinical protocol for patients presenting with oral ulceration. Most cases of clinical ocular
presentation are bilateral, although the disease often begins unilaterally and progresses to the
other eye over several years Ocular MMP begins as a non-specific chronic conjunctivitis
leading progressively to subconjunctival fibrosis with "symblepharon formation" and
forniceal shortening. "Ankeloplepharon" is adhesion between the eyelids lead to narrowing of
palpebral fissure
Skin lesions:
Two types of skin lesions are evident.
Recurrent vesicles and bullae, which rupture and heal without significant scarring
Brunsting Perry variant, in which lesions are predominantly localized to the head and neck
and consist of flaccid blisters that, after ulceration, heal slowly and leave atrophic scars. On
the scalp, recurrent blistering may result in cicatricial alopecia
Other site:
Nasal involvement usually consists of a crusted ulceration on the septum or turbinates.
Pharyngeal involvement is typically manifested by ulceration of the posterior or lateral
pharynx and presents with dysphagia. Involvement of the larynx is often clinically manifest
as hoarseness, and laryngeal erosions and adhesions may be seen on examination, Vesicle and
erosions of the labia majora or minora in women and of the glans penis and foreskin in men
can lead to fibrosis and adhesion formation. Complications include urethral stenosis and
narrowing of the vaginal orifice, and scarring in these areas may require surgical intervention.

Human leukocyte antigen associations in MMP

Most studies have looked at relatively small numbers of patients, and the earliest reports were
contradictory. More recent studies have shown an association between ocular cicatricial
pemphigoid (OCP) and human leukocyte antigen (HLA).
Pathophysiology
The pathophysiologic mechanism of MMP is complex and is not yet completely understood.
There is clearly in immune regulation involving the formation of autoantibodies, usually of
IgG class, directed against normal components of BMZ. This interactions trigger a
complicated web of immunologic events resulting in expression of inflammatory mediators
that induce migration of lymphocytes, esionophils, neutrophills and mast cells to BMZ. The
separation of epithelium from the underlying tissue within BMZ may result of direct
cytotoxic action or the effect of lysosomal proteolytic enzymes. Fibroblasts are also activated
secondary to production
of inflammatory cytokines. The collagen produced may lead to cicatrisation of eye or mucous
membrane. This process is of particular importance in MMP affecting the eyes where fibrosis
or subsequent cicatrisation can cause profound tear insufficiency, symbelpheron formation,
trichiasis, keratinization of comes and other defects. There are several components to the
BMZ that can be schematically divided into keratinocytes, lamina Lucida and densa,
sublamina densa. With in this zone hemidesmosomes anchor keratinocytes to basement
membrane. Components of hemidesmosomes are proteins bullous phemphigoid antigen
1(BPAG1), bullous phemphigoid antigen2 (BPAG2), plectin, laminin-5 also called epiligrin.
BPAG1 is an intracellular protein where as BPAG2 are transmembrane proteins. The major
ligand between the transmembrane proteins and anchoring filaments is thought to be laminin5. Laminin-5 serves as critical molecule in this adhesive structure. Anchoring fibrils
composed of type VII collagen are located deeper in lamina densa. Autoantibodies produced
in MMP target one of several different components of the BMZ causing immunologic events
that lead to epithelial separation from connective tissue at the BMZ. The most commonly
targeted autoantibody in MMP is BPAG2, however antibodies to BPAG1, laminin-5 have
been identified.102
Epithelial and basement membrane antigens

The oral epithelium is a complex structure consisting of a range of cells, mainly

keratinocytes, adherent to each other by desmosomes, and via hemidesmosomes and an
epithelial basement membrane to the underlying lamina propria. Each component is itself
complex and consists of several proteins with important functions not least the adherence of
cells to adjacent structures and cell-cell recognition and signaling. The basement membrane
zone comprises the basal cell plasma membrane, the lamina Lucida, the lamina densa, and the
sublamina densa. On the ventral surface of basal keratinocytes are small electron-dense
domains of the plasma membrane, the hemidesmosomes (HD). These are specialized
junctional complexes that contribute to the attachment of epithelial cells to the underlying
basement membrane. Several proteins implicated in the pathogenesis of subepidermal
blistering diseases are associated with the HD and include the bullous pemphigoid antigens
BP230 and BP180 and the a6b4 integrin.
The lamina Lucida is the electronlucent zone adjacent to the basal cell plasma membrane and
is 20-40 nm thick. Anchoring filaments transverse the lamina Lucida perpendicularly from
the basal cell membrane to the underlying lamina densa. Together with HD they form the HD
anchoring filament complex, which has an important role in cell-basement membrane
adhesion. The lamina densa is the electrondense layer below the lamina Lucida and is thought
to be thinner in female than in male skin and possibly mucosal epithelium.102
Immunofluorescence: Direct immunofluorescence (DIF) investigations using perilesional
mucosa show a linear continuous band at the BMZ, usually with IgG and C3 but often with
IgA in virtually 100% of patients with the clinical characteristics of MMP. DIF is essential for
the diagnosis of MMP and must be performed to complement the clinical findings. Once a
clinician suspects a diagnosis of a subepithelial blistering disease, tissue samples must be
obtained. Any patient suspected of having MMP must have two biopsy specimens taken for
pathologic evaluation. However, a diagnostic biopsy is difficult because of the fragility of the
tissue. The epithelium frequently detaches from the underlying connective tissue, rendering
the biopsy specimen useless. Routine histopathology of a properly obtained specimen will
demonstrate sub-basilar cleavage. But routine biopsy of a patient suspected of having MMP
is often not enough to differentiate the disease from other mucocutaneous disorders. Direct
immunofluorescence (DBF) is, in itself, often helpful in making a broad diagnosis of
pemphigoid. This procedure involves performing an incisional biopsy from a perilesional site
adjacent to a new vesicle or bulla. The specimen should be transferred in a specific transport
media (Michele's solution) and must be processed in a timely manner.The tissue is then

incubated with fluorescein-coupled antibodies against specific IgG's, complement and

fibrinogen, and examined under a fluorescent microscope.102 DIF shows a uniform, linear
deposition of IgG and/or complement along the BMZ of perilesional tissue. In some cases,
additional biopsies may be necessary to demonstrate the presence of immune deposits in the
BMZ. Biopsy specimens should not be obtained from lesional tissue, because a false-negative
interpretation may be given.
The following recommendations by the Consensus Statement may enhance positive results:
In patients with single-site mucosal involvement, a biopsy specimen should be obtained
from tissue next to the areas of inflammation.
When patients present with multiple-site involvement, the biopsy should be taken from
tissue adjacent to an inflamed non ocular site.
Patients who present with both skin and other mucosal involvement should have a skin
biopsy taken from an inflamed lesion.
For patients with ocular involvement requiring a biopsy, the procedure should be performed
cautiously to minimize both injury and additional scarring.
Drug-induced clinical manifestations of MMP should be considered when epithelial BMZimmune deposits are not demonstrated.
Indirect Immunofluorescence (IIF)
It can also be used to detect circulating antibodies in a patient's serum. IIF is performed by
incubating patient serum with an epithelial substrate and marking the specific antigens with
fluorescein-labeled, anti-human IgG. Using this method, antibody titers of MMP
autoantibodies can be determined. Autoantibody titers of IgG at initial presentation may be a
predictor of disease severity and may correlate to disease activity. To better determine exactly
which components of the BMZ are targeted by autoantibodies, a salt-split skin procedure may
be performed. In this analysis, normal human skin substrate is incubated with l mol/L of
sodium chloride solution, which results in a separation between the epithelium and the
connective tissue. This exposes the components of the BMZ, resulting in improved sensitivity
for detection of binding antibodies in serum directed against the substrate. Antigens on both
sides of the split can be identified. Most patients with MMP have auto antibodies against the
epidermal side of the salt-split skin, where the BPAG2 antigens are present, where as those
with auto antibodies to antigens on the dermal side of split side of the split are targeted
towards dermal side of the split targeted towards epiligrin.102

Differential diagnosis:
Other diseases that should be considered in differential diagnosis of benign mucous
Membrane phemphigoid are:
Phemphigus vulgaris
Bullous pemphigoid
Bullous lichen planus
Chronic ulcerative stomatitis
Early cases of erythema multiforme.
Benign mucous membrane pemphigoid and bullous pemphigoid are clinically, histologically
and immunologically similar but differ in sites of involvement.
Management
Management of MMP depends upon the severity of the disease. Topical high potency
costicosteroids like flucinonide 0.03% or clobetasol 0.05% and betamethasone dipropionate
0.05% can be used carefully. Gel based formulations are better than ointment and cream form
since the adherence & penetrance is better. Intralesional steroids are useful for recalcitrant
lesions. Injecting the steroids into the lesion with a steroid suspension will usually result in
healing. Care must give to inject the proper amount, as excessive steroid can result in tissue
necrosis.
Dapsone:
It is a synthetic sulfone with anti-inflammatory properties, is one such medication used for
MMP. There is evidence that dapsone suppresses neutrophil function and inhibits the
synthesis of prostaglandins (E2) by neutrophils. Dapsone may also inhibit neutrophil activity
by suppressing neutrophil adherence to the endothelium, and it appears to interfere with the
chemotaxis.
Minocycline:
A tetracycline-type antibiotic has also been effective in treating MPP. Minocycline has been
used as an effective anti-inflammatory agent, in low doses to treat periodontal diseases. The
benefit in treatment of MMP may be related to leukocyte chemotaxis and other antiinflammatory and immunosuppresant action. The dosage of minocycline is between 50 to
l00mg. Adverse side effects with minocycline include nausea, vomiting, dizziness,
photosensitivity and hyperpigmentation. Combination therapies consisting of tetracycline and

nicotinamide have also been reported as effective therapy for MMP. Potential adverse effects
reported with nicotinamide therapy may include hepatotoxicity, pruritis and flushing, even
though these have been reported in patients taking much higher doses than those used in
combination therapy.102
ERYTHEMA MULTIFORME
Synonym
Erythema multiforme minor
Erythema multiforme major
Erythema multiforme exudativum
Ectodermosis erosive pluriorificialis
Eruptive fever associated with stomatitis and opthalmia
Stevens Johns syndrome
Baaders dermato-stomatitis
Erythema multiforme is a term applied to an acute dermatitis of unknown etiology and
protean manifestation.36
It is an acute inflammatory disease, which may involve the skin and the mucous membranes
of the mouth, conjunctiva and genitalia. It occurs commonly in spring and autumn. It is
characterized by variety of eruptions, which may appear as red or papules, which by
peripheral extension and central clearing tend to form the characteristic iris lesions. These
lesions appear as concentric circular erythematous rings resembling a target or bulls eye
(target lesions).103 The lesions are frequently symmetrical. Common sites are face and lips.
Dorsal surfaces of hands, forearms, feet and legs. The mouth is often involved usually early
and may be the only part affected, according to Mauriello (1954) and lighterman (1958).
There is accompanying fever. After recovery there may be frequent recurrence during the
following 2-5 years, but the systemic upset is usually reduced or absent.103 The more severe
form of this condition is generally called erythema multiforme exudativum by Herba in
1866.103
Etiology:
EM is an immune-mediated disease that may be initiated either by deposition of immune
complexes in the superficial microvasculature of skin and mucosa. 36,

102

EM is almost

infectious in origin and HSV is the infectious agent in about 70 to 80% of cases. HSV I and II
are known to trigger EM. In contrast to EM drugs precipitate 80 to 95% of cases of TEN and
more than 50% of cases of SJS.

These drugs are sulfonamides, trimethoprim, sulfamethoxazole, NSAIDs, penicillin,

anticonvulsants such as barbiturates, carbamazipine, valproic acid, allopurinal and
terbinafine.
Other triggers for EM include progesterone, Mycoplasma, benign and malignant tumors,
radiotherapy, Crohn's disease, sarcoidosis, histoplasmosis, and infectious mononucleosis, and
graft versus host disease.36
Pathology:
The pathology of EM differs from that of SJS/TEN. In EM there is perivascular infiltrate of
CD4 and CD8 lymphocytes surrounding swollen blood vessels in upper dermis with papillary
dermal edema and vacuolar degeneration of basal layer, sub dermal blister formation and
epidermal necrosis of keratinocytes that increases with older lesions. The individual necrotic
keratinocytes are surrounded by CD8 cells termed as "satellite cell necrosis". In most cases
the attack is against HSV-DNA particles expressed on blood vessels and keratinocytes. In the
epidermis of EM there is an overproduction of interferon by CD4 T helper -1 cell. INFgamma is not found in drug-induced conditions. SJS/TEN exhibits much more widespread
necrosis of epidermis and little vascular inflammation of dermis. Presumably the drug
antigens are expressed only on keratinocyte, not the blood vessels. In fact there is remarkable
absence of significant lymphocytes around the vessels and few are seen in epidermis.
Clinical features: 36
It is commonly seen in young adults and found more frequently in males, has an acute onset
runs self-limited course for several weeks. Frequently associated with preceded upper
respiratory infection combined with headache, malaise, nausea and arthalgia. Often during
the early stage their fever.
Skin involvement:
The clinical appearance of skin EM differs from that of SJS/TEN. EM is characterized by
multiple target or iris lesions. All lesions typically present with in 3 days of onset. There may
be hundreds of lesions, but less than 10% of body surface is covered. The lesions are fixed
and symmetric. They present as circular erythematous plaques concentric area with lesion
size ranging from 2 to 20mm. A central blister of area of necrosis may be present initially the
lesions are seen acrally (dorsal surfaces of hands feet, elbows and knees). Face may also be
involved.36

Oral manifestations:
The disease usually occurs in younger individuals and males are frequently affected. The
frequency of oral manifestations may vary from about 40 to 100% (Gorlin, Pindborg and
Cohen, 1976). Oral lesions usually appear after skin eruption; some times it can be reverse.
Furthermore it has been reported that some patients never develop skin lesions (Cooke, 1960;
Shklar and Mc Carthy 1966)2 Oral lesions may be found on lips, labial mucosa, floor of the
mouth, soft palate buccal and gingival mucosa. Because of humid environment and
movements of mucosal tissues during mastication, the oral lesions are not well defined as
skin lesions.2,103The development of oral lesions can be divided into 5 distinctive stages:
macular,
vesicular, sloughing, pseudomembranous and healing (Wooten et al, 1967).2 The initial stage
in development of oral lesion is small erythematous plaques or macule, which is soon
followed by vesicle present but for brief time. Vesicles of oral mucosa tend to rupture more
easily than vesicles of the skin. The ruptured vesicles become confluent to form shallow
erosions with a peripheral erythema and covering of slough, giving rise to
pseudomembranous stage. The oral
lesion becomes extremely painful as vesicles rupture and ulcers get secondarily infected.
Swallowing may be difficult if lesions are present on oropharynx. Although the lesions may
occur in any area of mouth, the lips are invariably and extensively involved with crust
formation. The appearance of these crust areas can be helpful in diagnosis. Marked halitosis
may be present. When the gingival is affected by disease, peculiar mixture of catarrhal and
necrotic gingivitis may result. The lesions usually complete their course with in 2 weeks, but
recurrent attacks are common. The oral changes may be complicated by sialorrhoea,
dysphagia and enlarged cervical lymph nodes. In more severe cases epitaxis is an early sign,
the local glands are enlarged, but not so early as in acute herpetic stomatitis. Sometimes
patient is dehydrated because they are unable to ingest liquids as a result of mouth pain.103
Differential diagnosis:
Erythema multiforme may present diagnostic problems because of varied clinical picture.
Among the more important diseases, which may resemble EM, are benign mucous membrane
pemphigoid, behcets syndrome, and Reiters syndrome. In pemphigoid skin lesions are rare
and do not exhibit the iris sign. The slough covering the ulceration is usually thicker and
more glazed than the pemphigoid.36 In Behcets syndrome the clinical course is more chronic

and oral lesions more closely resemble aphthae, and are not wide spread as in EM. In Reiters
syndrome the presence of keratosis menorrhagica like lesions are characteristic.
Treatment of EM and SJS:
Mild cases of oral EM may be treated with supportive measures only, including topical
anesthetic mouthwashes and a soft or liquid diet. Moderate to severe oral EM may be treated
with a short course of systemic corticosteroids in patients without significant
contraindications to their use. Young children treated with systemic steroids for EM appear to
have a higher rate of complications than do adults, particularly gastrointestinal bleeding and
secondary infections. Adults treated with short-term systemic steroids have a low rate of
complications and a shorter course of EM. The protein-wasting and adrenal suppression
effects of systemic steroids are not
Significant when used short-term, and the clinical course of the disease may be shortened. An
initial dose of 30 mg/d to 50 mg/d of prednisone or methylprednisolone for several days,
which is then tapered, is helpful in shortening the healing time of EM particularly when
therapy is started early in the course of the disease. Patients with severe cases of recurrent
EM have been treated with dapsone, azathioprine, levamisole, or thalidomide. EM triggered
by progesterone, also referred to as autoimmune progesterone dermatitis and stomatitis has
been treated successfully with tamoxifen. In resistant cases, oophorectomy has been
necessary to cure the
disorder.

36

Early treatment of recurrent HSV infection is the recommended approach to

prevent
recurring attacks of EM. Systemic antiviral agent has abortive or suppressive actions.
Famciclovir 125mg BID for 5 days. Or Valacyclovir 500mg BID for 5 days. Effective therapy
depends on initiating treatment during the prodromal phase. For example tingling sensation
of lip may herald an attack of herpes labialis. If the drug therapy is started after the lesions
appear, EM may be aborted.60 When there is no prodrome present suppressive therapy may
be started. Famciclovir 125 to 250mg/day or valacyclovir 500mg to l000 mg/day for a year
may totally
prevent EM attacks. After 1 year attacks may be severe and frequent or may occur as before.
When suppressive treatment does not work, it may indicate a trigger other than HSV. In this
case suppressive treatment is a test to determine if HSV or some other trigger is involved. In
few cases where HSV does not seem to be trigger, Dapsone, Hydrochloroquine, Azathioprine

and Thalidomaide have been advocated. There are no standard guidelines for treatment of
SJS/TEN. Recognition and prompt discontinuation of offending agent is priority. Use of all
drugs should be stopped as quickly as possible, especially those taken within 8 weeks before
the onset of TEN symptoms. In SJS oral intake may be limited so patients may need to be
hospitalized to receive replacement IV fluids. Opthalmological consultation is imperative.
Ocular lubricants and elimination of new lid adhesions should be priority.
PERIODONTAL DISEASES RELATED TO PSYCHOGENIC
CAUSE
Although it is apparent that psychogenic insight is required for the proper management of
dental practice, other relationships between psychology and dentistry are also less obvious
but no less important. Psychoanalytic theory places great importance in the relationship of the
oral cavity to the psyche. Other data also support the hypothesis that psychologic and social
factors are involved in diseases of the oral cavity.104
Psychosomatic factors:
In periodontal diseases related to psychogenic causes. A study of hospitalized,- emotionally
ill population showed acutely disturbed patients had a higher incidence of periodontal
diseases than did apathetic patients.
PERIODONTAL DISEASES
1) Necrotizing ulcerative gingivitis: 104
It is a disease of special interest because it may have an emotional basis. Some evidence
exists to indicate that the suggested relationship between emotional stress of necrotizing
ulcerative gingivitis is more than conjectures of the hospitalized patients examined by
Mellars and Herms, the acutely mentally ill were more prone to necrotizing ulcerative
gingivitis than were the chronically mentally ill. The disease among military personnel may
be related to fatigue, nervousness and unusual dependence. A group of patients with this
disease examined by Moultan and Co-workers exhibited a pattern of oral dependence as a
central life problem.105 The attacks of necrotizing ulcerative gingivitis among this group were
brought on by acute anxiety, case histories indicate incidence that attacks of acute anxieties
are often the precipiting factor. Patients with necrotizing ulcerative gingivitis have tendency
to cutaneous vasodilatation in response to irritation and in addition show a longer latency
period for flare reaction.

2) Atypical gingivostomatitis
An unusual gingivitis, extending from gingival margin to the mucogingival junction and
limited almost entirely to the labial and buccal surfaces has been reported. Evidence of an
excessively dependence yet hostile relationship with either spouse or parent was found in the
patents studies.106
3) Excoriative gingivitis (Gingivitis artefeacta)
Self inflicted gingival excoriations that have a neurotic or unconscious habitual basis are
periodically reported. These may be so extensive as to involve self-extraction of teeth. It is
most seen in young individuals and women who are more likely to exhibit this condition.
Self-inflicted injuries can also be seen in Manchausens syndrome.

4) Thegosis and Somatization (Parafunctional occlusal traumatism)

Theogosis is the general term applied to embrace two aspects of jaw parafunctional activity
jaw clenching and tooth grinding. Somatization has been defined as " a tendency to
experience and communicate" somatic distress and symptoms unaccounted for by
pathological findings, to attribute them to physical illness and to seek medical help for
them.107
5) General Adaptation Syndrome108
Selye's General Adaptation Syndrome was based on the observation that stress significantly
influences endocrine function through the hypothalamus and anterior pituitary gland, leading
to enlargement and increased function of the adrenal cortex. Periodontal emotional stress
syndrome results in severe vertical and horizontal bone loss with associated pocket
formation, consistent involvement of the first molar teeth and a paucity of other local
etiological agent.
Stress and wound healing;
Decresed levels of IL-1, IL-8 and TNF results in delayed wound healing.
EFFECTS OF STRESS ON PERIODONTIUM:

Genco et al (1998)134 proposed a model, demonstrating the potential role that psychosocial
stressors may play in initiating a cascade of events in the corticotrophin releasing hormone/
hypothalamic-pituitary-adrenal axis, the autonomic nervous system and the central nervous
system, this resulted in depressed immunity, increasing the chances of infection and
specifically periodontal disease. Another important psychosocial stressors are behavioral and
emotional responses to common sequelae of advancing periodontal disease like pain,
swelling, tooth migration, impairing esthetics tooth mobility and perceived threat of losing
teeth early in the life. Treatment of periodontal disease is time consuming and expensive. All
these can act
as powerful negative emotional stressors. These factors may induce stress system responses
that are further harmful to periodontal health. The behavioral pathogens extending from
neglect of oral hygiene to dietary inadequacies, poor sleep patterns, use of tobacco products,
and other substance abuse constitute an important class of psychosocial stressors that
contribute to the vicious cycle, increasing severe forms of periodontal disease. Stress can also
influence periodontal disease through its effects on the course of diabetes and smoking
behavior.
EVIDENCE FOR THE ROLE OF STRESS IN PERIODONTAL DISEASE:
Monteiro da silva et al (1995)135 reported that evidence was strong for stress as a
predisposing factor to acute necrotizing ulcerative gingivitis. Shapira et al (1999) 109 in a study
in mice found that an emotional stressor (isolation) and a physical stressor (cold), compared
to control, had the effect of modifying the inflammatory response to Porphyromonas
gingivalis.
Factitious ulceration-stomatitis artefacta
This is the intraoral counterpart of the well recognized dermatitis artefacta (Sneddon, 1977).
The lesions will vary in their appearance according to the manner in which they are created.
The most common and least troublesome lesion is due to cheek chewing. Here, usually a
young, anxious, neurotic individual continually chews the buccal mucosa producing wide
areas of peeling, macerated, hyperkeratinized epidermis. Similarly, lip biting may produce
fissures, white areas of hyperkeratosis or a mucous extravasation cyst this presents as a
round, bluish, fluctuant swelling on the lower labial vermilion border which may vary in size
from time to time. Excision of the cyst must include the associated damaged mucous glands
to avoid recurrence. In the older anxious or agitated patient, lip chewing produces varicosities
so that the vermilion border becomes curiously cyanotic in appearance. Greater difficulty

may be experienced in recognizing the discrete lesion where local abrasion with a finger nail
or sharp instrument may produce a linear palatal or faucial ulcer or several gingival ulcers.
Rubbing the alveolar mucosa with a finger leaves an elongated erythematous patch. All of
these will be seen to be on accessible areas of the oral mucosa. Because of the hysterical
element in this condition, the condition may mimic a natural lesion, particularly if the patient
is associated with dentistry or medicine. Unfortunately, there appears to be no age,
intellectual or professional barrier to this problem, although women seem to be more prone
than men. The history is characteristically vague and the lesion either persists longer or recurs
more frequently than one would expect it is often associated with one of the pain syndromes,
and the patient appears to produce the lesion to validate an organic diagnosis for their pain.
Sneddon (1977) describes three groups:
1. True malingerers, where an injury is consciously aggravated for monetary gain or the
avoidance of some responsibility.
2. Munchausen's syndrome, which is a persistent incurable psychopathic way of life without
any obvious advantage, other than obtaining medical and nursing care.
3. Part of an emotional instability, such as a personality disorder where the underlying
problem is a disturbance in personal relationships.
It is rare to obtain an acknowledgement or explanation as to how the lesions are produced,
and it is frequently difficult to get the patient or her family to agree to psychiatric help.
Nevertheless, this is important in order to protect the patient from inappropriate
investigations and treatment.
Oral diseases in which psychologic factors may play some etiologic role
a. Erythema multiforme
b. Mucous membrane pemphigoid
c. Chronic periodontal disease
In both erythema multiforme and mucous membrane pemphigoid, emotional stress plays a
significant role in determining the severity of the disease as well as recurrent episodes.
Remissions and exacerbations of longstanding mucous membrane pemphigoid are often
related to specific periods of psychologic tension. Emotional factors also probably play a
significant role in the complex etiology of chronic periodontal disease, in which the gingiva
and underlying periodontal -tissue cannot respond adequately to the local irritation of
bacterial plaque and calcareous deposits upon the teeth (calculus). The loss of tissue
resistance has been attributed to a variety of systemic factors, including emotional
stress.110,111,94

Oral infections in which emotional stress serves as a predisposing factor

a. Recurrent herpes labialis
b. Necrotizing gingivitis
Recurrent herpes labialis appears to be related to either physical trauma or emotional stress.
The herpesvirus type I exists within the regional ganglia and under appropriate stimuli it can
leave the nerves and produce lesions of skin and labial mucosa despite the fact that
circulating antibodies already exist in the patient.Trauma, such as mechanical irritation or
sunlight, or emotional stress apparently serves to prevent the antibodies from acting at the
local mucosal site. Whatever therapy is used for herpes labialis, its success depends upon the
clinician assuming a positive psychologic Necrotizing gingivitis is a fusospirochetal infection
caused by normal oral bacterial flora. Some predisposing factor reduces the tissue response to
the normal flora and they become pathogenic. Among these predisposing systemic influences,
emotional
stress appears to be the most common, although debilitating diseases, nutritional deficiencies
and neurologic disease may play similar roles. 107
Oral disease induced by neurotic habit
1. Leukoplakia induced by smoking cigarettes, cigars, or pipes, or by chewing tobacco, snuff,
or betel nut.
2. Biting of oral mucosa
3. Physical or mechanical irritation of mucosa with foreign objects or substances
4. Dental and periodontal disease produced by bruxism
The psychologic significance of oral habits is well known. The gratification obtained from
stimulation of oral mucosa is essentially sexual, since the erotic relationship of the oral
tissues is now well understood and the concept universally accepted. Smoking is certainly the
most widely practiced of the oral neurotic habits, and it can produce leukoplakia in
susceptible individuals; apparently, there must also be some genetic or hormonal
predisposition. Holding tobacco, snuff, or betel nut against oral mucosa induces leukoplakia
in a high proportion of subjects.2 Biting the oral mucosa or tongue can induce severe trauma.
A history may be difficult to obtain because the highly neurotic subject may not wish to
divulge the nature of the
trauma, or the trauma may have been produced during sleep. Biopsies are taken of many of
these lesions to rule out carcinoma before their traumatic nature can be appreciated. Strong
sucking motions can also induce unusual oral lesions that may initially delay diagnosis.

Neurotic patients may also traumatize their mouths with foreign objects such as sharp pencils,
toothpicks, or even fingernails. In rare cases a mentally unstable patient might induce severe
necrotic oral lesions, as with caustic chemicals, to gain the attention of a doctor who may not
have been sufficiently impressed with other symptoms about which the patient
complained.112,113 Grinding teeth (bruxism, bruxomania) is a neurotic habit that usually occurs
during sleep. It may result in wear of teeth, trauma to periodontal tissues, and occasionally,
trauma to facial musculature and temporomandibular joint structures
PSYCHIATRIC AND PAIN RATING SCALES 7,11,16,13
The principal difficulty and criticism in making a diagnosis of a psychogenic disturbance
either for individuals or groups is measurement. In the absence of any neurotransmitter assay
the clinician has to resort to rating-scale questionnaires measuring behaviour and symptoms
in order to support his clinical diagnosis. Psychiatric rating scales are completed either by the
patient (self raring) or the clinician (observer rating).
The most common forms are:
1. Case finding' instruments;
2. Mood check lists;
3. Personality scales;
4. life-event scales;
5. Illness behaviour;
6. Pain.
1. Case finding instruments yield scores with cut-off points indicating the likelihood of the
patient receiving a psychiatric diagnosis. They also allow an investigator to establish the
incidence of psychiatric morbidity in a population. The best validated and widely used selfrating scale is the General Health Questionnaire (GHQ) (Goldberg, 1972) which comes in
three versions, 28, 30 and 60 items, and is translated into 25 languages. The scale is easily
accepted by patients who do not regard themselves as mentally ill.The Clinical interview
Scale (Goldberg, 1972) is a semi-structured clinician rating scale which has to be completed
by a trained psychiatrist.
2. Mood check-lists measure the severity of mood states such as anxiety or depression. It is
important that mood scales should be sensitive to change. The selfrating scale used widely in
general hospital situations is the Hospital Anxiety and Depression Scale (HAD) (Zigmond
and Snaith, 1983), which has been validated in English populations. The Montgomery Asberg
Depression Rating Scale (Montgomery and Asberg, 1979) is the most widely used observer

raring scale. This may be used by any health professional. The Spielberger State/Trait
Anxiety Scale consists of two 20-item scales. State anxiety indicates the patient's anxiety at a
particular moment in time, whereas trait anxiety is the patient's general level of anxiety
(Spielberger, 1975).
3. Personality questionnaires measure 'traits' such as neuroticism or extroversion. In the UK
the only established scale is the Eysenck Personality Questionnaire (EPQ) (Eysenck and
Eysenck, 1965). There is no generally accepted clinician rating scale of personality. American
scales such as the Minnesota Multiphasic Personality Inventory (MMPI) or the Cattell 16PF
(Personality Factors) are not recommended because they tend to confuse illness with
personality and have not been validated in an English population.
4. Life-event scales measure significant changes in the patient's life which may be positive in
the form of promotion, marriage, moving house, or negative in the form of bereavement,
financial loss or marital difficulties. A patient's mood may exaggerate the effect of any event
so that only ratings obtained by trained observers should be used. Recommended
questionnaires are the Paykel life Event's scale (Paykel et al., 1969) or the Brown Life Event's
Inventory (Brown and Harris, 1982).
5. Illness Behaviour Questionnaire (IBQ) comprises several scales measuring attitudes and
concerns (Pilowsky and Spence, 1976). The IBQ has 52- and 62-item versions. The factors
are: (i) general hypochondriasis, (ii) disease conviction, (iii) somatic versus psychological
concern, (iv) inhibition of affect, (v) affective disturbance or dysphoria, (vi) denial and (vii)
irritability.
Its validity for British populations is questionable.
6. Pain rating scales. The McGill Pain Questionnaire (Melzack, 1975) consists of 20 sets of
words describing sensory, affective and evaluative dimensions of the painful experience. The
questionnaire can discriminate between different types of pain. It is also a reliable and
sensitive measure of the effects of different therapies on chronic pain. The simplest are the
visual analogue, verbal analogue and numerical rating scales. With the former, a 10 cm line is
displayed with (each end being designated) 'no pain' and 'the most severe pain'. The patient is
asked to mark the severity of pain at the appropriate point on this axis. This is easy to
measure and surprisingly reproducible. Verbal analogue scales use a series of grades of pain
such as, nil, mild, moderate, severe and intolerable, and a numerical rating scale can be
designed from 0 to 5 or 0 to 10 in the same way. These scales are non-parametrie for
statistical analysis and are probably equally reliable (Keele, 1948).
EATING DISORDERS

Anorexia nervosa
Anorexia nervosa is a chronic disorder characterized behaviorally by self induced weight
loss, psychologically by body image and other perceptual disturbances and psychologic
alterations (eg; ammenorhoea) that results from nutritional depletion. Anorexia nervosa is a
pathological avoidance of food where the subject has a delusional body image. Despite
emaciation, they see themselves as being fat and, apart from limiting their food intake, there
is often a covert practice of vomiting. However, the bulimiae by self-induced vomiting
maintains a normal weight despite indulging in eating binges. Both groups eventually suffer
erosion of their teeth and
caries due to the regurgitated gastric juice. Treatment requires the cooperation of the patient,
a restorative dentist and a psychiatrist.96
Etiology of eating disorders: 96
Involves a complication of psychological, biologic and cultural risk factors. Risk factorssexual or physical abuse, family history of mood disturbances, substance abuse. Patients with
anorexia tend to be more obsessional and perfectionist than their peers. As weight loss
progress, the fear of gaining weight grows, dieting becomes stricter and psychological
behavior and medical aberrations increase.96 Bulimia nervosa begins during or following an
episode of dieting often in association with depressed mood. Patients who develop bulima
nervosa describe a higher than expected prevalence of childhood and parental obesity,
suggesting that predisposition towards obesity may increase vulnerability to the bulima
nervosa. There may be severe biological abnormalities and central nervous system
serotonergic function that is involved in the regulation of eating disorder and disruption of
peripheral satiety mechanics including the release of cholecystokinin from small intestine.
Genetic factors probably contribute to the development of eating disorders. Incidence is
greater in families with at least one member affected and occurrence in monozygomatic twins
is greater than dizygotic twins.
Clinical features
Onset

Anorexia nervosa
Mid adolescent

Bulimia nervosa
Late adolescence/

F:M ratio
Prevalence in women
Weight
Menstruation
Binge eating
Mortality

10:1
0.5%
Markedly decreased
Absent
25-30%
5% per decade

childhood
10:1
1-3%
Usually normal
Usually normal
Required for diagnosis
Low

Early

Detection and evaluation:

Physical examination shows the patient is hypotensive and bradycardiac with significant
orthostatic signs. Skin may appear yellow with languo hairs present. Irregular cardiac rhythm
and peripheral edema Mitral valve prolapse is common in anorexia nervosa as weight loss
leads to size disproportion between left ventricle and mitral valve.118
Laboratory evaluation118: Laboratory evaluation of anorectic should include the following,
1) Complete blood count
2) Electrolytes
3) Magnesium, calcium, phosphorus, urea nitrogen, creatinine, glucose and albumin.
4) Measuring FSH, LH, TSH and prolactin can be helpful in evaluating the cause of
amenorrhea.
5) Electrocardiogram is especially important in patients who are bingeing and purging and
who have metabolic abnormalities.
6) Bone densitometry should be considered to assess severity of bone loss especially if results
will affect the treatment.
Physical examination
Bulimics generally look healthy.
1) Patient will have erosions of teeth and or with many fillings.
2) Parotid gland hypertrophy
3) Examination of the patient's fingernails may disclose abnormalities related to the use of
fingers to initiate purging. Russell's sign where hypertrophy of knuckles from inducing
vomiting.
4) Peripheral edema
5) Rectal prolapse
Laboratory evaluation:
It shows hypokalemia, hypochloremic metabolic alkalosis.
Treatment:
Anorexia nervosa
The primary goal in the treatment is weight restoration of 90% of predicted weight
unfortunately most patients resist this goal. The physician should attempt to engage the
patient in treatment by eliciting the patients concern (eg; about osteoporosis, weakness,

fertility). If possible educate the patient regarding importance of normalizing nutritional

Status. Initial treatment is determined by patient's current weight, rapidity of recent weight
loss and severity of medical and psychological complication. Hospitalization is considered
for patients weighing less than 75% of expected, even if results of routing blood studies are
within normal limits. Acute medical problems like severe electrolyte imbalance should be
identified. Nutritional restoration by oral and parenteral method. For severely underweight
patients approximately 1500-1800Kcals/day should be provided initially in divided meals as
food or liquid supplements. Calories can then gradually increased to achieve a weight gain of
l-2Kg per week, required intake of 3000-4000Kcals/day. All patients should receive
multivitamins with iron and calcium, zinc supplements at 50mg daily is well tolerated and
may facilitate weight gain and improve affective symptoms. Metoclopramide may be helpful
if patients complain of abdominal bloating. Psychiatric treatment focuses on emotional
support and development of self-esteem for satisfying personal relationship and attainment of
reasonable academic and occupational goals. Less severely affected patients may be treated in
a partial hospitalization-program where medical and psychiatric supervision is available and
several meals can be monitored each day.119
Management of Bulimia nervosa
Cognitive behavioral therapy has emerged as the most effective therapy for bulimia nervosa
when compared to other psychological treatments and to medications (antidepressants). Non
depressed bulimics are generally treated first with cognitive behavior therapy; medication is
added if they continue to binge or purge. Walsh et al compared cognitive behavioral therapy
with psycho dynamically oriented supportive psychotherapy and also assessed whether
adding benefits. They found that cognitive behavioral therapy was superior to supportive
psychotherapy in reducing the number of binge/purge episodes and in increasing the
percentage of individuals becoming binge/purge free. Adding medication (either fluoxetine or
imipramide) to cognitive behavioral therapy was superior to cognitive behavioral therapy
alone.120
Medications:
Early studies suggested that imipramide was helpful in the treatment of bulimia nervosa.
More recently fluoxetine has emerged as an effective medication in bulimia. Two randomized
trials support the superiority of fluoxetine over placebo, although the dose of fluoxetine that

was effective was 60mg was significantly higher than the dose typically used for depression
20mg.
Cancerophobia:
Phobia- fear or anxiety that exceeds normal proportions or that has no basis in reality, a
obsessive or irritational dread.121 Cancerophobia is term frequently used when a patient
belives that innocuous pathology signs and symptoms of harmless disorders or even normal
anatomical features. Example fungiform papillae frequently causes this anxiety. It is a
persistent fear in the patients mind that they have contacted oral cancer these are usually well
read, educated patients who constantly change their toothpaste often use a multitude of
mouthwashes and are in general very finicky about the oral hygiene, but at the same time they
go from dentist to dentist seeking reassurance that all is fine. This has been noted to be
associated with depression.122.What is described clinically as cancerophobia can mild fears
that symptoms are suggestive of this to frank phobia. The former is a quite common and one
reinforced by health education propaganda, but after appropriate detailed examinations, for
the majority of patients reassurance is all that is required. It is apparent that significant
minorities dont accept reassurance and hence must be considered a suffering from true
phobic state. The latter patients need referral to a psychiatric or clinical pathologist for further
assessment and specific treatment. It is worth nothing that, if
symptoms persist referral by the dentist should be easily, not late, for this will not relieve
present symptoms, but will avoid further deterioration in the psychological state. 123 Creagan
ET in 1999 have given a wonderful review of the relationship between psychosocial,
emotional and attitudinal factors and aggravation of malignancy. They have left the debate
open with a note that the strong effect on different medical conditions cannot be ignored. 124
Rogus et al in 1999 have determined that edentulous patients after cancer treatment have
more psychological disturbances and these may complicate compliance with prosthetic
appliances. Bocca M et al in 1999 in their study of 28 oral cancer patients found almost all
subjects revealed the presence of anxiety symptoms and 60% of the subjects were affected by
minor depression.
Pyostomatitis vegetans:
Pyostomatitis vegetans is an uncommon inflammatory disease of oral cavity.36 The lesions of
oral pyostomatitis vegetans were first described as rare inflammatory disease of oral mucosa.
The cause of the disease is unknown, but pyostomatitis vegetans is consistently associated

with inflammatory bowel disease. Pyostomatitis vegetans is an oral ulcerative condition that
is considered to be highly specific marker for inflammatory bowel disease.125
History:
In 1949, McCarthy described three cases of extremely rare mouth conditions, two of whom
suffered from chronic ulcerative colitis. Another three patients were observed who had colitis
and presented the characteristic lesions of the oral cavity.126In 1963 McCarthy and Shklar first
described the syndrome of pyostomatitis vegetans and ulcerative colitis. They coined the term
"pyostomatitis vegetans" because the oral lesions resemble both macroscopically and
microscopically the skin lesions of pyodermite vegetans of Hallopeau, a variant of
phemphigus vegetans (Lever and Schaumberg, 1975). McCarthy also described it as
pyoderma vegetans, is an unusual pustular and vegetating condition of skin that may affect
the axilla, genital region and occasionally face and scalp. In two of the two original five cases
described by Hallopean, lesions were also described in the mouth.36
Etiology: 126
The cause of the disease is unknown, McCarthy and Shklar in 1963 suggested that
psychosomatic factors might be involved. Pyostomatitis vegetans has been described in great
detail by McCarthy and Shklar who pointed out that the oral lesions are one part of a
syndrome in which the patient also manifests ulcerative colitis and other GITdisturbances.111
In fact the history of colitis or GIT disturbance often points to diagnosis of oral lesions.
Regional enteritis or regional ileitis also known, as Crohn's disease is a granulomatous
inflammation of intestine of unknown etiology, which may be, associated with pyostomatitis
vegetans. This has been described by Cataldo and his associates who illustrated a case in
which the oral lesions ultimately led to the diagnosis of the intestinal disease.127

Oral manifestations:
No gender predilection has been reported and most cases range in age group of 15 to 47
years. The development of pyostomatitis vegetans usually follows the onset of inflammatory
bowel disease, and oral lesions regress when colitis is controlled. The oral lesions of
pyostomatitis vegetans (PV) are composed of large number of small, closely set papillary
projections with a broad base, usually on an intensely erythematous mucosa. Although the
small projections are red to reddish-pink, they may show tiny yellow pustules beneath the
epithelium. The lesions are painless. These lesions may occur in any part of oral cavity,

although tongue involvement appears to be uncommon. These tiny pustules beneath the
epithelium, which liberated purulent material when ruptured. These leave areas of ulceration,
which may coalesce, into large areas of ulceration.128 The lip and check mucosa are diffusely
swollen and inflamed, with deep fissure like ulcerations separating papillary projections of
mucus membrane. The gingival and palatal mucosa may also be involved. The submandibular
lymph node are swollen and tender and the patient may be pyrexic. The lesions develop over
period of six to eight weeks This is the only disease known to produce oral pustular
eruptions. The buccal mucosa is most commonly involved which presents as "cobble stone
appearance" while vestibular lesions appear as folds and ulcers. Lips appear to be swollen
and indurated, palatal lesions appear as multiple apthous ulcers. The chief complaint is
usually eruptions in mouth. The lesions may be present or month before the patient seeks
professional attention, and occasionally they may be found on routine examination. The
lesions rang in size from 2 -3mm, later confluency develop lesions on extensive areas of oral
mucosa, when the purulent discharge is wiped away it may express a hemorrhagic surface.
Serpentine pustules set on an erythematous mucosa termed as "snail tract ulcerations",
although in most instances the lesions are probably not truly ulcerated. The oral discomfort is
variable which may be related to the number of pustules that have ruptured to form ulcers.
The oral lesions may appear concurrently with the bowel symptoms or they may precede the
intestinal involvement.127 Pyostomatitis vegetans, a purulent inflammation of the mouth, may
also occur. These oral lesions are characterized by deep-tissue vegetating or proliferative
lesions that undergo ulceration and then suppuration. As the lesions disappear with total
colectomy, it is speculated that these manifestations are due to the effects of circulating
immunocomplexes induced by antigens that are derived from the gut lumen or the damaged
colonic mucosa.36
Differential diagnosis:
A diagnosis is possible only if following can be ruled out.
Generalized papillomatosis of oral mucosa
Crohns disease
Vesicular eruption like pemphigus vegetans
Viral and fungal infections
Systemic drug reactions
Allergic reactions such as erythema multiforme.

Management
The treatment is non specific, since the oral lesions are refractory to antibiotic therapy. It has
been found that the oral lesions tend to regress when the intestinal disturbances is brought
under control. However exacerbation of the GIT frequently results in exacerbation of the oral
lesions as well.129
MANAGEMENT OF PSYCHOSOMATIC ORAL DISEASES AND
NEUROTIC ORAL SYMPTOMS: 130
Pharmacotherapy
Many different psychiatric conditions are worsened by stressors. When major psychiatric
conditions like depression or psychosis are present, the most appropriate medications are
those for the Axis I diagnosis. However, more typically the picture is primarily one of anxiety
or, insomnia, perhaps not of as great a magnitude as that found typically in anxiety disorder,
but still very distressing to the patient in such settings pharmacological therapy with
anxiolytics or short-term hypnotic agents can be extremely helpful. 130 The field has lurched
from olle extreme to another in terms of prescription of such medication. Clearly, the
unsupervised long-term prescription of this type of medication brings with it risks for drug
dependence on the other hand, depriving patients of such medication. When they are in crisis
is unconscionable. Short-term use of low dose benzodiazepines is of considerable utility in
helping patients struggle with unusual stressors. This interventional in association with
supportive psychotherapy is extremely effective in crisis intervention.131 In psychosomatic
oral diseases, the placebo effect of systemic medicaments or locally applied ointments cannot
be discounted; in many instances it appears to be responsible for successful therapy. Whatever
medicament is to be used, it should be given to the patient with a positive approach.
Corticosteroid creams or ointments are helpful in oral ulcerative disease because they are
anti-inflammatory and relieve some of the painful sensations, so that the patient is convinced
initially that the substance will be helpful. If there is no response to the agent used, the patient
should be told that this agent does not work in all cases and that other agents may be more
successful in his particular case. If there is no response to any agents used and the patient's
complaints are severe, the anxiety factor can be discussed with the patient and antianxiety
drugs prescribed or psychiatric consultation suggested. 130When we believe that a significant
emotional factor is part of the etiology of a disease, we present this concept to the patient in
most cases such patients are relieved to know that they are affected with a "disease of

civilization" rather than an infection or neoplasm. We point out to the patient that "neurotic is
normal," that we are all neurotic to varying degrees, but that each person's subconscious
responds to emotional stress in different ways. This person's subconscious has "selected" the
mouth as a target area for me resolution of stress. The patient is told that his condition is one
that he will have to learn to live with for a prolonged period of time, and that treatment may
help to alleviate the severity of the lesions and the painful symptoms but may not completely
cure the disease or prevent recurrences. This approach is particularly applicable to oral lichen
planus of the bullous or erosive type.132 Recurrent herpes labialis can often be prevented if the
patient is told to rub some corticosteroid-antibiotic ointment, such as Terra-Cortril, into the
labial mucosa about 24 hours before the lesions erupt Most patients are aware of the probable
onset of disease by a tingling sensation that is a prodromal manifestation of herpes labialis.
Once the lesions have developed, the ointment may help to reduce discomfort, but it will not
significantly alter the course of the disease.133 Psychosomatic oral diseases do not appear to be
helped by tranquilizing or antianxiety drugs. Neurotic symptoms, on the other hand, may be
alleviated by the antianxiety
drugs. We have used agents such as those in the following list meprobromate (Miltown,
Equanil), 200 to 400 mg tid or qid diazepam (Valium), 2 to 5 mg tid or qid chlordiazepoxide
(Librium), 5 to 10 mg. qid oxazepam (Serax), 10 to 15 mg qid hydroxyzine (Atarax, Vistaril),
25 to 50 mg qid.134 These drugs seldom have serious side effects and are relatively safe. All of
these drugs can produce drowsiness and patients should be warned of this, particularly if they
drive car. Or are employed in occupations requiring alertness. These drugs should not be
prescribed to pregnant women owing to possible teratogenic effects, and they should not be
prescribed if the patient is also taking a CNS depressant or is an alcoholic. If the patient
suffers from insomnia and inflicts the oral trauma during these hours of half-sleep, various
sleeping preparations can be prescribed to be taken before retiring for the night We usually
prescribe flurazepam (Dalmane), 15 to 30 mg, or chloral hydrate, 500 mg (.5 gm).135 For
muscle pains or spasms caused by clenching or grinding of teeth, methocar bamol (Robaxin),
750 mg qid, is often helpful. Diazepam (Valium), 2 to 5 gm qid, may also be used for its
muscle relaxant effect as well as for its tranquilizing action. A single tablet of diazepam, 5
mg, or flurazepam, 30 mg, can be helpful if taken before bedtime.136
Cognitive-Behavioral Therapy: 116, 31
Cognitive-behavioral therapy methods are increasingly used to help individuals better
manage their responses to stressful life events. "These treatment methods are based on the

notion that cognitive appraisals of stressful events and the coping efforts related to these
appraisals play a major role in determining the response to stress. 137 A model of stress and
coping has been developed that serves as the conceptual foundation for most cognitivebehavioral stress management protocols. This model maintains that there are two types of
cognitive appraisal that are especially important in mediating reactions to stress. The first
primary appraisal, refers to the way in which an individual evaluates the significance or
meaning of a given event. When events (e.g., being diagnosed with a chronic illness such as
rheumatoid arthritis) are appraised as harmful and threatening (e.g., "Because of my
rheumatoid arthritis, I will never be able to do anything i really care about"), the individual is
more likely to become anxious, depressed, and withdrawn. However, If the same event is
viewed as challenging (e.g., Although my arthritis prevents me from doing some physically
demanding activities, there are many other important and meaningful activities that I can do
and enjoy"), then more positive outcomes are more likely to occur. Secondary appraisal refers
to the process of evaluating what can be done about the stressful event. Several factors can
influence such secondary appraisals including the breadth of individuals' repertoire of coping
skills, their mastery of specific coping skills and their expectation that their skills will be
effective. Cognitive-behavior therapy approaches to stress management have three major
aims. The first aim is to help individuals become more of their own cognitive appraisals of
stressful events. The third aim is to teach individuals how to develop and maintain the use of
a variety of effective cognitive and behavioral stress management skills. Self-observation one
of the most effective ways of helping individuals become more aware of how they respond to
problem situations is to have them keep a daily record of their behavior. A daily diary format
is often used with patients being asked to keep a record of how they responded to challenging
or stressful events that occurred each day. Entries are made in three columns: antecedents,
behaviors, and consequences. In the "antecedents" copatients record a specific environmental.
The event might be an interpersonal stressor such as having an argument with a spouse or a
confrontation with a coworker, or an intrapersonal stressor such as a flare in pain symptoms,
or a major natural disaster. To assess appraisals of the stressor, patients are asked to rate how
stressful they found this event on a 0 to 100 scale (e.g., 0 = not at all stressful; 100 = the most
stressful event I have ever experienced). In the column marked behavior, patients are
instructed to record their cognitive and behavioral reactions to the stressful event. The term
"behavior" is broadly divided so that it not only encompasses overt behavioral responses, but
also more covert cognitive, affective, and physiological responses. Thus, in the behavioral
response column individuals might indicate specific coping behaviors they engaged in (e.g.,

avoidance), cognitve(: responses to the stressor, negative emotions (e.g., anxiety, depression),
and physiological responses (e.g., increased sweating, heart rate, or nausea). In the column
marked "consequences," patients record the outcomes resulting from their behavior in this
situation. Self-observation is effective for several reasons. First, it makes individuals aware of
behaviors that they usually fail to notice. An individual whose style of dealing with social
anxiety is to use avoidance, for example, may avoid potentially stressful situations in a more
or less automatic fashion (e.g., routinely refuse invitations), use very subtle forms of
avoidance (e.g.. aniving late or leaving a party early), or arrange their lifestyle (e.g., work
alone) so that they have very few chances to confront their fears. Participants who keep daily
diaries are often struck by the variations in their own reactions across different events. For
example, while they may cope effectively with one stressful event (e.g., meeting an important
work deadline), they find themselves unable to deal with another stressful event (e.g., an
argument with their teenage son or daughter). Self observation highlights the role that coping
efforts, cognitive appraisals, and physiological responses play in explaining these very
different responses to stressful situations. Interestingly, individuals who keep daily diary
records of stress-related behaviors often make changes in their own behavior, even before
other stress management methods are introduced.
Cognitive restructuring: A hallmark of cognitive-behavioral therapy is its insistence that
cognition plays a central role in the stress and coping process. In cognitive behavioral therapy
cognitive appraisals about stressful events are considered to be the key factor in determining
stress-related responding. Given this emphasis on cognition, it is not surprising that a major
thrust of cognitive-behavioral therapy approaches to stress management is on helping
participants to become aware of and to change their maladaptive thoughts, beliefs, and
expectations. Cognitive therapists have developed protocols for helping distressed individuals
restructure dysfunctional, emotional reactions that are excessive or prolonged are often the
result of cognitions that are distorted or dysfunctional. The second step in cognitive
restructuring is monitoring and analyzing dysfunctional thoughts. As can be seen, each of
these thoughts can be linked to a negative emotion. A careful analysis of each thought also
reveals an inherent error in logic certain types of errors cognitive distortion, occur quite
frequently and individuals can thus be taught to recognize them. 135 The third step in cognitive
restructuring is to challenge and change cognitive distortions. Participants are often provided
with a list of key questions that can be applied to their own negative thoughts. They are asked
to select one or two questions that are useful in identifying the underlying logical problems in

their thinking. Finally, participants develop a rational response that represents a more accurate
and helpful cognitive response to the situation. If the rational response is to be effective, it
must be used frequently, ideally each time the negative thought occurs. To ensure that this
occurs, patients are given home practice assignments which they are asked to expose
themselves to stressful events, monitor their negative thoughts, and respond with a more
rational thought pattern. They are also asked to keep records of the resulting consequences,
both in terms of changes in emotions and behaviors.
Relaxation Training: 137
Relaxation skills can be very helpful in managing Stressful individuals to learn to relax; their
overall muscle tension is reduced, as is their overall level of autonomic arousal. In the 1920s
Edmund Jacobson developed progressive relaxation training as a way to help individuals to
control excessive muscle tension. Jacobson approached relaxation as a motor skill and
emphasized that, like any skill, repeated practice was necessary for skill mastery. In
traditional Jacobsonian relaxation training the goal is to heighten an individual's awareness of
very low levels of muscular tension. The patient is instructed to focus on sensations that
occur when tensing a single large muscle group (e, g the forearm flexors-tensed by bending
the left hand back at the wrist). The individual if then instructed to release the tension in that
muscle pull and study the resulting physical sensations. Traditional Jacobson relaxation
training is effective: however, it does require a substantial time commitment on the part of the
participant.137 in the 1950s Jacobsonian relaxation training was modified by behavior
therapists so that it could be more easily incorporated into treatment programs. The modified
training program was similar to Jacobson's in emphasizing that relaxation could be achieved
by using a series of exercises involving tensing and relaxing muscle groups, but differed in
that it, was much briefer. Numerous modified versions of Jacobson's original method have
been developed and refined over the years. One of the most important tasks in relaxation
training is helping patients learn how to generalize their skills in relaxation from home
practice sessions to stressful and demanding daily life events. Several techniques are used to
enhance generalization. The first is a method developed by Jacobson called differential
relaxation. In differential relaxation, the trainee is instructed to engage in a daily task and
only use the muscles that are necessary for carrying out the task. For example, while writing
one's name there needs to be activity in muscles of the hands and arms, but the muscles in the
face, lower trunk, legs, and feet can be deeply relaxed. Differential relaxation is initially
practiced in relatively easy situations (e.g., siuing or standing) where the demands are

minimal. Over time, however, patients learn how to use differential relaxation in situations
that are challenging and stressful. A seconn generalization method is termed the minipractice.
This consists of a brief relaxation procedure in which the trainee takes a deep breath, and then
while slowly exhaling focuses on sensations of relaxation flowing downward from the
muscles of the face to those of the neck, shoulders, trunk, and legs. The minipractice takes
approximately 30 seconds and thus can be done repeatedly over the course of a day.
Individuals are encouraged to develop innovative reminders to make themselves to perform
frequent minipractices every day. As individuals increase this frequency, they often report
that relaxation becomes more or less an automatic and habitual.
Time Management
A stressful event, (e.g., caring for a sick child), can place inordinate demands on time. When
exposure to such an event is prolonged oris combined with exposure to other stressors, the
demands on time and energy are multiplied. In such circumstances individuals often report
feeling that they have lost control of their daily activities. The first step in training in time
management skills is designed to enhance awareness of current patterns of time use. To
accomplish this goal, individuals might be asked to keep a record of how they spend their
time each day, noting the amount of time spent in important categories such as work, family,
exercise, or leisure activities. Alternatively, they may be asked to list the important areas-in
their lives and then asked to provide two time estimates: (1) the amount of time they currently
spend engaging in these activities, and (2) the amount of time they would like to spend'
engaging in these activities. 'Frequently, there is a substantial difference in the time
individuals would like to spend on important activities and the amount of time they actually
spend on them. With awareness of this difference comes increased motivation to make
changes.138 The second step in time management is designed to help individuals set their
priorities. In setting priorities an important distinction can be drawn between urgency and
importance. To explore this distinction it is helpful to envision a table that has the dimension
of importance along one axis and the dimension of urgency along the other axis. Patients are
then encouraged to enter into each quadrant of the table examples of activities from their own
lives and to reflect on the patterns they observe. Individuals may note that much of their time
is spent doing activities that are in the Urgent-Not important quadrant or the Not Urgent-Not
Important quadrant. Alternatively, they may report that they spend little or no time engaging
in activities in the Not Urgent- But Important quadrant. Patients are encouraged to discuss the
benefits that can come from increasing the priority they give to such important but less urgent

activities as exercising, resting, relaxing, or doing volunteer work. They are also encouraged
to try to match the time spent engaging in such meaningful activities with the priority they
place on the activity. Once participants have developed a better sense of their priorities, they
are ready to move on to the third step in time management: goal setting. Goal setting focuses
on specific behavior change targets that fit with an individual's long-term priorities. First, the
individual is asked to identify a goal to be accomplished in the next week. The goal, for
example might be to lose 2 pounds or to sign up for an exercise program. Second. Patients are
asked to critically analyze the goal to ensure that it is reasonable, specific, and personally
meaningful. Many of us set unrealistic goals (e.g.. losing 10 pounds in a week) when trying to
change our own behavior and as a result fail, feel frustrated, and give up. In the third step of
goal setting, individuals are asked to reconfirm a time frame (e.g., a week) in which they will
meet the goal. This step is important in reducing procrastination, a common obstacle to
effective time management the individual's efforts in reaching the goal are reviewed. Even if
the goal was not achieved, important information about goal setting can be achieved by
reviewing performance.
Problem Solving:
Problem solving is a skill that is introduced in the later stages of stress management training.
As trainees attempt to apply what they have learned about stress management, they may find
that some problem situations are particularly challenging and difficult to manage using only
one or two stress management techniques. Problem solving involves several basic steps. The
first is problem identification during which the key problematic aspects of a stressful event
such as problematic behaviors, thoughts, feelings, and physiological responses are identified.
For example, dealing with the aftermath of a hurricane may be perceived as stressful because
it is associated with particular (1) behavioral problems-having to clean up while
simultaneously caring for one's children, (2) overly negative thoughts-"We will never recover
from responses-muscle tension, fatigue, and sleep problems. Helping an individual
understand the various facets of their problematic responses is often helpful because it
suggests what skills might be particularly useful. For example, if the problem is mainly a
somatic one (Increased tension) relaxation-based strategies may be the most effective. The
second step in problem solving is generatim alternatives. Brainstorming is used to generate a
wide range of alternative problem solution. The rule of brainstorming include: (1) the
individual should offer as many solutions as they can. Even if the solutions do not
immediately seem reasonable; (2) no criticism is allowed: and (3) there should be an attempt

to mix and match solutions in creative ways. One reason that brainstorming is effective in
problem solving is that because of its rules it reduces
the tendency to prematurely judge and reject possible coping options. Using this approach a
participant can often generate a list of 5 to 10 potential solutions. The third step in problem
solving involves evaluating the alternatives and selecting the best solution. To begin this
process a participant can be asked to rate the likelihood that each solution will have a positive
outcome. It is often helpful to discuss some of the factors that influence how the participant
makes these ratings. This case history demonstrates the confluence of adverse life events,
physical illness and emotional distress and the pharmacologic and psychotherapeutic
treatment of stress-related psychopathology.116,31
CONCLUSION
Knowledge of the basic psychology is fundamental for effective and efficient practice in that
it helps the doctor in management of both. The fear that most patients have, as well as this
varied group of oral disorders result from the interaction of soma and the psyche. A
knowledgeable dentist a should be able to recognize and refer the selected cases to
psychiatrist and use the services of the medical social worker in long term follow up and total
health care to his patient.

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