PROBLEM 1

GASTROINTENSTINAL SYSTEM BLOCK

Agustina Cynthia Cesari S
405140066
 LO 1
ANATOMY, PHYSIOLOGY, HISTOLOGY,
BIOCHEMISTRY
ANATOMY
Mouth
 TheVestibule (vestibulum oris) is a slit-like space, bounded
externally by the lips and cheeks, internally by the gums and
teeth.
 It communicates with the surface of the body by
the rima or orifice of the mouth.
 Mouth Cavity Proper (cavum oris proprium) is bounded
laterally and in front by the alveolar arches with their
contained teeth; behind, it communicates with the pharynx
by a constricted aperture termed the isthmus faucium.
Mucous Membrane
 Lining the mouth is continuous with the integument at the
free margin of the lips, and with the mucous lining of the
pharynx behind
 It is of a rosepink tinge during life, and very thick where it
overlies the hard parts bounding the cavity.
 It is covered by stratified squamous epithelium.
Lips (Labia Oris)
 Two fleshy folds which surround the rima or orifice of the mouth
 externally of integument
 internally of mucous membrane
 There are :
 Orbicularis oris muscle
 the labial vessels
 some nerves, areolar tissue, and fat, and numerous small labial glands.
 The inner surface of each lip  corresponding gum by a fold of
mucous membrane, the frenulum—the upper being the larger
Cheek (Buccae)
 form the sides of the facecontinuous in front with the lips.
 External :integument
 Internal :mucous membrane; and between the two of a
muscular stratum, besides a large quantity of fat, areolar
tissue, vessels, nerves, and buccal glands.
Gums (gingivoe)
 Composed of dense fibrous tissue
 Closely connected to the periosteum of the alveolar
processes, and surrounding the necks of the teeth.
 Covered by smooth and vascular mucous membrane.
 Around the necks of the teeth this membrane presents
numerous fine papillæ, and is reflected into the alveoli,
where it is continuous with the periosteal membrane lining
these cavities
Palatum
 Hard Palate (Palatum  Soft Palate (Palatum Molle) :
Durum) : front back
 covered by a dense structure  is a movable fold
 formed by the periosteum  suspended from the posterior
and mucous membrane of the border of the hard palate, and
mouth, which are intimately forming an incomplete
adherent. septum between the mouth
 it is covered with stratified and pharynx.
squamous epithelium, and  It consists of a fold of mucous
furnished with numerous membrane enclosing
palatal glands lie between muscular fibers, an
the mucous membrane and aponeurosis, vessels, nerves,
the surface of the bone. adenoid tissue, and mucous
glands.
Teeth (dentes)
 The deciduous teeth/milk teeth 
20four incisors, two canines, and
four molars, in each jaw.
 The permanent teeth 32four
incisors, two canines, four premolars,
and six molars, in each jaw.
Tongue (Lingua)
 Function:
 organ of the sense of taste
 of speech
 assists in the mastication and deglutition of the food.
 It is situated in the floor of the mouth, within the curve of the
body of the mandible.
 Classification:
 Root :directed backward, and connected with the hyoid bone by the
Hyoglossi and Genioglossi muscles and the hyoglossal membrane1
 Apex :directed forward against the lingual surfaces of the lower
incisor teeth.
 Dorsum :is convex and marked by a median sulcus, which divides it
into symmetrical halves
 Extrinsic Muscle:
 M. hyoglosus, genioglossus dan styloglossus for
mastication,to make the food that we eat become a solid mass,
guide the food to the posterior to be swallowed
 Intrinsic Muscle:
 M. longitudinalis superior, longitudinalis inferior,lingualis
transversus dan lingualis vertikalisTo control the tongue on
speech and swallowing system
Salivary Gland
 Parotid  Stensen’s duct  oral cavity dealing with Molar II
 Submandibula Wharton’s duct  lateral frenulum
lingualis
 Sublingual  Rivinus’ duct  posterior papilla manibularis’
duct
Laring and Pharing
 Food  was swallowed  pharing
 Pharing : composed by skeletal muscle and coated by
mucosal membrane 3 parts: nasofaring,
orofaring,laringofaring.
 Nasofaring’s function only for respiratory system.
 Orofaring and laringofaring also have function for digestion
system  contraction  propelling the food to
esophagus gaster
PHYSIOLOGY
Digestive system
 The primary function of the digestive system: to transfer
nutrients, water and electrolytes from the food we eat into
the body’s internal environment
 There are four basic digestive processes:
 Motility
 Secretion
 Digestion
 Absorption
Basic digestive processes
 Motility: muscular contractions that mix and move forward
the contents of the digestive tract
 Secretion: a number of digestive juices secreted into the
digestive tract lumen by exocrine glands along the route,
each with its own specific secretory product. Each digestive
secretion consists of water, electrolytes, and specific organic
contituents important in the digestive process, such as
enzymes, bile salts, or mucus.
 Digestion: biochemical breakdown of the structurally
complex foodstuffs of the diet into smaller, absorbable units
by the enzymes produced within the digestive system
 Absorption: in the small intestine, digestion is completed and
most absorption occurs. Through the process of absorption,
the small absorbable units that result from digestion, along
with water, vitamins, and electrolytes, are transferred from
the digestive tract lumen into the blood or lymph
Digestive system
 The digestive system consists:  Acessory digestive organs:
 Digestive tract  Salivary glands
 Accessory digestive organs  Exocrine pancreas
 Digestive tract:  Biliary system (liver and
 Mouth galbladder)
 Pharynx
 Esophagus
 Stomach
 Small intestine (duodenum,
jejunum, and ileum)
 Anus
Digestive tract wall
 The digestive tract wall has the same general structure
through-out most of its length from the esophagus to the
anus, with some local variations characteristics for each
region
 From the innermost layer outward they are:
 Mucosa
 Submucosa
 Muscularis externa
 Serosa
Regulation of digestive function
 Digestive motility and secretion carefully regulated to
maximize digestion and absorption of ingested food
 Four factors are involved in regulating digestive system
function:
 Autonomous smooth muscle function
 Intrinsic nerve plexuses
 Extrinsic nerves
 Gastrointestinal hormones
 The digestive tract wall contains three types of sensory
receptors that respond to loval changes in the digestive tract:
 Chemoreceptors sensitive to chemical components within the
lumen
 Mechanoreceptors sensitive to stretch or tension within the
wall
 Osmoreceptors sensitive to the osmolarity of the luminal
contents
Mouth (motility)
 Entry to the digestive tract is through the mouth or oral
cavity
 The first step in the digestive process is mastication, or
chewing, the motility of the mouth that involves the slicing,
tearing, grinding, and mixing of ingested food by the teeth
 The functions of chewing are:
 To grind and break food up into smaller pieces to facilitate
swallowing and to increase the food surface area on which
salivary enzymes will act
 To mix food with saliva
 To stimulate the taste buds
Mouth (secretion)
 Saliva, the secretion associated with the mouth, is produced
largely by three major pairs of salivary glands that lie outside
the oral cavity and discharge saliva through short ducts into
the mouth
 Saliva is about 99,5% H2O and 0,5% electrolytes and
protein
 The most important salivary proteins are amylase, mucus,
and lysozyme
Mouth
Digestion Absorption
 Digestion in the mouth  No absorption of foodstuff
involves the hydrolysis of occurs from the mouth
polysaccharides into  Importantly some drugs
diaccharides by amylase can be absorbed by the oral
mucosa, a prime example
being nitroglycerin
Pharynx and esophagus (motility)
 The motility associated with the pharynx and esophagus is
swallowing
 Swallowing is the entire process of moving food from the
mouth through the esophagus into the stomach
Esophagus (secretion)
 Esophageal secretion is entirely mucus
 Mucus is secreted throughout the length of the digestive tract
by mucus-secreting gland cells in the mucosa
 By lubricationg the passage of food, esophageal mucus lessens
the likelihood that the esophagus will be damaged by any
sharp edges in the newly entering food
 Furthermore, it protects the esophageal wall from acid and
enzymes in gastric juice if gastric reflux occurs
Esophagus (digestion & absorption)
 The entire transit time in the pharynx and esophagus
averages a mere 6-10 seconds, too short a time for any
digestion or absorption in this region
HISTOLOGY
Tongue
Teeth

Blood vessels - carry nutrients to the tooth.

Bone - alveolar bone forms the tooth socket and provides it with
support.
Cementum - the layer of hard bone-like tissue covering the root
of the tooth.
Cemento-enamel junction - the line where the enamel and
cementum meet.
Dentin - the hard yellow tissue underlying the enamel and
cementum, making up the main bulk of the tooth.
Enamel - the hard, white outer layer of the tooth.
Gingiva - the gum tissue surrounding the tooth.
Ligament - the connective tissue that surrounds the tooth and
connects it to bone.
Nerves - relay signals such as pain to and from your brain.
Pulp - located in the center of the tooth, it contains the arteries,
veins and nerves.
Root canal - canal in the root of the tooth where the nerves and
blood vessels travel through.
Teeth Circumvallatae Papillae
GI-Tract
 The gastrointestinal tract has 4 distinct functional layers :
 Mucosa :
 Made up of three components :
 Ephitelium  supporting lamina propria and a thin muscle layer the muscularis mucosae 
produces local movement and folding of the mucosa.
 Undergoes abrupt transition from one form to another  the gastro-esophageal junction, the
gastroduodenal junction, the ileocaecal junction and the rectoanal junction.
 Submucosa :
 Layer of loose collagenous connective tissue supports the mucosa.
 Contains : the larger blood vessels, lymphatics and nerves.
 Muscularis propria :
 Muscular wall proper consists of smooth muscle that is usually arranged as an inner circular layer and an
outer longitudinal layer.
 In the stomach only  inner oblique layer of muscle.
 The action of the two layers, at right angles to one another  basis of peristaltic contraction.
 Adventitia :
 Outer layer of loose supporting tissue conducts  the major vessels, nerves and contains variable adipose
tissue.
 The gut lies within the abdominal cavity (peritoneal cavity), the adventitia is referred to as the serosa
(visceral peritoneum) and is lined by a simple squamous epithelium (mesothelium).
 Elsewhere  the adventitial layer merges with retroperitoneal tissues.
 Esophagus

Wheater’s functional histology p.255

Esophagus
 Esophagus

Wheater’s functional histology p.255

 Esophago-gastric junction

Wheater’s functional histology p.256

BIOCHEMISTRY
Biochemistry
Biochemistry
 Saliva is the watery and  Saliva is composed of:
usually frothy substance  Ions (Na+, K+, Ca2+, F¯,
produced in the mouths of Mg2+, PO43-, HCO3¯)
humans.  pH (6.2 – 8.0)
 Saliva is produced in and  Glycoprotein (Mucin)
secreted from the salivary  Digestive enzymes (alpha-
glandsmostly of water, amylase, lipase)
but also includes  Antibacterial agents
electrolytes, mucus, (thiocyanate,
antibacterial compounds, sialoperoxidase, lysozyme,
and various enzymes. lactoferrin)
 Immunoglobulins
 LO 2
PHYSIOLOGY OF SWALLOWING
Swallowing
 Swallowing initiated when a bolus, or ball chewed or liquid
food, is voluntarily forced by the tounge to the rear of the
mouth into the pharynx
 The pressure of the bolus stimulates pharyngeal pressure
receptors, which send afferent impulses to the swallowing
center located in the medulla of the brain stem
 Swallowing is divided into the oropharyngeal stage and the
esophageal stage
Oropharyngeal stage
 When the bolus enters the pharynx, it must be directed into
the esophagus and prevented from entering the other
openings that communicate with the pharynx
 The esophagus is guarded at both ends by sphincters.
 The upper: pharyngesophageal sphincter
 The lower: gastroesophageal sphincter
 Except during a swallow, the pharyngoesophageal sphincter
remains closed as a result of neurally induced contraction of
the sphincter’s circular skeletal muscle
 During swallowing, this sphincter opens and allows the bolus
to pass into the esophagus. Once the bolus has entered the
esophagus, the pharyngoesophageal sphincter closes.
 The oropharyngeal stage is complete
The esophageal stage
 The swallowing center triggers a primary peristaltic wave
that sweeps from the beginning to the end of the esophagus,
forcing the bolus ahead of it through the esophagus to the
stomach
 The term peristalsis refers to ringlike contractions of the
circular smooth muscle that move progressively forward,
pushing the bolus into a relaxed area ahead of the contraction
 Except during swallowing, the gastroesophageal sphincter,
which is smooth muscle in contrast to the upper esophageal
sphincter, stays tonically contracted by means of myogenic
activity to maintain a barrier between the stomach and
esophagus
 As the peristaltic wave sweeps down the esophagus, the
gastroesophageal sphincter relaxes so that the bolus can pass
into the stomach
 The swallow is complete and this lower esophageal sphincter
again contracts
 LO 3
TERMINOLOGY AND
PATHOPHYSIOLOGY OF SWALLOWING
DIFFICULTY (DYSPHAGIA AND
ODYNOPHAGIA)
Swallowing difficulty
 Dysphagia is difficulty with swallowing refers to problems
with the transit of food or liquid from the mouth to the
hypopharynx or through the esophagus
 Odynophagia refers to painful swallowing, typically resulting
from mucosal ulceration within the oropharynx or
esophagus. It commonly is accompanied by dysphagia, but
the converse is not true.
 Be subclassified :
 Location: oral, pharyngeal, or esophageal dysphagia
 Circumstances in which it occurs.
 Dysphagia caused by
 an oversized bolus
 a narrow lumen is called structural dysphagiaabnormalities of
peristalsis
 impaired sphincter relaxation after swallowingpropulsive or
motor dysphagia.
 More than one mechanism may be operative in a patient with
dysphagia.
Oro-pharyngeal
 Oral-phase dysphagia is associated:
 poor bolus formation and control  prolonged retention
within the oral cavity and may seep out of the mouth.
 Poor bolus control also may lead to premature spillage of food
into the hypopharynx with resultant aspiration into the trachea
or regurgitation into the nasal cavity
 Pharyngeal-phase dysphagia is associated with retention of food
in the pharynx due to poor tongue or pharyngeal propulsion or
obstruction at the UES
Esophageal
 Solid food dysphagia  lumen is narrowed  poorly masticated
food or motor dysfunction
 Circumferential lesions are more likely to cause dysphagia than are
lesions that involve only a partial circumference of the esophageal
wall.
 The most common structural causes:
 Schatzki's rings, eosinophilic esophagitis, and peptic strictures.
 Dysphagia also occurs in the setting of gastroesophageal reflux disease
without a stricture, perhaps on the basis of altered esophageal
sensation, distensibility, or motor function.
 Propulsive disorders  abnormalities of peristalsis and/or
deglutitive inhibition, potentially affecting the cervical or thoracic
esophagus.
 LO 4
DYSPHAGIA & ODYNOPHAGIA
ACHALASIA
Achalasia
 Achalasia is a rare disease caused by loss of ganglion cells
within the esophageal myenteric plexus
 Epidemiology:
 Population incidence of about 1:100.000
 Usually presenting between age 25 and 60
Etiology
 Increasing evidence suggests that the ultimate cause of
ganglion cell degeneration in achalasia is an autoimmune
process attributable to a latent infection with human herpes
simplex virus 1 combined with genetic susceptibility
Pathophysiology
 The disease involves both excitatory (cholinergic) and
inhibitory (nitrit oxide) ganglionic neurons
 Functionally, inhibitory neurons mediate deglutitive lower
esophageal sphincter (LES) relaxation and the sequential
propagation of peristalsis. Their absence leads to impaired
deglutitive LES relaxation and absent peristalsis
 Long-standing achalasia is characterized by progressive
dilatation and sigmoid deformity of the esophagus with
hypertrophy of the LES
Clinical manifestations
 Dysphagia (solid and liquid food)
 Regurgitation, occurs when food, fluid, and secretion are
retained in the dilated esophagus, or lung abcess from
chronic regurgitation and aspiration
 Chest pain, result from esophageal spasm. Patients describe a
squeezing, pressure-like retrosternal pain, sometimes
radiating to the neck, arms, jaw, and back
 Weight loss
Differential diagnosis
 Diffuse esophageal spasm (DES)
 Chagas’ disease
 Pseudoachalasia
Examination
 Achalasia is diagnosed by barium swallow x-ray and/or
esophageal manometry
 The diagnostic criteria for achalasia with esophageal
manometry are impared LES relaxation and absent peristalsis
Therapy
 Therapy is directed at reducing LES pressure so that gravity and
esophageal pressurization promote esophageal emptying
 LES pressure can be reduced by pharmacologic therapy, pneumatic
balloon dilatation, or surgical myotomy
 Pharmacologic therapies are relatively ineffective but are often
used as temporizing therapies:
 Nitrates or calcium channel blockers are administered before eating
 Botulinum toxin, injected into the LES under endoscopic guidance,
inhibits acetylcholine release from nerve endings and improves
dysphagia
 Sildenafil and alternative phosphodiesterase inhibitors effectively
decrease LES pressure
 The only durable therapies for achalasia are pneumatic
dilatation and Heller myotomy
 Pneumatic dilatation is an endoscopic technique using a
noncompliant, cylindrical balloon dilator positioned across
the LES and inflated to a diamtere 3-4 cm
 The most common surgical procedure for achalasia is
laparoscopic Heller myotomy, usually performed in
conjunction with an antireflux procedure
Complication & prognosis
 In untreated or inadequately treated achalasia, esophageal
dilatation predisposes to stasis esophagitis
 Prolonged stasis esophagitis is the likely explanation fot the
association between achalasia and esophageal squamous cell
cancer
REFLUX ESOPHAGITIS
Reflux esophagitis
 Etiology: Reflux of gastric contents into the lower esophagus
is the most frequent cause of esophagitis. The associated
clinical condition is termed gastroesophageal reflux disease
(GERD)
Pathophysiology
 The most comon cause of gastroesophageal reflux is transient
lower esophageal sphincter relaxation. This thought to be
mediated via vagal pathways, and can be trigerred by gastric
distention, by gas or food, mild pharyngeal stimulation that
does not trigger swallowing, and stress
 Gastroesophageal reflux can also occur following swallow-
induced lower esophageal sphincter by ans abrupt increase in
intraabdominal pressure, such as that due to coughing,
straining, or benidng
 Other conditions that decrease lower esophageal sphincter
tone or increase abdominal pressure and contribute to GERD
include alcohol and tobacco use, obesity, central nervous
system depressant, pregnancy, hiatal hernia, delayed gastric
emptying, and increased gastric volume
 Reflux of gastric juices is central to the development of
mucosal injury in GERD
Clinical manifestations
 Heartburn
 Dysphagia
 Regurgitation of sour-tasting gastric contents
Therapy
 Treatment with proton pump inhibitors, which have
repleaced H2 histamine receptor antagonists, to reduce
gastric acidity typically provides sympomatic relief
Complication
 Ulceration
 Hematemesis
 Melena
 Structure development
 Barrett esophagus
DENTAL CARIES
Dental caries
 Dental caries usually begin asymptomatically as a destructive
infectious process of the enamel
Etiology and pathophysiology
 Etiology: bacteria, principally Streptococcus mutans colonize
the organic buffering biofilm (plaque) on the tooth surface. If
not removed by brushing or by the natural cleansing and
antibacterial action of saliva, bacterial acids can demineralize
the enamel.
 Fissures and pits on the occlusal surfaces are the most
frequent sites of early decay
 Overtime, dental caries extend to the underlying dentin,
leading to cavitation of the enamel
 Without management, the caries will penetrate to the tooth
pulp  acute pulpitis
 At this stage, when the pulp infection is limited, the tooth
may become sensitive to percussion and to hot or cold, and
pain resolves immediately when the irritating stimulus is
removed
 Should the infection spread throughout the pulp, irreversible
pulpitis occurs  pulp necrosis
 At this later stage, pain can be severe and has a sharp or
throbbing visceral quality that may be worse when the
patient lies down
Therapy
 Treatment of caries involves removal of the softened and
infected hard tissue and restoration of the tooth structure
with silver amaglam, glass ionomer, composite resin, or gold
 Once irreversible pulpitis occurs, root cannal therapy
becomes necessary, removal of the contents of the pulp
chamber and root canals is followed by thorough cleaning and
filling with an inert material
 The tooth may be extracted
ORAL CANDIDIASIS
Oral candidiasis
 Candida albicans is a normal component of the oral flora in
approximately 50% of the population and is the most
common fungal infection of the oral cavity
 Several factors seem to influence the likelihood od a clinical
infection, these include the immune status of the individual,
the strain of C. albicans present, and the composition of an
individual’s oral flora
Clinical manifestations
 There are three major clinical forms of oral candidiasis:
 Pseudomembranous
 Eruthematous
 Hyperplastic

PSEUDOMEMBRANOUS
 Most common and is also known as thrush
 Superficial, gray to white inflammatory membrane composed
of matted organisms enmeshed in a fibrinosuppurative
exudate that can be eradily scraped off to reveal and
underlying erythematous inflammatory base
LEUKOPLAKIA
Leukoplakia
 White patches form on gums, the insides of cheeks, the
bottom of mouth and tongue. These patches can't be scraped
off.
 Doctors don't know what causes leukoplakia but consider
tobacco — whether smoked, dipped or chewed
 Leukoplakia usually isn't dangerous, but it can sometimes be
serious. Although most leukoplakia patches are noncancerous
(benign), some show early signs of cancer. Many cancers on
the floor of the mouth — beneath the tongue — occur next
to areas of leukoplakia.
Symptoms
Leukoplakia may appear:
 White or grayish in patches that can't be wiped away
 Irregular or flat-textured
 Thickened or hardened in areas
 Along with raised, red lesions (erythroplakia), which are more likely to show
precancerous changes
 A type of leukoplakia called hairy leukoplakia primarily affects people whose
immune systems have been weakened by medications or disease, especially
HIV/AIDS. Hairy leukoplakia is a white patches that resemble folds or ridges
on the sides of your tongue.
Causes
 Leukoplakia
 Although the cause of leukoplakia is unknown, tobacco use, including smoking and
chewing, appears to be responsible for most cases. Often, regular users of smokeless
tobacco products eventually develop leukoplakia where they hold the tobacco against
their cheeks. Long-term alcohol use and other chronic irritants also may contribute to
leukoplakia.
 Hairy leukoplakia
 Hairy leukoplakia, sometimes called oral hairy leukoplakia, results from infection with
the Epstein-Barr virus (EBV). Once you've been infected with EBV, the virus remains in
your body for life. Normally, the virus is dormant, but if your immune system is
weakened, either from disease or certain medications, the virus can become reactivated,
leading to conditions such as hairy leukoplakia.
 People with HIV/AIDS are especially likely to develop hairy leukoplakia. Although the
use of antiretroviral drugs has reduced the number of cases, hairy leukoplakia still affects
a number of HIV-positive people and it may be one of the first signs of HIV infection.
The appearance of oral hairy leukoplakia may also be an indication that antiretroviral
therapy is failing.
Risk factors
 Tobacco use puts you at high risk of leukoplakia and oral
cancer. Drinking alcohol combined with smoking further
increases your risk.
Complications
 Leukoplakia usually doesn't cause permanent damage to
tissues in your mouth. However, oral cancer is a potentially
serious complication of leukoplakia. Oral cancers often form
near leukoplakia patches, and the patches themselves may
show cancerous changes. Even after leukoplakia patches are
removed, the risk of oral cancer remains.
 Hairy leukoplakia, on the other hand, isn't painful and isn't
likely to lead to cancer. But it may indicate HIV infection or
AIDS.
Tests & diagnosis
 Most often, your dentist diagnoses leukoplakia by examining the
patches in your mouth and ruling out other possible causes. To test
for early signs of cancer, your dentist may:
 Remove a tissue sample (biopsy) for analysis. This involves
removing cells from the surface of the lesion with a small, spinning
brush (oral brush biopsy) or surgically removing the entire
leukoplakia patch (excisional biopsy) if the patch is small.
 Send the tissue for lab analysis. A highly specialized imaging
system allows a pathologist to detect abnormal cells.
 If the biopsy is positive and your dentist performed an excisional
biopsy that removed the entire leukoplakia patch, you may not
need further treatment. If the patch is large, your dentist may
refer you to an oral surgeon or ENT specialist for treatment.
Treatment
 For most people, stopping tobacco or alcohol use clears the condition. When
this isn't effective or if the lesions show early signs of cancer, your dentist may
refer you for treatment, which involves:
 Removal of leukoplakia patches.
 Patches may be removed using a scalpel & a laser
 Follow-up visits. Recurrences are common.
 Leukoplakia treatment is most successful when a lesion is found and treated
early, when it's small. Regular checkups are important, as is routinely inspecting
your mouth for areas that don't look normal.
 Treating hairy leukoplakia
 Usually, you don't need treatment for hairy leukoplakia. The condition often
causes no symptoms and isn't likely to lead to mouth cancer.
 If your doctor or dentist recommends treatment, you may take a pill that affects
your whole system (systemic medication), such as the antiviral medicine
acyclovir (Zovirax) or antiretroviral medicine zidovudine (Retrovir). Or you
may use a medication solution that you apply directly to the lesions in your
mouth (topical medication), such as podophyllum.
Prevention
 Avoid all tobacco products. Talk to your doctor about
methods to help you quit. If friends or family members
continue to smoke or chew tobacco, encourage them to have
frequent dental checkups. Oral cancers are usually painless
until fairly advanced.

 Avoid or limit alcohol use. Alcohol is a factor in both

leukoplakia and oral cancer. Combining alcohol and smoking
may make it easier for the harmful chemicals in tobacco to
penetrate the tissues in your mouth.
MOUTH ULCERS (APHTHOUS ULCERS)
Aphthous Ulcers (Canker Sores)
 Apthous ulcers are common, often recurrent, exceedingly
painful, superficial oral mucosa ulcerations of unknown
etiology
 Aphthous ulcers tend to be prevalent within certain families
and may also be associated with immunologic disorders
including celiac disease, inflammatory bowel disease, and
Behcet disease
 The lesions appear as single or multiple, shallow, hyperemic
ulcerations covered by a thin exudate and rimmed by a
narrow zone of erythema
 The underlying inflammatory inflitrate is at first largely
mononuclear, but secondary bacterial infection may result in
a neutrophilic infiltrate
 The lesions typically resolve spontaneously in 7-10 days, but
may sometimes persist stubbornly for weeks, particulary in
immunocompromised patients.