Periodontal Diseases in Children

and Adolescents

Dr. Hasham Khan

Professor of Paediatric Dentistry
Khyber College of Dentistry
Peshawar
Periodontal Diseases in Children
Periodontal diseases can be viewed as a group of infections
in which there is a selective proliferation of certain
components of the normal flora.
The organisms involved may be:

* Streptococci

* Actinomyces

* Bacteroids

* Fusiform

* Spirochetes
Periodontal Screening in Children and Adolescents
using Basic Periodontal Examination(BPE)
Periodontal screening using BPE should be a routine part of
the dental examination in children:
 After the eruption of the permanent incisors and first permanent molars in
children, the BPE can be used for screening the indexed teeth UR6, UR1,
UL6, LL6, LL1 and LR6 (one tooth from each of the six sextants).
 The WHO621 probe with the 0.5mm spherical ball on the tip and shaded
band at 3.5 – 5.5mm is used to detect normal sulcus and periodontal
pockets. Each index tooth is probed at 6 sites (mesiobuccal, mid-buccal,
distobuccal, mesiopalatal, mid-palatal, distopalatal).The worst finding on
each index tooth is recorded using a six-box grid.
 To identify incipient periodontitis, it is necessary to asses whether or not
the base of the ‘pocket’ is apical to the cemento-enamel junction. To
determine small amounts (1mm or so) of attachment loss, a useful
technique is to locate (using tactile sensation) the cemento-enamel
junction using the tip of the probe, gently advance the probe to the
connective tissue attachment level and note the distance moved by the
probe – a one –step measuring technique.
Continues:
 BPE codes 0-2 should be used up to the age of 11 years because of the
probability of pseudopockets associated with newly erupting teeth.
 Presence of a deep pocket in which the 3.5 – 5.5mm black band
disappears would necessitate further periodontal investigation
irrespective of the age.
 In adolescents aged 12 years or over, the full range of scores can be
used on the index teeth so that periodontal pockets can be detected as
early as possible, although care should be exercised to distinguish true
pockets from pseudopockets.
 If pockets are detected, then full-mouth periodontal measurements and
subsequent monitoring should be undertaken.
 Periodontal screening of new patients and at the 4 or 6-monthly recalls
in children and adolescents is recommended so that periodontal
problems are detected early and treated appropriately.
 This BPE screening system typically takes less than 1-2 minutes in
children and adolescents.
 The ball end on the WHO 621 probe can also be used to detect
subgingival calculus.
WHO 621 Periodontal Probe
 UR6 UR1 UL6

LR6 LL1 LL6

Six-box Grid for Index Teeth

WHO 621 Periodontal Probe Used in BPE
 What is BPE and How to Record it
The BPE is a simple and rapid screening tool that is used to
indicate the level of examination needed and to provide basic
guidance on treatment need. It does not provide a diagnosis.
How to Record:
• The dentition is divided into 6 parts called sextants:
upper right (17 to 14), upper anterior (13 to 23), upper left (24 to 27)
lower right (47 to 44), lower anterior (43 to 33), lower left (34 to 37)
• All teeth in each sextant are examined.
• For a sextant to qualify for recording, it must contain at least 2 teeth (if only one
tooth, its score will be included in the recording for the adjoining sextant.
• A WHO 621 probe is used. This has a “ball end” 0.5 mm in diameter, and a black
band from 3.5 to 5.5 mm.
• The probe should be “walked around” the sulcus/pockets in each sextant, and the
highest score recorded. As soon as a code 4 is identified in a sextant, the clinician
may then move directly on to the next sextant, though it is better to continue to
examine all sites in the sextant. If a code 4 is not detected, then all sites should be
examined to ensure that the highest score in the sextant is recorded before moving
on to the next sextant.
 Basic Periodontal Examination (BPE) Scoring Criteria
Code 0 In deepest sulcus of sextant, Gingival tissue healthy, does Treatment: Preventive care
probe’s coluored band not bleed on gentle probing. required.
remains completely visible. No calculus or defective
margins found.

Code 1 In deepest sulcus of sextant, No calculus or defective Treatment: Subgingival plaque

probe’s coluored band margins found, but some removal; appropriate oral hygiene
remains completely visible. bleeding after gentle probing instructions
detected.

Code 2 The probe’s coluored band Bleeding on probing may be Treatment: Plaque and calculus
is still completely visible. present and supragingival or removal; correction of plaque-
subgingival calculus and/or retentive margins of restorations;
defective margins found oral hygiene instructions.

Code 3 The coloured band is Need for a comprehensive periodontal examination and charting of
partially submerged. the affected sextant to determine the necessary treatment.
If two or more sextant score code 3, a comprehensive full-mouth
examination and charting is indicated.

Code 4 The coloured band Comprehensive full-mouth periodontal examination, charting, and
completely disappears in the treatment planning are needed.
pocket (depth >5.5mm).
Code * An asterisk (*) is entered in addition to code number when furcation involvement, tooth mobility,
mucogingival problem or gum recession is present [extending to the coloured band of the probe
(≥ 3.5mm)].
 2 0 3

1 2* 1

BPE score grid might look like the above - Example

Radiographs for periodontal screening and
diagnosis
 Radiographs for detection and assessment of periodontal diseases in
children and adolescents should be taken only when clinically justified.
 The opportunity to assess bone levels should always be taken on intraoral or
panoramic films, even if these were not taken primarily for periodontal
purposes (bone loss may be horizontal or vertical). Individuals with angular,
vertical bone loss affecting at least one molar have been considered as
periodontal risk subjects.
 In children a BPE code of 3, 4 or *, or full periodontal charting indicating
the presence of pockets or furcation involvement, would warrant
radiographic examination.
 Intraoral and extraoral radiographs suitable for detection and monitoring of
bone loss include bitewings, periapicals and panoramic views (OPG etc).
The intraoral films which are taken in routine recalls can be used for
longitudinal monitoring of bone changes.
 A distance of 2mm and above between the cemento-enamel junction and the
alveolar crest in the absence of local factors (caries, fillings, open contacts
etc) could be an indication of periodontitis. In primary molars, this distance
may be 0.8 – 1.4mm.
 Periodontal Indices used for Baseline
Measurements
 At the start of treatment periodontal indices appropriate to the
BPE codes and diagnosis should be used. These provide a baseline
against which change (whether improvements or deteriorations)
can be measured.
 Monitoring involves measuring the periodontal condition using a
chosen index and remeasuring it after a defined period. All
periodontal assessments should be recorded in the patient’s notes.
 For BPE codes of 1 or 2 in a child with gingivitis, only plaque
index and marginal gingival bleeding index need to be recorded.
 Marginal gingival bleeding is a measure of gingivitis and it correlates with
supragingival plaque control. The presence or absence of marginal gingival
bleeding elicited by gently running a blunt periodontal probe around the
gingival margin should be recorded. It is done on four sites per tooth (buccal,
mesial, distal, lingual) to give the percentage of surfaces with gingival bleeding.
 Plaque can then be disclosed and measured at the same sites.
 As a motivational tool give the child a score based on plaque-free surfaces or
marginal bleeding-free surfaces so that the score gets higher as they improve
their tooth cleaning.
 For a less cooperative child, only six teeth can be used designated for the BPE.
Continues:

 For BPE codes of 3, 4 or * , the following periodontal indices need

to be used in the affected area:
 Probing depths / clinical attachment levels in millimeters, traditionally at six
sites per tooth using a graduated periodontal probe.
 Bleeding on probing from the base of the pocket at the same six sites per tooth.
This indicates inflammation at the base of the pocket and the percentage of
sites with bleeding on probing can be calculated (in approximately 30 % of
sites with bleeding on probing attachment loss progresses).
 Mobility (I = upto 1mm movement horizontally; II = more than 1mm
movement horizontally: III = movement of tooth both horizontally and
vertically).
 Furcation involvement ( horizontal probe penetration into furcation: F1 =
upto 3mm: F2 = over 3mm; F3 = through and through between two roots).
 Suppuration.
 Recession of the gingival margin (in mm) apical to the cemento-enamel
junction.
Periodontal Diseases in Children and Adolescents
[International workshop for the classification of periodontal diseases (1999)]
1. Chronic Marginal Gingivitis (caused by dental plaque & other local irritating factors)
2. Incipient Chronic Periodontitis
a. Localized
b. Generalized
3. Aggressive Periodontitis
a. Localized
b. Generalized
4. Periodontal Disease Associated with Systemic Conditions
a. Associated with Haematological Disorders
b. Associated with Genetic Disorders
c. Associated with Endocrine Factors
d. Associated with Drugs
e. Associated with Malnutrition
f. Not Otherwise Specified (NOS)
5. Necrotizing Periodontal Diseases
a. Necrotizing Ulcerative Gingivitis (NUG)
b. Necrotizing Ulcerative Periodontitis (NUP)
6. Other Periodontal Lesions in Children
a. Localized Gingival Recessions
b. Gingivitis Artefacta
Periodontal Disease Associated with Systemic Conditions
a. Associated with Haematological Disorders
1. Acquired neutropenia
2. Leukemias
3. Other e.g; HIV
b. Associated with Genetic Disorders
1. Familial and cyclic neutropenia 2. Down’s syndrome
3. Leukocyte adhesion deficiency syndromes 4. Papillon-Lefevre syndrome
5. Chediak- Higashi syndrome 6. Histiocytosis syndromes
7. Glycogen storage disease 8. Infantile genetic agranulocytosis
9. Ehlers-Danlos syndrome (Type IV and VIII) 10. Cohen syndrome
11. Hereditary gingival fibromatosis 12. Hypophosphatasia
c. Associated with Endocrine Factors
1. Puberty-associated gingivitis
2. Diabetes mellitus-associated periodontal disease
d. Associated with Drugs
1. Drug-induced gingival enlargements
i. Phenytoin
ii. Cyclosporin
iii. Nifedipine
e. Associated with Malnutrition
1. Ascorbic acid-deficiency gingivitis
f. Not Otherwise Specified (NOS)
Management of Periodontal Diseases in
Children and Adolescents
Aims:
Periodontal therapy aims to preserve the natural dentition and
periodontium and to improve comfort, aesthetics and function.

Healthy Periodontium:
The clinical signs of a healthy periodontium comprise the
absence of redness, swelling, suppuration and bleeding on
probing; maintenance of a functional periodontal attachment
level; minimal or no recession in the absence of inter-proximal
bone loss.
 Periodontal Therapy

Periodontal therapy is usually undertaken in three

phases:

 Initial cause-related therapy.

(To remove the cause if possible)

 Corrective therapy (additional therapeutic measures).

(To correct the defect or problem if possible)

 Supportive therapy (maintenance therapy).

(To prevent disease recurrence and progression with follow-up recalls
appropriate to the diagnosis)
 Chronic marginal gingivitis
• Widespread in children.

• Often associated with erupting primary and permanent teeth,

and with exfoliating primary teeth (resolve spontaneously).

• Mostly associated with the presence of plaque, materia alba

and calculus (result of inefficient oral hygiene).

• Other common local irritants include rough edges of carious

cavities and overhanging margins of restorations.

Treatment:
1. Remove local irritating factors by carrying out a prophylaxis,
restoring carious cavities, and replacing or smoothing
unsatisfactory restorations. Scaling if calculus present.

2. Give oral hygiene instructions and dietary advice.

 Incipient Chronic Periodontitis

Chronic periodontitis can be classified on the basis of the

number of sites affected:
Localized: when less than 30% of sites are affected
Generalized: when more than 30% of sites are affected

The severity of the disease (localized or generalized) can be

categorized on the basis of Clinical Attachment Loss (CAL):
Mild: CAL 1-2 mm
Moderate: CAL 3-4 mm
Severe: CAL 5 mm or more
Clinical Features of Incipient Chronic Periodontitis
 Most prevalent in adults but can occur in children and adolescents
(13-14 years).
 There do not appear to be defects in host response, therefore the key
causative factor is microbial plaque.
 The amount of periodontal destruction is proportionate to local factors.
 Clinical attachment loss of 1-2 mm.
 True periodontal pockets of 4-5 mm.
 Incipient crestal alveolar bone loss ≥ 0.5 mm. (the early bone loss is
typically of the horizontal crestal type affecting only a few sites).
 Mesial and distal sites on first molars and incisors commonly affected
but can affect any other site/sites as well.
 Slow progression but may have periods of rapid progression. However,
prevalence and extent increase from early to late teenage years.
 Progression has been associated with presence of subgingival calculus,
plaque and gingival inflammation.
 Progression can only be confirmed by repeated clinical examinations.
 Treatment
 The primary aim of the treatment of chronic periodontitis is the
resolution of inflammation and arrest of disease progression.

 Scaling and root planing and adjunct antimicrobial therapy may

be used for management of chronic periodontitis.

 A surgical treatment of chronic periodontitis:

 Provides better access for removal of aetiologic factors.

 Reduces deep probing depths.

 Regenerates or reconstructs lost periodontal tissues.

 Regenerative therapies with bone grafting and guided tissue

regeneration (GTR) techniques, with or without bone replacement
grafts, may be successful at selected sites with advanced bone loss.
 Aggressive Periodontitis
• Severe, often rapidly destructive forms of periodontitis.
• Have familial tendency (aggregate in families).
• Affected individuals are systemically healthy.
• May have a virulent periodontal pathogenic microflora.
• Impaired host response (chemotactic and phagocytic abnormalities
in neutrophils).
• Multifactorial nature, possibly genetic element.
• Severity of periodontal destruction inconsistent with level of plaque.
• Elevated proportions of Aggregatibacter Actinomycetemcomitans.
• Hyper-responsive macrophage phenotype, including elevated
production of PGE2 and interleukin-1β in response to bacterial
endotoxins.
• Progression of attachment loss and bone loss may be self-arresting.
 Aggressive Periodontitis

Classified as:

• Localized Aggressive periodontitis

• Generalized Aggressive periodontitis

 Localized Aggressive periodontitis
Clinical Features:
• Onset around puberty.
• Affects less than 1 % of otherwise healthy children and adolescents.
• Localized first permanent molar/incisor presentation on at least
two teeth (one of which is a molar) and involving no more than two
teeth other than first molars/incisors.
• Attachment loss of at least 3mm, usually with associated deep
pockets.
• Radiographs may show angular defects on incisors and arc-shaped
bone defects on affected first permanent molars.
• Aggregatibacter actinomycetemcomitans usually, although not
invariably, is present in subgingival plaque.
• Robust serum antibody response (IgG2 in particular) to the
infecting organism.
 Generalized Aggressive periodontitis

Clinical Features:
• Usually affects people under 30 years of age, but patients may
be older.
• Generalized interproximal attachment loss of 3 mm or more.
• Affects at least three permanent teeth other than first molars
and incisors.
• Pronounced episodic nature of destruction of periodontal
attachment and alveolar bone.
• Organisms include Porphyromonas gingivalis, Prevotella
intermedia, Camplyobacter rectus, Bacteroides forsythus,
Fusobacterium nucleatum and Aggregatibacter
actinomycetemcomitans.
• Poor serum antibody response to infecting agents.
 Treatment
Periodontal screening has a vital role in early detection and
treatment of the disease.
 The initial cause-related therapy is undertaken by carrying out scaling and root
planing. This will non specifically reduce the mass of microbial deposits.
 The non-responding sites is re-root planed (preferably by taking flap) and
systemic antibiotic therapy is given. Systemic antibiotic therapy should not be
given without prior mechanical therapy (debridement) because the undisturbed
biofilm prevents the antibiotic from reaching the target organisms.
 There is no consensus on the use of antibiotics. However the most effective and
commonly used antibiotic regimen is to give metronidazole and amoxicillin three
times daily for 7-10 days. Lab tests of plaque samples may be carried out if
antibiotics normally used in periodontitis do not work.
 These principles of treatment are equally applicable to both the localized and
generalized form of aggressive periodontitis.
 In generalized form of aggressive periodontitis, the microflora may be more
diverse than the localized form. Surgery can be successful in reducing A.
actinomycetemcomitans.
 If surgical treatment is undertaken, a biopsy of granulation tissues is
recommended to rule out certain other pathological entities (e.g; Langerhans cell
histiocytosis). ND:YAG laser may be used as an alternative to surgical approach.
It has a significant antibacterial action.
Periodontal Disease Associated with
Systemic Conditions

 There is a delicate balance between periodontal tissues

defense mechanisms and the bacterial flora. A small
defect on host side allows pathogenic microorganisms
to colonize and destroy periodontal tissues.

 Systemic disorders can change the host’s response to

bacterial challenge and ‘tip the balance’ in favour of
bacteria.
 Cyclic Neutropenia

• Nine-year-old child.
• Parents complained that her gums get swollen and bleed
at intervals.
• In between the episodes her gums are completely normal.
• Her peripheral smear showed:
• Neutrophils 06 %
• Lymphocytes 67 %
• Eosinophils 7%
• Basophils 22 %
 Neutropenias
(Acquired and Genetic)

• Quantitative deficiencies (agranulocytosis or neutropenia) of

leukocytes are generally accompanied by destruction of the
periodontium of all teeth, whereas qualitative (chemotactic or
phagocytic) defects are often associated with localized destruction
affecting only the periodontium of certain teeth.
• Patients with neutropenia present with diverse periodontal
manifestations. Usually there is bleeding from gums and in the
severe form, there may be ulceration and necrosis of the marginal
gingiva. Sometimes attached gingiva may become involved.
• Familial and cyclic neutropenia (genetic) results in reduction of
neutrophils at regular intervals. Since polymorphs constitute an
important component of the host defence mechanism, an upset in
the ‘balance’ can occur and gingival ulceration and inflammation
can develop cyclically. Sometimes the lesions may show deep
periodontal pockets and extensive generalized bone loss.
 Leukemias

• Leukemias are the commonest form of childhood cancer, ALL

accounting for 76% of all childhood leukemias.

• Periodontal lesions have been frequently observed in patients with

leukemia.

• Bleeding of the gingiva may be present in both acute and chronic

leukemia and may relate to the associated thrombocytopenia.
Gingival ulceration is also a common feature.

• Sometimes there is generalized swelling and enlargement of

gingiva due to infiltration by leukemic cells, particularly in AML.
 HIV / AIDS
• Rapid and aggressive periodontal destruction in
children and adolescents, particularly when oral
candidiasis is present, may be indicative of infection
with HIV.
• Linear gingival erythema presents as a distinct band of
intense marginal gingival erythema (disproportionate
to the quantity of plaque present and not responding to
plaque removal). May be due to candidal infection.
• Necrotizing ulcerative periodontitis:
• Necrosis and loss of papillary and marginal gingiva and bone.
• Spontaneous gingival bleeding.
• Deep, aching pain.
• May progress to cancrum oris or noma in undernourished or
debilitated individuals.
 Down’s Syndrome
• Show a generalized early periodontitis which starts in the
deciduous dentition and continues into the permanent dentition.

• Periodontal disease very prevalent and more severe than in age-

matched controls especially in lower anteriors.

• Differences not explained by plaque levels.

• Rapid progression of the disease.

• The short roots of the mandibular incisors and the bone loss in the
mandibular anterior region can lead to the premature loss of these
teeth.

• Possible factors include:

Disorders in the connective tissue
Abnormal capillary or tooth morphology
Functional defects of polymorphs and monocytes
Decline in T-cell function after the age of 10 years
 Leukocyte Adhesion Deficiency
Syndrome
• A rare autosomal recessive disease.
• Young patients with this syndrome present with severe
inflammatory periodontal disease.

• Defects in numbers of cell-cell adhesion receptors on the

neutrophil surface may lead to increased susceptibility to
periodontitis and other infectious diseases.

• The disease is generally fatal.

 Papillon-Lefevre Syndrome
• A rare hereditary (autosomal recessive) condition
characterized by early onset aggressive periodontitis
affecting the deciduous, and subsequently the permanent,
dentitions.
• Rapid attachment loss and bone loss in both the dentitions
resulting in tooth loss.
• There is palmar-plantar hyperkeratosis.
• The reasons underlying the severe periodontal destruction
are unclear and management of the disease is often
unsuccessful.
 Chediak-Higashi Syndrome

• An autosomal recessive disease associated with severe

periodontitis.

• Patients are extremely susceptible to bacterial infections

because there are defects in neutrophils in this syndrome
(abnormal chemotaxis and phagocytosis).

• Common features include generalized severe gingivitis,

extensive loss of alveolar bone and premature loss of teeth.
 Histiocytosis Syndromes
• A group of syndromes in which there is abnormal increase in the number of
histocytes (immune cells) and may affect infants, children and adults.
• Three major classes of histiocytosis:
• Langerhans cell histiocytosis (Histiocytosis X).
• Malignant histiocytosis syndrome (T-cell lymphoma).
• Non-Langerhans cell histiocytosis (haemophagocytic syndrome).
• Histiocytosis X is important because oral soft tissue and bony lesions are
common in this condition.
• Gingival inflammation and ulceration may be present due to invasion by
Langerhans cells. The periodontal lesions may clinically resemble necrotizing
ulcerative periodontitis. There is considerable granulation tissue, tissue
necrosis and marked bone loss.
• Lesions in weight bearing bones may cause the bones to fracture without
apparent reason. When jaw lesions are present ( 10-20%of cases), frequent
symptoms include swelling, tenderness, pain and loosening of teeth. Primary
teeth may be lost prematurely. Radiographs may show a ‘punched out’
appearance in the bone.
• Tests in children may include:
• Biopsy of skin and bone marrow to check for the presence of Langerhans cells. Biopsy of
the granulation tissue can also help in diagnosis.
• Complete blood count.
• Skeletal X-rays.
 Glycogen Storage Disease

• An autosomal recessive condition associated with

defective carbohydrate metabolism.

• Clinical features include:

• Reduced neutrophil numbers.
• Impaired neutrophil function.
• Periodontal disease.
 Infantile Genetic Agranulocytosis

• A rare autosomal recessive disorder.

• There is severe neutropenia in this disease.
• The periodontitis linked with this disease is similar to early
onset aggressive periodontitis.
 Ehlers-Danlos Syndrome
• An autosomal dominant disorder characterized by defective
collagen synthesis.
• Collagen disorder affecting joints (loose jointedness) and skin
(fragile and hyperextensible). May have flat feet and vision
problems.
• Types IV and VIII have an increased susceptibility to
periodontitis.
• Type VIII is linked with fragile oral mucosa and blood vessels.
Also associated with generalized aggressive early onset
periodontitis leading to premature loss of permanent teeth.
• Tests to be performed for diagnosis:
• Collagen typing (performed on a skin biopsy sample).
• Collagen gene mutation testing.
• Echocardiogram.
• Lysyl hydroxylase or oxidase activity.
 Cohen’s syndrome

• An autosomal recessive condition.

• There is frequent and extensive alveolar bone loss.
• The patients also suffer from non-progressive mental and
motor retardation, obesity and neutropenia.
 Hereditary Gingival Fibromatosis
• An autosomal dominant condition.
• There is a slow, progressive, benign, usually generalized but
sometimes local fibrous enlargement of the gingival tissues.
• The gingival tissues begin to enlarge with the eruption of the
primary teeth and continues to enlarge (more with the eruption of
permanent teeth). Therefore the condition is usually seen in young
children but may remain un-noticed (mild) until adolescence or
adulthood.
• Gross enlargement may interfere with the occlusion of teeth and
look unsightly.
• The dens fibrous tissue often causes displacement of the teeth and
malocclusion.
• Treatment:
• Excision of excess tissue, but it tends to recur.
• Excellent plaque control is stressed to the patient because it delays the
recurrence.
 Hypophosphatasia
• Hypophosphatasia is an inherited disorder and is associated with
deficiency of serum alkaline phosphatase and increased urinary
excretion of phospho-ethanolamine. There is abnormal
mineralization of bone and cementum hypoplasia or aplasia.

• Periodontal destruction may affect deciduous dentition, resulting

in premature exfoliation (acute periodontal manifestations may
not be seen).

• Diagnosis is made by:

» Clinical and radiological examinations.

» Serum alkaline phosphatase.

» Molecular biology alone can establish the diagnosis.

 Puberty-associated gingivitis

• The rise in steroid hormone levels during puberty in both sexes

has a transitory effect on gingivitis.

• There is an increase in gingival inflammation in circumpubertal

age individuals of both sexes without a simultaneous increase in
plaque levels.

• The inconsistency in the level of gingival inflammation and the

amount of plaque present help in the differentiation of the disease.

• The incidence and severity of gingivitis in adolescents is also

influenced by dental caries, mouth breathing, crowding of the
teeth and tooth eruption.
 Diabetes mellitus-associated
periodontal disease
• Diabetes mellitus-associated gingivitis is found in children with
poorly controlled type 1 diabetes mellitus (insulin dependent or
juvenile onset).
• Features of gingivitis are similar to plaque induced gingivitis.
• The level of diabetes control along with plaque control determine
the severity of the gingival inflammation.
• Effects of poorly controlled diabetes:
• Increased attachment loss and bone loss.
• Incidence increases after puberty and with age.
• Altered (decreased) neutrophil function.
• Collagen effects, including formation of advanced glycation end products.
• Increased susceptibility to infections.
• Reduced wound healing.
Drug-induced gingival enlargements

Gingival enlargements associated with various drugs may

develop in children and adolescents, therefore the medical
history is pertinent to the diagnosis.

The drugs involved are usually:

 Phenytoin

 Cyclosporin

 Nifedipine
Phenytoin-induced gingival hyperplasia

• Phenytoin is a drug used in the treatment of epilepsy. The most

common side effect of its chronic use is gingival hyperplasia.
All patients on the drug do not develop this side effect. Almost
50% of chronic users of phenytoin may develop gingival
hyperplasia within three months of starting the drug.

• The incidence and severity of hyperplasia are related to the

dosage of phenytoin and the amount of plaque present.

• Younger individuals develop more severe cases of hyperplasia.

Sex of the patient or duration of therapy have no effect.
 Mechanism of gingival enlargement

• The enlargement of gingiva is due to the proliferation of the

connective tissue rather than the epithelial component.

• Gingival enlargement may be due to sensitization of the high

activity fibroblasts.

• Other report suggests that phenytoin selects for a subpopulation

of gingival fibroblasts which produce an inactive collagenase.
This interfere with the turnover of gingival collagen which
could subsequently lead to gingival enlargement.
Treatment
• There is evidence that gingival inflammation is necessary for the
clinical development of gingival hyperplasia in users of phenytoin. If
excellent plaque control, gingival hyperplasia can be largely prevented.

• If the drug is changed, much of the existing gingival hyperplasia

disappears. But it is a remarkably effective and safe drug.

• If change of drug is not possible, the most effective treatment for cases
of phenytoin-induced gingival hyperplasia is removal of local irritants
followed by rigorous daily plaque control. Use of 0.2 % chlorhexidine
mouth rinse helpful.

• Surgical option is reserved only for severe cases where the

hyperplastic tissues interfere with function , make plaque control
impossible or cause esthetic problems for the patient. After surgery
good plaque control is essential.

• Along with good plaque control, the use of positive pressure

appliances will help in preventing recurrence.
 Cyclosporin
•Cyclosporin is another drug associated with gingival
overgrowth, particularly if used in combination with the
calcium-channel blocker nifedipine.

•This drug is used as an immuno-suppressant in patients

who have had organ transplants (to prevent organ
rejection).

•The incidence and severity of the enlargement are dose-

dependent and correlated to blood levels of the drug.

• Treatment is the same as for Phenytoin.

 Nifedipine
• Nifedipine is a calcium-channel blocker that is used in
adults for the control of cardiovascular problems.
• Also given to post-transplant patients to reduce the
nephrotoxic effects of cyclosporin.
• The incidence of gingival enlargement in dentate subjects
taking nifedipine is 10-15%.
• The drug blocks the calcium channels in cell membranes ⎯
intracellular calcium ions are a prerequisite for the
production of collagenases by fibroblasts.
• The lack of these enzymes could be responsible for the
accumulation of collagen in the gingiva.
 Ascorbic acid-deficiency gingivitis
• There may be gingival swelling, sponginess, bleeding and
ulceration in Vitamin C deficiency.

• These signs and symptoms are due to impaired production

of collagen and intercellular ground substance and weak
capillary walls.

• Uncommon in children in developed countries.

• Treatment : Vitamin C rich food and supplements.
 Treatment of Periodontal Disease
Associated with Systemic Conditions
• Treatment includes non-surgical or surgical mechanical
debridement and antimicrobial therapy.

• The management of periodontal disease associated with

systemic conditions is almost similar to the management of
aggressive periodontitis in the permanent dentition.

• Localized lesions may resolve successfully with this

treatment but the extent of success is usually limited in the
case of generalized periodontitis.

• Extraction of affected teeth may be the line of treatment in

many cases.
Necrotizing Periodontal Diseases

Recurrent periodontal diseases of microbial

origin with a complex and poorly understood
etiology. Necrotizing periodontal diseases
are divided into:

• Necrotizing ulcerative gingivitis

• Necrotizing ulcerative periodontitis
 Necrotizing Ulcerative Gingivitis
Clinical Features: The three most important diagnostic
features are:
• Interproximal gingival necrosis and ulceration presenting as
‘punched-out’ papilla.
• Gingival pain of rapid onset, spontaneous, constant and
exacerbated by eating and tooth brushing.
• Gingival inflammation and bleeding.
Other Signs and Symptoms:
• A characteristic halitosis (fetid odour).
• A pseudomembrane (containing fibrin, bacteria, sloughed
epithelial cells and other debris) covering the ulcerated areas of
gingiva (easily wiped off).
• Other signs occasionally associated with the disease include:
lymphadenopathy, increased salivation, fever, malaise, and
anorexia.
 Differential Diagnosis

Includes primary herpetic gingivostomatitis caused by

primary contact with herpes simplex virus type -1 but

can be easily distinguished from necrotizing ulcerative

gingivitis.
 Host Resistance and NUG
• Children who develop the disease have compromised and
overburdened immune systems (immunosuppression is a predominant
factor).

• Other predisposing factors include poor oral hygiene, stress, poor diet,
smoking and HIV infection. Children with the disease usually suffer
from either malnutrition or may have serious viral or parasitic
infections.

• Lowered host resistance allows certain components of the normal flora

to proliferate and cause the disease. Bacteriologic smears of the
microflora suggest that the lesions are dominated by spirochetes and
fusiform bacilli (anaerobes).

• Children who are highly susceptible to infections, such as those with

Down Syndrome, run an increased risk of developing NUG (may be
due to defective phagocytic, chemotactic, and bactericidal capacities of
the neutrophils).
Necrotizing ulcerative periodontitis
Necrotizing ulcerative gingivitis may become recurrent or
progress to necrotizing ulcerative periodontitis if treatment
is not sought or the predisposing factors remain.
Clinical Features:
• Necrosis and loss of papillary and marginal gingiva and
bone.
• Deep, aching pain.
• Spontaneous gingival bleeding.
• May progress to cancrum oris or noma in undernourished
or debilitated individuals.
• The lesions are most commonly observed in individuals
with systemic conditions like HIV infection, severe
malnutrition and immunosuppression.
 Cancrum Oris

NUG (fusospirochetal infection) is usually limited to the

interproximal papillae and marginal gingivae. In some severely

debilitated individual the infection can locally spread to adjacent

sites. The ulcerative lesions can involve the buccal mucosa, nose,

and other facial structures. These advanced forms of facial

fusospirochetal infections are called noma or cancrum oris.

 Prevalence

• The frequency of necrotizing periodontal diseases is higher in

developing countries as compared to the developed countries. Probably
less than 1% of the world’s population is affected.

• In developed countries, about 70% of cases occur in individuals

15 – 30 years of age. It is very rare in children under 10 yr old.

• In contrast, 60 - 75 % of cases in underdeveloped countries are

children under 10 years of age.
 Treatment
• Identify and eliminate factors (if possible) which may predispose to the
disease. Factors which predispose children to NUG include malnutrition,
emotional stress, lack of sleep and a variety of systemic illnesses. Children
with serious viral infections, such as measles and hepatitis, are more
susceptible to NUG and NUP.

• Careful local debridement and complete removal of plaque and calculus

deposits. OHI should be reinforced.

• Systemic antibiotics to control infection (metronidazole and penicillin) and

pain killers. Oxidizing mouthrinse (3 % hydrogen peroxide and equal
volume warm water) and chlorhexidine 0.2 % mouthwash are also helpful.

• Recommend supportive therapy, such as adequate rest and a balanced diet.

• Once the acute phase is over, the patients should be followed for several
months. Special attention should be given to the interproximal soft tissue
craters. If these craters are not eliminated recurrent bouts of the disease
may occur.

• In most children, the interproximal papillae completely regenerate.

Other periodontal lesions in children

Include:

 Localized gingival recession

 Gingivitis artefacta
Localized Gingival Recession
• Found in approximately 10% of children under the age of 15 years.

• Occur most frequently on the labial surfaces of the mandibular incisors.

Causes: Malaligned teeth, injurious tooth brushing habits, history of

orthodontic therapy, poor plaque control, habits (gingivitis artefacta),
trauma, high frenal attachment, shallow buccal sulcus, traumatic
occlusion etc.

• Of these, malalignment of teeth is the most common cause of gingival

recession (80-90% of all cases). Labially placed teeth are particularly
susceptible to these lesions.

• Plaque-induced inflammation or vigorous tooth brushing can easily

destroy the thin gingival tissue covering the roots of labially placed
(prominent) teeth. This is because the labial plate of alveolar bone
normally covering the root is often absent in labially placed teeth.
Localized Gingival Recession Continues

• Orthodontic therapy may cause thinning of the labial gingiva and

alveolar bone during labial movement of teeth, thus predisposing to
gingival recession.

• Individuals who require orthodontic therapy are already predisposed

to gingival recession because of malaligned teeth. The addition of
orthodontic appliances (brackets and wires) make oral hygiene
procedures more difficult, and many individuals either give up on
plaque control or become toothbrushing zealots. Either extreme can
promote the development of gingival recession.
Treatment
• Identify the etiologic and predisposing factors and if possible,
eliminate them.

• Many cases of gingival recession can be arrested by good plaque

control and maintenance therapy.

• Some cases may require surgical intervention, such as free gingival or

lateral sliding grafts. Main objective of these procedures is to increase
the width of the attached gingiva so that plaque control can be
effectively practiced.

• However, in children mucogingival surgery should be avoided until

adulthood and recession should be arrested by nonsurgical means.
Gingivitis artefacta

• Gingivitis artefacta is a self-inflicted lesion, most commonly on a

gingival margin or papilla usually with a finger nail.

• The lesion may be an ulcer or a localized stripping of the gingival

margin from the tooth, which may expose the root surface.

• This behaviour is usually initiated by minor gingival irritation (e.g;

from an inflamed papilla) or an exfoliating tooth but sometimes
psychological factors are involved.
Treatment

• Examine for any possible source of local irritation, and treat as

necessary.

• Inform the child that the finger is aggravating the soreness. Attempt
to break the habit with the child and parents cooperation. Adhesive
bandage on the finger may serve as a reminder.

• Patients with psychological disturbances may be referred for treatment.