PERIODONTAL DISEASE IN

CHILDREN
Introduction

• Although gingivitis is not uncommon in children, periodontitis with

alveolar bone loss is usually a manifestation of a serious underlying
immunological deficiency.
• Periodontal diseases peak their destructive stages in the middle age , but
many of them have their inception during childhood.
• The early detection and early treatment are important from a preventive
aspect since, the prevention of most periodontal diseases are relatively
simple and very effective, providing lifetime benefits.
Anatomy of the periodontium in children

• Marginal gingival tissues around the primary dentition are more highly
vascular and contain fewer connective tissue fibres than tissues around
the permanent teeth.
Anatomy:
• junctional epithelium
• marginal gingiva
• attached gingiva
• alveolar bone
• differences between the primary and permanent dentitions.
 Anatomy of the periodontium in
children
Features Children Adults

Gingival colour More reddish Coral pink

contour Free gingival margin- Gingival margin-

rounded knife edge

Consistency Flabby due to less CT Firm and resilient

density and lack of
organized collagen fiber
bundles
Surface texture Stippling absent in Stippling present
infancy.
`Mostly seen by age of 6
yrs
feaatures Children Adults

Interdental area Saddle shaped gingiva Papillary gingiva

Gingival sulcus Newly erupted teeth 1-2mm

sulcus depth is greater
than deciduous
predecessor

Attached gingiva Width increases with Greater in adults

age and concomitant
decrease in sulcus
depth

7
A classification of periodontal diseases in children
Gingival conditions without
loss of connective tissue
attachment
Acute gingivitis
• Herpetic gingivostomatitis
• Necrotizing ulcerative gingivitis
Chronic gingivitis
• Plaque induced
• Puberty gingivitis
Gingival enlargement
Drug-induced (generalized)
Traumatic gingivitis
Mucogingival problems
Periodontal conditions
with loss of connective
tissue attachment
Chronic periodontitis
• Plaque induced
• Complication of orthodontic treatment
Aggressive periodontitis
Periodontitis as a manifestation
of systemic disease
Papillon–Lefèvre syndrome
Ehlers–Danlos syndrome
Hypophosphatasia
Chediak–Higashi syndrome
Leucocyte adhesion deficiency syndrome
Neutropenias
Langerhans cell histiocytosis
Acute gingival conditions

• The principal acute gingival conditions that affect children are

primary herpetic gingivostomatitis and necrotizing ulcerative
gingivitis.
Primary herpetic gingivostomatitis

CLINICAL:
•Primary/Recurrent
•Viral
•Vesicular Lesions
•Complications Rare.
TREATMENT:
•Symptomatic
•Rest And Soft Diet
•Fluids
•Paracetamol Suspension
•Acyclovir.
Ulcerative stage of primary herpetic
gingivostomatitis:

(a) palatal gingiva;

(b) lower lip mucosa

Necrotizing ulcerative gingivitis

CLINICAL:
•Yellow-grey Ulcers
•Fusospirochaetal Infection
•Possible Viral etiology
•Well-established Predisposing Factors.
treatment:
•Intense Oral Hygiene
•Remove Predisposing Factors A 5-year-old Ethiopian boy with
necrotizing ulcerative
•Mechanical Debridement gingivitis.
•Metronidazole
Chronic gingivitis:

• Plaque-associated
• Lymphocyte-dominated
• Linked To The Onset Of Puberty
• Potentially A Key Role In Predicting Future Attachment And Tooth
Loss.
Drug-induced gingival enlargement

• Gingival enlargement:
• Drug-induced
• Collagen Accumulation
• Surgical Treatment
• Superimposed Gingivitis.

Drug- (phenytoin-) induced gingival

enlargement in a
12-year-old boy
Traumatic gingivitis (gingivitis artefacta/factitious gingivitis)

• Gingivitis artefacta:
• Minor/Major
• Self-inflicted
• Habitual
• Psychological
Mucogingival problems in children

• Gingival recession:
Narrow Keratinized Gingiva
Local Trauma
Post Orthodontics
Conservative Treatment Approach.
Screening for periodontal diseases in children

• The Basic Periodontal Examination (BPE). The system involves

recording the single most severe code for each sextant of the
dentition after probing the gingival and periodontal pockets with a
0.5mm ball-ended WHO 621 probe which has a black band 3.5–
5.5mm from the tip of the ball end.
Basic Periodontal Examination
(BPE)

0 Healthy gingiva with no pockets or bleeding after probing

1 Bleeding after probing but no calculus present and the entire black
Band remains visible
2 Calculus and other plaque retentive factors such as overhanging or
Deficient restoration margins; bleeding after probing may also be
Present and the black band remains completely visible
3 Shallow pockets with the band only partly visible above the gingival
Margin
4 Deep pocket where the band disappears entirely subgingivally.
Risk factors for periodontal conditions and diseases

Risk factors or periodontal disease can be classified as local or general.

• Local risk factors:
Malocclusions
Traumatic dental injury
Plaque retentive factors
Ectopic eruption
• General risk factors:
General risk factors for periodontal disease may have a genetic basis,with
certain inherited conditions possessing periodontal manifestations (e.g.
Papillon–Lefèvre syndrome).
Periodontal complications of orthodontic
treatment

Orthodontic Problems:
• Gingivitis
• Enlargement
• Root Resorption
• Gingival Trauma.
(a) Gingival enlargement on the palatal
aspect of retracted maxillary incisors.

(b) Appliance in situ.

Aggressive periodontal diseases:

• Aggressive periodontal diseases comprise a group of rare, but rapidly

progressing, infections that affect the primary and permanent
dentitions.
• The disorders are associated with a more specific microbial challenge
and an inherent defect in the host’s immunological response.
• The nature of these diseases can lead to premature tooth loss at an
early age.
• Prompt diagnosis is essential if treatment is to be successful, and the
periodontal status must be monitored regularly to ensure that the
treated disease remains quiescent.
Primary dentition

• The disease may present immediately after the teeth have

erupted.
• Localized/Generalized
• aggressive pathogens
Aggregatibacter (previously Actinobacillus)
actinomycetemcomitans, Porphyromonas gingivalis, Fusobacterium
nucleatum, and Eikenella corrodens.
Localized

• Localized disease progresses more slowly than the generalized

form
• Bone loss characteristically affects only incisor–molar teeth.
• Plaque levels are usually low.
• Soft tissue changes are minimal with gingivitis and proliferation
involving only the marginal tissues.
Generalized

• In the generalized form the gingiva appear fiery red, swollen, and
hemorrhagic.
• Extensive areas of recession.
• Gross deposits of plaque are inevitable.
• The disease progresses extremely rapidly, with primary tooth loss
occurring as early as 3–4 years of age.
• The bone loss may be restricted to one arch.
• Susceptible to recurrent general infections, e.G otitis media and
upper respiratory tract infections.
 Treatment

• Oral hygiene instruction, scaling, and root surface instrumentation

• Bacterial culturing of the pocket.
• If pathogens persist after oral debridement, an antibiotic such as metronidazole or
amoxicillin should be given systemically, after sensitivity testing, as a short course
over 1–2weeks.
• Generalized disease responds poorly to treatment.
• Extraction of the involved teeth has produced some improvement
• in severe cases of generalized periodontitis, extraction of all primary teeth can
limit the disease to the primary dentition.
• When the permanent teeth erupt, bacterial culturing of the subgingival flora
ensures that re-infection is detected early.
Permanent dentition

• In the permanent dentition, aggressive periodontitis involves

severe periodontal destruction with an onset around puberty.
• onset around puberty
• localized/generalized
• Aggregatibacter actinomycetemcomitans
• neutrophil chemotaxis defect.
Localized Aggressive
periodontitis(LAP):

• characterized by “localized loss of attachment and bone around

permanent incisors and first permanent molars”
• Prevelence is 1%
• It is linked to presence of Actinobacillus actinomycetemcomitans
and successful treatment outcomes correlate well with eradication
of bacteria.
Clinical and radiographic features

• The clinical features are pocket formation and loss of attachment

associated with the permanent incisors and first molar teeth.
• The radiographic pattern of bone loss is quite distinctive. Bilateral
angular bone defects are identified on the mesial and/or distal
surfaces of molars.
• The gingiva can appear healthy when the levels of plaque are low,
but a marginal gingivitis will be present if a good standard of
plaque control is not evident.
(a) Clinical appearance of a 13-year-old girl with
localized
aggressive periodontitis.

(b) Radiographic appearance of vertical bone loss on the

mesial aspect of 26.
Generalized aggressive
periodontitis (GAP):

• It sometimes occurs in adolescents and teenagers.

• Characterized by generalized interproximal attachment loss
affecting at least three permanent teeth other than incisor and
first molar.
Clinical and radiographic features

• Severe generalized bone loss is the characteristic feature.

• The pattern may be a combination of angular and horizontal resorption,
producing an irregular alveolar crest.
• When patients have good plaque control the degree of bone resorption is
not commensurate with the level of oral hygiene.
• The more generalized nature of the disease predisposes to multiple and
recurrent abscess formation, which is a common presenting feature.
• Invariably, one of the presenting signs is tooth migration or drifting of
incisors.
• Unexpected loosening of teeth.
Aggressive periodontitis with generalized bone loss in a 16-year-old male.
Treatment

• Plaque control.
• Mechanical debridement.
• Systemic antimicrobials. tetracycline therapy (250mg,four times
daily) for 2 weeks, combination of metronidazole (250mg) and
amoxicillin (375mg), three times daily for one week.
• Periodontal surgery.
Periodontitis as a manifestation of systemic
disease

• Papillon–Lefèvre syndrome
• Ehlers–Danlos syndrome
• Hypophosphatasia
• Chediak–Higashi syndrome
• Leucocyte adhesion deficiency syndrome
• Neutropenias
• Langerhans cell histiocytosis
• Down syndromde
Papillon Lefevre Syndrome

• -Papillon-Lefevre Syndrome
• (Palmoplantar Keratoderma with Periodontosis)
-Inherited as an autosomal recessive trait
-Mutation of the gene that produces the enzyme Cathespin C.
• -Greater frequency in consanguineous offspring.
Clinical features

• -Children are born looking completely normal.

• They may have redness on palms of hands and soles of feet.
• -Teeth erupt in normal sequence, position, and time.
• -At age 1, when primary teeth starting to erupt, the gum tissue is severely
inflamed and generalized aggressive periodontitis accompany the teeth.
• -By age 4, the child has lost all of there primary dentition.
• -Gingival tissue in mouth goes back to healthy & normal.
• -Eruption of the permanent dentition begins at normal age and in normal sequence
• -Patient will loose their permanent teeth and be completely edentulous by age 14-
17
Neutropenias

• The neutropenia's comprise a heterogeneous group of blood disorders.

• Neutropenias can be drug-induced or be secondary to severe bacterial or viral
infections or autoimmune diseases
• heritable conditions transmitted as autosomal dominant traits,
• diagnosed between 6 and 24 months
• characterized by frequent and multiple pyogenic infections of the skin and
mucous membranes
• primary dentition may not be involved
• gingiva inflamed and oedematous; gingival recession, ulceration, and
desquamation can also occur
Clinical features & treatment

• Gingiva are inflamed

• Edematous
• Gingival recession
• Ulceration,
• Desquamation
TREATMENT:
• Local removal of plaque and calculus.
• Strict plaque control measures are difficult to achieve in younger children,
so use of an antibacterial mouth. Rinse may prove useful.
Chediak–Higashi syndrome

• Inherited as an autosomal recessive trait.

Clinical features
• Partial albinism
• Photophobia
• Nystagmus.
• Recurrent pyogenic infections
• Malignant lymphoma,
• Neutropenia, anemia.
• Thrombocytopenia.
• Severe gingival inflammation
• Premature exfoliation.
Leucocyte–adhesion deficiency
syndrome (LAD)
• Autosomal recessive trait
• Severe recurrent bacterial infections
• Impaired wound healing
• Formation of pus.
• Aggressive gingivitis
Ehlers–Danlos syndrome
• An autosomal dominant trait
CLINICAL FINDINGS
• Excessive joint mobility
• Skin hyper-extensibility
• Susceptibility to scarring
• Bruising of the skin and oral mucous membranes
• Fragile gingival tissues
• Advanced periodontal disease
• Abnormalities of the amelodentinal junction
• Vascular inclusions in dentine
• Fibrous degeneration of
• The pulp, and disorganization of cementum.
Langerhans cell histiocytosis

• Non-malignant granulomatous
• Can affect the pituitary gland
• Marginal gingivitis
• Bleeding gingiva
• Abscess formation
• Pain
• Drifting and mobility of the teeth
• ‘Floating teeth’ radiographic appearance
• Local lesions that are confined to bone respond well to curettage and excision.
Hypophosphatasia
• Deficiency of alkaline phosphatase (ALP) activity.
• Increased excretion of phosphoethanolamine in the urine.
• Childhood hypophosphatasia become apparent before 2 years of age.
• Dental features
• Resorption of alveolar bone.
• Premature exfoliation of anterior primary teeth
• Hypoplasia or complete absence of cementum
• Small teeth
• Enlarged pulp chambers
• Aplastic or hypoplastic cementum
• Periodontal attachment.
• The diagnosis of hypophosphatasia is confirmed biochemically by low activity of serum alp
and a raised level of phosphoethanolamine in a 24-hour urine sample.