juvenile periodontitis

:Contents:IntroductionClassificationLocalized Juvenile Periodontitis: Etiology Clinical Features Radiographic FeaturesGeneralized Juvenile Periodontitis Etiology Clinical Features Radiographic FeaturesMicrobiologyImmunologyDifferential DiagnosisTreatmentConclusionReferences

PERIODONTIUM:

The normal healthy periodontium consists of several tissues namely: 1. Gingiva , 2. Periodontal ligaments(PDL) , 3. Cementum , 4. Alveolar bone

For the maintenance of the tooth in the oral cavity, the health of the periodontium as a whole is of paramount importance.

Cementum

Gingiva

Early onset Periodontitis, Aggressive Periodontitis

INTRODUCTION:

Juvenile Periodontitis is the most uncommon severe form of the Periodontal disease Described by Wannenmacher(1938) as destruction of the supporting tissues of the teeth that becomes clinically significant during adolescence or early adulthood.

CLASSIFICATION:

Ranney,1993,classified the disease in Localized & Generalized form

1.Localized aggressive periodontitis: - Characterized by bone loss around the first molars & incisors

- Occurring in otherwise healthy individuals

2.Generalized aggressive periodontitis: - Characterized by a more widespread pattern of periodontal destruction

- Associated with a variety of diseases of other systems

1.LOCALIZED JUVENILE PERIODONTITIS

ETIOLOGY:-

• Actinobacillus actinomycetemcomitans are the most commonly found bacteria at the diseased sites .

• Other micro-organisms found are: P. gingivalis, E.corrodens, Capnocytophaga, Spirochetes ,Bacillus,etc.

• Elevated levels of A.a. found in active sites (low in numbers at healthy sites)

•Produce leukotoxins, collagenase,bone resorbing factors & other immunosuppressive factors that help in invasion of host tissues,evasion of host defences leading to the destruction of periodontal tissue.

•Incidence of A.a. found to be greater in younger persons compared to older clients

•Younger patients experience more destruction in a shorter period of time

CLINICAL FEATURES:-

Onset around the time of puberty .

Occur in an otherwise healthy individual, clinical inflammation may not be obvious.

Localized almost exclusively to the incisors & first molars, less than 30% of sites are involved. Females are affected more than males

Blacks affected more than whites

Abnormality in the phagocyte function.

Self arresting disease progression.

Earliest Sign Drifting of teeth in a patient having a good oral hygiene

Affected teeth becomes mobile followed by pocket formation.

Progression of bone loss is 3-5 times faster than adult periodontitis.

Maxillary incisors migrate in distolabial direction diastema.

Sensitive root surfaces

Deep,dull,radiating pain may occur with mastication (irritation of the supporting tissues)

Periodontal abscess formation

Diastema

Denuded root surface

Some reasons why disease activity affects certain teeth:

A.a. colonize first perm. teeth to erupt

- Evade host defenses - Following initial attack, host

responds - Antibodies produce which

improve phagocytosis of bacteria - This may prevent colonization at

other sites

A.a. may lose its ability to produce leukotoxin

- This may slow or arrest the disease process

Antagonistic bacteria - Anti-A.a. bacteria may colonize

sites & prevent A.a. from colonizing other sites in mouth

- Localizes the infection & tissue destruction

Denuded root surfaces - The root surfaces of patients

with LJP are often denuded (absence of

cementum) - Allows bacteria to penetrate

the root and colonize the site

RADIOGRAPHIC FEATURES:

1.A localized vertical bone loss with widening of PDL space

2. Arc shaped bone destruction starting from the distal margin of the second premolar & extending to the mesial margin of the second molar

2. GENERALIZED JUVENILE PERIODONTITIS

ETIOLOGY:

• Actinobacillus actinomycetemcomitans along with the diverse microbiota.

• Defective neutrophil or monocyte function.

• Poor serum antibody response to infecting agent is seen.

• Subgingival tissues shows the presence of gram negative rods including P.Gingivalis & exhibit suppressed neutrophil chemotaxis.

CLINICAL FEATURES: Usually affect an individual under 30 years of age

Generalized involvement of permanent teeth, more than 30 percent.

Affects atleast 3 permanent teeth other than first molar & incisors

The destruction often appears episodically, with periods of advanced destruction followed by stages of quiescence of variable length.

Patients often have small amounts of bacterial plaque associated with the affected teeth.

Destructive phase:Tissue appears severely inflamed, ulcerated & fiery redBleeding with or without stimulationSuppurationAttachment & bone loss usually occurs

Non-destructive phase:Tissues appear pink with some stipplingLack of inflammationProbing will reveal deep pocketsBone & attachment levels relatively stable

Some patients with GAP may exhibit: Weight loss, Mental depression, General malaise.

Systemic conditions may predispose patient to GAP, these include:

Chronic neutrophil defects, leukocyte adherence deficiency,etc.

Destructive phase

Non destructive phase

Pus formation

RADIOGRAPHIC FEATURES:

1.Severe bone loss associated with minimal no. of teeth to advanced bone loss affecting the majority of the teeth

MICROBIOLOGY:

Actinobacillus actinomycetemcomitans appears to be primarily associated with the disease. - Gram negative anaerobes - Rod shaped organisms - Localized predominantly at the base of the defect

The presence of a recently discovered genus termed Capnocytophaga, has been associated with the progression of periodontitis lesions.

IMMUNOLOGY:

Defective function or production of circulating neutrophils & monocytes is often associated with an increased frequency & severity of bacterial infection.

DIFFERENTIAL DIAGNOSIS:

Conditions that could contribute to alveolar bone loss in the primary dentition & premature loss of primary teeth:

1. Hypophosphatasia 2. Papillon – Lefevre syndome

3. Cyclic Neutropenia

HYPOPHOSPHATASIA:

TREATMENT:

1.Early diagnosis aids in successful treatment.

2.Extraction of involved teeth (depends on severity of tissue loss)

3.Antibiotics can be provided against infective microorganisms: Tetracycline is consider the drug of choice (1g/day orally for 14 days ) Tetracycline+Metronidazole Doxycycline

4. Periodontal therapy: Scaling & root planning

Plaque control instruction Debridement with or without flap surgery Subgingival Irrigation with iodine & hydrogen peroxide Bone grafts, root resections, hemi sections

CONCLUSION:

Periodontal Disease accounts for a majority of missing teeth in adults & results in tremendous economic & social burdens both to the individual & the society.

Periodontal disease is so prevalent that only possible solution to the problem is its “prevention” by maintaining the good oral hygiene.

REFERENCES:

1.Essential of Pediatric Oral Pathology By Mayur Chaudhary, Sweta Dixit Chaudhary

2.Textbook of Pedodontics By Shobha Tandon

3.Textbook of Oral Pathology By Shafer’s

4.Principle & practice of Pedodontics By Aarthi Rao