AGGRESSIVE PERIODONTITIS

Aggressive periodontitis Introduction: It generally affects systemically healthy individuals less than 30 years old or older. It may be universally distinguished from chronic periodontitis by the age of onset, the rapid rate of disease progression, the nature and composition of the associated subgingival microflora, alteration in the host immune response and a familial aggregation of diseased individuals.

Older terminology Juvenile periodontitis Early onset periodontitis

Classification Aggressive periodontitis is broadly classified as: Localized aggressive periodontitis Generalized aggressive periodontitis

Localised aggressive periodontitis Clinically it is characterised as having “localised first molar/ incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar and involving no more than two teeth other than first molars and incisors.

3) Presence of bacteria antagonistic to AA influences its action. Reasons for localization of aggressive periodontitis to certain teeth: 1) Actinobacillus actinomycetemcomitans evades host defences by different mechanisms.A strong antibody response is characteristic. 2)The organism may loses it’s leukotoxin producing ability for unknown reasons. 3) Presence of bacteria antagonistic to AA influences its action. 4)a defect in cementum formation

Clinical features Lack of clinical inflammation despite presence of deep periodontal pockets. Presence of minimal plaque. Distolabial migration of maxillary incisors with diastema formation. Increasing mobility of first molars Sensitivity of denudes root surfaces to thermal and tactile stimuli. Deep dull radiating pain during mastication.

Radiographic features : Vertical loss of alveolar bone around first molars and incisors beginning around puberty is a classic sign. “Arc shaped angular bone loss extending from distal aspect of 2nd premolar to the mesial aspect of 2nd molar”.

Generalized aggressive periodontitis: It affects individuals under the age of 30, but older patients also may be affected. They produce a poor antibody response to the pathogens present. Clinically it is characterised by generalised interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors. Destruction appears episodically.

Like localised aggressive periodontitis , patients have small amounts of plaque with affected teeth. Qualitatively ,P.gingivalis, A. actinomycetemcomitans and B.forsythus frequently are detected in plaque.

Clinical features Two types of gingival responses can be found: One is a severe,acutely inflamed tissue, often proliferating, ulcerated and fiery read. Bleeding may occur spontaneously or with slight stimulation.

Contd.. The other is that gingival tissues may appear pink, free of inflammation and occasionally with some degree of stippling, although the last feature may be absent. Deep pockets can be demonstrated by probing.

Systemic manifestations Weight loss Mental depression General malaise. Medical histories should be reviewed and updated.

Radiographic findings It can range from severe bone loss to advanced bone loss affecting majority of teeth in dentition.

Risk factors for aggressive periodontitis Microbiologic factors Immunologic factors Genetic factors Environmental factors.

Prognosis The prognosis for patients with aggressive periodontitis depends on wether the disease is generalized or localised and the degree present. The generalized form which are usually associated with some systemic diseases have a worse prognosis. Early radiographs have to be obtained to get a prognosis of the disease.

Treatment for Localised aggressive Periodontitis Early form responds to standard periodontal treatment. Extraction- after the involved teeth have been extracted, uneventful healing ensues Standard periodontal therapy- Includes scaling and root planing, curettage, flap surgery with and without bone grafts,hemisections. Strict plaque control and frequent maintenance visits

Contd.. Chlorhexidine rinses should be prescribed. Antibiotic therapy- Tetracycline 250mg 4 times daily for 14 days every 8 weeks. Lindhe treated patients with tetracycline 250mg, four times daily for two weeks, modified widman flaps and periodic recall visits(one visit every month for 6 months) Doxycycline: loading dose 200mg/day 100 mg / day cotinued. Chlorhexidine rinses should be prescribed.

Surgical Therapy Modified widman flaps + tetracycline 250mg 4 times daily for 2 weeks + periodic recall. Tetracycline+ flap surgery + placement of grafts : excellent bone fill Chlorhexidine rinses for several weeks. Refractory LAP – antibiotic susceptibility tests

Treatment of Generalized aggressive periodontitis Diagnostic tests to determine organisms sensitivity to specific antimicrobials. Mechanical debridement with scaling and root planing to reduce supra and sub gingival bacterial masses.

Combination therapy Metronidazole + amoxycillin for AA commitans associated periodontitis Amoxycillin + doxycycline for treatment of AA + P.gingivalis associated periodontitis Metronidazole + ciprofloxacin

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