Aggressive periodontitis

Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis:

1. Localized aggressive periodontitis (LAP)
2. Generalized aggressive periodontitis (GAP)

Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form.

The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis.

Characteristics

In contrast to chronic periodontitis, primary features that are common to both LAP and GAP are as follows:

• except for the presence of periodontal disease, patients are otherwise healthy
• rapid loss of attachment and bone destruction
• familial aggregation
• Depressed neutrophil function.
• Neutrophils (PMN's) are defective, resulting in depressed chemotaxis and phagocytosis.

Moreover, aggressive periodontitis often presents with the following secondary features:

• Amounts of microbial deposits are inconsistent with the severity of the periodontal tissue destruction
• elevated proportions of Aggregatibacter actinomycetemcomitans, and in some cases, of Porphyromonas gingivalis as well
• phagocyte abnormalities
• hyperresponsive macrophage phenotype, including elevated levels of prostaglandin E₂ (PGE₂) and interleukin 1β
• progression of pathogenesis may be self-limiting

Localized vs. generalized forms of aggressive periodontitis

The 1999 Consensus Report published by the American Academy of Periodontology permitted the subdivision of aggressive periodontal disease into localized and generalized forms based on enough individually specific features, as follows:

• Localized aggressive periodontitis
  • circumpubertal (around the time of puberty) onset
  • robust serum antibody response to infective agents: the dominant serotype antibody is IgG2
  • localized first molar/incisor presentation
  • Gingival inflammation, edematous, bleeding, pocketing
• Generalized aggressive periodontitis
  • usually affects patients under 30 years of age
  • poor serum antibody response to infective agents
  • pronounced episodic nature of periodontal destruction
  • generalized presentation affecting at least 3 permanent teeth other than first molars and incisors.
  • More bony destruction and more rapid than the LAP
  • Bleeding, deep pocketing (BPE 4), Periodontal abscess. No gingival inflammation

Severity of periodontal tissue destruction is subclassified in the same fashion as is chronic periodontitis.

Treatment

Treatment generally involves mechanical therapy (non-surgical or surgical debridement) in conjunction with antibiotics. Several studies suggest that these types of cases respond best to a combination of surgical debridement and antibiotics. Regenerative therapy with bone grafting procedures are often selected in these cases due to the favorable morphology of the bony defects which result from the disease.

Aggregatibacter actinomycetemcomitans (Aa) is one of the most efficient causative pathogens in this disease, Tetracycline seems affecting Aa better (250 mg 3 times daily for 2 weeks). However some suggests the use of Metronidazole 400 mg and Amoxicillin 250 mg 4 times daily for 1 week in severe cases. Root planing and maintaining good oral hygiene is required and Periodontal surgery to gain more access to the roots is needed occasionally.