- Localized aggressive periodontitis (LAP)
- Generalized aggressive periodontitis (GAP)
The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis.
- 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 phogocytosis.
The first feature mentioned is to say that patients may not exhibit any disorder that predisposes one to another form of periodontitis.
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
- 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 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.
- Armitage GC (December 1999). "Development of a classification system for periodontal diseases and conditions". Ann. Periodontol. 4 (1): 1–6. doi:10.1902/annals.1918.104.22.168. PMID 10863370.
- Albandar JM, Tinoco EM (2002). "Global epidemiology of periodontal diseases in children and young persons". Periodontol. 2000 29: 153–76. PMID 12102707.
- Papapanou PN (November 1996). "Periodontal diseases: epidemiology". Ann. Periodontol. 1 (1): 1–36. PMID 9118256.
- American Academy of Periodontology (1999). "Consensus report: Aggressive Periodontitis". Ann. Periodontol. 4 (1): 53. doi:10.1902/annals.1922.214.171.124.
- AAP In-Service Exam, 2008-B40