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Aggressive periodontitis

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Periodontitis refers to the inflammation of the supporting periodontal tissues surrounding the tooth. It is caused by specific groups of micro-organisms and results in progressive destruction of the periodontal fibres and the alveolar bone. Chronic periodontitis is the most common form of periodontitis, has a slow rate of progression and most commonly affects adults and sometimes even children and adolescents. It is associated with accumulation of plaque and calculus but the rate of disease progression also depends on local (morphology of teeth, restorations), systemic (diabetes mellitus, HIV/AIDS) and environmental factors (cigarette smoking). Aggressive periodontitis (AP) on the other hand, differs from the chronic form by 1) occurring primarily in adolescents and young adults, 2) causing rapid destruction of the periodontium with very little or no plaque and calculus accumulation, 3)occurring in healthy individuals with no systemic disease and 4) having a genetic predisposition.

AP is further classified as localized (LAP) and generalized aggressive periodontitis (GAP). As the name implies, the localized form of the disease is characterized by destruction of periodontal tissues and bone loss localized only around the incisors and first molars. GAP however, has a more generalized widespread destruction. LAP was previously called localised juvenile periodontitis and the generalized aggressive form encompasses what were previously called generalizied juvenile and rapidly progressive periodontitis.


LAP is very rare and its prevalence is estimated to be less than 1%. It does not have any gender predilection and affects both males and females usually around puberty before 20 years of age. One of the striking features of the disease is the amount of periodontal destruction with minimal to no plaque accumulation. LAP is characterized by attachment loss being restricted to the incisors and first molars. In fact the disease does not involve any other teeth other than incisors and molars. This disease has a 2-3 times faster rate of bone loss compared to chronic periodontitis. Teeth mobility and migration are common signs. Many patients have distolabial migration of teeth leading to a diastema formation. Patients may also complain of a dull pain during mastication. Of importance is the fact that patients otherwise are healthy and do not have signs or symptoms of any systemic disease.

Radiographically, the disease shows vertical bone loss in the incisor and molar area. Characteristic sign is an arc shaped bone loss, extending from the distal surface of the second premolar to the mesial surface of the second molar. There may be a similar arc shaped bone loss in the incisor regions.

So what makes this disease restrict itself to these teeth?

It is speculated that incisors and first molars are primarily involved due to the fact that they are the first permanent teeth to erupt. So A.actinomycetemcomitans evades host immune responses, colonizes and starts inflicting damage. However, the body then elicits a robust immune response and develops a high serum antibody titre against A.actinomycetemcomitans, thereby restricting growth and spread. Other organisms also simultaneously proliferate, competing and antagonising growth of A.actinomycetemcomitans.


GAP affects persons younger than 30 years but could appear in patients who are older. Similar to LAP, the periodontal destruction occurs with little or no plaque accumulation. It is characterized by interproximal attachment loss in at least three teeth apart from incisors and first molars. Teeth mobility and migration are common signs. Like LAP, patients do not have signs of any systemic disease. Clinical signs are known to occur episodically with periods of periodontal destruction and periods of quiescence. It also differs from LAP in having a poor antibody response against A.actinomycetemcomitans. This is the reason speculated for the more generalized spread of attachment loss unlike LAP. In fact many patients of GAP are patients who have progressed from LAP, though there are patients who develop GAP from the onset. Unlike LAP, GAP has a microbiological environment that is diverse and also has increased quantities of organisms like P.gingivalis, P.intermedia and F.nucleatum.


Since A.actinomycetemcomitans invades the connective tissue and the patient may have neutrophil functional defects, routine scaling and root planning would not suffice. Periodontal debridement has to be complemented with antibiotics like tetracycline, amoxicillin and minocycline. Chlorhexidine also has to be prescribed and should be used by patients for several weeks post treatment. Patients are to be kept under follow up and re-evaluated every 3-4 weeks. Patients with LAP have a good prognosis but patients presenting with GAP and advanced bone loss usually have a bad prognosis and respond less reliably to treatment.


Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology. 10 th ed. Elsevier; 2009.

Nibali L. Aggressive Periodontitis: microbes and host response, who to blame? Virulence. 2015;6(3):223-8.

Noack B, Hoffmann T. Aggressive periodontitis. Perio. 2004;1(4):335-44.

Lindhe J, Lang NK, Karring T. Clinical periodontology and implant dentistry. 5th ed. Blackwell Munksgaard;2008.

Neville BW, Damm DD, Allen CM, Chi A. Oral and Maxillofacial Pathology. South Asian ed. Elsevier; 2016.


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