AGGRESSIVE PERIODONTITIS: INTRODUCTION, CLASSIFICATION AND PATHOGENESIS
AUTHOR: Sanketh DS, MDS
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.
ETIOLOGY AND PATHOGENESIS
The pathogenesis of AP is attributed mainly to microbiological factors and genetic predispositions to certain immunologic abnormalities.
Although specific microorganisms like Porphyromonas gingivalis, Prevotella intermedia, Capnocytophaga sp and Eikenella corrodens have been reported, Aggregatibactor actinomycetemcomitans is thought to be the primary pathogen involved in the disease.
So, why do researchers believe A.actinomycetemcomitans to be the primary pathogen causing the disease?
1. Well for starters, almost 97% of the patients with this disease harbour a very high number of A.actinomycetemcomitans. Compared to this only 21% of patients with chronic form of periodontitis may harbour this microorganism.
2. Another interesting fact is that LAP patients show elevated levels of A.actinomycetemcomitans in sites of destruction or disease progression, compared to the low numbers or complete absence in other healthy sites.
3. LAP patients have elevated serum antibody levels against A.actinomycetemcomitans.
4. It has also been found that reducing the load of A.actinomycetemcomitans in patients during treatment correlates positively with clinical success of the treatment.
So, how does this microorganism cause the disease?
1. Well, first of all A.actinomycetemcomitans has the ability to translocate itself through the junctional epithelium invading into the connective tissue. So, just scaling or root planing to remove plaque or diseased/inflamed periodontal tissue is not going to solve the problem.
2. One of the main weapons in its arsenal is a protein toxin called leukotoxin!Leukotoxin helps A.actinomycetemcomitans thrive in this micro-environment.
a) Leukotoxin can potentially kill neutrophils which form the first line of defence in an inflammatory response.
b) It can also cause non-lethal suppression of lymphocytic activity.
3. A.actinomycetemcomitans release chemotactic inhibitory factors that inhibit the ability of neutrophils to respond to chemotactic factors. This prevents neutrophils from migrating to the diseased site!
4. The microorganism releases factors that help it evade the host immune response.
5. Apart from causing havoc to the host immune response, the bacteria also produce collagenases that destroy the connective tissue and bone resorbing factors, causing rapid resorption of bone.
6. There is also the host inflammatory response to take into consideration. It is elicited by the bacteria and causes damage to the host tissues while trying to protect it. In fact it has been reported that patients have hyper-responsive monocytes and macrophages, which release bone resorbing factors like IL-1 and PGE2 in excess thus helping rapid bone resorption.
Apart from the damage caused by A.actinomycetemcomitans individuals with this disease are also known to have genetic predispositions to immunologic abnormalities that could amplify the disease response.
1. 70-75% of patients with this disease are known to have defective neutrophil chemotaxis. It was found that LAP tended to occur among family members and the neutrophil defect had a genetic predisposition.
2. Another defect in LAP patients was that antibodies could not bind efficiently to the bacterial antigens, which meant that these micro-organisms could not be removed through complement mediated responses. It is speculated that, for this reason, LAP patients tend to have a rather robust and increased antibody response to counter its inefficient binding to bacterial antigens.
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