ETIOPATHOGENISIS OF AgP

Etiology

In aggressive periodontitis, the following four factors play distinct roles in the susceptibility of
the host and thus in the manifestation of disease:

Bacteria–host interactions.

Host defences in aggressive periodontitis.

Deficiencies in host defences.

Genetic predisposition.

The term aggressive periodontitis was suggested by the International Workshop on the
Classification of Periodontal Diseases and Conditions, which was organized by the American
Academy of Periodontology in 1999

According to the consensus report of the above workshop, patients may present certain
secondary features, such as elevated proportions of A.a and, in some populations, P g

The gram-negative, capnophilic coccobacillus, A. a, has been considered, for over 30 years,
as the most likely etiologic agent in aggressive periodontitis (Socransky, Muller HP, Slots J.)

Serotype b most strongly associated with the disease (Zambon JJ, Slots J, and Genco RJ.)

Specific JP2 clone, representing serotype b important role in the development of aggressive
periodontitis in certain populations (Haubek D)

Takeuchi for detection of microorganisms in sub gingival flora of Japanese population using
PCR it was found that the prevalence of A.a was less in patients with LAP whereas elevated
levels of P.g, Tannerella forsythia, T.denticola, P.intermedia, and Campylobacterrectus
was detected.

Filifactor alocis is gram positive anaerobic rod which has the potential of being periodontal
pathogen and the levels of these bacteria is elevated in aggressive periodontitis patients.
(Schlafer S)

Treponema lecithinolyticum and Treponema socranskii are elevated in GAP (Takeuchi Y)

Desulfomicrobium orale, has been suggested to be involved in various categories of
periodontal destruction, possibly synergistically with the red complex periodontal pathogens
(Langendijk)

Yamabe suggested Archaea a methanogenic organism, especially Methanobrevibacter

oralisas putative periodontal pathogen for aggressive periodontitis.

Herpes viruses, especially Epstein-Barr virus and human cytomegalovirus, have been
suggested to play a role in the onset of aggressive periodontitis by interacting with
periodontitis-associated bacteria, such as A.a, P.g, T. forsythia, C. rectus, (slots j)

Mombelli et al conducted a systematic review 2002 to decide whether A.a can be used for the
detection of AgP. Found that A.a was found in both CGP and AgP. Any Aa Positive
individual with periodontitis was three times more likely to be suffering from Chronic than
AgP. So concluded presence or absence of A.a could not discriminate between CGP and AgP.

Immunologic Factors

HLA antigen, which regulate immune response, have been evaluated as a candidate markers
for AgP. Although the findings with many HLA antigens have been inconsistent, HLA-A9 and
B-15 antigens are consistently associated with aggressive periodontitis.

Polymorphonuclear neutrophils (PMNs) play an important role in host immune response

qualitative and quantitative deficiency in PMNs can lead to increased periodontal destruction.

AgP display functional defects in PMN`s, monocytes or both. These defects can impair either
chemotactic attraction of PMN to site of infection or the ability of phagocytosis.

Kinane et al.performed an extensive study of polymorphonuclear neutrophil chemotaxis from

a series of these patients with aggressive periodontitis and found not only no defect, but rather
an overactivation of these cells in the peripheral blood of patients with aggressive periodontitis.

Hyper-responsiveness of monocyte from LAP patients with respects to their production of

PGE2 in response to LPS. This hyper-responsive phenotype could lead to increased CT or Bone
loss due to excessive production of these catabolic factors.

Poorly functional form of monocytes FcyR11 receptor seen in AgP.

Increased expression of MHC 2, HLA DR43, altered helper or suppressor T cell function,
polyclonal activation of B cells by microbial plaque etc predisposes AgP.
GENETIC FACTORS

Read genetics notes

Results from several studies support the concept that all individuals are not equally susceptible
to AgP specifically, several authors have described familial pattern of ABL and have
implicated gene factors in AgP.

Genetic factors regulate the innate immune system and that certain genetic polymorphisms may
render the immune system defective and unable to successfully fend off assaults by infecting
microorganisms.

Genetic factors may play a more significant role in the pathogenesis of aggressive periodontitis
than in chronic periodontitis.

Segregational analyses and linkage analyses of families with a genetic predisposition for LAP
suggest that a major gene plays a role in disease which is of Autosomal Dominant mode of
inheritance.

Van dyke et al reported a familial clustering of the neutrophil abnormalities seen in LAP.

Antibody response to periodontal pathogens A.a is under genetic control

Tonetti and Mombelli concluded “It seems that specific genes may be different in various
populations and /or ethnic groups and therefore true heterogeneity in disease susceptibility may
be present. The role of specific genes remains to be elucidated.

Environmental Factors

Amount of duration of smoking

Smokers have more affected teeth ad more loss of clinical attachment than non-smoking
patients with GAP.