Literature Review | Periodontosis
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Zambon, J, Christersson, R, Genco: Diagnosis and Treatment of Localized Juvenile Periodontitis. JADA, 113:295, 1986


Review Article. Proposed treatment modalities directed to reduce subgingival AA
(AA=HA=Haemophilus actinomycetemcomitans).

Hypothesis about the pattern of destruction

  1. Immune response limit disease process: The first molars and incisors are the first teeth to erupt. AA colonized (transmitted from other family member), and then the immune system produce opsonizing antibodies against AA. Antibodies control the numbers of AA at initial sites of infection and prevent spreading of AA to other periodontal sites.
  2. Absence of bacterial antagonism to AA in infected sites. (Presence of inhibitory bacteria can prevent spread of AA to other sites).

VIRULENCE of AA is due to production of: Leukotoxins, chemotaxis inhibiting factor, lipopolysaccharides that can cause bone resorption, collagenase (destroy gingival connective tissue), epitheliotoxins, lymphotoxins.

There is evidence to suggest that AA is the causative agent for LJP and other forms of periodontitis:

PROPOSED TX: Mechanical debridement and systemic use of tetracycline. In order to avoid "under" or "over tx", the presence of AA should be monitor by laboratory technique. Immunologic techniques such as immunofluorescent microscopy seems to be better and faster than culture, and could be obtained in a dental office.


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