Journal of Clinical Periodontology

Actinobacillus actinomycetemcomitans in human periodontal disease


  • Joseph J. Zambon

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    1. Departments of Oral Biology and Periodontology, State University of New York at Buffalo, School of Dentistry, New York, USA
      Department of Oral Biology, Room 222 Foster Hall, State University of New York at Buffalo, 3435 Main Street, Buffalo. New York 14214, USA
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Department of Oral Biology, Room 222 Foster Hall, State University of New York at Buffalo, 3435 Main Street, Buffalo. New York 14214, USA


Abstract Recent evidence implicates Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis. This paper reviews the morphological, biochemical and serological characteristics of A. actinomycetemcomitans, evidence incriminating it as a periodontopathogen, its importance in human nonoral infections, and virulence factors which may be involved in the pathogenesis of A. actinomycetemcomitans infections.

A. actinomycetemcomitans is a non-motile, gram-negative, capnophilic, fermentative coccobacillus which closely resembles several Haemophilus species but which does not require X or V growth factors. The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose and into 3 serotypes on the basis of heat stable, cell surface antigens.

A. actinomycetemcomitans primary human ecologic niche is the oral cavity. It is found in dental plaque, in periodontal pockets, and buccal mucosa in up to 36% of the normal population. The organism can apparently seed from these sites to cause severe infections throughout the human body such as brain abscesses and endocarditis.

There is a large body of evidence which implicates A. actinomycetemcomitans as an important microorganism in the etiology of localized juvenile periodontitis including: (1) an increased prevalence of the organism in almost all localized juvenile periodontitis patients and their families compared to other patient groups; (2) the observation that localized juvenile periodontitis patients exhibit elevated antibody levels to A actinomycetemcomitans in serum, saliva and gingival crevicular fluid; (3) the finding that localized juvenile periodontitis can be successfully treated by eliminating A. actinomycetemcomitans from periodontal pockets; (4) histopathologic investigations showing that A. actinomycetemcomitans invades the gingival connective tissue in localized juvenile periodontitis lesions; (5) the demonstration of several pathogenic products from A. actinomycetemcomitans including factors which may: (a) facilitate its adherence to mucosal surfaces such as capsular polysaccharides; (b) inhibit host defense mechanisms including leukotoxin, a polymorphonuclear leukocyte chemotaxis inhibiting factor, and a lymphocyte suppressing factor (c) cause tissue destruction such as lipopolysaccharide endotoxin, a bone resorption-inducing toxin, acid and alkaline phosphatases, collagenase, a fibroblast inhibiting factor and an epitheliotoxin.

Although A. actinomycetemcomitans is an apparently important micro-organism in the etiology of localized juvenile periodontitis, additional research is needed to pinpoint subjects at risk of contracting this disease, to develop means of preventing localized juvenile periodontitis, and to examine the role of this organism in other forms of periodontal disease.