Abstract
The Gram-negative bacterium Aggregatibacter actinomycetemcomitans is part of the HACEK group that causes infective endocarditis, a constituent of the oral flora that promotes some forms of periodontal disease and a member of the family of species that secrete a cytolethal distending toxin (Cdt). The family of bacteria that express the cdt genes participate in diseases that involve the disruption of a mucosal or epithelial layer. In vitro studies have shown that human gingival epithelial cells (HGEC) are native targets of the Cdt that typically induces DNA damage that signals growth arrest at the G2/M interphase of the cell cycle. The gingival epithelium is an early line of defense in the oral cavity against microbial assault. When damaged, bacteria collectively gain entry into the underlying connective tissue where microbial products can affect processes and pathways in infiltrating inflammatory cells culminating in the destruction of the attachment apparatus of the tooth. One approach has been the use of an ex vivo gingival explant model to assess the effects of the Cdt on the morphology and integrity of the tissue. The goal of this review is to provide an overview of these studies and to critically examine the potential contribution of the Cdt to the breakdown of the protective gingival barrier.
Highlights
Aggregatibacter actinomycetemcomitans is a member of the taxonomic family Pasteurellaceae that includes the genera Actinobacillus/Aggregatibacter [1], Haemophilus, Mannheimia and Pasteurella
Aggregatibacter actinomycetemcomitans has been strongly implicated in the development of localized aggressive periodontitis (LAP) and possibly contributes to chronic periodontitis (CP), two derivatives of periodontal disease
Along with factors released from recruited inflammatory cells, induce degradation of connective tissue and bone resulting in damage to the supporting structures of the teeth
Summary
Aggregatibacter actinomycetemcomitans is a member of the taxonomic family Pasteurellaceae that includes the genera Actinobacillus/Aggregatibacter [1], Haemophilus, Mannheimia and Pasteurella. All fresh clinical isolates of A. actinomycetemcomitans obtained from a large geographically homogeneous population of LAP families contain a chromosomal locus for the Cdt [20,21] Some of these isolates have cdt gene deletions of various lengths, all members of one restriction fragment length polymorphism (RFLP) cluster group contain a complete cdt operon [7]. Fifty-three percent of the Cdt+ isolates correlated with attachment loss indicative of LAP In another recent study, A. actinomycetemcomitans isolated from 255 subgingival samples from aggressive and chronic periodontitis and clinically healthy sites in 30 Chinese subjects were screened for only the cdtB gene sequence [24]. The goal of this review is to present and critically analyze current information supporting the hypothesis that the AaCdt plays a role in early events associated with periodontal disease
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