The aim of this study was to evaluate the histologic and cellular response to A.actinomycetemcomitans (A.a) infection, and how diabetes-enhanced TNF-? production and diabetes-enhanced apoptosis contribute to the periodontal disease progression and bone coupling. Conclusion. The results link A. a infection with important characteristics of periodontal destruction and provide new insight into how diabetes aggravates A. a induced periodontal destruction in rats by significantly increasing the inflammatory response, leading to increased bone loss and enhancing apoptosis of gingival epithelial and connective tissue cells through a caspase-3-dependent mechanism. Antibiotics had a more pronounced effect on many of these parameters in diabetic than in normoglycemic rats, suggesting a deficiency in the capacity of diabetic animals to resist infection. In addition, diabetes prolongs inflammation and osteoclastogenesis in periodontitis and through TNF limits the normal reparative process by negatively modulating factors that regulate bone.
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