Despite wide discussion in the literature regarding an association between diabetes and 28-demethyl-beta-amyrone periodontal disease, the periodontal histological alterations induced by diabetes are poorly known. Diabetes seems to interfere in extracellular matrix metabolism in periodontium, reducing collagen synthesis and increasing collagenolytical activity. Histological studies also demonstrated increased vessel wall thickening in gingival tissue of diabetic patients. In addition, some studies suggest diabetes seems to interfere in host defense mechanisms such as chemotaxis, adherence, phagocytosis and apoptosis, contributing therefore to tissue destruction. Although some authors have not found significant association between diabetes and periodontal disease in humans experimental models have demonstrated that the prevalence and severity of bone resorption in periodontal disease induced by ligatures or bacterial inoculation was higher in the presence of diabetes. Experimental studies demonstrate that the increased severity of periodontal disease in diabetic animals was due to an exacerbated inflammatory response triggered by advanced glycation end products. However, in all this previous experimental studies, the putative effect of diabetes over the periodontal tissues was always investigated in a scenario resultant of the deliberated Armepavine induction of periodontal disease by means of bacterial inoculation or by silk ligatures. Nevertheless, recent studies suggest that diabetes could also favor, or even trigger, the establishment of periodontal disease, and not only exacerbate the established disease. Therefore, considering that diabetes presents a great influence on periodontal health, and the putative diabetes effects over periodontium were never previously investigated without simultaneous intentional induction of periodontal disease, in this study we investigated the kinetics of radiographic and histological changes in periodontal tissues after diabetes induction in rats. The experimental group showed evidence of development and progression of periodontal disease, observed from the third month of diabetes induction.