Alveolar bone response in an experimental model of renal failure and periodontal disease: a histomorphometric and histochemical study.

Abstract

Chronic destructive periodontal disease is characterized by gingival inflammation, periodontal pocket formation, and bacterial plaque that lead to alveolar bone destruction. Polymorphonuclear neutrophil leukocytes (PMNs) are the first line of defense against infection caused by dental plaque bacteria. Renal patients present functional abnormalities of PMN, including impaired chemotaxis, phagocytosis, and intracellular killing of bacteria. In view of the above, the aim of this work was to evaluate the effect of renal failure on bone damaged by periodontal disease using histomorphometric and histochemical parameters. Twenty male Wistar rats weighing 250 g were assigned to one of the following four groups: 1) control (no treatment); 2) renal failure (RF); 3) periodontal disease (PD); and 4) renal failure plus periodontal disease (RF+PD). All the animals were sacrificed 31 days after the onset of the experiment. Mesio-distally oriented sections of the first lower molar were obtained for histomorphometric and histochemical evaluation. Total erosion, active erosion, and total number of tartrate-resistant acid phosphatase-positive (TRAP+) osteoclasts were found to be increased in the RF+PD group compared with the PD group. Our results demonstrate increased bone resorption in animals with untreated renal failure and periodontal disease, and thus indicate that the release of different factors by inflammatory cells is magnified, accelerating the progression of the disease in this animal model.