Apoptosis of periodontium cells in streptozototocin- and ligature-induced experimental diabetic periodontitis in rats

Abstract

Objective. The aim of this study was to investigate the presence of apoptosis of periodontium cells in streptozototocin- and ligature-induced experimental diabetic periodontitis in rats. Materials and methods. Sixty-two 6-week-old male Sprague-Dawley (SD) rats were randomly divided into three groups: the diabetic periodontitis group (group DP; n = 22), periodontitis group (group P; n = 20) and normal control group (group N; n = 20). Diabetes was induced by intraperitoneal injection of streptozototocin (STZ). Periodontitis was initiated by ligating floss around maxillary second molars. The animals were sacrificed at 3 and 6 weeks after ligature placement in the P and DP groups. Maxillary dentoalveolar segments were isolated and were prepared for morphometric analysis of alveolar bone loss (ABL) and for histological analysis. Results. ABL was significantly increased in group DP compared with group P (p < 0.05). The number of PDL fibroblasts, osteoblasts and osteocytes in group DP was decreased compared with group P (p < 0.05). Inter-group analysis revealed higher osteoclast numbers in the inflammatory area of group DP and group P when compared with group N (p < 0.05). Also, compared with group P, group DP had more higher osteoclast numbers (p < 0.05). Periodontitis and diabetic periodontitis also increased apoptosis of fibroblasts, osteoblasts and osteocytes. The percentage of these apoptotic cells was ∼ 2-fold higher in group DP vs group P. Conclusions. The results of these studies suggest that diabetes may have a negative effect on the periodontium by increasing the formation of osteoclasts and enhancing apoptosis of fibroblasts, osteoblasts and osteocytes in the periodontal tissue.

Key Words::

• animal model
• apoptosis
• diabetes
• periodontitis

Acknowledgments

The authors thank Baocai Dong for technical assistance.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.