Diabetic characteristics and alveolar bone loss in streptozotocin- and streptozotocin-nicotinamide-treated rats with periodontitis

• Published in: Journal of periodontal research 2014-12, Vol.49 (6), p.792-800
• Main Authors: Kim, J-H., Lee, D-E., Choi, S-H., Cha, J-H., Bak, E-J., Yoo, Y-J.
• Format: Article
• Language: English
• Subjects: Alveolar Bone Loss - etiology; Animals; Blood Glucose - analysis; Body Weight; bone loss; Bone Matrix - pathology; Bone Resorption - etiology; Dentistry; Diabetes Mellitus, Experimental - blood; Diabetes Mellitus, Experimental - complications; Furcation Defects - etiology; Gingiva - pathology; Glucose Tolerance Test; Hyperglycemia - blood; Hyperglycemia - complications; Insulin - blood; Insulin-Secreting Cells - drug effects; Leukocytes, Mononuclear - pathology; Male; Molar - pathology; Neutrophils - pathology; Niacinamide - administration & dosage; nicotinamide; periodontitis; Periodontitis - complications; RANK Ligand - analysis; Rats; Rats, Inbred F344; Streptozocin; streptozotocin; Tibia - pathology; Vitamin B Complex - administration & dosage; Weight Loss; X-Ray Microtomography - methods
• ISSN: 0022-3484; 1600-0765
• DOI: 10.1111/jre.12165

Background and Objective Experimental models showing variable diabetic status are necessary to understand the relationship between diabetes and periodontitis. The streptozotocin (STZ)‐induced diabetes model allows control of diabetic status by nicotinamide (NA), which protects against STZ‐induced β‐cell necrosis. Therefore, we compared diabetic characteristics and alveolar bone loss in STZ‐ and STZ‐NA‐treated rats with periodontitis. Material and Methods STZ‐treated rats were generated by intravenous (IV) administration of STZ (50 mg/kg). STZ‐NA‐treated rats were induced by intraperitoneal administration of NA (270 mg/kg) 15 min before IV administration of STZ (65 mg/kg). Periodontitis was induced by ligature around the left mandibular first molar 1 wk after injection. Blood glucose level, glucose tolerance and serum insulin levels were determined at day 0 and/or 20 after ligature. At day 20, tibia bone loss was assessed using micro‐computed tomography and hematoxylin and eosin staining. Alveolar bone loss was histologically measured as the distance of the cementoenamel junction to the alveolar bone crest in distal and the percentage of periodontal ligament area in the first molar furcation, respectively. The number of inflammatory cells, receptor activator of nuclear factor kappa‐B ligand (RANKL)‐positive cells and the area of osteoid were determined. Results In STZ‐treated rats, obvious hyperglycemia over 300 mg/dL and severe body weight loss were observed. The insulin level was approximately 14% compared to that of control rats. STZ‐NA‐treated rats were impaired in glucose tolerance compared to control rats; however, body weight and insulin levels were not significantly different. Tibia bone loss was increased in STZ‐treated rats, but significant change was not observed in STZ‐NA‐treated rats compared to control rats. In ligatured teeth, alveolar bone loss was increased in both STZ‐ and STZ‐NA‐treated rats compared to control rats. Alveolar bone loss, the number of inflammatory cells and RANKL‐positive cells in STZ‐treated rats were greater than in STZ‐NA‐treated rats. The area of osteoid decreased in STZ‐treated rats compared to control, but not STZ‐NA‐treated rats. Conclusion These results indicate that STZ‐ and STZ‐NA‐treated rats exhibit diabetic characteristics similar to type 1 diabetes mellitus and a pre‐diabetic state, respectively. In addition, alveolar bone loss in response to periodontitis and tibia loss depend on diabetic status. Diabetic st