Mechanisms linking periodontitis and diabetes

Background + Aims

• Periodontitis is a chronic inflammatory disease that affects the supporting structures of teeth, and its prevalence is notably higher in patients with diabetes.
• This study investigates the role of nitrosative stress in the progression of experimental periodontitis in diabetic rats.
• Nitrosative stress, characterised by the overproduction of reactive nitrogen species, can exacerbate inflammation and tissue damage.
• The primary aim of this research is to elucidate the mechanisms by which diabetes influences periodontal disease, focusing on the expression of inflammatory markers such as tumor necrosis factor-alpha (TNF-α) and inducible nitric oxide synthase (iNOS).
• By employing an experimental model, the study seeks to provide insights into the pathophysiological changes that occur in periodontal tissues under diabetic conditions, ultimately contributing to better management strategies for periodontal disease in diabetic patients.

Materials + Methods

• The study utilised male Sprague-Dawley rats, which were divided into 2 groups: diabetic and normal.
• Diabetes was induced in the diabetic group through a single intraperitoneal injection of streptozotocin (STZ).
• 2 weeks post-injection, periodontitis was induced by ligating a nylon thread around the cervical portion of the second molar (M2) on one side, while the contralateral side served as a control.
• Gingival tissues were collected for mRNA and protein analyses, including assessments of TNF-α and iNOS expression using quantitative PCR and Western blotting.
• Micro-computed tomography (micro-CT) was employed to evaluate alveolar bone resorption.
• Blood glucose levels and body weights were monitored throughout the study.
• Statistical analyses were performed using one-way ANOVA with Bonferroni correction to determine significant differences between groups, with a significance threshold set at p < 0.05.

Results

• Diabetic rats exhibited a marked reduction in body weight, averaging 222.5 ± 15.5 g, compared to 313.4 ± 8.1 g in normal rats (p < 0.01).
• Blood glucose levels were significantly elevated in diabetic rats, measuring 348.0 ± 30.0 mg/dl, while normal rats had levels of 113.3 ± 12.3 mg/dl (p < 0.001).
• Histological analysis showed that ligature-induced periodontitis led to a significant increase in the expression of TNF-α and iNOS mRNA in the gingival tissues of diabetic rats. The expression levels of TNF-α were significantly higher in the periodontitis side of diabetic rats compared to normal rats, indicating an exacerbated inflammatory response.
• Micro-CT analysis demonstrated significant alveolar bone loss in diabetic rats, with a reduction of approximately 30% in bone volume compared to the control side. The number of nitrotyrosine-positive cells, a marker of nitrosative stress, was significantly higher in the periodontitis side of diabetic rats (193.8 ± 28.6/mm²) compared to normal rats (52.6 ± 10.7/mm², p < 0.05).
• Gingival blood flow measurements indicated that diabetic rats had a baseline blood flow of 8.8 ± 2.8 ml/min/100 g tissue, significantly lower than the 14.8 ± 6.1 ml/min/100 g tissue observed in normal rats (p < 0.05). The ligature-induced periodontitis resulted in a 2.1-fold increase in gingival blood flow in diabetic rats, compared to a 1.3-fold increase in normal rats, highlighting the altered vascular response in diabetic conditions.

Limitations