Abstract
Objectives Diabetes mellitus (DM) is a major risk factor for periodontitis. Susceptibility to periodontitis increases approximately three times in people with DM. There is a clear relationship between the degree of hyperglycemia and the severity of periodontitis. This study aimed to analyze the reduction of tumor necrosis factor-α (TNF-α) in diabetics who came for periodontitis examination to prevent exacerbations.
Materials and Methods This was an analytic observational study using a cross-sectional approach at health centers in Surabaya, Indonesia. Measurement of periodontal status used the community periodontal index of treatment needs by measuring bleeding at probing and pocket depth. TNF-α was measured using enzyme-linked immunosorbent assay, and behavior and lifestyle using a questionnaire.
Statistical Analysis The Kolmogorov–Smirnov test was performed to identify data normality (p < 0.05). A nonparametric test was used to measure the degree of association between different characteristics and the incidence of periodontitis in type 2 DM patients with and without periodontitis. Spearman's test was done to examine the correlation between TNF-α level and severity of periodontitis in diabetics. The significant level was at p <0.05.
Results There was a correlation between age, predisposing factors, reinforcing factors, drug consumption, and TNF-α levels in patients with type 2 DM and the incidence of periodontitis.
Conclusions Poor glycemic control can induce oxidative stress on the gingiva, thereby aggravating damage to periodontal tissue. An important factor in preventing periodontitis for type 2 DM patients is controlling blood sugar levels through regular consumption of drugs and regular maintenance of oral cavity health. Knowledge is a predisposing factor that affects adherence of people with type 2 DM to consuming drugs regularly, which can be strengthened by family support. These will ultimately play a role in reducing TNF-α levels.
Effects of Tumor Necrosis Factor-α on Glucose Metabolism in Cultured Human Muscle Cells from Nondiabetic and Type 2 Diabetic Subjects1