Comparative evaluation of tumor necrosis factor-α levels in gingival crevicular fluid, HbA1c levels, and homeostatic model assessment for insulin resistance in nondiabetic subjects with and without periodontitis.

BACKGROUND

Diabetes mellitus is a well-recognized risk factor for periodontitis and there is ample evidence that untreated periodontitis can worsen glycemic control in the diabetic population. However, the effect of untreated periodontitis on glycemic status of nondiabetic population is less explored. The aim of the study is to estimate and correlate glycemic control and inflammatory status with periodontal parameters of nondiabetic subjects with and without generalized periodontitis.

MATERIALS AND METHODS

Nondiabetic subjects between 18 and 60 years were divided into two groups: Group 1: periodontally healthy controls ( = 50) and Group 2: nondiabetic participants with chronic periodontitis ( = 50). Probing pocket depth (PPD), clinical attachment level (CAL), and modified Sulcus Bleeding Index were recorded for all the individuals. Blood samples for the estimation of HbA1c (glycated hemoglobin) and Homeostatic Model Assessment for Insulin Resistance (HOMA IR) and gingival crevicular fluid (GCF) samples for the estimation of tumor necrosis factor alpha (TNF-α) were collected. The GCF and the serum samples were processed using the ELISA kits.

RESULTS

There was a statistically significant difference ( = 0.001) between the test and control groups in the values of glycemic indicators; HbA1c (Group A - 5.19% ±0.47% and Group B - 5.90% ±0.46%), TNF-α (Group A - 15.52 ± 7.35 pg/ml and Group B - 35.25 ± 18.26 pg/ml), and HOMA IR (Group A - 3.45 ± 2.29; Group B - 5.78 ± 1.82). A lack of correlation was observed between periodontal parameters (PPD and CAL) and glycemic indicators such as HbA1c, TNF α, and HOMA IR in both the groups.

CONCLUSION

There is a significant difference in the HbA1c, HOMA IR, and TNF α between nondiabetic subjects with and without periodontitis indicating that untreated periodontal disease worsens the glycemic control and increases the risk of developing diabetes mellitus in nondiabetic individuals.