Abstract

Treating periodontitis with metronidazole (MET) as an adjunct to scaling root planing (SRP) is suggested to have inconsistent effects on insulin resistance (IR) in type 2 diabetes mellitus (T2DM). This paper will present the effects of MET, in addition to SRP, on the homeostatis model assessment of IR (HOMA-IR). A three-arm clinical trial was conducted and analyses were performed on T2DM participants with periodontitis (n = 74) who completed follow-up visits at 3 and 6 months after the intervention. The observed between-group and within-group mean changes in IR were found using ANOVA with repeated measures, followed by a post-hoc analysis, and a p-value of ≤0.05 was considered significant. Between-group analyses showed no difference in the HOMA-IR at 3 months, but at 6 months the difference was significant (p = 0.046). Within-group analyses showed that the HOMA-IR was significantly reduced in both test groups (p ≤ 0.05) over the period of time. Adjunct use of MET may result in a sudden short-term lowering of the HOMA-IR level within 3 months that may not be retained over 6 months when compared to the sustained lowering of the HOMA-IR levels in T2DM when intervened with SRP without MET.

Highlights

  • Uncontrolled type 2 diabetes mellitus (T2DM) with raised levels of glucose is represented by higher levels of HbA1c

  • The periodontitis of all recruited participants was found with a pocket depth of 3.48 ± 0.87 mm and a mean clinical attachment loss (CAL) of 3.87 ± 1.03

  • Adjunct use of MET may result in a sudden lowering of the HOMA-insulin resistance (IR) levels in 3 months within the group, but the reduction may not be retained over a longer period of 6 months, especially when compared to the sustained lowering of homeostatis model assessment of IR (HOMA-IR) levels as observed in the scaling root planing (SRP) without MET group

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Summary

Introduction

Uncontrolled type 2 diabetes mellitus (T2DM) with raised levels of glucose is represented by higher levels of HbA1c. The hormone called insulin, produced by the human pancreas, helps to utilize this glucose in the body. In an uncontrolled condition, the patients suffer from insulin resistance (IR) that does not allow cells to absorb and utilize glucose, thereby causing increased glucose levels in the body. Insulin resistance is commonly initiated due to a reduced sensitivity to insulin-mediated glucose clearance and an inability to produce glucose by liver enzymes [1]. Insulin resistance is said to be established as a result of low-grade inflammation [3,4] that further deteriorates the systemic functions and eventually increases the risk of T2DM [5]. It is theorized that the persistent Gram-negative bacterial challenge and host-mediated release of pro-inflammatory cytokines may have consequences extending beyond the periodontal tissues, leading to increased IR and poor glycemic control [6]

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