Role of Cluster of Differentiation 163 in Diabetes-Periodontitis Interplay.

Daliah Ruth,Anilkumar Kumar,Ambalavanan Namasivayam,Jaideep Mahendra,Little Mahendra,Nalini Devarajan

doi:10.7759/cureus.8523

Abstract

BackgroundThe aim of the present study was to assess and quantify cluster of differentiation 163 (CD163) protein levels and CD163 messenger RNA (mRNA) gene expression in subgingival plaque samples of generalized chronic periodontitis subjects with and without type II diabetes mellitus (DM).Materials and methodsEighty chronic periodontitis subjects were selected and divided into 40 systemically healthy, generalized chronic periodontitis subjects (Group I) and 40 generalized chronic periodontitis subjects diagnosed with type II diabetes mellitus (Group II). Age, body mass index (BMI), income, plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were recorded. CD163 protein and gene expressions were quantified and compared between the groups.Results The mean age, BMI, income, PI, BOP %, and CD163 protein and gene expression were higher in Group II (p< 0.05) as compared to Group I. In Group I, CD163 protein levels showed a negative correlation with respect to BMI and PI, and this was statistically significant. In Group II, all the periodontal parameters showed a positive correlation with CD163 protein levels. Overall, PI and BOP % were significantly correlated with CD163 protein levels. Both CD163 protein and gene expression showed a negative correlation with each other (p= 0.001).ConclusionThe elevated protein levels of CD163 in the subgingival plaque samples of generalized chronic periodontitis individuals with type II diabetes mellitus signify the involvement of CD163 in the pathogenesis of both periodontitis and diabetes mellitus. CD163 can play a challenging role as a diagnostic, as well as a prognostic biomarker, in both these inflammatory diseases.

Highlights

Periodontitis is a microbial-induced chronic inflammatory disease of supporting periodontal structures resulting in progressive destruction of the periodontium with an increase in probing pocket depth, recession, or both, leading to tooth loss
The mean age, body mass index (BMI), income, plaque index (PI), bleeding on probing (BOP) %, and cluster of differentiation 163 (CD163) protein and gene expression were higher in Group II (p< 0.05) as compared to Group I
In Group I, CD163 protein levels showed a negative correlation with respect to BMI and PI, and this was statistically significant

Summary

Introduction

Periodontitis is a microbial-induced chronic inflammatory disease of supporting periodontal structures resulting in progressive destruction of the periodontium with an increase in probing pocket depth, recession, or both, leading to tooth loss. Periodontal disease results from a complex interplay between subgingival biofilm and the host immune-inflammatory events. It is important to understand the cause and pathological process of periodontal diseases and their chronic inflammatory nature to reveal the possible way through which it may activate several infectious events in the body [1]. The elevated inflammatory state in diabetes contributes to both microvascular and macrovascular complications and it is clear that hyperglycemia can result in the activation of pathways that increase inflammation, oxidative stress, and apoptosis. The aim of the present study was to assess and quantify cluster of differentiation 163 (CD163) protein levels and CD163 messenger RNA (mRNA) gene expression in subgingival plaque samples of generalized chronic periodontitis subjects with and without type II diabetes mellitus (DM)

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