Abstract

Aim:The aim of the present study was to investigate gingival crevicular fluid (GCF) calprotectin, osteocalcin and cross-linked N-terminal telopeptide (NTx) levels in health along with different periodontal diseases.Material and methods:Twenty chronic periodontitis (CP), 20 generalized aggressive periodontitis (G-AgP), 20 gingivitis and 20 healthy subjects were included. Probing depth, clinical attachment level, plaque index and papillary bleeding index was recorded. GCF calprotectin, osteocalcin and NTx levels were analyzed by enzyme-linked immunosorbent assay (ELISA).Results:CP, G-AgP and gingivitis groups had higher GCF calprotectin total amount compared to healthy subjects (p< 0.008). CP and G-AgP groups had similar, but higher levels compared to gingivitis groups (p< 0.008). CP and G-AgP groups had lower GCF osteocalcin total amount compared to gingivitis and healthy groups (p< 0.008). CP group had higher GCF NTx but lower osteocalcin total amount and osteocalcin/NTx ratio than the G-AgP group (p< 0.008)Conclusions:Our results suggest that elevated GCF calprotectin levels play a role as a reliable inflammatory marker in the pathogenesis of periodontal disease. Fluctuating GCF levels of osteocalcin and NTx might point out to the abnormal bone turnover in periodontitis. Our data document for the first time the role of NTx in the pathogenesis of different periodontal diseases.

Highlights

  • Current knowledge about the pathogenesis of periodontal disease suggests that the central cause of periodontal disease is the loss of a healthy balance between microbial virulence agents and host inflammatory response [1,2]

  • Chronic periodontitis (CP) group had higher scores compared to generalized aggressive periodontitis (G-AgP) group and both groups had higher probing depth (PD) scores than the gingivitis group (p < 0.008)

  • CP groups had elevated clinical attachment loss (CAL) scores compared to G-AgP group (p < 0.008)

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Summary

Introduction

Current knowledge about the pathogenesis of periodontal disease suggests that the central cause of periodontal disease is the loss of a healthy balance between microbial virulence agents and host inflammatory response [1,2]. Inflammation and tissue destruction are early and continuing events during host- mediated process in response to the bacterial infection [3]. Periodontal diseases may differ in their etiological factors and pattern of progression. This variability can be attributed to differences in the presence of factors that might modify the host response to microbial pathogens. Chronic periodontitis (CP) and aggressive periodontitis, two forms of inflammatory periodontal disease, differ from each other in terms of the magnitude, sequel and control of the response [4]

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