Abstract

The study of host response in periodontal disease may provide a mechanism to monitor disease progression. The purpose of the present research was to determine the levels of IL-1α, IL-1β, TNF-α, IL-6, IL-6sR, IL-8, IL-10, MMP-3 and MMP-8 in gingival crevicular fluid (GCF), before and after non-surgical periodontal treatment (NSPT) in order to evaluate therapy response. Methodology: Eleven patients diagnosed with chronic periodontitis and eleven healthy subjects were selected for this study. Clinical measurements, including probing depth (PD) and clinical attachment loss (CAL) were carried out in patients diagnosed with chronic periodontitis and periodontal healthy controls. The clinical indexes evaluated were: gingival index (GI) and plaque index (PI). Samples of GCF were taken from one tooth per quadrant before and 45 days after NSPT. The levels of inflammatory mediators were measured by ELISA. Results: The values of all clinical parameters decreased significantly after treatment. The concentration levels of all cytokines and MMP-3 and MMP-8 in the GCF sample were higher in patients diagnosed with chronic periodontitis compared to the healthy group. All inflammatory mediators decreased after therapy, but did not reach control values; IL-6, Il-6sR, IL-10 and TNF-α, attained the highest reduction (70% -54%); the vales of MMP3, IL-1α, IL-1β and IL-8 were reduced between 50% - 34%; and MMP-8 showed the lowest decrease (28%). Conclusion: All clinical parameters and cytokines levels decreased after NSPT. The mediators TNF-α IL-6, IL-6sR, and IL-10 showed the largest variation between before and after NSPT and could thus be used to evaluate therapy response.

Highlights

  • Periodontitis is characterized by chronic infection, inflammation, and destruction of supporting periodontal tissues.[1]

  • Data collection Clinical measurements, including probing depth (PD), clinical attachment loss (CAL), gingival index (GI) and plaque index (PI), were carried out in patients diagnosed with chronic periodontitis (9 females and 2 males) and periodontally healthy controls (8 females and 3 males)

  • Strong negative correlation was found between PI with IL-10 (r=-0.847; p

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Summary

Introduction

Periodontitis is characterized by chronic infection, inflammation, and destruction of supporting periodontal tissues.[1] Disease manifestation results from the interaction between host defense mechanisms, microbial agents, and environmental and genetic factors.[2] The host response to pathogens results in the production of inflammatory mediators by cells like neutrophils, macrophages, T-cells, mast cells and fibroblast. Pro-inflammatory cytokines like interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor (TNF-α) and prostaglandin E2 (PGE2) can promote extracellular matrix destruction by matrix metalloproteinases (MMPs) in the periodontium and stimulate bone resorption.[3] Increased levels of several cytokines, including interleukin IL-1, IL-2, IL-6, IL-8 and TNF-α have been observed in GCF from patients with periodontal disease. Cytokines and MMPs levels in gingival crevicular fluid from patients with chronic periodontitis before and after non-surgical periodontal therapy

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