Abstract

Objective: The protective mechanisms that maintain periodontal homeostasis in gingivitis and prevent periodontal tissue destruction are poorly understood. The aim of this study was to identify changes in the salivary proteome during experimental gingivitis.Study design: We used oral neutrophil quantification and whole saliva (WS) proteomics to assess changes that occur in the inflammatory and resolution phases of gingivitis in healthy individuals. Oral neutrophils and WS samples were collected and clinical parameters measured on days 0, 7, 14, 21, 28, and 35.Results: Increased oral neutrophil recruitment and salivary cytoprotective proteins increased progressively during inflammation and decreased in resolution. Oral neutrophil numbers in gingival inflammation and resolution correlated moderately with salivary β-globin, thioredoxin, and albumin and strongly with collagen alpha-1 and G-protein coupled receptor 98.Conclusions: Our results indicate that changes in salivary cytoprotective proteins in gingivitis are associated with a similar trend in oral neutrophil recruitment and clinical parameters.Clinical relevance: We found moderate to strong correlations between oral neutrophil numbers and levels of several salivary cytoprotective proteins both in the development of the inflammation and in the resolution of gingivitis. Our proteomics approach identified and relatively quantified specific cytoprotective proteins in this pilot study of experimental gingivitis; however, future and more comprehensive studies are needed to clearly identify and validate those protein biomarkers when gingivitis is active.

Highlights

  • Periodontal diseases are a diverse group of inherited or acquired conditions that affect the tooth-supporting tissues in more than half of world population

  • Worsening of clinical inflammatory parameters and biofilm accumulation were evident in all experimental gingivitis (EG) participants by day 21, including Bleeding on Probing (BOP), and Gingival Index (Löe, 1967)

  • Changes in clinical parameters were detected by day 7, and increased significantly by day 14 reaching a peak on day 21 and returned to baseline levels by day 35, after subjects returning to regular OH on day 21

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Summary

Introduction

Periodontal diseases are a diverse group of inherited or acquired conditions that affect the tooth-supporting tissues in more than half of world population. Different pathogenic mechanisms including inflammatory, traumatic, genetic, and neoplastic contribute to the onset and progression of periodontal diseases (Madianos et al, 2005). The main etiologic factor for these conditions is the bacterial biofilm while the most common forms of periodontal diseases are plaque-induced gingivitis (GI) and chronic periodontitis (CP). The causative relationship between bacterial plaque (biofilm) and gingival inflammation was well demonstrated in experimental gingivitis (Loe et al, 1965). CP is characterized by extension of gingival inflammation to the alveolar bone, connective tissue degradation, and net loss of tooth attachment to periodontium (American Academy of Periodontology, 2000). Clinical studies have demonstrated that in some individuals GI never progresses to CP, regardless of periodontal care (Pihlstrom et al, 2005)

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