Abstract

Diagnosis of periodontopathy is complex and includes defining the cause, type, stage, and grade of periodontitis. Therefore, alternative diagnostic methods are sought to indicate the progression of inflammation or to determine the effectiveness of therapy. Gingival crevicular fluid (GCF) biomarkers can be particularly useful because they most likely reflect the disease process of the periodontal tissues. However, the difficulty of collecting GCF for testing is the reason for the limited use in diagnostics. Because periodontitis is the primary source of nitrogen free radicals in the oral cavity, the aim of the study was to evaluate the biomarkers of nitrosative stress (nitric oxide, peroxynitrite, and S-nitrosothiols) in GCF, non-stimulated and stimulated saliva of 90 patients with periodontitis. The study group was divided into two subgroups, depending on the stage of the disease severity. We showed a significantly higher concentration of all assessed biomarkers in the non-stimulated and stimulated saliva of patients with periodontitis. However, significant changes in GCF has been shown only for peroxynitrite. The studied biomarkers did not correlate with clinical periodontal status, which probably results from their short-duration activity and the impact on a few factors in the oral cavity. Saliva and gingival fluid are not very useful in the differential diagnosis of periodontitis.

Highlights

  • The most recent definition of periodontitis indicates that it is a chronic and multifactorial inflammatory disease associated with dysbiosis in bacterial biofilm and leading to progressive destruction of the attachment apparatus [1]

  • The picture of periodontopathy is influenced by the effects of the immune-inflammatory response, contained in the gingival crevicular fluid (GCF) and saliva, as well as the impact of environmental and behavioral factors

  • The research involved 60 patients treated for periodontitis in the Department of Periodontology at the Medical University named after Piastów Ślaskichin Wrocław

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Summary

Introduction

The most recent definition of periodontitis indicates that it is a chronic and multifactorial inflammatory disease associated with dysbiosis in bacterial biofilm and leading to progressive destruction of the attachment apparatus [1]. The lesions associated with periodontitis can be tracked at the level of periodontal pathogens of the biofilm in the periodontal pocket (microbiome), markers of an immune-inflammatory response in the connective tissue of the gingiva, peridentium and cells, as well as mediators of alveolar bone remodeling and expression of multiple genes (genome and epigenome). Evidence has shown that interaction of phagocytic cells with invading pathogens results in the nitric oxide (NO) formation (primarily form inducible nitric oxide synthases—iNOS) and superoxide anion, leading to the formation of peroxynitrite, responsible for the destruction of microorganisms [2]. Since NO has a limited ability to react with cellular elements, most of the deleterious effects associated with

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