Abstract
Non-surgical periodontal therapy (NSPT) is the first essential step for the management of any periodontitis patient. This study aims to evaluate the impact of NSPT on pro-inflammatory mediators’ regulation and on clinical parameters in periodontitis patients who suffer from chronic hepatitis C. At baseline, selected patients were clinically evaluated for their periodontal status. A subsequent quantitative assessment of C-reactive protein and pentraxin-3 in samples of gingival fluid was performed by Enzyme-Linked Immunosorbent Assay (ELISA). Afterwards, NSPT was performed. Three months after NSPT, the clinical and ELISA assessments were repeated. The results show an improvement of the clinical parameters in periodontitis patients at the three-month recall. In chronic hepatitis C patients with periodontitis, the gingival fluid levels of pro-inflammatory markers reduced significantly. The targeted markers also expressed significant correlations with the clinical parameters used for the assessment of periodontitis’ severity. The results suggest that, while chronic hepatitis C patients exhibited a more negative periodontal status at baseline as compared to non-hepatitis ones, NSPT is effective in decreasing the local periodontal inflammatory reaction and in proving the periodontal status of this type of patients. Given the limitation of the study, periodontal screening and NSPT should be included in the integrated therapeutical approach of chronic hepatitis C patients, for its impact on the local inflammatory response.
Highlights
Periodontitis is an inflammatory disease caused by the subgingival accumulation and growth of bacterial biofilm [1]
gingival crevicular fluid (GCF) C-reactive protein (CRP) value was higher for the Hepatitis C Virus (HCV)+P group than the P group, but not statistically significant (p = 0.1243)
Periodontitis and Chronic hepatitis C (CHC) are characterized by chronic inflammatory reactions, which can mainly lead to the accumulation of their clinical consequences in adult patients
Summary
Periodontitis is an inflammatory disease caused by the subgingival accumulation and growth of bacterial biofilm [1]. Periodontitis is triggered when the accumulated subgingival bacterial biofilm is left undisrupted for extended time periods, which allows its colonization with highly pathogenic bacteria [3]. These bacteria and their toxins enter the gingival tissues, triggering the inflammatory reaction which characterizes periodontitis [4]. Periodontitis can influence the systemic health status of a patient and the clinical manifestation of certain diseases [7] This bi-directional relationship of periodontitis with systemic health and disease has been studied over the last decade, leading to the development of the “periodontal medicine” concept [8]. The concept is taken into account by the new 2018 classification of periodontal diseases, stating that, for example, a poorly controlled diabetes mellitus can significantly modify the staging and grading of periodontitis, in terms of severity and rate of progression [10]
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