Abstract
Several studies have recently highlighted the implication of B cells in physiopathogenesis of periodontal disease by showing that a B cell deficiency leads to improved periodontal parameters. However, the detailed profiles of circulating B cell subsets have not yet been investigated in patients with severe periodontitis (SP). We hypothesised that an abnormal distribution of B cell subsets could be detected in the blood of patients with severe periodontal lesions, as already reported for patients with chronic inflammatory diseases as systemic autoimmune diseases. Fifteen subjects with SP and 13 subjects without periodontitis, according to the definition proposed by the CDC periodontal disease surveillance work group, were enrolled in this pilot observational study. Two flow cytometry panels were designed to analyse the circulating B and B1 cell subset distribution in association with the RANKL expression. A significantly higher percentage of CD27+ memory B cells was observed in patients with SP. Among these CD27+ B cells, the proportion of the switched memory subset was significantly higher. At the same time, human B1 cells, which were previously associated with a regulatory function (CD20+CD69-CD43+CD27+CD11b+), decreased in SP patients. The RANKL expression increased in every B cell subset from the SP patients and was significantly greater in activated B cells than in the subjects without periodontitis. These preliminary results demonstrate the altered distribution of B cells in the context of severe periodontitis. Further investigations with a larger cohort of patients can elucidate if the analysis of the B cell compartment distribution can reflect the periodontal disease activity and be a reliable marker for its prognosis (clinical trial registration number: NCT02833285, B cell functions in periodontitis).
Highlights
Periodontitis is a bacterial biofilm-induced chronic inflammatory disease leading to the destruction of tooth-supportive structures
Our pilot study showed for the first time that severe periodontitis (SP) patients presented an altered distribution of peripheral blood B cells with a higher proportion of memory B cells, especially switched memory B cells, and a lower proportion of regulatory CD11b+ B1 cells
The proportion of CD19+ B cells decreases until age 35, B cells remains steady up to age 65 [25] and when young healthy donors (HD) and mild-aged HD are compared, similar percentages of CD27+IgD- switched memory B cells were found [26]
Summary
Periodontitis is a bacterial biofilm-induced chronic inflammatory disease leading to the destruction of tooth-supportive structures (gingiva, alveolar bone and periodontal ligament). B cell distribution in severe periodontitis diabetes mellitus or artherosclerosis [2]. Inflammatory processes are mediated by various inflammatory and stromal cell types that lead to tissue destruction. These bacteria-induced inflammatory mechanisms are the suspected links between periodontitis and inflammatory systemic syndromes [3,4]. The requirement for reliable biomarkers to distinguish progressive periodontitis from normal biological processes is considered fundamental to conduct the appropriate treatment
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