B cell subset distribution is altered in patients with severe periodontitis

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).

CD19+ CD24hi CD38hi Regulatory B Cells and Memory B Cells in Periodontitis: Association with Pro-Inflammatory and Anti-Inflammatory Cytokines

“…In the clinically healthy sulcus, memory B cell trafficking may occur together with the polymorphonuclear cell emigration [ 14 , 15 ]. Such gingival memory B cells are obviously functional, as they can secrete IgG and IgA after in vitro polyclonal stimulation [ 16 ]. B cell subsets in gingivitis and periodontitis were initially described by Mahanonda et al, who published that patients of periodontitis show a characteristic distribution of different B cell populations.…”

Osteoimmunology of Oral and Maxillofacial Diseases: Translational Applications Based on Biological Mechanisms

“…During periodontitis, stromal cells and immune cells express different cytokines and chemokines such as IL-4, IL6, IL-5, CXCL13, and APRIL that induce B cell migration and support their survival in the periodontium (65, 66). Patients with periodontitis have a significantly higher percentage of CD19 + CD27 + CD382 − memory B cells and CD138 + HLA-DR low plasma cells while B1 cells, which have been previously described as a regulatory type of B cell (CD20 + CD69 − CD43 + CD27 + CD11b + ) are decreased (67, 68). B cells/plasma cells are well-known for their humoral immunity.…”

Osteoimmunology: Inflammatory osteolysis and regeneration of the alveolar bone

“…Thus, B cells can contribute to inflammatory osteolysis but not under all circumstances. Moreover, even though in periodontally diseased gingival tissue, more than 90% of B cells expressed RANKL (Kawai et al., ) and RANKL expression is increased in circulating B‐cell subsets from periodontitis patients (Demoersman et al., ), mice with a conditional knockout of RANKL in B cells showed no inflammatory alveolar bone loss (Tsukasaki et al., ). Thus, there is a controversy as to under what conditions B cells are involved in inflammatory osteolysis.…”