Department of Stomatology, Shengjing Hospital of China Medical University, Shenyang, China.
J Periodontal Res. 2019 Feb;54(1):73-80. doi: 10.1111/jre.12606. Epub 2018 Oct 22.
Periodontitis is a bacteria-induced disease that often leads to alveolar bone damage. Its mechanisms were considered to be complicated, involving an imbalance of the formation and resorption of bone. We sought to disclose the antibody-independent function of B cells during periodontitis.
Production of receptor activator for nuclear factor-κB ligand (RANKL) by total lymphocytes or sorted B-cell subsets in gingiva from healthy or experimental periodontitis animals was examined by flow cytometry, real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. To define the effects of lymphocytes or B-cell subsets on osteoclastogenesis induction, bone marrow mononuclear cells were culture in culture medium of lymphocytes or cocultured with B-cell subsets. Osteoclasts were enumerated by tartrate-resistant acid phosphatase staining. Constituent ratio of B-cell subsets in healthy or experimental periodontitis was also detected by flow cytometry.
Gingiva B cells produce more RANKL and support more osteoclastogenesis than T and other lymphocytes, and this potential improved in periodontitis. Memory B cells (CD27+CD38-) decreased their percentage in periodontitis. Memory B cells have the highest propensity for RANKL production. Remarkably, memory B cells from periodontitis animals expressed significantly more RANKL compared to healthy controls. Memory B cells supported osteoclast differentiation in vitro in a RANKL-dependent manner, and the number of osteoclasts was higher in cultures with memory B cells from periodontitis animals than in those derived from healthy ones. Other B-cell subsets have limited impact on osteoclast formation.
Findings of this study further disclose the roles of B cells engaged in periodontal immunomodulation and reveal the considerable importance of memory B cells in alveolar bone homeostasis and their likely contribution to alveolar bone destruction in periodontitis.
牙周炎是一种由细菌引起的疾病，常导致牙槽骨损伤。其机制被认为较为复杂，涉及骨形成和吸收的失衡。本研究旨在揭示牙周炎中 B 细胞的抗体非依赖性功能。
通过流式细胞术、实时聚合酶链反应和酶联免疫吸附试验检测来自健康或实验性牙周炎动物牙龈的总淋巴细胞或分选 B 细胞亚群产生核因子-κB 配体（RANKL）的情况。为了明确淋巴细胞或 B 细胞亚群对破骨细胞诱导的影响，将骨髓单核细胞在淋巴细胞培养基中培养或与 B 细胞亚群共培养。通过抗酒石酸酸性磷酸酶染色计数破骨细胞。通过流式细胞术检测健康或实验性牙周炎中 B 细胞亚群的组成比例。
与 T 细胞和其他淋巴细胞相比，牙龈 B 细胞产生更多的 RANKL 并支持更多的破骨细胞生成，这种潜能在牙周炎中增强。记忆 B 细胞（CD27+CD38-）在牙周炎中的比例降低。记忆 B 细胞具有最强的 RANKL 产生倾向。值得注意的是，与健康对照组相比，来自牙周炎动物的记忆 B 细胞表达了更高水平的 RANKL。记忆 B 细胞以 RANKL 依赖的方式支持破骨细胞分化，并且来自牙周炎动物的记忆 B 细胞培养物中的破骨细胞数量高于来自健康动物的培养物。其他 B 细胞亚群对破骨细胞形成的影响有限。
本研究的结果进一步揭示了 B 细胞在牙周免疫调节中的作用，并揭示了记忆 B 细胞在牙槽骨稳态中的重要性及其在牙周炎中对牙槽骨破坏的可能贡献。
