双相磷酸钙和富血小板纤维蛋白的协同作用通过抑制/信号通路抑制慢性牙周炎中炎症和破骨细胞分化的标志物。
Synergistic Effect of Biphasic Calcium Phosphate and Platelet-Rich Fibrin Attenuate Markers for Inflammation and Osteoclast Differentiation by Suppressing / Signaling Pathway in Chronic Periodontitis.
机构信息
Department of Periodontology, Meenakshi Ammal Dental College and Hospital, Meenakshi Academy of Higher Education and Research, Chennai 600095, India.
Maktoum Bin Hamdan Dental University College, Dubai 213620, United Arab Emirates.
出版信息
Molecules. 2021 Oct 30;26(21):6578. doi: 10.3390/molecules26216578.
BACKGROUND
Periodontitis is characterized by excessive osteoclastic activity, which is closely associated with inflammation. It is well established that MAPK/NF-kB axis is a key signaling pathway engaged in osteoclast differentiation. It is stated that that biphasic calcium phosphate (BCP) and platelet-rich fibrin (PRF) have significant antiostoeclastogenic effects in chronic periodontitis.
OBJECTIVE
We aimed to elucidate the synergetic effect of PRF/BCP involvement of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and the mitogen-activated protein kinase () signaling pathway in osteoclast differentiation in chronic periodontitis.
METHODS
We induced osteoclast differentiation in vitro using peripheral blood mononuclear cells (PBMCs) derived from patients with chronic periodontitis. We assessed osteoclast generation by tartrate-resistant acid phosphatase (TRAP) activity, proinflammatory cytokines were investigated by ELISA and NF-κB, and by immunoblot, respectively. MAPK proteins and osteoclast transcription factors were studied by Western blot analysis and osteoclast transcriptional genes were assessed by RT-PCR.
RESULTS
The results showed that the potent inhibitory effect of PRF/BCP on osteoclastogenesis was evidenced by decreased TRAP activity and the expression of transcription factors, NFATc1, c-Fos, and the osteoclast marker genes, TRAP, MMP-9, and cathepsin-K were found to be reduced. Further, the protective effect of PRF/BCP on inflammation-mediated osteoclastogenesis in chronic periodontitis was shown by decreased levels of proinflammatory cytokines, NF-kB, IKB, and MAPK proteins.
CONCLUSIONS
PRF/BCP may promote a synergetic combination that could be used as a strong inhibitor of inflammation-induced osteoclastogenesis in chronic periodontitis.
背景
牙周炎的特征是破骨细胞过度活跃，这与炎症密切相关。MAPK/NF-kB 轴是参与破骨细胞分化的关键信号通路，这一点已得到充分证实。有研究表明，双相磷酸钙（BCP）和富含血小板的纤维蛋白（PRF）在慢性牙周炎中具有显著的抗破骨细胞生成作用。
目的
本研究旨在阐明 PRF/BCP 参与核因子 kappa-轻链增强子的激活 B 细胞（NF-kB）和丝裂原活化蛋白激酶（MAPK）信号通路在慢性牙周炎破骨细胞分化中的协同作用。
方法
我们通过体外诱导慢性牙周炎患者外周血单个核细胞（PBMC）分化为破骨细胞来评估破骨细胞的生成。通过抗酒石酸酸性磷酸酶（TRAP）活性来评估破骨细胞的生成，通过酶联免疫吸附试验（ELISA）来检测促炎细胞因子，通过免疫印迹法分别检测 NF-κB 和 MAPK，通过 Western blot 分析研究 MAPK 蛋白和破骨细胞转录因子，通过 RT-PCR 评估破骨细胞转录基因。
结果
结果表明，PRF/BCP 对破骨细胞生成具有强烈的抑制作用，表现为 TRAP 活性降低，转录因子 NFATc1、c-Fos 以及破骨细胞标志物基因 TRAP、MMP-9 和组织蛋白酶-K 的表达降低。此外，PRF/BCP 对慢性牙周炎炎症介导的破骨细胞生成具有保护作用，表现为促炎细胞因子、NF-kB、IKB 和 MAPK 蛋白水平降低。
结论
PRF/BCP 可能促进协同组合，可作为慢性牙周炎炎症诱导的破骨细胞生成的强抑制剂。
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