Mineral deposition intervention through reduction of phosphorus intake suppresses osteoarthritic lesions in temporomandibular joint
Mineral deposition intervention through reduction of phosphorus intake suppresses osteoarthritic lesions in temporomandibular joint
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DOI：
10.1016/j.joca.2021.05.061
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发表时间：
2021-08-15
影响因子：
7
通讯作者：
Wang, M.
中科院分区：
文献类型：
--
作者：
Duan, J.;Zhang, J.;Wang, M.
目的：探讨低磷饮食对骨关节炎颞下颌关节的抑制作用及软骨细胞核酸损伤的可能机制。实验设计：软骨细胞在有或无低磷培养液的情况下承受流体流动剪切应力（FFSS）。72只小鼠（3、7、11周取样，n = 6）和48只大鼠（12周取样，n = 6）在低磷饮食和非低磷饮食的条件下进行单侧前牙反牙合（UAC）。在FFSS模型中，检测软骨细胞中的Ca和P含量、核酸降解相关分子以及矿物质产生反应。测定培养皿硬度对软骨细胞成骨分化的影响。在UAC模型中，测定血清Ca、P含量。应用显微CT、扫描电镜、原子力显微镜观察髁突软骨骨化情况及刚度。结果如下：FFSS诱导软骨细胞核酸降解、Pi积累和矿物质生成反应，低磷培养基可减轻FFSS诱导的软骨细胞核酸降解、Pi积累和矿物质生成反应。较硬的培养皿底部促进培养软骨细胞的成骨分化。低磷饲料可抑制UAC引起的软骨退变和软骨细胞核酸损伤，增加PARP 1和血清P含量，促进软骨的骨化和硬化（均P < 0.05）。结论：核酸损伤在骨关节炎软骨中的磷产生中起作用，有助于软骨的矿化和硬度增强，这反过来促进软骨降解，这可以通过低磷摄入来缓解。(c)2021国际骨关节炎研究学会。由爱思唯尔有限公司出版。保留所有权利。
Objective: To explore the suppressing impact of low phosphorus intake on osteoarthritic temporomandibular joint and the possible mechanisms of nuclear acid injury in the insulted chondrocytes. Design: Chondrocytes were loaded with fluid flow shear stress (FFSS) with or without low phosphorus medium. Seventy-two mice (sampled at 3-, 7- and 11-wk, n = 6) and forty-eight rats (sampled at 12-wks for different testing purpose, n = 6) were applied with unilateral anterior crossbite (UAC) with or without low phosphorus diet. In the FFSS model, the Ca and P content, molecules related to nucleic acid degradation and the mineral-producing responses in chondrocytes were detected. The effect of culture dish stiffness on chondrocytes osteogenic differentiation was measured. In the UAC model, the content of Ca and P in serum were tested. The condylar cartilage ossification and stiffness were detected using micro-CT, scanning electron microscope and atomic force microscope. Results: FFSS induced nucleic acid degradation, Pi accumulation and mineral-producing responses in the cultured chondrocytes, all were alleviated by low P medium. Stiffer dish bottoms promoted the osteogenic differentiation of the cultured chondrocytes. UAC stimulated cartilage degeneration and chondrocytes nucleic acid damage, increased PARP 1 and serum P content, and enhanced ossification and stiffening of the cartilage, all were suppressed by low phosphorus diet (all, P < 0.05). Conclusion: Nucleic acid damage takes a role in phosphorus production in osteoarthritic cartilage, contributing to the enhanced mineralization and stiffness of the cartilage that in turn promotes cartilage degradation, which can be alleviated by low phosphorus intake. (c) 2021 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.