Elevated cross-talk between subchondral bone and cartilage in osteoarthritic joints.
Elevated cross-talk between subchondral bone and cartilage in osteoarthritic joints.
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DOI：
10.1016/j.bone.2011.11.030
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发表时间：
2012-08
期刊：
影响因子：
4.1
通讯作者：
Wang, Liyun
中科院分区：
文献类型：
--
作者：
Pan, Jun;Wang, Bin;Li, Wen;Zhou, Xiaozhou;Scherr, Thomas;Yang, Yunyi;Price, Christopher;Wang, Liyun
骨关节炎（OA）是一种退行性关节疾病，是美国和世界各地残疾的主要原因之一。作为一种全关节疾病，OA表现出复杂的病因学，风险因素包括但不限于老化、关节负荷改变和损伤。假设软骨下骨参与OA的发展。然而，缺乏支持这一点的直接证据。我们先前检测到可测量的溶质运输通过正常关节中的矿化钙化软骨，这表明软骨下骨和软骨之间存在潜在的串扰。这种串扰是否存在于OA中尚未确定。使用两种模型，诱导OA的老化或手术（内侧半月板，DMM的不稳定），我们测试的假设，增加串扰发生在OA。我们使用我们新开发的光漂白诱导的荧光损失（FLIP）方法定量了钙化关节基质内荧光素钠（376 Da）（小尺寸信号分子的标记物）的扩散率。老年人钙化软骨内示踪剂扩散系数为0.30±0.17和0.33±0.20 μm2/s，骨软骨界面内示踪剂扩散系数为0.12±0.04和0.07±0.03 μm2/s（20-24月龄，n=4）和DMM OA关节（5月龄，n=5），分别与DMM小鼠中对侧未手术关节的值（0.48±0.13和0.12±0.06 μm2/s）相当。虽然我们没有检测到OA关节组织基质渗透性的显著变化，但我们发现i）侵入钙化软骨的血管数量增加（有时接近潮标）在老年（+100%）和DMM（+50%）关节相对于正常年龄对照;和ii）老年关节中的软骨下骨和钙化软骨层变薄60%（在DMM关节中未检测到显著变化）。这些结果表明，软骨下骨和关节软骨之间的串扰的能力可以在OA中升高。需要进一步的研究来确定串扰的方向，涉及的信号分子，并测试软骨下骨的变化是否启动OA的发展，并可以作为OA治疗的药物靶点。
Osteoarthritis (OA) is a degenerative joint disease and one of the leading causes of disability in the United States and all over the world. As a disease of the whole joint, OA exhibits a complicated etiology with risk factors including, but not limited to, ageing, altered joint loading, and injury. Subchondral bone is hypothesized to be involved in OA development. However, direct evidence supporting this is lacking. We previously detected measurable transport of solute across the mineralized calcified cartilage in normal joints, suggesting a potential cross-talk between subchondral bone and cartilage. Whether this cross-talk exists in OA has not been established yet. Using two models that induced OA by either ageing or surgery (destabilization of medial meniscus, DMM), we tested the hypothesis that increased cross-talk occurs in OA. We quantified the diffusivity of sodium fluorescein (376Da), a marker of small-sized signaling molecules, within calcified joint matrix using our newly developed fluorescence loss induced by photobleaching (FLIP) method. Tracer diffusivity was found to be 0.30±0.17 and 0.33±0.20 μm2/s within the calcified cartilage and 0.12±0.04 and 0.07±0.03 μm2/s across the osteochondral interface in the aged (20–24-month-old, n=4) and DMM OA joints (5-month-old, n=5), respectively, comparable to the values for the contralateral non-operated joints in the DMM mice (0.48±0.13 and 0.12±0.06 μm2/s). Although we did not detect significant changes in tissue matrix permeability in OA joints, we found i) an increased number of vessels invading the calcified cartilage (and sometimes approaching the tidemark) in the aged (+100%) and DMM (+50%) joints relative to the normal age controls; and ii) a 60% thinning of the subchondral bone and calcified cartilage layers in the aged joints (with no significant changes detected in the DMM joints). These results suggested that the capacity for cross-talk between subchondral bone and articular cartilage could be elevated in OA. Further studies are needed to identify the direction of the cross-talk, the signaling molecules involved, and to test whether subchondral bone changes initiate OA development and could serve as a pharmaceutical target for OA treatment.
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作者：
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通讯作者：
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通讯作者：
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DOI：
10.1302/0301-620x.62b3.7410471
发表时间：
1980-01-01
影响因子：
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作者：
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通讯作者：
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