关键词: articular cartilage collagen collagen crosslinking genipin glutaraldehyde interstitial lubrication tribological rehydration

Mesh : Humans Cartilage, Articular Lubrication Glutaral Collagen Osteoarthritis / drug therapy Friction Stress, Mechanical Iridoids

来  源:   DOI:10.1115/1.4064663   PDF(Pubmed)

Abstract:
Healthy articular cartilage is a remarkable bearing material optimized for near-frictionless joint articulation. Because its limited self-repair capacity renders it susceptible to osteoarthritis (OA), approaches to reinforce or rebuild degenerative cartilage are of significant interest. While exogenous collagen crosslinking (CXL) treatments improve cartilage\'s mechanical properties and increase its resistance to enzymatic degradation, their effects on cartilage lubrication remain less clear. Here, we examined how the collagen crosslinking agents genipin (GP) and glutaraldehyde (GTA) impact cartilage lubrication using the convergent stationary contact area (cSCA) configuration. Unlike classical configurations, the cSCA sustains biofidelic kinetic friction coefficients (μk) via superposition of interstitial and hydrodynamic pressurization (i.e., tribological rehydration). As expected, glutaraldehyde- and genipin-mediated CXL increased cartilage\'s tensile and compressive moduli. Although net tribological rehydration was retained after CXL, GP or GTA treatment drastically elevated μk. Both healthy and \"OA-like\" cartilage (generated via enzymatic digestion) sustained remarkably low μk in saline- (≤0.02) and synovial fluid-lubricated contacts (≤0.006). After CXL, μk increased up to 30-fold, reaching values associated with marked chondrocyte death in vitro. These results demonstrate that mechanical properties (i.e., stiffness) are necessary, but not sufficient, metrics of cartilage function. Furthermore, the marked impairment in lubrication suggests that CXL-mediated stiffening is ill-suited to cartilage preservation or joint resurfacing.
摘要:
健康的关节软骨是一种卓越的轴承材料,针对近乎无摩擦的关节关节进行了优化。因为其有限的自我修复能力使其容易患骨关节炎,加强或重建退化软骨的方法是非常感兴趣的。而外源性胶原交联(CXL)处理改善软骨的机械性能和抵抗其酶降解的敏感性,它们对软骨润滑的影响尚不清楚。这里,我们研究了胶原蛋白交联剂京尼平(GP)和戊二醛(GTA)如何使用会聚固定接触面积(cSCA)构型影响软骨润滑。与经典配置不同,cSCA通过间隙和流体动力增压的叠加来维持生物静力动摩擦系数(µk)(即,摩擦学补液)。不出所料,戊二醛和京尼平介导的CXL增加软骨的拉伸和压缩模量。尽管CXL后仍保留了净摩擦学补液,GP或GTA处理急剧升高µk。在盐水(=0.02)和滑液润滑接触(=0.006)中,健康和“OA样”软骨(通过酶消化产生)均保持极低的µk。在CXL之后,µk增加到30倍,达到与体外软骨细胞明显死亡相关的值。这些结果表明,机械性能(即,刚度)是必要的,但还不够,软骨功能的指标。此外,润滑方面的显著损害提示CXL介导的硬化不适用于软骨保存或关节表面修复.
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