Institute of Anatomy, Paracelsus Medical University (PMU), Salzburg and Nuremberg, Prof-Ernst Nathan Strasse 1, 90419 Nuremberg, Germany.
Cells. 2019 Aug 27;8(9):990. doi: 10.3390/cells8090990.
Osteoarthritis (OA) induces inflammation and degeneration of all joint components including cartilage, joint capsule, bone and bone marrow, and ligaments. Particularly intraarticular ligaments, which connect the articulating bones such as the anterior cruciate ligament (ACL) and meniscotibial ligaments, fixing the fibrocartilaginous menisci to the tibial bone, are prone to the inflamed joint milieu in OA. However, the pathogenesis of ligament degeneration on the cellular level, most likely triggered by OA associated inflammation, remains poorly understood. Hence, this review sheds light into the intimate interrelation between ligament degeneration, synovitis, joint cartilage degradation, and dysbalanced subchondral bone remodeling. Various features of ligament degeneration accompanying joint cartilage degradation have been reported including chondroid metaplasia, cyst formation, heterotopic ossification, and mucoid and fatty degenerations. The entheses of ligaments, fixing ligaments to the subchondral bone, possibly influence the localization of subchondral bone lesions. The transforming growth factor (TGF)β/bone morphogenetic (BMP) pathway could present a link between degeneration of the osteochondral unit and ligaments with misrouted stem cell differentiation as one likely reason for ligament degeneration, but less studied pathways such as complement activation could also contribute to inflammation. Facilitation of OA progression by changed biomechanics of degenerated ligaments should be addressed in more detail in the future.
骨关节炎(OA)可引起包括软骨、关节囊、骨和骨髓以及韧带在内的所有关节成分的炎症和退化。特别是连接关节的关节内韧带,如前交叉韧带(ACL)和半月板胫骨韧带,将纤维软骨半月板固定在胫骨上,容易受到 OA 炎症关节环境的影响。然而,韧带退化在细胞水平上的发病机制,很可能是由 OA 相关炎症引发的,目前仍知之甚少。因此,本综述深入探讨了韧带退化、滑膜炎、关节软骨降解和失衡的软骨下骨重塑之间的密切相互关系。已经报道了伴随关节软骨降解的韧带退化的各种特征,包括软骨样化生、囊肿形成、异位骨化以及黏液样和脂肪变性。固定韧带与软骨下骨的韧带附着点可能会影响软骨下骨病变的定位。转化生长因子 (TGF)β/骨形态发生 (BMP) 途径可能是连接骨软骨单位和韧带退化的纽带,因为干细胞分化错误是韧带退化的一个可能原因,但研究较少的途径,如补体激活,也可能导致炎症。未来应更详细地研究退化韧带的生物力学变化对 OA 进展的促进作用。