Department of Orthopedic Surgery and Sports Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL.
Department of Orthopaedic Surgery, Duke University, School of Medicine, Durham, NC.
J Orthop Trauma. 2019 Jun;33 Suppl 6:S6-S12. doi: 10.1097/BOT.0000000000001472.
The goals of all orthopaedic surgeons treating articular cartilage injuries have been anatomic reduction and stable fixation of the articular cartilage surface with restoration of limb alignment and/or reestablishment of the joint stability, all while minimizing the risk of surgical complications. Recent developments in the study of articular cartilage injury have shown that there is a robust cellular response to joint injury. This response has been shown to involve the synoviocytes, chondrocytes, and osteocytes in and around the injured joint and if these responses are left unchecked, they can lead to the development of posttraumatic osteoarthritis (PTOA). Therefore, to predictably and successfully treat articular cartilage injuries, it is not sufficient to just restore articular congruity, limb alignment, and joint stability, but we must also recognize and attempt to mitigate this associated cellular response. Understanding not only the mechanical aspects of these joint injuries but also the biological aspects is paramount to giving our patients the best opportunity to heal their injuries, recover full function, and avoid the potential devastating development of PTOA. Gone is the simplistic view that if one can achieve articular congruity after intraarticular fracture, as well as joint stability after ligamentous injury, that our patients will do just fine. This review sheds new light on the molecular response to cartilage injury, how residual joint incongruity and instability affect the joint's ability to recover from injury, and how chondrocyte apoptosis in response to injury can influence joint. This article then briefly reviews how cellular and growth factors may be beneficial to the treatment of articular cartilage injury and how ultimately cartilage regeneration may be used in the future to salvage the joints ravaged by PTOA in response to injury.
所有治疗关节软骨损伤的骨科医生的目标都是使关节软骨表面解剖复位和稳定固定，恢复肢体对线和/或重建关节稳定性，同时最大限度地降低手术并发症的风险。关节软骨损伤研究的最新进展表明，关节损伤后会有强烈的细胞反应。这种反应已被证明涉及受伤关节内和周围的滑膜细胞、软骨细胞和成骨细胞，如果这些反应不受控制，它们可能导致创伤后骨关节炎（PTOA）的发展。因此，为了可预测和成功地治疗关节软骨损伤，仅仅恢复关节吻合度、肢体对线和关节稳定性是不够的，我们还必须认识到并试图减轻这种相关的细胞反应。了解这些关节损伤的机械方面和生物学方面同样重要，这是为我们的患者提供最佳治愈损伤、恢复全部功能并避免 PTOA 潜在破坏性发展的机会的关键。现在已经不再是那种简单的观点，即如果在关节内骨折后能够实现关节吻合度，在韧带损伤后能够实现关节稳定性，那么我们的患者就会没事。这篇综述揭示了软骨损伤的分子反应、残余关节不吻合和不稳定如何影响关节从损伤中恢复的能力，以及软骨细胞对损伤的凋亡如何影响关节。本文简要回顾了细胞和生长因子如何有益于治疗关节软骨损伤，以及最终软骨再生如何在未来用于修复因损伤而受到 PTOA 蹂躏的关节。
