Centre of Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London, Queen Mary's School of Medicine and Dentistry, II floor John Vane Building, Charterhouse Square, London EC1M 6BQ, UK.
Eur Cell Mater. 2010 Sep 28;20:210-7. doi: 10.22203/ecm.v020a17.
Joint surface defects (JSD) involving the articular cartilage and the subchondral bone are a common clinical problem in rheumatology and orthopaedics. The recent availability of accurate imaging for diagnosis and efficacious therapeutic options has stirred new interest in their natural history and biology. The evidence that some of these lesions can heal spontaneously whereas others precipitate osteoarthritis has raised important questions as to which lesions should be treated, when, and how. Evidence of repair of some of these lesions has also stimulated research into which factors contribute to successful healing and which ones determine chronic evolution and development of osteoarthritis (OA). Older anatomical observations, together with novel molecular tools and experimental models, have revealed a complex cellular and molecular response of cartilage to focal defects, which could explain differences in healing responses between individuals, and may provide clues to stimulating intrinsic tissue repair. In the first part of this review we will discuss clinical aspects of these lesions in the patient, with particular emphasis on their biology and natural history. In the second part we will summarize the data coming from in vitro and in vivo models of cartilage injury and regeneration, focussing on the molecular control of cartilage homeostasis after creation of cartilage surface defects.
关节表面缺损（JSD）涉及关节软骨和软骨下骨，是风湿病学和矫形外科学中的一个常见临床问题。最近，准确的成像诊断和有效的治疗选择已经激发了人们对其自然史和生物学的新兴趣。一些这些病变可以自发愈合，而另一些则会引发骨关节炎的证据，提出了关于哪些病变应该治疗、何时治疗以及如何治疗的重要问题。这些病变中有一些可以修复的证据也激发了对哪些因素有助于成功愈合以及哪些因素决定了慢性演变和骨关节炎（OA）发展的研究。更古老的解剖学观察结果，加上新的分子工具和实验模型，揭示了软骨对局灶性缺损的复杂细胞和分子反应，这可以解释个体之间愈合反应的差异，并可能为刺激内在组织修复提供线索。在这篇综述的第一部分，我们将讨论患者中这些病变的临床方面，特别强调它们的生物学和自然史。在第二部分，我们将总结来自软骨损伤和再生的体外和体内模型的数据，重点关注软骨表面缺损形成后软骨内稳态的分子控制。
