The Department of Spinal Surgery, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 111, Dade Road, Yuexiu District, Guangzhou 510120, China; The Laboratory Affiliated to Orthopaedics and Traumatology of Chinese Medicine of Linnan Medical Research Center of Guangzhou University of Chinese Medicine, No. 12, Jichang Road, Baiyun District, Guangzhou 510405, China.
The Department of Spinal Surgery, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 111, Dade Road, Yuexiu District, Guangzhou 510120, China; Guangzhou University of Chinese Medicine, No. 12, Jichang Road, Baiyun District, Guangzhou 510405, China.
Med Hypotheses. 2018 Dec;121:183-187. doi: 10.1016/j.mehy.2018.08.023. Epub 2018 Aug 27.
Osteoarthritis (OA) is one of the most common degenerative disease which causes pain and disability of joint and brings heavy socioeconomic burden in the world. However, the pathogenesis of OA has not been fully understood. Articular cartilage degradation or loss was often regarded as the characteristic of osteoarthritis. But we believe that there may had a illusion that OA was simply considered to be a process of wear and tear because evidences have supported all joint tissues remodeling including cartilage, subchondral bone, synovium, ligament, fat pad, and etc, were engaged in OA, in particular the cartilage and subchondral bone. Many factors such as mechanics, inflammation and immunological abnormality could drive the joint tissues metabolic and disturb the steady state of cartilage and bone, which further devoted to a serial pathological manifestations, consisting of hypertrophy and apoptosis of articular chondrocytes, degradation of cartilage matrix, angiogenesis and calcification of hyaline cartilage, replication of tidemark, formation of osteophytes, degeneration of ligaments and, in the knee, the menisci, hypertrophy of the joint capsule and remodeling of subchondral bone along with increased permeability of the osteochondral interface. The thickening of calcified cartilage, the thinning of superficial hyaline cartilage and the remodeling of subchondral bone indicated that the cartilage degradation could be a procedure of enchondral ossification similar to the growth plate, of driven by a host of cytokines within the affected joint. Articular cartilage loses stable state from normal resting to a high turnover in the stimulation of abnormal mechanical stresses and cytokines would subsequently contributed to slowly sustained remodeling and calcification, which might be the key features of the initiation and development of OA. In this article, the development and structural comparison of articular cartilage and growth plate as well as the major pathologic features of OA will be discussed to explain that cartilage degeneration in OA might be a process of enchondral ossification similar to growth plate. This would provide a new perspective for understanding OA's pathogenesis and the treatment in the future.
骨关节炎(OA)是最常见的退行性疾病之一,它会导致关节疼痛和功能障碍,并给全球带来沉重的社会经济负担。然而,OA 的发病机制尚未完全阐明。关节软骨的降解或丢失通常被认为是 OA 的特征。但我们认为,人们可能存在一种误解,即 OA 仅仅被认为是一种磨损过程,因为有证据表明,包括软骨、软骨下骨、滑膜、韧带、脂肪垫等在内的所有关节组织都参与了 OA 的重塑,特别是软骨和软骨下骨。许多因素,如力学、炎症和免疫异常等,都可以驱动关节组织的代谢,并扰乱软骨和骨的稳定状态,从而进一步导致一系列病理表现,包括关节软骨细胞的肥大和凋亡、软骨基质的降解、透明软骨的血管生成和钙化、潮线的复制、骨赘的形成、韧带的变性,以及在膝关节中,半月板的变性、关节囊的肥大和软骨下骨的重塑,同时伴随着骨软骨界面的通透性增加。钙化软骨的增厚、浅层透明软骨的变薄和软骨下骨的重塑表明,软骨降解可能是一种类似于生长板的软骨内成骨过程,受关节内多种细胞因子的驱动。关节软骨从正常静止状态到异常机械应力和细胞因子刺激下的高转换状态的不稳定会导致缓慢持续的重塑和钙化,这可能是 OA 起始和发展的关键特征。本文将讨论关节软骨和生长板的发育和结构比较以及 OA 的主要病理特征,以解释 OA 中的软骨退化可能是一种类似于生长板的软骨内成骨过程。这将为理解 OA 的发病机制和未来的治疗提供一个新的视角。
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