Steinhagen J, Niggemeyer O, Bruns J
Klinik und Poliklinik für Orthopädie, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg.
Orthopade. 2001 Jan;30(1):20-7. doi: 10.1007/s001320050569.
Osteochondritis dissecans of the talus is a particular form of osteochondral lesions of the talus. A trauma with subsequent osteochondral defect detected immediately by radiology has to be differentiated from osteochondritis dissecans of the talus. Osteochondritis dissecans (o.d.) is primarily a disease of the subchondral bone and can affect almost every joint in the human organism. After the knee and elbow, the talus is the third most common site of the disease accounting for 4% of all cases. It mostly arises in the 2nd decade but can occur at almost any age. Different etiological factors of osteochondritis dissecans (vascular, traumatic, infectious, endogenous, genetic) are discussed in general and in particular for the talus. In the literature, the etiopathogenetic mechanism of trauma is favored. Several studies show an anamnestic coincidence of distortsion and/or supination trauma prior to the onset of o.d. at the talus. The most common localization of the o.d. lesion is the middle and posterior third of the medial and less frequently anterior and middle third of the lateral talus. Biomechanical experiments demonstrated that these areas are those with the highest load under varus/valgus and pronation/supination stress. Trauma is held responsible for both the more frequent medial, cup-shaped lesion and the less frequent lateral, wafer-shaped lesion. Taking into consideration the complex motion patterns of the ankle joint, these conceptions should be abandoned and the exact pathomorphogenetic mechanism assessed more closely in future. Other possible etiological factors such as genetic, metabolic or infectious causes are discussed but are not yet substantiated by scientific and experimental evidence. The different stages of o.d. do not differ from the stages in other joints and from aseptic osteonecrosis. Theoretically, it seems that o.d. is initiated when an imaginary threshold value is reached so that a subchondral osteonecrosis occurs (stage I). Repetitive mechanical forces possibly interfere with the regeneration process of the lesions, resulting in the development of a subchondral sclerosis (stage II). Further disturbance of the regenerative process may lead to a demarcation of the osteochondral area (stage III) and eventually dissecation (stage IV) of the fragment with loose bodies in the joint. Clinical symptoms are nonspecific. Periarticular swelling, hydrarthrosis, reduced range of motion and sometimes joint locking are the most common clinical signs. Differentiation of o.d. from posttraumatic osteochondral lesions of the talus is sometimes difficult or even impossible. In contrast, other entities of the tibiotalar joint (such as talar necrosis or subchondral ganglion) can be easily distinguished.
距骨剥脱性骨软骨炎是距骨骨软骨损伤的一种特殊形式。必须将伴有放射学检查立即发现的继发骨软骨缺损的创伤与距骨剥脱性骨软骨炎相鉴别。剥脱性骨软骨炎主要是一种软骨下骨疾病，几乎可累及人体的每个关节。仅次于膝关节和肘关节，距骨是该疾病的第三大常见发病部位，占所有病例的4%。它大多发生在20岁左右，但几乎可发生于任何年龄。本文将对剥脱性骨软骨炎的不同病因（血管性、创伤性、感染性、内源性、遗传性）进行概述，尤其针对距骨的病因进行讨论。在文献中，创伤的病因发病机制备受青睐。多项研究表明，距骨剥脱性骨软骨炎发病前存在扭曲和/或旋后创伤的既往史。剥脱性骨软骨炎病变最常见的部位是内侧的中后三分之一处，外侧距骨的前中三分之一处则较少见。生物力学实验表明，在内外翻和旋前/旋后应力作用下，这些区域是负荷最高的部位。创伤被认为是内侧较常见的杯状病变和外侧较罕见的片状病变的病因。考虑到踝关节复杂的运动模式，这些观念应被摒弃，未来需更深入地评估确切的病理形态发生机制。还讨论了其他可能的病因，如遗传、代谢或感染因素，但尚未得到科学和实验证据的证实。剥脱性骨软骨炎的不同阶段与其他关节以及无菌性骨坏死的阶段并无差异。理论上，当达到一个假想的阈值导致软骨下骨坏死（I期）时，似乎就引发了剥脱性骨软骨炎。反复的机械力可能会干扰病变的再生过程，导致软骨下硬化的发展（II期）。再生过程的进一步紊乱可能导致骨软骨区域的分界（III期），最终导致碎片分离（IV期），关节内出现游离体。临床症状不具有特异性。关节周围肿胀、关节积液、活动范围减小，有时还有关节交锁是最常见的临床体征。将距骨剥脱性骨软骨炎与距骨创伤后骨软骨损伤相鉴别有时很困难，甚至不可能。相比之下，胫距关节的其他病变（如距骨坏死或软骨下囊肿）则很容易区分。
