Etiology and pathogenesis of osteochondrosis dissecans tali

Abstract

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.