Etiology and pathogenesis of osteochondritis dissecans of the talus

Citation
J. Steinhagen et al., Etiology and pathogenesis of osteochondritis dissecans of the talus, ORTHOPADE, 30(1), 2001, pp. 20-27
Citations number
45
Categorie Soggetti
Ortopedics, Rehabilitation & Sport Medicine
Journal title
ORTHOPADE
ISSN journal
00854530 → ACNP
Volume
30
Issue
1
Year of publication
2001
Pages
20 - 27
Database
ISI
SICI code
0085-4530(200101)30:1<20:EAPOOD>2.0.ZU;2-A
Abstract
Osteochondritis dissecans of the talus is a particular form of osteochondra l lesions of the talus. A trauma with subsequent osteochondral defect detec ted 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 kne e and elbow, the talus is the third most common site of the disease account ing for 4% of all cases. It mostly arises in the 2nd decade but can occur a t almost any age. Different etiological factors of osteochondritis dissecans (vascular, traum atic, infectious, endogenous, genetic) are discussed in general and in part icular for the talus. In the literature,the etiopathogenetic mechanism of t rauma is favored. Several studies show an anamnestic coincidence of distors ion 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 l ateral talus. Biomechanical experiments demonstrated that these areas are t hose with the highest load under varus/valgus and pronation/supination stre ss. Trauma is held responsible for both the more frequent medial, cup-shaped le sion and the less frequent lateral, wafer-shaped lesion. Taking into consid eration the complex motion patterns of the ankle joint, these conceptions s hould be abandoned and the exact pathomorphogenetic mechanism assessed more closely in future. Other possible etiological factors such as genetic, met abolic 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 initia ted when an imaginary threshold value is reached so that a subchondral oste onecrosis 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 regenera tive 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, r educed range of motion and sometimes joint locking are the most common clin ical signs. Differentiation of o.d. from posttraumatic osteochondral lesion s of the talus is sometimes difficult or even impossible. In contrast, othe r entities of the tibiotalar joint (such as talar necrosis or subchondral g anglion) can be easily distinguished.