Difficulties in definition of equine osteochondrosis; differentiation of developmental and acquired lesions
1993; Wiley; Volume: 25; Issue: S16 Linguagem: Inglês
10.1111/j.2042-3306.1993.tb04847.x
ISSN2042-3306
Autores Tópico(s)Ruminant Nutrition and Digestive Physiology
ResumoSummary This paper reviews most of the important clinical syndromes currently considered as examples of articular osteochondroses based on the belief that they arise from a primary lesion in the articular cartilage that produces failure in endochondral ossification. Arguments are made why a number of syndromes are not osteochondroses. Because morphological lesions resembling osteochondrosis can be produced at osteochondral junctions from primary disorders centred in the growth cartilages (dyschondroplasia) or in the capillary bed that replaces the cartilage model during endochondral ossification, the definition of osteochondrosis in horses needs to be reexamined. Because the morphology of an individual lesion of osteochondrosis provides little insight into its fundamental cause, this paper suggests that the pattern of skeletal distribution of the lesions in affected individuals may help distinguish between foals with the idiopathic (constitutional defects in the cartilage model) and acquired forms of osteochondrosis. In foals with acquired osteochondrosis when the cause of the defect in endochondral ossification is known, the cause of the disorder should be included in naming the clinical syndrome, e.g. traumatic osteochondrosis or zinc‐induced osteochondrosis. The search for the key to the pathogenesis of osteochondrosis in horses can only begin after the fundamental mechanisms causing perturbations of endochondral ossification are better understood.
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