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Veterinary pathology, 2007-07, Vol.44 (4), p.429-448
2007
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Autor(en) / Beteiligte
Titel
Etiology and pathogenesis of osteochondrosis
Ist Teil von
  • Veterinary pathology, 2007-07, Vol.44 (4), p.429-448
Ort / Verlag
United States
Erscheinungsjahr
2007
Quelle
MEDLINE
Beschreibungen/Notizen
  • Osteochondrosis is a common and clinically important joint disorder that occurs in human beings and in multiple animal species, most commonly pigs, horses, and dogs. This disorder is defined as a focal disturbance of enchondral ossification and is regarded as having a multifactorial etiology, with no single factor accounting for all aspects of the disease. The most commonly cited etiologic factors are heredity, rapid growth, anatomic conformation, trauma, and dietary imbalances; however, only heredity and anatomic conformation are well supported by the scientific literature. The way in which the disease is initiated has been debated. Although formation of a fragile cartilage, failure of chondrocyte differentiation, subchondral bone necrosis, and failure of blood supply to the growth cartilage all have been proposed as the initial step in the pathogenesis, the recent literature strongly supports failure of blood supply to growth cartilage as being the most likely. The term osteochondrosis has been used to describe a wide range of different lesions among different species. We suggest a refinement of this terminology to include the modifiers latens (lesion confined to epiphyseal cartilage), manifesta (lesion accompanied by delay in endochondral ossification), and dissecans (cleft formation through articular cartilage). The purpose of this review is to provide an overview of the disease, focusing on the most commonly cited theories, recent research findings, and our own views regarding the etiology and pathogenesis of osteochondrosis, in order to provide a better understanding of this apparently complex disease.
Sprache
Englisch
Identifikatoren
ISSN: 0300-9858
eISSN: 1544-2217
DOI: 10.1354/vp.44-4-429
Titel-ID: cdi_pubmed_primary_17606505

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