期刊
EQUINE VETERINARY JOURNAL
卷 54, 期 3, 页码 601-613出版社
WILEY
DOI: 10.1111/evj.13486
关键词
condyle; cyst; horse; juvenile osteochondral trauma; osteochondral junction; osteochondrosis; subchondral radiolucency
资金
- Fonds en Sante Equine de la Faculte de Medecine Veterinaire de l'Universite de Montreal et Zoetis
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Quebec Cell, Tissue and Gene Therapy Network - TheCell (Fonds de recherche du Quebec-Sante)
The research on equine medial femoral condyle (MFC) subchondral bone radiolucencies (SR) in Thoroughbreds found that these lesions are not caused by osteochondrosis, but may be attributed to trauma.
Background The aetiology of equine medial femoral condyle (MFC) subchondral bone radiolucencies (SR) is unknown. Objectives Characterise the microstructural structural features of MFC SR in juvenile Thoroughbreds with microcomputed tomography (mu CT) and histology. Study design Cross-sectional post-mortem study. Methods Distal femurs were collected at post-mortem. Conventional tomodensitometry was employed to scout for MFCs with and without SR lesions (SR+ and SR-, respectively). Group 1 were CT MFC SR+ and Group 2 age-matched SR- controls. Both underwent mu CT and histological analysis. Group 3 CT MFC SR- foals, <6 months, were selected to search for chondronecrosis. Histological sections, processed from the lesion (Group 1) and a corresponding site in Groups 2 and 3, were assessed for chondronecrosis, fibrin, fibroplasia and osteochondral separation. Group 3 sections were surveyed for chondronecrosis alone. Results A total of 178 femurs from 89 Thoroughbreds were harvested. Of these horses 19.1% (95% CI: 10.9%-27.3%) were CT MFC SR+ (17/23; 7.46 +/- 4.36 months) and met the inclusion criteria for Group 1. Group 2 included 30 CT MFC SR- specimens (5.00 +/- 2.73 months) and Group 3 had 44 CT MFC SR- s (2.68 +/- 1.74 months). SR were located axially in foals <7 months of age, and centrally thereafter. All SRs had areas of thickened cartilage on histology and separation at the osteochondral junction containing fibrin (acute event) and fibroplasia (chronicity) in 73.9% (17/23; 95% CI: 56%-91.9%). In Group 1 specimens, chondronecrosis was present in 82.6% (19/23; 95% CI: 67.1%-98.1%) but four MFC SR+ had no evidence of chondronecrosis. Chondronecrosis was not detected in the Group 3 foal MFCs. Main limitations No longitudinal follow-up. Conclusions The absence of chondronecrosis, pathognomic of osteochondrosis, in four MFC SR+s and in all of the CT MFC SR- foals suggests that osteochondrosis is not the cause, or the only cause, of these lesions and favours trauma as an alternate aetiological hypothesis.
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