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Subchondral bone failure in an equine model of overload arthrosis.
Bone. 1998 Feb; 22(2):133-9.BONE

Abstract

Gross examination of metacarpo-/metatarsophalangeal (fetlock) joints from racehorses revealed defects on the condylar surface that ranged from cartilage fibrillation and erosion to focal cartilage indentations and cavitation in subchondral bone characteristic of traumatic osteochondrosis. Because these lesions represented a spectrum of mechanically induced arthrosis in which microdamage is thought to play a role, a histologic study of sagittal sections was made to study the morphogenesis. Subchondral bone failure developed beneath a flattened section of the condyle where the margin of the sesamoid bone produces compression as well as shear on impact of the foot with the ground. Milder lesions had thickening of subchondral bone and underlying trabeculae. With advancing sclerosis an increased amount of osteocyte necrosis was present. Occasional vascular channels with plugs of matrix debris and cells were present just beneath the cartilage. There was increased prominence of subchondral vessels, and osteoclastic remodeling was seen in and around the sclerotic zone. Apparent fragmentation lines in the subchondral bone suggested increased matrix fragility. Irregular trabecular microfractures developed at a depth of a few millimeters. Increased vascularity with hemorrhage, fibrin, and fibroplasia could be seen in enlarged marrow spaces at this more advanced stage. The overlying articular cartilage was variably indented but remained largely viable with degeneration and erosion limited to the superficial layers. Focally, breaks in the calcified layer appeared to lead to collapse and cartilage infolding. In metacarpal condyles from experimental horses run on a treadmill, there were milder changes at the site. The subchondral bone was increased in volume and there was increased diffuse staining with basic fuchsin, but no increase in the number of microcracks was seen. The findings in the racehorses indicate that the equine fetlock condyle is a consistent site of overload arthrosis in which microfracture and failure in subchondral bone may occur. Controlled exercise in treadmill horses may provide a model in which to study the pathogenesis.

Authors+Show Affiliations

Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins 80523, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9477236

Citation

Norrdin, R W., et al. "Subchondral Bone Failure in an Equine Model of Overload Arthrosis." Bone, vol. 22, no. 2, 1998, pp. 133-9.
Norrdin RW, Kawcak CE, Capwell BA, et al. Subchondral bone failure in an equine model of overload arthrosis. Bone. 1998;22(2):133-9.
Norrdin, R. W., Kawcak, C. E., Capwell, B. A., & McIlwraith, C. W. (1998). Subchondral bone failure in an equine model of overload arthrosis. Bone, 22(2), 133-9.
Norrdin RW, et al. Subchondral Bone Failure in an Equine Model of Overload Arthrosis. Bone. 1998;22(2):133-9. PubMed PMID: 9477236.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Subchondral bone failure in an equine model of overload arthrosis. AU - Norrdin,R W, AU - Kawcak,C E, AU - Capwell,B A, AU - McIlwraith,C W, PY - 1998/2/26/pubmed PY - 1998/2/26/medline PY - 1998/2/26/entrez SP - 133 EP - 9 JF - Bone JO - Bone VL - 22 IS - 2 N2 - Gross examination of metacarpo-/metatarsophalangeal (fetlock) joints from racehorses revealed defects on the condylar surface that ranged from cartilage fibrillation and erosion to focal cartilage indentations and cavitation in subchondral bone characteristic of traumatic osteochondrosis. Because these lesions represented a spectrum of mechanically induced arthrosis in which microdamage is thought to play a role, a histologic study of sagittal sections was made to study the morphogenesis. Subchondral bone failure developed beneath a flattened section of the condyle where the margin of the sesamoid bone produces compression as well as shear on impact of the foot with the ground. Milder lesions had thickening of subchondral bone and underlying trabeculae. With advancing sclerosis an increased amount of osteocyte necrosis was present. Occasional vascular channels with plugs of matrix debris and cells were present just beneath the cartilage. There was increased prominence of subchondral vessels, and osteoclastic remodeling was seen in and around the sclerotic zone. Apparent fragmentation lines in the subchondral bone suggested increased matrix fragility. Irregular trabecular microfractures developed at a depth of a few millimeters. Increased vascularity with hemorrhage, fibrin, and fibroplasia could be seen in enlarged marrow spaces at this more advanced stage. The overlying articular cartilage was variably indented but remained largely viable with degeneration and erosion limited to the superficial layers. Focally, breaks in the calcified layer appeared to lead to collapse and cartilage infolding. In metacarpal condyles from experimental horses run on a treadmill, there were milder changes at the site. The subchondral bone was increased in volume and there was increased diffuse staining with basic fuchsin, but no increase in the number of microcracks was seen. The findings in the racehorses indicate that the equine fetlock condyle is a consistent site of overload arthrosis in which microfracture and failure in subchondral bone may occur. Controlled exercise in treadmill horses may provide a model in which to study the pathogenesis. SN - 8756-3282 UR - https://www.unboundmedicine.com/medline/citation/9477236/Subchondral_bone_failure_in_an_equine_model_of_overload_arthrosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S8756-3282(97)00253-6 DB - PRIME DP - Unbound Medicine ER -