Characterization of experimentally induced post-traumatic osteoarthritis in the medial femorotibial joint of horses

Courtney J. Bolam Ontario Veterinary College, Comparative Orthopaedic Research Group, University of Guelph, Guelph, ON N1G 2W1, Canada.

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 DVM
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Mark B. Hurtig Ontario Veterinary College, Comparative Orthopaedic Research Group, University of Guelph, Guelph, ON N1G 2W1, Canada.

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 DVM, MVSc
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Antonio Cruz Ontario Veterinary College, Comparative Orthopaedic Research Group, University of Guelph, Guelph, ON N1G 2W1, Canada.

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Beverly J. E. McEwen Department of Clinical Studies, and Department of Pathobiology, University of Guelph, Guelph, ON N1G 2W1, Canada.

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 DVM, PhD

Abstract

Objective—To study osteoarthritis in the equine medial femorotibial (MFT) joint after a single traumatic injury.

Animals—10 mature horses.

Procedure—In vitro explant cultures were used to determine injury threshold for stifle joint cartilage. Contusive impacts were applied to the medial femoral condyle (MFC), and horses were followed for 84 (n = 5) and 180 days (5). Synovial fluid samples were collected every 14 days for determination of sulphated glycosaminoglycan (sGAG) concentrations. Radiographic and lameness evaluations were performed. Gross and histologic descriptions, and immunohistochemistry, cartilage sGAG content determination, and cartilage aggregate modulus determination were performed at the MFC impact site (MFCi), MFC nonimpact site (MFCn), and medial tibial plateau (MTP).

Results—Synovial fluid sGAG concentration decreased significantly on days 14, 28, 42, and 56 in all horses. Macroscopic and microscopic articular lesions developed within all MFT joints. No radiographic abnormalities were observed. Mild lameness was evident in several horses. No significant differences were found between short-term and longterm cohorts of horses with respect to histologic scores and TUNEL results. On immunohistochemistry, MFCi was positive for COL2–¾Cshort. International Cartilage Repair Society scores differed significantly between short-term and long-term cohorts of horses. In all horses, sGAG concentrations were significantly decreased at the MFCi, compared with the MFCn.

Conclusions and Clinical Relevance—Use of contusive impacts on the MFC of horses results in cartilage lesions that are similar to those described clinically, supporting trauma as a contributing factor in the natural pathogenesis of osteoarthritis.

Abstract

Objective—To study osteoarthritis in the equine medial femorotibial (MFT) joint after a single traumatic injury.

Animals—10 mature horses.

Procedure—In vitro explant cultures were used to determine injury threshold for stifle joint cartilage. Contusive impacts were applied to the medial femoral condyle (MFC), and horses were followed for 84 (n = 5) and 180 days (5). Synovial fluid samples were collected every 14 days for determination of sulphated glycosaminoglycan (sGAG) concentrations. Radiographic and lameness evaluations were performed. Gross and histologic descriptions, and immunohistochemistry, cartilage sGAG content determination, and cartilage aggregate modulus determination were performed at the MFC impact site (MFCi), MFC nonimpact site (MFCn), and medial tibial plateau (MTP).

Results—Synovial fluid sGAG concentration decreased significantly on days 14, 28, 42, and 56 in all horses. Macroscopic and microscopic articular lesions developed within all MFT joints. No radiographic abnormalities were observed. Mild lameness was evident in several horses. No significant differences were found between short-term and longterm cohorts of horses with respect to histologic scores and TUNEL results. On immunohistochemistry, MFCi was positive for COL2–¾Cshort. International Cartilage Repair Society scores differed significantly between short-term and long-term cohorts of horses. In all horses, sGAG concentrations were significantly decreased at the MFCi, compared with the MFCn.

Conclusions and Clinical Relevance—Use of contusive impacts on the MFC of horses results in cartilage lesions that are similar to those described clinically, supporting trauma as a contributing factor in the natural pathogenesis of osteoarthritis.

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