Influence of methylprednisolone acetate on osteochondral healing in exercised tarsocrural joints of horses

Abstract

Objective. To evaluate joint function and healing of surgically created full-thickness articular cartilage defects in exercised horses after intra-articular administration of methylprednisolone acetate (MPA; 120 mg) and sterile saline solution in the contralateral limb. Design. Experimental investigation. Sample Population. 12 healthy, sound, radiographically normal horses with induced full-thickness osteochondral lesions on the medial and lateral trochlear ridges of the tali. Procedure. Two 8.4-mm-diameter full-thickness articular cartilage lesions were created in each tarsocrural joint (12 horses [24 tarsocrural joints]); 1 was in a weight-bearing (WB) position and the other in a less weight-bearing (LWB) position. Each horse was maintained on a standardized exercise protocol (stall rest, days 0-6; walking, days 7-12; and treadmill, days 13-42) and evaluated throughout the study for changes in joint circumferences, synovial fluid, radiographs, lameness, and scintigraphy. 6 horses were euthanatized onday 42, and 6 on day 180. Gross morphometric assessment was performed, using an image analysis system on a projected color slide of the defect. The type of repair tissue, based on gross appearance, was expressed as a percentage of the total defect for each osteochondral defect. Histochemical assessment was performed, using safranin-O staining for proteoglycans and an image analysis system to express the area of stain uptake. Histomorphometric assessment was performed on H and E-stained sections, using an image analysis system. The repair tissue filling the defect was categorized as to tissue type and expressed as a percentage of the total defect area. Synovial membrane specimens were assessed semiquantitatively on H and E-stained sections for changes in character. Significance was established at P < 0.05. Results. Joint circumference was significantly increased in the saline, compared with the MPA-treated, limbs on days 7, 12, and 42. Synovial fluid WBC oounts were significantly increased in the MPA-treated limbs on day 42. Cross osteochondral defects had a greater percentage of mature repair tissue in saline-treated joints (30.8% LWB, 23% WB), compared with MPA-treated joints (0% LWB, 0% WB) at 42 days. Histomorphometric assessment of the repair tissue indicated significant differences with regard to the quality of repair in the saline-treated (34% fibrous tissue LWB, 19.4% fibrous tissue WB) versus MPA-treated (2.5% fibrous tissue in LWB and WB) joints at 42 days. Microscopically, the percentage of fibrocartilage in the LWB (MPA, 23.7%; saline, 24.8%) was significantly greater than that in the WB (MPA, 14.6%; saline, 15.4%) site at day 180. The MDA-treated limbs had greater villous hyperplasia, edema, and extent of inflammation within the synovial membrane than did saline-treated limbs (days 42 and 180). Conclusion. MPA inhibits the development and maturation of repair tissue at 42 days and incites potential long-term (180 days) detrimental synovial membrane inflammation. Furthermore, a single dose of MPA does not cause long-term detrimental effects (180 days) in quality of repair tissue.