Effects of intra-articular administration of methylprednisolone acetate on normal articular cartilage and on healing of experimentally induced osteochondral defects in horses.
1992
Shoemaker R.S. | Bertone A.L. | Martin G.S. | McIlwraith C.W. | Roberts E.D. | Pechman R. | Kearney M.T.
The effects of intra-articular administration of methylprednisolone acetate (MPA) on the healing of full-thickness osteochondral defects and on normal cartilage were evaluated in 8 horses. In group-1 horses (n = 4), a 1-cm-diameter, full-thickness defect was created bilaterally in the articular cartilage on the dorsal distal surface of the radial carpal bone. Cartilage defects were not created in group-2 horses (n = 4). One middle carpal joint was randomly selected in each horse (groups 1 and 2), and treated with an intra-articular injection of 100 mg Of MPA, once a week for 4 treatments. Injections began 1 week after surgery in group-1 horses. The contralateral middle carpal joint received intra-articular injections of an equivalent volume of 0.9% sodium chloride solution (SCS), and served as a control. Horses were evaluated for 16 weeks, then were euthanatized, and the middle carpal joints were examined and photographed. Synovial and articular cartilage specimens were obtained for histologic and histochemical evaluation. Gross morphometric evaluation of the healing defects in group-1 horses revealed that 48.6% of the defect in control joints and 0% of the defect in MPA-treated joints was resurfaced with a smooth, white tissue, histologically confirmed as fibrocartilage. This replacement tissue was a firmly attached fibrocartilage in control joints and a thin fibrous tissue in MPA-treated joints. The articular cartilage in joints treated with MPA had morphologic changes, including chondrocyte cluster formation, loss of palisading architecture, and cellular necrosis in both groups of horses. Histochemical (safranin-0) staining intensity was reduced significantly (P < 0.05) in all layers of articular cartilage in MPA-treated joints in groups 1 and 2. In the replacement tissue, intense safranin-O staining was found only in the chondrocyte clusters deep in the tissue of control joints, confirming fibrocartilage repair. Intra-articular administration of MPA in this dosing regimen thus induced degenerative changes in normal articular cartilage and resulted in histomorphologic changes in the repair of full-thickness articular osteochondral defects in horses.
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