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.

Neoplastic cells were isolated from 2 sibling Great Dane/Labrador Retriever mixed-breed dogs in which telangiectatic type osteosarcomas arose concurrently. Cells from various sites in the same osteosarcoma appeared similar in culture, but there were differences between the 2 osteosarcomas in growth characteristics and appearance of cells. Cells from 1 osteosarcoma had a small, but significant (P less than 0.05), cyclic adenosine monophosphate response to parathyroid hormone stimulation, indicating a low order of osteoblastic differentiation. Cells from the other osteosarcoma had no response to parathyroid hormone stimulation. Cells from both osteosarcomas and a concentrated cell-free filtrate from the osteosarcoma with osteoblastic differentiation were injected into nude mice, but osteosarcomas were not induced. Results of ultrastructural examination of osteosarcoma samples for viral particles were negative and supernatant fluids from cultured cells were considered negative for viral reverse transcriptase activity.

We compared the frequency and severity of osteochondrosis lesions in young Thoroughbred horses with cervical stenotic myelopathy (CSM) vs that in clinically normal Thoroughbreds of the same age. All lesions of the cervical vertebrae and appendicular skeleton were classified histologically as osteochondrosis or nonosteochondrosis and were measured for severity. Minimal sagittal diameter was significantly smaller in horses with CSM from C2 through C6; no difference was detected at C7. Severity of cervical vertebral osteochondrosis was greater in the horses with CSM, however frequency was not different. Frequency and severity of nonosteochondrosis lesions were not different in cervical vertebrae or appendicular skeleton. Frequency and severity of appendicular skeleton osteochondrosis lesions were both greater in horses with CSM. Osteochondrosis and nonosteochondrosis lesions were more severe on facets at sites of compression than on facets at noncompressed sites in horses with CSM. However, compression was also observed at sites with no articular facet lesions. The association of widespread osteochondrosis and spinal canal narrowing with CSM suggests CSM may represent a systemic failure in the development or maturation of cartilage and bone.

Lumbar and thoracic vertebrae of the extinct horse, Equus occidentalis, were examined for gross and radiographic evidence of overriding spinous processes. Of 2,661 vertebrae examined, 580 had intact spinous processes. Thirty-six intact spinous processes, which appeared grossly similar to overriding spinous processes in the modern domestic horse, E caballus caballus, were radiographed. Of these 36 vertebrae, 2 had radiographic signs compatible with a radiographic diagnosis of overriding spinous processes, ie, radiographically observed lysis and/or sclerosis. Seemingly, weight bearing or other stresses imposed by human beings may not have induced the signs of overriding spinous processes.

Osteoporosis is defined as a decrease in bone mass that leads to an increased risk of fracture. The therapeutic effect of 1alpha,25 dihydroxycholecalciferol, the hormonal form of vitamin D3 that mediates calcium translation in intestine and bone, on the healing process of fracture has still been controversial. These studies were designed to understand the healing process of normal fibular fracture, the osteoporotic changes after ovariectomy, and the theraqeutic effects of 1alpha,25 dihydroxycholecalciferol on the osteoporotic fracture in rats. The simple transverse fractures of rat fibulae were produced with a rotating diamond saw. The changes of the biochemical and mechanical indices of rats were investigated. The mechanical study based on bending test revealed the healing of the fibular fracture in the 5th week after simple transverse fracture. The osteoporosis impaired more the healing of osteoporotic fibular fracture than normal non-osteoporotic fibular fracture. The healing process of osteoporotic fracture was facilitated by the treatment with 1alpha,25 dihydroxycholecalciferol, however was delayed more than the healing process of normal fracture. The bone strength based on the bending test also confirmed this tendency. The bone strengths in the 5th week after fracture of normal bone, osteoporotic bone, and 1alpha,25 dihydroxycholecalciferol-treated osteoporotic bone were 75%, 41% and 67%, respectively, in comparison with those of intact bone. In conclusion, 1alpha,25 dihydroxycholecalciferol was effective in promoting the osteroporotic fracture healing.