The ACLT variant of the surgical instability model in rabbits is a reproducible and effective model of OA. The cartilage lesions in this model and their response to therapy can be graded according to an adapted histological and histochemical grading system, though also this system is to some extent subjective and, thus, neither objective nor entirely reproducible.

Objective. To determine whether oral glucosamine alleviates cartilage degradation in an animal model of osteoarthritis (OA).Methods. The effect of 8 weeks of daily oral glucosamine hydrochloride on degeneration of articular cartilage was evaluated in rabbits in which anterior cruciate ligament transection (ACLT) was performed to induce OA. Animals were treated with glucosamine (n ‫؍‬ 16) or a placebo (n ‫؍‬ 16) and necropsied at 11 weeks. Seven unoperated rabbits served as controls. The articular cartilage was evaluated macroscopically and histologically and analyzed for total type II collagen and glycosaminoglycan (GAG) content.Results. Histologic analysis revealed that loss of proteoglycan, based on Safranin O-fast green staining, was significantly reduced in the lateral tibial plateau cartilage of ACL-transected limbs in the glucosamine group compared with ACL-transected limbs in the placebo group, with a similar, but not significant, trend for the lateral femoral condylar cartilage. Likewise, macroscopic analysis of cartilage showed that the lateral tibial plateau alone had a significantly lower rate of disease in the glucosamine group, which was consistent with the results of the independent histologic assessment. However, no significant treatment effect was detected when composite histologic scores were analyzed. A significant reduction in GAG content was observed in the femoral condyles of placebo-treated ACL-transected joints, but not in the same region of glucosamine-treated ACLtransected joints, compared with their respective contralateral unoperated joints.Conclusion. Oral administration of glucosamine had a detectable, site-specific, partial disease-modifying effect in this model of OA. From a clinical perspective, the administration of glucosamine did not prevent fibrillation and/or erosions of the articular cartilage in all of the treated animals, and no effects were detected in the medial joint compartments.In addition to decreasing pain, an ideal therapeutic agent for osteoarthritis (OA) would also prevent or retard the progression of established OA by reducing or, preferably, reversing the underlying pathologic processes (structure modifying), resulting in the retention or restoration of more normal articular cartilage function. The most common pharmacologic therapeutic agents currently used for OA are primarily palliative and include acetaminophen, nonsteroidal antiinflammatory drugs, corticosteroids, and hyaluronic acid (1,2). None of these drugs for OA are disease modifying.Analyses of many randomized clinical trials of oral glucosamine in OA patients support the contention that glucosamine is a symptom-modifying agent in OA (3-5), while investigators in many other trials have

The data reveal corresponding, progressive degenerative changes in articular cartilage and subchondral bone, including striking focal resorptive lesions, in the third carpal bone of racehorses subjected to repetitive, high impact trauma.

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Matrix and ossification front changes were frequently observed and significantly associated with cartilage canals suggesting that they may be physiological changes associated with matrix remodelling and development. The collagen structure was variable through the growing epiphysis and a differential in biomechanical properties at focal sites may predispose them to injury.