Establishment and Evaluation of a Sheep Model of Full-thickness Osteochondral Defect.

Abstract

Aging, trauma, genetic predisposition, and lifestyle impact the human body´s cartilage degradation. Once injured, continuous insults resulting from daily activities can trigger pathological conditions such as osteoarthritis, the primary cause of disability and socioeconomic loss worldwide. The main goal of all orthopedic surgeons treating joint cartilage injuries has been to reduce the extent of the lesion anatomically, repair the cartilage surface, and reestablish joint stability. Animal models are essential for the development of therapeutic drugs, but current models for cartilage defects are unsatisfactory. Osteochondral lesions in sheep are a valuable model for testing new therapies and biomaterials that can aid in the recovery of cartilage and bone in human joint environments. This study established an efficient protocol for inducing acute osteochondral defects in large animals. A standardized lesion was created in both medial femoral condyles. One knee was randomly assigned to receive gelatin-methacryloyl treatment, while the contralateral knee served as a control. Six months after the surgical procedure, the femoral condyle area was removed, the dissected knee joints were decalcified, embedded in paraffin, and cut into sections, which were stained with hematoxylin and eosin. Scores were used to evaluate the lesion. This methodology allows immediate macroscopic observation after injury induction. Additionally, this model effectively replicates clinical cartilage defects, providing a valuable model for studying their pathology and developing innovative therapeutic approaches.