In juvenile osteochondritis dissecans (JOCD), the patient’s cartilage disintegrates, primarily in the knees. Although the disorder is rare, it is occurring with increasing frequency, with close to 80 percent of cases being found in high-level athletes. These athletes, most often participating in the popular sports of soccer and basketball, are required to refrain from participating in activities, including sports, for long periods of time. Even with the time off, treatment success rates are only 60-70 percent, claims Eric Wall, MD, director of Orthopaedic Sports Medicine at Cincinnati Children’s.

Despite the fact that the condition was discovered 100 years ago, physicians still know little about its cause, and previous animal models have focused on surgically created lesions.¹ To further search for a cause of JOCD, Wall and his team conducted a controlled laboratory study of juvenile rabbits who were subjected to repetitive loading forces on one limb over a period of five weeks. Subsequent examination of the rabbits showed that all had developed osteochondral lesions in the loaded limbs, while the unloaded limbs did not demonstrate lesions. This research, which has been ongoing for close to seven years, was completed and published in FY16.

Histopathological analysis identified multiple structural changes in the cartilage of loaded limbs compared to control limbs. (a) Normal control histology. (b) Discrete areas of change in loaded limbs had a maximum cartilage thickness twice that of the control limb (arrow). (c,d) Joint surface irregularities including cracks and vertical fissure-like clefts, and focal articular surface depressions or elevations in most animals. (e) Nuclear drop out present in loaded limbs. (f) Chondrocyte cloning.

This animal model supports the hypothesis that repetitive stress to immature knees may contribute to the development of human JOCD, and may be useful in understanding the pathophysiology and healing of human JOCD. These injuries to the interface between bone and cartilage resemble those seen in JOCD patients. Consequently, this model may now be used to assess the efficacy of nonoperative treatments such as bracing, or operative drilling of the lesion which may bring in new bone and blood supply to heal the lesions.

“Our research supports the hypothesis that repetitive stress may be the cause of osteochondritis dissecans in immature bone structures,” says Wall. “Eventually, of course, the goal is to cure the disease – but before we can do that, we must identify the cause.”

Reference: 1. Stone AV, Little LJ, Glos DL, Stringer KF and Wall EJ. Repetitive stresses generate osteochondral lesions in skeletally immature rabbits.Am J Sports Med. 2016 Jul 26.