Little evidence is available on the natural course of osteoarthritis (OA) development and the genes that protect and predispose individuals to it. This study was designed to compare strain-dependent development of OA and its association with tissue regeneration in mice. Two recombinant inbred lines LGXSM-6 and LGXSM-33 generated from LG/J and SM/J intercross were used. Previous studies indicated that LGXSM-6 can regenerate both articular cartilage and ear hole punch while LGXSM-33 cannot.
Transection of the medial meniscotibial ligament was performed on 10-week-old male mice to induce OA. Cartilage damage was analyzed by histology and bone morphology was evaluated using micro-computed tomography (CT). Ear punches were performed and evaluated by measurement of residual hole diameter.
Osteoarthritis (OA) is a degenerative joint disease resulting in articular cartilage fibrillation and loss and is estimated to affect 70–90% of the population aged 60 years and older. Knee OA is thought to be dependent on multiple factors with mechanical overload, obesity and trauma being the most prominent risk factors. The variation in OA susceptibility may be due to a variation in responsiveness to these factors. Emerging evidence indicates that 50–75% of variation in OA in humans is genetic, however, little evidence is available on the genes that cause and protect individuals from OA4–6. Evidence from genome-wide association studies in humans has shown that OA appears to be highly polygenic with multiple risk alleles conferring small effects6.
Clinical options for patients with cartilage defects and OA are limited to symptomatic treatment, unless the patient is qualified for osteotomy or total joint replacement. In recent years, treatments that attempt to repair or restore the cartilage lesions have been developed with limited success. Thus, the knowledge of the genetic contribution to the susceptibility or protection from OA would greatly contribute to our understanding of OA and would provide not only potential treatment strategies but may also help predict individuals who are at risk for developing OA.