Effect of Low-level Laser Therapy on Osteoarthropathy in Rabbit

The aim of this study was to determine whether low- level laser therapy (LLLT) aided the recovery of damaged articular cartilage in joints with artificially induced osteoarthropathy (OA). OA was induced by injecting hydrogen peroxide (H2O2) into the articular spaces of both knees in rabbits, twice a week for 4 weeks. The induction of OA and the effect of LLLT were evaluated by biochemical, radiological and histopathological analysis. Superoxide dismutase (SOD) activity increased about 40% in the OA group, as compared to the controls. Although SOD activity in the OA group was not significantly different from the 2-week groups, it was significantly different from the 4-week control and treatment groups. There was also a significant difference between the 4- week control and treatment groups. Simple radiographs and three-dimensional computed tomographs (3D CT) did not show detectable arthropathy in the OA group, nor any paricular changes in the 2-week groups. In contrast, distinct erosions were seen in the distal articular cartilage of the femur, with irregularity of the articular surface, in the 4-week control group, while the erosions were reduced and arthropathy improved slightly in the 4-week treatment group. Grossly, erosions formed on the articular surface in the OA group. In comparison, severe erosions damaged the articular cartilage in the 4-week control group, but not in the 2-week control and treatment groups. Regeneration of articular cartilage was seen in gross observations in the 4-week treatment group. Histopathologically, there was slight irregularity of the articular surface and necrosis in the OA group, and serious cartilage damage, despite slight chondrocyte regeneration, in the 4-week control group. Conversely, the 4-week treatment group showed chondrocyte replacement, with sometimes close to normal articular cartilage on the articular surface. These results suggest that LLLT was effective in the treatment of chemically-induced OA. Although it is a common non-inflammatory, degenerative disease occurring in synovial joints, the pathology of osteoarthropathy (OA) is still uncertain (1). This disease induces cartilage damage and deformity, mainly due to weakened articular cartilage, and brings about local degenerative changes characterized by secondary inflammation with abnormal bone formation on the joint surface and surrounding area (2,3). The degenerative changes are thought to be due to cartilage metabolic dysfunction in joints that support the body weight (4,5).