The Effect of Low-Magnitude High-Frequency Vibration on Osteoarthritic Cartilage and Subchondral Bone in Anterior Cruciate Ligament Transection-Induced Osteoarthritic Rat Model.

摘要

Osteoarthritis (OA) is the most common degenerative joint disease. Mechanical loading plays an important role on the onset and progression of OA. Abnormal mechanical load due to obesity, joint mal-alignment, previous injury and weakened quadriceps strength associate with the onset and development of OA. However, regular moderate-level physical activity and aerobic exercise do not exacerbate but benefit knee OA. Chondrocytes synthesize articular cartilage matrix and maintain cartilage function. They respond to a wide array of mechanical stimuli including compression, shear, tension and hydrostatic pressure. Previous studies found that mechanical stimulation not only enhanced collagen and chondrogenic markers expression in normal cartilage, but also increased matrix accumulation and decreased matrix metalloproteinase production in osteoarthritic chondrocytes. In contrast, some other studies showed controversial results, reporting that mechanical stimulation increased aggrecan mRNA and decreased MMP3 mRNA expression in normal cartilage but this effect was not observed in osteoarthritic chondrocytes. Lowmagnitude high-frequency vibration (LMHFV) is a non-invasive biophysical modality, which the vibration signals are mild and provide systemic vibration to musculoskeletal system. The biological effects of systemic vibration include enhanced lubricin expression in articular cartilage and muscle strength, reduced plasma inflammatory marker concentration and self-perception of pain, which are of potential beneficial effects for OA patients. Systemic vibration also showed retention effect on improving muscle performance for a long time after discontinuing therapy. Meanwhile, increased bone loss and porosity in the subchondral region was considered a common phenomenon in early stage of OA. LMHFV also showed positive effects on enhancing bone mineralization, vascularization and maturation during osteoporotic bone fracture healing, which may have good potential in preventing bone loss in OA.;In this study, we hypothesized LMHFV could delay osteoarthritic cartilage deterioration, prevent subchondral cancellous bone loss and subchondral sclerosis, thus protecting from OA progression and resulting in better limb function in OA rat model. The effects of LMHFV on osteoarthritic cartilage, distal femur epiphysis, subchondral bone plate and limb function were compared between control (CTL) and treatment (VIB) groups at 6, 12 and 18 weeks after LMHFV treatment. The VIBS group that gave LMHFV treatment for 12 weeks only and followed-up till 18 weeks would be compared with CTL and VIB groups at 18 weeks time point, to observe the retention effect of LMHFV on osteoarthritic knee joint. Histological, morphological, biomechanical and functional assessments were performed.;Histological study showed that LMHFV accelerated cartilage degradation with faster increase in histological score. Cartilage volume also increased after LMHFV treatment and most significantly increased at 12 weeks, which might be attributed to cartilage swelling. These findings were also reflected in the worse functional results in treatment group with lower duty cycle, lower regularity index and higher Limb Idleness Index. In contrast, bone formation of epiphysis in distal femur was improved by LMHFV treatment with increased bone volume fraction (BV/TV), trabecular number (Tb.N) and decreased trabecular spacing (Tb.Sp). Subchondral bone plate density increased significantly along with OA progress in both groups. Biomechanical properties including integrated reflection coefficient (IRC) and roughness of cartilage surface, elastic modulus of cartilage in medial tibial plateau did not show significant difference between CTL and VIB groups. All the assessments results of VIBS group did not show significant difference with neither CTL nor VIB group at 18 weeks time point.;In conclusion, LMHFV accelerated cartilage degeneration and caused functional deterioration of OA in an unstable knee induced by ACLT. In contrast, LMHFV promoted bone formation in OA affected distal femur epiphysis, but did not reverse OA progression. Biomechanical properties of the osteoarthritic cartilage did not change after LMHFV treatment, in accordance with the unchanged collagen and aggrecan contents. The retention effect of LMHFV was not observed in this study. These findings indicate that the clinical application of LMHFV on OA patients with unstable knees should be cautious and further work to study the effect of LMHFV on spontaneous OA in a stable knee joint is needed in the future.