目的:骨关节炎(OA)是由于机械应力引起的关节软骨退化和破坏的组合,继发性滑膜炎,和骨骼重塑。近年来,早期膝关节OA,OA结构失效的初步阶段,作为预防OA发作的潜在治疗靶点引起了人们的关注。一碘乙酸(MIA)的关节内给药诱导OA样症状,和低剂量的MIA诱发早期OA样症状。在这个实验中,低剂量MIA诱导早期OA模型小鼠,然后用低强度脉冲超声(LIPUS)照射,以检查LIPUS是否改善早期OA的症状。
方法:LIPUS照射4周后,在1周和4周时观察到关节软骨。使用Safranin-O染色结果计算国际骨关节炎研究协会(OARSI)评分。使用变性胶原检测试剂(DCDR)检测软骨变性。
结果:在第4周,我们观察到LIPUS照射组的OARSI评分显着降低。非LIPUS组显示广泛的II型胶原和DCDR双阳性区域,而LIPUS组仅显示少量DCDR阳性区域.此外,第1周时在关节囊中计数的巨噬细胞数量在LIPUS照射组中显示出显着减少。润滑素检测显示,在第4周,LIPUS照射可显著增加润滑素阳性细胞数。
结论:这些结果表明,LIPUS通过减轻炎症和增强润滑素对软骨退变的抑制作用来减轻早期OA的软骨退变。
OBJECTIVE: Osteoarthritis (OA) is a combination of degeneration and destruction of articular cartilage due to mechanical stress, secondary synovitis, and bone remodelling. In recent years, early knee OA, a preliminary stage of structural failure in OA, has attracted attention as a potential target for therapy to prevent the onset of OA. Intra-articular administration of monoiodoacetic acid (MIA) induces OA-like symptoms, and low doses of MIA induce early OA like symptoms. In this experiment, a low-dose of MIA was induced to early OA model mice, which were then irradiated with low-intensity pulsed ultrasound (LIPUS) to examine whether LIPUS improves symptoms of early OA.
METHODS: After 4 weeks of LIPUS irradiation, articular cartilage was observed at 1 and 4 weeks. The Osteoarthritis Research Society International (OARSI) scores were calculated using Safranin-O staining results. Cartilage degeneration was detected using Denatured Collagen Detection Reagent (DCDR).
RESULTS: We observed a significant decrease in OARSI scores in the LIPUS irradiated group at week 4. The non-LIPUS group showed widespread areas of double positivity for Type II collagen and DCDR, whereas the LIPUS group showed only a small number of DCDR-positive areas. In addition, macrophage numbers counted in the articular capsule at week 1 showed a significant decrease in the LIPUS irradiated group. Lubricin detection showed that lubricin positive cell number was significantly increased by LIPUS irradiation at week 4.
CONCLUSIONS: These results suggest that LIPUS attenuates cartilage degeneration in early OA by relieving inflammation and enhancing the inhibitory effect of lubricin on cartilage degeneration.