Avascular necrosis (AVN) of the femoral head (AVNFH) is a disease caused by injury to the blood supply of the femoral head, resulting in a collapse with osteonecrosis and damage to the articular cartilage. Extracorporeal shockwave therapy (ESWT) has been demonstrated to improve AVNFH owing to its anti-inflammation activity, angiogenesis effect, and tissue regeneration in clinical treatment. However, there are still so many pieces of the jigsaw that need to be fit into place in order to ascertain the mechanism of ESWT for the treatment of AVNFH. The study demonstrated that ESWT significantly protected the trabecular bone volume fraction BV/TV () and the trabecular thickness (), while in contrast, the trabecular number and trabecular separation were not significantly different after treatment as compared with AVNFH. ESWT protected the articular cartilage in animal model of AVNFH. The levels of IL1-β and IL33 were significantly induced in the AVNFH group () as compared with Sham and ESWT groups and reduced in ESWT group () as compared with AVNFH group. In addition, the expression of the receptor of IL33, ST2, was reduced in AVNFH and induced after ESWT (). The expression of IL17A was induced in the AVNFH group () and reduced in the ESWT group (). Further, the expression of the receptor of IL17A, IL17RA, was reduced in the AVNFH group () and improved to a normal level in the ESWT group as compared with Sham group (). Taken together, the results of the study indicated that ESWT modulated the expression of IL1-β, pro-inflammatory cytokines IL33 and IL17A, and their receptors ST2 and IL17RA, to protect against loss of the extracellular matrix in the articular cartilage of early AVNFH.

中文翻译：

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体外冲击波治疗调节大鼠模型早期股骨头缺血性坏死关节软骨内促炎细胞因子 IL33 和 IL17A 及其受体 ST2 和 IL17RA 的表达

股骨头缺血性坏死（AVN）（AVNFH）是一种由于股骨头血供受损，导致股骨头塌陷和骨坏死和关节软骨损伤的疾病。体外冲击波疗法 (ESWT) 已被证明可改善 AVNFH，因为其在临床治疗中具有抗炎活性、血管生成作用和组织再生。然而，为了确定 ESWT 治疗 AVNFH 的机制，仍然有很多拼图需要安装到位。研究表明，ESWT 显着保护了骨小梁体积分数 BV/TV（)和小梁厚度 ()，而相比之下，与 AVNFH 相比，治疗后小梁数量和小梁分离没有显着差异。ESWT 保护 AVNFH 动物模型中的关节软骨。IL1- β和IL33水平在AVNFH组显着诱导（)与 Sham 和 ESWT 组相比，ESWT 组减少 ()与 AVNFH 组相比。此外，IL33 受体 ST2 的表达在 AVNFH 中降低，并在 ESWT 后被诱导。）。AVNFH组诱导IL17A表达（)并在 ESWT 组中减少 (）。此外，IL17A 受体 IL17RA 的表达在 AVNFH 组中降低（)与 Sham 组相比，ESWT 组改善至正常水平 (）。总之，研究结果表明，ESWT 可调节 IL1 - β、促炎细胞因子 IL33 和 IL17A 及其受体 ST2 和 IL17RA 的表达，以防止早期 AVNFH 关节软骨中细胞外基质的损失。