背景:颞下颌关节骨关节炎(TMJOA)的特征是关节软骨退变和进行性滑膜炎。如何在早期有效抑制TMJOA一直是生物医学领域的研究热点。作为一种非侵入性物理治疗,脉冲电磁场(PEMF)治疗在治疗四肢关节骨关节炎(OA)方面显示出巨大的潜力。
目的:本研究旨在探讨PEMF干预对TMJOA早期TMJ软骨退变和滑膜炎症的生物学效应。
方法:PEMF(2.0mT,15Hz,2小时/天)对大鼠进行治疗,其中通过应用单侧前反咬合(UAC)诱导了TMJOA。组织学和免疫组织化学染色,TUNEL检测,采用real-timePCR和Westernblotting法检测髁突软骨和滑膜的形态变化以及促炎和降解因子的表达。
结果:髁突软骨明显退变,以软骨厚度减少为特征,降解的软骨细胞外基质,促炎和降解因子的表达增加(TNF-α,IL-1β,MMP-13,ADAMTS-5,IL-6,MMP-3,MMP-9和COL-X)和软骨细胞死亡增加,在UAC组中观察到,伴有滑膜增生和滑膜促炎和降解因子的上调。PEMF干预在3周时逆转了软骨厚度的降低,在6周时逆转了软骨细胞外基质的降解。此外,促炎症的上调,在一定程度上抑制了UAC诱导的con突软骨中的降解和增生因子以及软骨细胞死亡。此外,在3周和6周时,滑膜增生和滑膜促炎和降解因子的上调被抑制。
结论:适当的PEMF刺激可以逆转软骨细胞外基质的损失,软骨细胞死亡,软骨中促炎和降解因子的表达增加,在TMJOA早期,UAC在一定程度上降低了软骨厚度和滑膜炎症。PEMF刺激可能是临床TMJOA治疗中一种有前途的方法。
BACKGROUND: Temporomandibular joint osteoarthritis (TMJOA) is characterized by articular cartilage degeneration and progressive synovitis. How to effectively inhibit TMJOA in the early stage has been a hot topic in the biomedical field. As a non-invasive physiotherapy, pulsed electromagnetic field (PEMF) treatment has shown great potential in the treatment of osteoarthritis (OA) in extremity joints.
OBJECTIVE: This study aims to investigate the biological effect of PEMF intervention on TMJ cartilage degeneration and synovium inflammation at the early stage of TMJOA.
METHODS: PEMF (2.0 mT, 15 Hz, 2 h/day) treatment was given to rats in which TMJOA was induced by applying the unilateral anterior crossbite (UAC). Histological and immunohistochemical staining, TUNEL assay, real-time PCR and western blotting assay were performed to detect the changes of the morphology and the expression of pro-inflammatory and degradative factors in condylar cartilage and synovium.
RESULTS: Obvious condylar cartilage degeneration, characterized by decreased cartilage thickness, degraded cartilage extracellular matrix, increased expression of pro-inflammatory and degradative factors (TNF-α, IL-1β, MMP-13, ADAMTS-5, IL-6, MMP-3, MMP-9 and COL-X) and increased chondrocytes death, was observed in UAC group, accompanied by synovium hyperplasia and up-regulation of pro-inflammatory and degradative factors in synovium. PEMF intervention reversed the decreased cartilage thickness at 3 weeks and degraded cartilage extracellular matrix at 6 weeks. Moreover, the up-regulation of pro-inflammatory, degradative and hypertrophyic factors and chondrocytes death in condylar cartilage induced by UAC were inhibited to some extent. In addition, the synovium hyperplasia and the up-regulation of pro-inflammatory and degradative factors in synovium were inhibited at 3 weeks and 6 weeks.
CONCLUSIONS: Appropriate PEMF stimulation can reverse the loss of cartilage extracellular matrix, the chondrocytes death, the increased expression of pro-inflammatory and degradative factors in cartilage, the decreased cartilage thickness and synovium inflammation induced by UAC at the early stage of TMJOA to some extent. PEMF stimulation may be a promising method in clinical TMJOA treatment.