Abstract
BACKGROUND & AIMS: Myofascial trigger points (MTrPs) are highly sensitive irritated points within a tense belt of skeletal muscle, and are the main cause of muscle pain and dysfunction. MTrPs can also cause paraesthesia and autonomic nervous dysfunction. Furthermore, long-term and chronic MTrPs can cause muscle atrophy and even disability, seriously affecting the quality of life and mental health of patients, and increasing the social and economic burden. However, to date, there have been few studies on fibrogenesis and changes in MTrPs. Therefore, this study investigated whether transforming growth factor beta1 (TGF-β1)-Smad2/3 participates in the formation of MTrPs and how it affects fibrosis using point shear wave elastography. METHODS: Forty Sprague‒Dawley rats were randomly divided into the MTrPs group and the control group. Blunt injury combined with eccentric exercise was used to establish an MTrPs model. Electromyography (EMG), haematoxylin and eosin (H&E) staining and transmission electron microscopy (TEM) were used to verify the model. The collagen volume fraction was measured by Masson staining, the protein expression of TGF-β1 and p-Smad2/3 was measured by Western blotting (WB) and immunohistochemistry (IHC), and the shear wave velocity (SWV) was measured by point shear wave elastography. RESULTS: EMG, H&E and TEM examination indicated that the modelling was successful. The collagen volume fraction and the protein expression of TGF-β1 and p-Smad2/3 were higher in the MTrPs group than in the control group. The SWV of the MTrPs group was also higher than that of the control group. These differences suggest that MTrPs may exhibit fibrosis. The correlations between the collagen volume fraction and SWV and between the collagen volume fraction and TGF-β1 were positive. CONCLUSION: Fibrotic conditions may be involved in the formation of MTrPs. Ultrasound point shear wave elastography and assessment of TGF-β1 and p-Smad2/3 expression can reflect the degree of MTrPs fibrosis to some extent. Further exploration of the important role of TGF-β1 and Smad2/3 in the pathogenesis of MTrPs will be of great significance for clinical treatment.