The pathophysiological nature of sarcomeres in trigger points in patients with myofascial pain syndrome: A preliminary study.

Abstract

BackgroundMyofascial pain syndrome (MPS) has a high global prevalence and is associated with myofascial trigger points (MTrPs) in taut bands or nodules. Little is known about the aetiology. The current study assessed the pathophysiological characteristics of MTrPs in MPS patients.MethodsBiopsies of the trapezius muscle were collected from the MTrPs of MPS patients (MTrP group; n = 29) and from healthy controls (control group; n = 24), and their morphologies were analysed via haematoxylin‐eosin (H&E) and Masson staining. A protein microarray was used to detect the receptor tyrosine kinase (RTK) family proteins. mRNA and long non‐coding RNA (lncRNA) sequencing and analysis were conducted, and immunohistochemistry and Western blotting were used to examine the expression of EphB and Rho family proteins.ResultsAbnormally contracted sarcomeres showed enlarged, round fibres without inflammation or fibrosis. An lncRNA‐mRNA network analysis revealed activation of muscle contraction signalling pathways in MTrP regions. Among RTK family proteins, 15 exhibited increased phosphorylation, and two exhibited decreased phosphorylation in the MTrP regions relative to control levels. In particular, EphB1/EphB2 phosphorylation was increased on the muscle cell membranes of abnormal sarcomeres. RhoA and Rac1, but not cell division control protein 42 (Cdc42), were activated in the abnormal sarcomeres.ConclusionsEphB1/EphB2 and RhoA/Rac1 might play roles in the aetiology of abnormally contracted sarcomeres in MTrPs without inflammatory cell infiltration and fibrotic adhesion.SignificanceContracted sarcomeres were found in MTrP regions, which is consistent with the MTrP formation hypothesis. EphB1/EphB2 and RhoA/Rac1 might play roles in the sarcomere contractile sites of MTrPs, which may be promising therapeutic targets.