Background: Muscle imbalance has long been recognized as one of the possible pathogeneses for adolescent idiopathic scoliosis (AIS). PIEZO2, the susceptibility gene of AIS, has been identified to play an important role in neuromuscular activities.
Objective: This study aims to compare the mRNA expression of PIEZO2 between concave and convex paraspinal muscles of AIS patients and to identify the relationship between the ratio of PIEZO2 expression and curve magnitude.
Methods: Twenty female AIS patients (right thoracic curve) who underwent spinal correction surgery were divided into moderate (n= 12) and severe (⩾ 70 degrees) curve groups (n= 8). The morphology of the paraspinal muscles was assessed with spinal MRI. Multifidus specimens were collected during surgical operations from the concave and convex sides of the apical region, and mRNA expression of the PIEZO2 gene was compared between sides. The localization of PIEZO2 protein expression was confirmed with the markers PAX7 and PAX3, and the percentage of PIEZO2+ cells was also investigated.
Results: In the moderate curve group, fatty infiltration in the deep paraspinal muscle was significantly higher on the concave side than on the convex side. There were no differences in deep muscle area, superficial muscle area, or fatty infiltration of superficial paraspinal muscle. The mRNA expression of PIEZO2 was significantly increased on the concave side, and the asymmetric expression predominantly occurred in moderate curves rather than severe ones. PIEZO2 was expressed on satellite cells instead of fibers of the muscle spindle. The percent of PIEZO2+PAX7+ cells in myofibers was significantly higher on the concave side in the moderate curve group, but not in the severe curve group.
Conclusions: Asymmetric morphological changes occur in the deep paraspinal muscles of AIS. The PIEZO2 is asymmetrically expressed in the multifidus muscle and is preferentially expressed in satellite cells.
Keywords: PIEZO2; adolescent idiopathic scoliosis; paraspinal muscle; satellite cells.