Belt electrode–skeletal muscle electrical stimulation (B-SES) has been reported to influence bone remodeling and muscle function. However, its potential role in fracture healing remains incompletely understood. This study aimed to evaluate the effects of B-SES on fracture repair in a rat femoral fracture model. Twelve male Sprague–Dawley rats with surgically induced femoral fractures were randomly assigned to either a B-SES group or a control group (n = 6 per group). B-SES was initiated immediately after fracture induction and applied for 20 min per day, 5 days per week, for 4 weeks. At 4 weeks post-fracture, femora, tibiae, periosteum, and vastus medialis muscle were harvested for radiographic assessment, micro-computed tomography (micro-CT), histological analysis, biomechanical testing, and reverse transcription polymerase chain reaction (RT-PCR) analysis. Radiographic evaluation demonstrated improved cortical bone continuity and greater callus formation in the B-SES group. Micro-CT analysis revealed significantly increased callus bone volume, trabecular bone thickness, and trabecular bone number in fractured femora, as well as improved trabecular bone microarchitecture in non-fractured tibiae. Biomechanical testing showed significantly higher yield load and toughness in the B-SES group. Histological analysis confirmed increased callus area in B-SES–treated rats. At 4 weeks post-fracture, RT-PCR analysis of the periosteum showed no significant between-group differences in runt-related transcription factor 2 (Runx2), receptor activator of nuclear factor kappa-B ligand (Rankl), or secreted protein acidic and cysteine rich (Sparc) expression, whereas Sclerostin (Sost) expression was significantly higher in the B-SES group. In skeletal muscle, Myostatin (Mstn) expression was significantly reduced in the B-SES group, while insulin-like growth factor 1 (Igf1) expression did not differ significantly between groups. B-SES was associated with improved fracture healing parameters, enhanced bone microarchitecture, and increased mechanical strength in this preclinical model. Reduced Mstn mRNA expression suggests a potential contribution of muscle–bone interactions; however, given the single time-point and transcription-level analyses, these findings should be considered preliminary. Further studies are required to clarify the underlying mechanisms and translational relevance of B-SES in fracture management.
Tsubouchi et al. (Fri,) studied this question.