Maxillary expansion is the most common procedure in orthodontics for correcting maxillary transverse deficiency. Despite its widespread use, standardized clinical protocols often neglect age-related differences in cellular responses, which may significantly impact treatment outcomes. To investigate these variations, we conducted comprehensive experiments on 6-week-old and 12-month-old mice, representing young and middle-aged groups, respectively. We employed 0.012-inch Australian orthodontic wire attached to the maxillary first and second molars on both sides, delivering a force of 25g. The outcomes were monitored at key intervals post-intervention (days 0, 3, 7, and 14; n = 8 per group) to capture the dynamic changes in bone remodeling over time. Our evaluation methods included MicroCT analysis, tartrate-resistant acid phosphatase (TRAP) stain, immunofluorescence stain using antibodies to RUNX2, osteocalcin, Gli1, and Ki67, and TUNEL assay to assess midpalatal suture gap, osteoclastogenesis, osteogenesis, and mesenchymal stem cell (MSC) proliferation/apoptosis. Both 6-week- and 12-month-old mice exhibited successful midpalatal suture opening, but young mice demonstrated earlier and more intense osteoclast activity, along with higher expression of RUNX2 and osteocalcin. Young mice also exhibited a higher percentage of Gli1+Ki67+immunopositive cells, while middle-aged mice showed a higher percentage of Gli1/TUNEL-positive cells on day 3 after maxillary expansion. Our findings suggest that aging negatively impacts mechanical force-induced bone remodeling by reducing osteoclastogenesis, osteogenesis, and MSC proliferation while increasing MSC apoptosis.