Long-term axial tissue remodeling following posterior lumbar ligament complex injury in SKG mice

Background Local injury may contribute to persistent remodeling of spinal ligament-associated tissues. We examined long-term axial tissue changes after posterior lumbar ligament complex injury in autoimmune-prone SKG mice, using curdlan-treated mice as a comparator with peripheral inflammatory manifestations. Methods Thirteen male SKG mice were allocated to Control (n = 3), curdlan (n = 5), or structural injury (n = 5) groups and followed for 15 months. Control mice received no pharmacological or surgical intervention. Monthly clinical and rotarod assessments and serial micro-computed tomography were complemented by terminal histology, immunofluorescence, and serum cytokine measurements in the two intervention groups. Endpoint comparisons used two-sided exhaustive permutation tests of the Mann–Whitney statistic, with Holm adjustment for defined imaging and histology families. Longitudinal outcomes were summarized descriptively. Results Curdlan-treated mice developed sustained peripheral arthritis. Posterior lumbar total histology scores were higher after injury than after curdlan treatment (median 6 versus 0; Holm-adjusted p = 0.0476). Fibrosis, fibrocartilage metaplasia, and new bone/bridging-tendency scores were also higher (adjusted p = 0.0397 for each domain). Sacroiliac total histology scores were higher (median 5 versus 1; adjusted p = 0.0476), although individual sacroiliac domains and regional micro-computed tomography scores did not differ after adjustment. Exploratory serum analysis showed higher interleukin-23 after injury (nominal p = 0.0079). Conclusions Posterior lumbar ligament complex injury was associated with long-term axial tissue remodeling in SKG mice, with the clearest histological differences in the posterior lumbar region. These observations support further investigation of injury-associated remodeling and its relationship to inflammation and repair. They do not establish a validated model of axial spondyloarthritis or a specific effect of autoimmune susceptibility.