Relationship between serum β-catenin mRNA expression and femoral fracture healing after head trauma: an experimental rat study.

Abstract

BACKGROUND: Fracture healing may be influenced by concomitant traumatic brain injury (TBI). Both clinical and experimental studies have reported accelerated union and enhanced callus formation in the presence of TBI. The Wnt/&#x3b2;-catenin signaling pathway is thought to play a role in this process; however, the relationship between serum &#x3b2;-catenin mRNA relative expression and fracture healing in the context of TBI remains unclear. METHODS: Thirty-six female Wistar albino rats were randomly assigned to four groups: control, TBI only, femoral fracture only, and combined TBI + femoral fracture. Radiographic healing was evaluated using the Radiographic Union Scale for Tibial fractures (RUST) at weeks 3 and 6. Serum &#x3b2;-catenin mRNA relative expression was quantified by real-time polymerase chain reaction at baseline (week 0) and during follow-up (weeks 3 and 6). Histological analysis was performed at week 6. RESULTS: Radiographic evaluation demonstrated progressive healing in all fracture groups, with significantly higher RUST scores in the TBI + fracture group compared to the fracture-only group at both time points (p<0.05). Serum &#x3b2;-catenin mRNA relative expression decreased significantly over time in both fracture groups, whereas no significant temporal changes were observed in the control or isolated TBI groups. Because this decline occurred in both fracture groups, it did not indicate a TBI-specific molecular effect. Histologi-cal analysis showed a tendency toward more mature osseous callus formation in the TBI + fracture group; however, these differences were not statistically significant. CONCLUSION: Concomitant TBI was associated with enhanced radiographic fracture healing and showed a non-significant trend toward more advanced osseous callus formation. The observed decline in serum &#x3b2;-catenin mRNA relative expression in the fracture groups suggests phase-dependent regulation of Wnt/&#x3b2;-catenin-related activity during repair. However, serum &#x3b2;-catenin mRNA represents an indirect systemic marker and does not establish a mechanistic, TBI-specific pathway. These findings highlight the complex systemic influence of TBI on skeletal repair and support further mechanistic studies-particularly those incorporating fracture-site (local) analyses-to clarify the biological pathways underlying the observed radiographic association.