Xuan Cheng, Yun Ling, Jun Xie, Lianbo Xiao, Xiong Shi, Chenxin Gao
CIA induced early deterioration of bone mass and trabecular microarchitecture, characterized by significant reductions in BMD and Tb.Th. No statistically significant between-group differences in Tb.N or Tb.Sp were identified at individual time points after multiplicity correction. Mechanical impairment of both femoral and vertebral bone was also observed during disease progression. These findings indicate that microarchitectural deterioration and loss of bone strength may follow partly distinct temporal patterns in CIA rats and underscore the importance of early assessment of skeletal changes in inflammatory arthritis.
AIM: This study aimed to characterize the temporal progression of bone loss, trabecular microarchitectural deterioration, and mechanical impairment in a rat model of collagen-induced arthritis (CIA).
METHODS: CIA was induced in Wistar rats via subcutaneous injection of bovine type II collagen. Following CIA induction, rats with a clinical arthritis score of ≥2 were considered to have successfully developed arthritis and were allocated to six experimental groups (n = 8 per group) for tissue collection at 2, 3, 4, 6, 8, and 10 weeks after enrollment. In parallel, three non-immunized normal control rats were euthanized at each corresponding observation time point. Bone quality was assessed using micro-computed tomography (micro-CT) of the proximal tibia and biomechanical testing of the femur and L5 vertebrae.
RESULTS: Micro-CT analysis revealed a significant decrease in bone mineral density (BMD) and trabecular thickness (Tb.Th) as early as 2 weeks post-induction (p < 0.05). After multiplicity correction, trabecular number (Tb.N) and trabecular separation (Tb.Sp) did not differ significantly between the model and corresponding normal groups at any individual time point. Biomechanical testing demonstrated significant reductions in both femoral bending strength and vertebral compressive strength from the earliest examined model time point at 2 weeks, and these impairments persisted through the final 10-week observation point.
CONCLUSION: CIA induced early deterioration of bone mass and trabecular microarchitecture, characterized by significant reductions in BMD and Tb.Th. No statistically significant between-group differences in Tb.N or Tb.Sp were identified at individual time points after multiplicity correction. Mechanical impairment of both femoral and vertebral bone was also observed during disease progression. These findings indicate that microarchitectural deterioration and loss of bone strength may follow partly distinct temporal patterns in CIA rats and underscore the importance of early assessment of skeletal changes in inflammatory arthritis.