Estudio de la microestructura femoral de pacientes con coxartrosis y con fractura de cadera mediante micro-TAC / Study of the microstructure of femoral patients with hip osteoarthritis and hip fracture by microCT

La disminución de la densidad mineral ósea (DMO), es decir, del volumen de tejido óseo por unidad de volumen del esqueleto, es característica de la osteoporosis, mientras que se ha sugerido que la artrosis se acompaña de un aumento de la DMO a nivel local y sistémico. Para comprobar esta hipótesis analizamos mediante microTAC el hueso trabecular de la cabeza femoral de 10 pacientes con fractura de cadera y 9 con coxartrosis. El análisis no reveló diferencias significativas entre ambos grupos en el volumen de tejido óseo trabecular, ni en los demás parámetros estructurales analizados. Tampoco se encontró una caída significativa del volumen de hueso trabecular con la edad. Esto indica que el hueso de esta región tiene una evolución peculiar. Los mecanismos responsables de ese comportamiento son desconocidos, pero su esclarecimiento podría, quizás, abrir la puerta a nuevos abordajes en el tratamiento de la pérdida de hueso asociada al envejecimiento (AU)

Whereas bone mineral density (BMD) is characteristically low in osteoporosis, it has been postulated that in osteoarthritis BMD is increased. We aimed to check this concept by analyzing bone volumen and structure in the femoral heads of patients with hip fractures (n=10) and with hip osteoarthritis (n=9). Unexpectedly, the analysis of microstructural parameters by microCT did not reveal significant differences between both groups. In addition, we did not find a significant decline in the trabecular bone volume across the age range studied. These results suggest that the evolution of the trabecular bone of the femoral head is different from the age-related decrease of bone mass in other regions of the skeleton. Elucidating the mechanism involved could suggest new approaches to treat the bone loss associated with aging (AU)

Comparative study of the effect of PTH (1-84) and strontium ranelate in an experimental model of atrophic nonunion.

UNLABELLED: This study aimed to set up an experimental model of long bone atrophic nonunion and to explore the potential role of PTH-1-84 (PTH 1-84) and strontium ranelate (SrR). A model of atrophic nonunion was created in Sprague-Dawley rats at the femoral midshaft level. The animals were randomised into four groups. Group A1: control rodents, fracture without bone gap; Group A2: rodents with subtraction osteotomy (non-union model control) treated with saline; Group B: rodents with subtraction osteotomy treated with human-PTH (PTH 1-84); and Group C: rodents with subtraction osteotomy treated with strontium ranelate (SrR). The groups were followed for 12 weeks. X-rays were be obtained at weeks 1, 6 and 12. After sacrificing the animals, we proceeded to the biomechanical study and four point bending tests to evaluate the resistance of the callus and histological study. In second phase, the expression of genes related to osteoblast function was analysed by reverse transcription-quantitative PCR in rats subjected to substraction osteotomy and treated for 2 weeks. The animals were randomised into three groups: Group A2: rodents treated with saline; Group B: rodents treated with PTH 1-84 and Group C: rodents treated with SrR. RESULTS: No significant histological differences were found between animals subjected to subtraction osteotomy and treated with either saline or PTH (p=0.628), but significant difference existed between animals receiving saline or SrR (p=0.005). There were no significant differences in X-ray score between the saline and PTH groups at either 6 or 12 weeks (p=0.33 and 0.36, respectively). On the other hand, better X-ray scores were found in the SrR group (p=0.047 and 0.006 in comparison with saline, at 6 and 12 weeks, respectively). In line with this, biomechanical tests revealed improved results in the SrR group. Gene expression analysis revealed a slightly decreased levels of DKK1, a Wnt pathway inhibitor, in rats treated with SrR. CONCLUSIONS: SrR increases has a beneficial effect in this atrophic non-union model in rats. This suggests that it might have a role may have important implications for the potential clinical role in the treatment of fracture nonunion.