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Study design:This cross-sectional study compared the androgen and growth factor profiles and the bone turnover of patients with spinal cord injury (SCI) versus able-bodied controls (AB).Objective:Determine whether androgens, GH, or either IGF-I or IGFBP-3, are implicated in bone turnover alteration in patients with recent SCI.Setting:Propara Center, Montpellier, France.Methods:In all, 16 men (31.3 years) with complete SCI, seven paraplegics and nine tetraplegics, who had sustained injury an average of 3 months earlier, and 12 AB who served as controls (27.5 years) participated. Androgens, growth hormone and its mediators were investigated. The bone resorption process was evaluated by urinary and plasma type I collagen C-telopeptide (CTXu, CTXp), while bone formation was evaluated by osteocalcin (OC) and bone alkaline phosphatase.Results:Total testosterone (TT) and the free androgen index (FAI) were significantly lower in the SCI patients, whereas FSH was significantly higher (P<0.05). These hormonal variations were not related to the level of neurological lesion. There was no significant difference in GH, IGF-I, or IGFBP-3 levels. CTXu and CTXp indicated high bone resorption activity in the SCI patients (P<0.05). Regarding bone formation markers, only OC was affected by neurological lesion (P<0.05). Basal hormone levels did not correlate with markers of bone turnover.Conclusion:The high bone resorption process observed in SCI patients did not seem directly related to testicular endocrine abnormalities or an altered growth factor profile. Nevertheless, the reduced TT and FAI levels could be aggravating factors in the development of acute bone loss.Spinal Cord (2006) 44, 791–797. doi:10.1038/sj.sc.3101922; published online 28 March 2006 [ABSTRACT FROM AUTHOR]

Study design:Review article on bone metabolism and therapeutic approach on bone loss in patients with spinal cord injury (SCI).Objective:The first part aims to describe the process of bone demineralization and its effects on bone mass in patients with SCI. The second part describes and discusses the therapeutic approaches to limiting the alteration in bone metabolism related to neurological lesions.Setting:Propara Rehabilitation Center, Montpellier, France.Results:During the first 24 months postinjury, demineralization occurs exclusively in the sublesional areas and predominantly in weight-bearing skeletal sites such as the distal femur and proximal tibia, both of which are trabecular-rich sites. Reduced bone mass, in association with a modified bone matrix property and composition, is very likely at the origin of pathological fractures after minor trauma to which these patients are frequently exposed. Since these fractures may be asymptomatic yet may lead to complications, preventing and managing ‘neurological osteoporosis’ remains a considerable challenge. Two main approaches are considered: the first consists in applying a mechanical stimulus to the bone tissue by standing, orthotically aided walking or functional electrical stimulation (FES). The second uses medications, particularly antiresorptive drugs such as calcitonin or diphosphonates.Conclusion:To develop well-adapted treatments, a more precise understanding of bone loss etiology is needed. The current rehabilitation programs are based on the idea that the bone physiological changes observed in patients with SCI are due to immobility, but results indicate that alterations inherent to neurological damage may play an even greater role in inducing osteoporosis.Spinal Cord (2006) 44, 203–210. doi:10.1038/sj.sc.3101832; published online 13 September 2005 [ABSTRACT FROM AUTHOR]

This study analyzed the temporal and regional variations in bone loss and explored bone cell activities via biochemical markers during an extended follow-up in patients with spinal cord injury (SCI). In parallel, the possible role of the osteoprotegerin (OPG)/RANKL system in disuse osteoporosis was investigated. Seven male patients with acute and complete SCI (31.3 ± 9.5 years) and 12 able-bodied (AB) men (26.9 ± 4.2 years) participated in the study. Measurements were performed 16, 24, 36, 48, and 71 weeks after injury. At week 16, marked calcium homeostasis disturbance and a concomitant increase in bone resorption markers were observed, reflecting an intense bone degradation process. Resorption activity decreased continuously with time. Contrasting with the great rise in the resorption markers, the bone formation markers showed little variation. During the period of investigation, a loss in bone mineral density (BMD) was demonstrated for the total body (−4.3%), pelvis (−15.7%) and lower limbs (−15.2%), whereas BMD did not change at the lumbar spine, upper limbs, or skull. At all stages, SCI patients had lower serum RANKL levels and higher serum OPG levels than did AB controls, but no significant variation with time was observed for either cytokine. These findings suggest that bone resorption persisted long after SCI and specifically affected BMD at sublesional sites. The marked modification of serum OPG/RANKL levels in SCI patients suggests that this system is affected, in disuse osteoporosis. However, the precise biologic role of the OPG/RANKL system in the bone tissue of SCI patients has yet to be determined. [ABSTRACT FROM AUTHOR]

A method for analysis of growth activity in long bones is presented. An external device composed of two force transducers was fixed on the femur of young rabbits on both sides of the epiphyseal plate. Periodical measurements of axial force variation and bone elongation have been made. Preliminary results have been presented and analysed. The possibility of clinical application, especially in control of the bone growth rate, has been discussed. [ABSTRACT FROM AUTHOR]