We present the results of a 1 year longitudinal study of bone mineral measurements and soft tissue composition in supra-and infra-lesional areas of 31 patients with a spinal cord injury (level D2-L3)_ Like others, we observed a rapid decrease of BMC in the paralysed areas, of -4%/month during the first year in areas rich in trabecular bone and of -2%/month in areas containing mainly compact bone. Lean soft tissue mass (muscle mass) decreases dramatically during the first months post injury in the legs, while fat content tends to increase. Though lean mass is better maintained in patients who develop spasticity, the evolution of BMC does not differ significantly between the groups of flaccid and spastic patients. In patients with partial or complete neurological recovery, a deficit in BMC of -10% with regards to the initial value is still observed at 1 year in the lower limbs. The lean mass of the upper limbs increases early after the cord injury, because of intensive rehabilitation. No significant change in BMC was observed in the supra-lesional areas. These data confirm the rapid loss of bone in the paralysed areas of paraplegic patients, which occurs independently of the presence of spontaneous muscle activity or of passive verticalisation. In patients with recovery, BMC does not return to pre-injury values within 1 year. Thus, there would be an interest in preventing bone loss early in the course of the disease.
Patients with a spinal cord section loose a significant amount of bone. After paraplegia, bone loss occurs below the lesional level and is the more dramatic in iliac bones and in the metaphyseal area of long bones. A peak of urinary calcium and hydroxyprolinuria is observed approximately 6 weeks after their lesion. To further understand the mechanisms underlying the bone damage, we used long-term bone marrow cultures to compare osteoclast-like (OCL-like) cell formation above and below the lesional level. Seven paraplegic, one quadriparetic, one quadriplegic patients and five normal subjects were investigated. Six weeks after their spinal cord section, the number of OCL-like cells formed in iliac bone marrow cultures was significantly greater than those formed in sternal bone marrow cultures for all paraplegic patients tested. No significant differences were seen between iliac and sternal bone marrow cultures for the quadriparetic, the quadriplegic patient, or for the five normal subjects. Conditioned media (CM) from iliac marrow of paraplegic patients increased OCL-like cell formation in normal bone marrow cultures. IL-1, TNF-alpha, IL-6, and PGE2 were measured in the CM after 3 weeks of culture. IL-6 was found to be significantly higher in iliac CM compared with sternal CM in six out of seven paraplegic patients. In two patients, addition of an anti-IL-6 monoclonal antibody to the marrow cultures significantly decreased the number of OCL-like cells formed at 3 weeks. We conclude that paraplegia caused by a cord section locally induces an increase in the capacity of progenitors to form OCL-like cells in long-term bone marrow cultures. A locally increased IL-6 production in the marrow below the lesional level could be partly responsible for this observation.
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