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Anselme, K and Noel, B and Limosino, D and Bianchi, F and Morin, C and Hardouin, P;
2000
October
Spinal Cord
Comparative study of the in vitro characteristics of osteoblasts from paralytic and non-paralytic children
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38
10
622
629
Study design: Cerebral palsy is known to provoke a high loss of bone in children and adults. The potential interest of human osteoblastic cell culture for assessing the osteoblastic function in metabolic bone disorders has been demonstrated by many previous studies. Few studies have attempted to evaluate the capacities of osteoblasts isolated from immobilized or normal bones by in vitro culture methods. Moreover, a few teams did make the distinction between young spastic and flaccid patients. Objectives: We attempted to characterize mature osteoblasts (OB) and bone marrow-stromal cells (BM) originating from 56 immobile and normal children. Spastic and flaccid patients formed the paralytic group. Setting: France. Methods: Osteoblasts and bone marrow cells were isolated from iliac crests obtained during pelvic osteotomies of young control and paralytic patients. The in vitro viability, proliferation and differentiation parameters of the cells from paralytic patients were compared with those of cells coming from normal controls. Results: No significant differences in the cell proliferation parameters were observed between the two groups. Only initial cell viability before inoculation was lower for the paralytic group, compared to the control group. On the other hand: contrary to expectations, we found that fresh and thawed OB cells from flaccid patients synthesized more osteocalcin and more collagen respectively than those of the spastic and control groups. Opposite results were obtained from BM cultures. Conclusion: A negative feedback mechanism by systemic or local factors, which is not conserved in vitro but controls the in vivo osteocalcin and collagen synthesis of flaccid paralytic OB cells, is hypothesized. Because these flaccid patients are known to have a high fat/lean mass, we suggest that leptin may be the potential regulating factor implicated in the hypothesized negative feedback mechanism.
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