ASGSB 1999 Annual Meeting Abstracts

EVIDENCE THAT PARATHYROID HORMONE (PTH) AND MECHANICAL LOADING EXERT THEIR EFFECTS ON THE SKELTON VIA INDEPENDENT PATHWAYS. J.D. Sibonga, E. Morey-Holton, M. Zhang, G.L. Evans, A. Maran and R.T. Turner. Dept. of Orthopedic Research, Mayo Clinic, Rochester, MN.

There is a belief that mechanical loading and PTH mediate their respective skeletal effects through common signaling pathways. Our laboratory has evaluated the putative interaction between PTH and mechanical loading in a 2x2 experimental design (± skeletal loading, ± PTH). In this study, rats are skeletally unloaded by hind-limb elevation and tibial histomorphometry is statistically analyzed by Two-way Analysis of Variance. Reported data reveal that cancellous bone area is significantly increased both by PTH (33.8±1.9 % PTH vs 28.7±2.8% Vehicle, p<0.05) and by loading (34.1±2.4% loading vs. 28.2±2.3% unloading, p<0.05), but no significant interaction is detected between the two factors. Our laboratory subsequently compared the cellular mechanisms behind the skeletal actions of PTH and mechanical loading in the rat by analyzing the gene expression of selected cytokines and bone matrix proteins with Northern analysis and RPA. PTH and mechanical loading each increased mRNA levels for osteocalcin, type 1 collagen and osteonectin within 24h but the time courses differed, as did the effect of the two treatments on expression of specific cytokines. In conclusion, these data all indicate that the effects of PTH and mechanical loading on bone formation are mediated through different pathways. As a result, PTH can stimulate bone formation in the absence of mechanical stimulation. (Supported by NAGW 496-3 and through a NASA Cooperative Agreement NCC 9-58 with the National Space Biomedical Research Institute.)

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