Novel effects on material's properties and pre- and post-yield behavior of rat bones - II. Effects of recombinant human growth hormone on bones and muscles after ovariectomy

GUSTAVO ROBERTO COINTRY; JOSÉ LUIS FERRETTI; RICARDO FRANCISCO CAPOZZA; PAOLA REINA; NÉSTOR MATÍAS FRACALOSSI; SARA FELDMAN

Calcidica (Grecia)

Congreso; IV International Workshop on Musculoskeletal and Neuronal Interactions; 2004

International Society of Musculoskeletal and Neuronal Interactions

Doses of 150 IU/kg/d of human recombinant growth hormone (rhGH, BioSidus, Buenos Aires) were sc given during 3 months to 3-month old rats, either intact or OX at that age. At the end of the study their diaphyses were scanned by pQCT and tested in bending. The fresh gastrocnemius muscles were weighed. OX reduced bone tissue´s mineralization and stiffness. A significant enhancement of bone growth in width improved significantly the diaphyseal architecture (cross-sectional moment of inertia, CSMI). This geometric improvement overcompensated the negative impact of the OX-induced impairment on bone material´s mineralization and stiffness, thus the diaphyseal strength was increased. The assayed rhGH dose rhGH was little effective in intact rats. However, it prevented the OX-induced impairment in bone tissue´s mineralization (not stiffness) and improved additively the OX-enhanced geometric variables. These effects of OX and rhGH were correlative with additive increases in muscle mass. Simple regression analyses showed that the impact of muscular improvement was more evident on bone architecture than on bone strength. The positive OX and rhGH effects on cortical bone mass and architecture may have derived from the induction of an "anabolic" shift of bone mechanostat threshold for triggering bone modeling during growth, with a positive biomechanical impact on the diaphyses (larger CSMI and fracture load than controls). The apparent incongruence between the repercussion of the additive improvement in muscle mass induced by OX and rhGH on bone geometry (large impact) and strength (relatively low impact) can be explained because rhGH did not prevent the OX-induced impairment in bone material´s stiffness because rhGH did not act on the microstructure of mineralized tissue. Based on original arguments, these evidences suggest the ability of rhGH to improve human post-menopausal osteopenias in which a relatively large impairment in cortical bone mass and/or distribution occurs. However, the actual benefit of the positive rhGH effects on bone mass and architecture in any species would remain uncertain as long as the nature of rhGH effects on the OX-impaired bone´s material stiffness is unknown. These results are interesting because they defy the prevailing view that the remaining bone tissue in metabolic osteopenias is normal.