Effects of gravitational changes on the bone system in vitro and in vivo.

Spaceflight data obtained on bone cells, rodents, and humans are beginning to shed light on the importance of gravitational loading on the skeletal system. The space environment is a relevant model to explore the bone cell response to minimal strains. However, whether there is a direct effect of gravity on the cell rather than changes related to lack of convection forces in cell cultures performed in microgravity is unknown. In vitro studies carried out using osteoblastic cell cultures in space show changes in cell shape, suggesting that cell attachment structures as well as cytoskeleton reorganization might be involved. Valuable information is expected from in vitro models of an increase or decrease in mechanical stress in order to identify the different pathways of mechanoreception and mechanotransduction in the osteoblastic lineage. Results obtained from both humans and rodents after spaceflights indicated that bone mass changes are site specific rather than evenly distributed throughout the skeleton, thus emphasizing the need to perform measurements at different bone sites: weight- and non-weight-bearing bones, and cancellous and cortical envelopes. Bone mass measurements and biochemical parameters of bone remodeling are currently under evaluation in cosmonauts. Histomorphometric studies of bones from rats after space missions of various periods provided the time course of the cancellous bone cellular events: transient increase in resorption and sustained decrease in bone formation. The underlying bone loss occurred first in weight-bearing bones and later in less weight-bearing bones. During the postflight period, time required to recover the lost bone was greater than the mission length. Thus, the postflight period deserves more attention than it is currently receiving. On earth, the rat tail-suspension model is currently used to mimic spaceflight-induced bone loss. Data from the model confirmed the impairment of osteoblastic activity and showed an alteration in osteoblast recruitment with skeletal unloading. However, this model needs to be further validated.