Published online Dec 26, 2020. doi: 10.4252/wjsc.v12.i12.1667
Peer-review started: September 3, 2020
First decision: September 15, 2020
Revised: September 30, 2020
Accepted: October 20, 2020
Article in press: October 20, 2020
Published online: December 26, 2020
Processing time: 114 Days and 8.9 Hours
Bone mass and strength decline with aging. Mesenchymal stem cells (MSC) are precursors of osteoblasts and adipocytes. Osteoblastogenesis decreases, and adipogenesis increases, in bone-marrow MSC with aging. Receptor activator for nuclear factor kappa B ligand (RANKL) induces osteoclastogenesis, whereas Osteoprotegerin (OPG) represses it. Therefore, the OPG/RANKL ratio regulates bone resorption. Hypoxia induces the HIF-1A gene, encoding a transcription factor which regulates, among others, genes involved in angiogenesis and osteogenesis. Chronic hypoxia has negative effects on bone. Yet, cyclic exposure to hypoxia for short periods, followed by long times in normoxia, may have beneficial effects.
Cyclic hypoxia can be a non-pharmacological method for the prevention and treatment of different clinical conditions, such as loss of bone mass with age.
Investigate the effects of cyclic hypoxia exposure on differentiation of human MSC, derived from bone-marrow, into osteoblasts or adipocytes. Conduct a pilot study on the cyclic hypoxia effect on bone-mineral density and fat mass in elderly.
MSC were induced to differentiate into osteoblasts or adipocytes, in cyclic hypoxia (3% O2 for 1, 2 or 4 h, 4 d a week). Osteogenic and adipogenic markers were measured. In addition, elderly were exposed to either low oxygen concentration in air (simulating an altitude of 2500 m above sea level) in a hypoxia chamber, or to normoxia, for 18 wk (36 CH sessions of 16 min each). Percentages of fat mass and bone mineral-density from whole body, trunk and right proximal femur were assessed, using dual-energy X-ray absorptiometry.
Cyclic hypoxia with 4 h of hypoxia exposure inhibited osteogenesis and adipogenesis. Osteocalcin, vascular endothelial growth factor A and LRP (5/6)/ dickkopf-1 gene expressions were upregulated in osteoblasts. Yet, the latter decreased in adipocytes. Cyclic hypoxia treatments increased the OPG/RANKL ratio, in both cell types. Elderly exposed to cyclic hypoxia increased total bone mineral-density, although the percentage of fat did not vary between groups.
Cyclic hypoxia affects MSC differentiation into osteoblasts or adipocytes. It can increase bone mass, by inhibiting osteoclastic activity, through upregulating the OPG/RANK ratio.
The potential of using cyclic hypoxia to prevent and treat bone-mass loss associated with ageing is promising. Yet, its mechanisms of action need to be further explored. Trials with a larger number of participants should be carried out to evaluate different patterns and times of exposure to cyclic hypoxia.