Since the beginning of the manned missions, microgravity was supposed to induce a bone fragility in the astronauts. In 2000, the first research on astronauts' osteoporosis started and showed that the adaptation to microgravity did not stop after the astronauts returned. Nowadays, the studies are still on and are about monitoring the astronauts who spent more than six months in space because the point of no-return to equilibrium is still unknown.
Space hosts extreme conditions and in microgravity the musculoskeletal system is used in a different way. As Jean Baptiste Lamarck said in the 18th century, “the function creates the organ”. So we could expect "structure-function" adaptations of the support tissues.
The adult bone is an active tissue which is submitted to a remodelling by bone resorption and formation. Due to this renewal, it is possible to:
- regulate many metabolic pathways;
- replace the damaged bone by a new one;
- adapt the body to the mechanical constraints which it must locally face by reinforcing the bone where the constraints increase (such as impact sports) and decreasing the bone matrix otherwise.
The bone is composed of two structure types: trabecular and cortical bones. The trabecular bone is made up of lattice-shaped spicules and occurs at the ends of long bones and within the interior of vertebrae, pelvis and flat bones. It is 20 % of the skeleton. The cortical or compact bone is 80 % of the skeleton and covers every bone. Both osseous compartments (cortical and trabecular) are different. In the case of bone fragility (astronauts and osteoporotic patients), the fracture has to be prevented. The diagnostic is currently based on densitometry measuring the global bone mineral density (BMD). An individual score is so established to be compared with the scores obtained by a referent population of healthy young adults.
In order to distinguish the osseous compartments, pQCT analysis (Densiscan, Scanco Medical, Switzerland) can be carried out on board, firstly for the needs of the astronauts. The first version of this tomographic devise separately measured the cortical and trabecular BMD of a non weight-bearing bone (the radius) and a weight-bearing one (the tibia).
Astronauts under pressure
So a cohort of astronauts who stayed from 1 to 6 months on board the MIR space station were tested. The results showed an important osseous loss in the weight-bearing bones (nothing in the radius) and particularly in the trabecular.
|•||Astronaut 5 (174 days)|
|•||Astonaut 7 (0 day)|
|•||Astronaut 9 (198 days)|
|•||Astronaut 11 (0 day)|
|•||Astronaut 13 (0 day)|
|•||Astronaut 15 (60 days)|
|•||Astronaut 6 (180 days)|
|•||Astronaut 8 (0 day)|
|•||Astronaut 10 (460 days)|
|•||Astronaut 12 (126 days)|
|•||Astronaut 14 (0 day)|
Even worth, six months after returning from a stay of the same length, there was no recovery. Other densitometry studies suggested that the osseous loss was effective in the lower half of the body.
It is interesting to compare the re-distribution of physiological liquids (blood flowing to the thoracocephalic regions at the expense of the lower limbs) with the minerals in the skeleton.
It has been shown that, in rats, the osseous loss due to immobilisation came with a diminution of the intraosseous vessel number and that the osseous gain resulting from physical exercise was combined with angiogenesis (development of new blood vessels from existing ones); this gain was completely inhibited if the animals were treated with a blocking major angiogenic factor, the VEGF (Vascular Endothelial Growth Factor).
What are the different mechanisms responsible for the accelerated and localised osseous loss after a space flight?
The BIOCOSMOS series of Russian flights showed a decrease in both the osseous formation and long-bones' growth. It also showed an early and transitory increase of the bone resorption resulting from a osseous loss in rats.
With the astronauts, the bone cell activities could be measured thanks to serum and urinary bone markers. They both showed a bone remodelling's uncoupling but the systemic characteristic made impossible to know where the osseous loss was located.
A higher performance version of Densiscan, called Xtreme CT, was mounted in Star City. It gave the opportunity to analyse the bone microarchitecture and so characterize the cortical envelope and trabecular network as well as predict biomechanical specifications. The measurements started on astronauts before and after (long-length monitoring) staying on board the ISS.
It appeared that our skeleton was adapting to these new mechanical functions. So the problem did not only exist during the exposure to microgravity but also back on Earth all the more so as the recovery seemed to be much longer than the flight time.
However, it should be noted that if some astronauts experienced spectacular osseous losses, others seemed to be insensitive. Why? Is there a genetic factor? Will we, one day, select only "osteoporosis-resistant" astronauts? Such individual variabilities can also be found during bed rest tests when healthy volunteers remain in bed in order to mime some space effects.
Finally, the problematics and studies carried out in microgravity first allowed us to better understand our own problem on Earth.