- New rodent study uncovers novel mechanism by which chronic stress leads to bone loss
- Study also finds the phenomenon restricted to males
May 18, 2016, Rome, Italy. Press Dispensary. A new study has helped to unveil the mystery of why chronic stress and depression can lead to bone loss and increase the risk of fractures. The effect of chronic stress on the health of bones is already known but how one leads to the other is not entirely understood. The study, whose results have just been announced by Holger Henneicke of the University of Sydney, set out to investigate the mechanism.
Dr Henneicke was speaking to an audience of specialists at ECTS 2016, the 43rd annual congress of the European Calcified Tissue Society (ECTS) being held in Rome. He described how the study examined the impact of chronic stress on skeletal metabolism and structure in mice, comparing a group of wildtype mice with a group in which the signals of a hormone, suspected of being responsible, had been disrupted.
Holger Henneicke said: “We know stress and depression are linked to poor bone health but not how one results in the other, so we set out to determine the role played by stress hormones, known as glucocorticoids, in the cells which synthesise bone.
“Eight week old male and female mice were exposed to chronic but mild stress. In some mice, the glucocorticoid signalling was selectively disrupted in bone-forming osteoblasts, while their littermates were left ‘wild’.”
There was also a control group not exposed to the mild stress.
Dr Henneicke continued: “After four weeks of stress exposure, the mice were examined and a portion of the spine – the L3-vertebrae – plus tibia and blood were analysed.
“When compared to the non-stressed control group, the wildtype mice, with normal intact stress hormone signalling, experienced a loss of bone mass in the analysed vertebrae and a reduction in the area of the tibial cortex, as well as an increase in the activity of osteoclasts, a type of bone cell that breaks down bone tissue for maintenance and repair purposes. Meanwhile, the stressed mice whose glucocorticoid signalling had been disrupted did not experience this effect.
“And interestingly, this only applied to males. In stressed females, neither the vertebral nor tibial structures were affected.”
Mr Henneicke concluded: “So in male mice, glucocorticoid signalling in osteoblasts and the subsequent activation of osteoclasts is part of what lies behind bone loss during chronic mild stress.
“In female mice, it is a different story altogether, chronic stress did not seem to influence bone health and we are currently looking into why not.”
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