How stress and depression can lead to unhealthy bones – but only for males
• New rodent study uncovers novel mechanism by which chronic stress leads to bone loss
May 18, 2016, Rome, Italy. Press Dispensary.
• Study also finds the phenomenon restricted to males
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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Notes for editors
About ECTS 2016
ECTS 2016 is the 43rd annual congress of the European Calcified Tissue Society (ECTS), held in Rome, Italy on May 14-17, 2016, in collaboration with the Cancer and Bone Society.
ECTS 2016 gives delegates the opportunity to collaborate with leading international researchers and clinical colleagues. Main discussion points are the latest in high quality science and research to benefit clinical practice.
ECTS 2017, the 44th congress, will be held in Salzberg, Austria, May 13-16, 2017.
See http://ects2017.org .
About The European Calcified Tissue Society
The European Calcified Tissue Society (ECTS) is the major organisation in Europe for researchers and clinicians working in the field of calcified tissues and related fields. ECTS acts as a forum for the dissemination of high quality research through its annual meeting, the European Symposium on Calcified Tissues, and through training courses and workshops.
Calcified tissues are central to a healthy skeleton and to bone disorders - such as osteoporosis, back pain and fractures - that make life a misery for countless people. Children can inherit some forms of bone diseases causing bone pain, shortness and deformed limbs.
About the study
The study, titled "Exposure to Chronic Stress Induces Bone Loss via Glucocorticoid Signalling in Osteoblasts", was carried out by Holger Henneicke and colleagues at the ANZAC Research Institute, University of Sydney, Australia.
After the four week exposure to forms of chronic stress, L3-vertebrae and tibiae were analysed by micro-CT and histomorphometry, and blood was collected for markers of bone turnover.
Compared to the non-stressed controls, exposure to chronic stress resulted in loss of vertebral trabecular bone mass in male wild-type mice but not in their male littermates in which glucocorticoid signalling was selectively disrupted in mature osteoblasts and osteocytes (wt:-15.9% tg:ư.8%, p < 0.05). Bone loss in mice with intact osteoblastic glucocorticoid signaling was due to a decrease in trabecular number (wt:-14.3% tg:Ʈ.8%, p < 0.01) and an increase in trabecular separation (wt:ი.1% tg:Ư.2%, p < 0.05). While trabecular bone in the tibia was unaffected in stress-exposed wild-type and HSD2OB-tg males, tibial cortical area (wt:-11.1% tg:Ư.3%, p < 0.05) as well as cortical area fraction (wt:-9.5% tg:-2.6%, p=0.054) were reduced in stressed wild-type but not in the stressed male mice with glucocorticoid signalling disruption. Histomorphometry and measurements of serum TRAP5b revealed an increase in osteoclast activity in wild-type males following stress exposure, an effect that was absent in their treated littermates. In female mice, both vertebral and long bone structural parameters remained unaffected by chronic mild stress.
For further information, please contact:
Roberta Mugnai, ECTS executive director
European Calcified Tissue Society (ECTS)
Tel: + 32 476 520 716
ECTS 2016: http://2016.ectscongress.org/
Event hashtag: https://twitter.com/hashtag/ECTS2016