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Age-related mechanism may be most responsible for osteoporosis
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Investigators from the University of Arkansas for Medical Sciences have identified an age-related loss of certain proteins that defend against bone-damaging molecules — not estrogen deficiency — as the main cause of osteoporosis.
The findings of the animal study were published in Cell Metabolism, and a review of the research was published at the online home of Endocrine Reviews.
“We feel like we have turned a page in our understanding of osteoporosis,” Stavros Manolagas, MD, PhD, researcher and director of the division of endocrinology and metabolism in the University of Arkansas for Medical Sciences College of Medicine, said in a press release. “This emerging evidence provides a paradigm shift from the ‘estrogen-centric’ view of what causes osteoporosis to one in which these age-related mechanisms are the main protagonists and other changes — including the reduction of estrogen — accentuate them.”
Paradigm shift
Manolagas and colleagues discovered that aging and the body’s decreased ability to defend against oxidative stress are most responsible for osteoporosis and possibly other age-related conditions, such as hardening of the arteries, stroke and Parkinson’s disease.
The researchers identified a specific family of proteins that defend against oxidative stress, according to the release. When the proteins, called forkhead box transcription factors, were removed from young mice, oxidative stress and bone weakness increased. When the proteins were increased, oxidative stress decreased and bone mass improved.
Forkhead box transcription factors
“These proteins that defend against oxidative stress are indispensable for maintaining bone mass,” Manolagas said in the release.
The proteins provide constant defense against oxidative stress to ensure a normal healthy life span but, with age, the bone-damaging molecules begin to overwhelm the body’s natural defenses.
“Now we will look for what specifically causes the defense mechanisms against oxidative stress to fail over time,” Manolagas said in the release.
Ambrogini E. Cell Metab. 2010;11:136-146.
Manolagas SC. Endocr Rev. 2010;doi:10.1210/er.2009-0024.
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