A handful of brain cells deep in the brain may play a surprising role in controlling women’s bone density, according to new research by UC San Francisco and UCLA scientists.
In a study published January 11, 2019 in Nature Communications, researchers showed that blocking a particular set of signals from these cells causes female (but not male) mice to build extraordinarily strong bones and maintain them into old age, raising hopes for new approaches to preventing or treating osteoporosis in older women.
“Our collaborators who study bone for a living said they’d never seen bone this strong,” said study senior author Holly Ingraham, Ph.D. “Our current understanding of how the body controls bone growth can’t explain this, which suggests we may have uncovered a completely new pathway that could be used to improve bone strength in older women and others with fragile bones.”
Participation in organized sport during childhood and adolescence is associated with bone mass at 20 years of age, according to a Journal of Bone and Mineral Research study.
In the study that followed 984 children into young adulthood, males who were ‘consistent sport participators’ from ages 5-17 years had significantly greater whole body and leg bone mineral content at age 20 years than those who dropped out of sport, whereas males who ‘joined sports’ had significantly greater leg bone mineral content than those who dropped out of sport.Females who were ‘consistent sport participators’ had significantly greater leg bone mineral content at 20 years of age than those who dropped out.
Because attainment of optimal peak bone mass in young adulthood is protective against osteoporosis later in life, participation in organized sport may have long-term skeletal benefits.
A group of steroid hormones could provide new insight into the bone loss and deterioration that occurs with aging, researchers at the Medical College of Georgia at Augusta University report.
Previous research has shown that the protein histone deacetylase 3, or HDAC3, turns off the genes that encourage the stem cells in our bone marrow to make and store fat instead of making bone. As HDAC3 levels decrease naturally with age, bones become less dense and easily breakable.
Now scientists looking further upstream to hopefully explain the mechanism behind that process are finding some conflicting results.