Some risk factors for osteoporosis such as being older and female or having a family history of the condition cannot be avoided. But others can, like smoking cigarettes, consuming alcohol, taking certain medications, or being exposed to environmental pollutants. But until now researchers haven’t gained a firm picture of how these exposures link up with bone loss.
A new study led by researchers from Penn’s School of Veterinary Medicine reveals a mechanism by which these factors and osteoporosis may be linked. Damage to mitochondria—key cellular organelles and energy generators—leads to a surge in the creation of cells called osteoclasts, which are responsible for breaking down bone, the researchers report in FASEB Journal. They uncovered these effects in cells in culture as well as in an animal model.
“In a normal individual, the process of bone degradation and rebuilding proceeds in a very balanced way, but in some people they somehow produce a lot more osteoclasts, and this leads to bone loss and osteoporosis,” said Narayan Avadhani, a biochemist at Penn Vet and senior author on the work. “We show in this paper that, when mitochondrial function is affected, it not only affects energy production but also triggers a type of stress signaling that induces the overproduction of osteoclasts.”
A combination of powerful tools has helped scientists identify two new genes that could contribute to osteoporosis through their effect on bone density. The finding could lead to better treatments for the bone-weakening disease.
The study, by researchers at the Children’s Hospital of Philadelphia (CHOP) in Pennsylvania, highlights the importance of understanding the 3D geography of the genome in locating genes that cause disease.
The team points out that identifying DNA variants, or differences, behind diseases, is not necessarily enough to locate the genes that cause the disease. The variants, for example, could be triggers of genes in other parts of the genome.
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.”
A large study has produced strong evidence that a drug commonly used to treat the bone-thinning disease osteoporosis could safely prevent fractures in elderly women who have bones that aren’t as weak.
The study of 2,000 women age 65 and older at earlier stages of bone loss — a condition known as osteopenia — found the drug zoledronatereduced by about one-third the risk they would suffer a break.
“This is an extremely important paper,” says Dr. Ethel Siris, a Columbia University medical professor who specializes in thinning bones and wasn’t involved in the study. “We now know that we have a therapy that has been shown to be highly effective.”
Women 65 and older should keep getting screened for osteoporosis, or porous, fragile bones that are prone to fractures, U.S. doctors recommend.
Some younger women who have an increased risk of osteoporosis might also benefit from bone tests, according to guidelines released today from the U.S. Preventive Services Task Force. This might include smokers, women who drink excessively, and women who are underweight or have a parent who has fractured a hip.
“Since many people don’t know they have osteoporosis until they have a fracture, screening gives us a chance to prevent these fractures from happening,” said task force member Dr. Chien-Wen Tseng of the University of Hawaii John A. Burns School of Medicine in Honolulu.
Hip fracture is a major public health problem, associated with high morbidity and mortality, and high costs to the healthcare system. With the aging of populations worldwide, the socioeconomic burden of hip fracture is set to rise dramatically.
A new Australian study published in Archives of Osteoporosis, looks at the 12-month mortality of older persons presenting to hospitals in Australia with hip fracture. It is the first large population-based matched cohort study exploring excess mortality risk from hip fracture in the Australian population while accounting for pre-injury comorbid conditions.
The researchers linked hospital and mortality data from four Australian states. 9748 Individuals aged 65 years and older who had a hospital admission with a primary diagnosis of hip fracture in 2009 were matched 1:1 on age, sex, and postcode of residence with a cohort of non-injured individuals selected from the electoral roll. Adjusted mortality rate ratios and attributable risk percent were calculated, and Cox proportional hazard regression was used to examine the effect of risk factors on survival.
Authors of a small-scale study are asserting that resistance training may increase testosterone levels in older men. Researchers believe that increased levels of the hormone may help guard against osteoporosis and increase resistance to injury from falls.
The study (abstract only available for free) is published online in the FASEB Journalfrom the Federation of American Societies for Experimental Biology and documents a research project that involved 6 young men and 13 older men. Levels of testosterone were measured before and after a 12-week resistance training program focused on knee extension and flexion. Biopsies were taken from the vastus lateralis.