Researchers Tackle Age-associated Bone Loss Using Stem Cells

04/10/2017

Everyone ages; it’s a fact of life. And, with age, there is more risk of illness and with a weaker immune system as the body becomes frailer, your body opens itself up to attracting diseases and infections. ‘Becoming old’ is something that scientists have tried to combat since science began; with little success.

Everyone ages; it’s a fact of life. And, with age, there is more risk of illness and with a weaker immune system as the body becomes frailer, your body opens itself up to attracting diseases and infections. ‘Becoming old’ is something that scientists have tried to combat since science began; with little success.

One of the major health problems in older people is osteoporosis which affects more than 200million people worldwide. Age-related osteoporosis (type II) is the most common type in the older generation which entrails thinning of the bone and loss of density. This, in turn, increases the likelihood of breaks and fractures significantly. Around 8.9m fractures a year are a result of this chronic disease.

University of Alabama, Birmingham (UAB) researchers have detailed an underlying mechanism that leads to people generating osteoporosis. When this mechanism malfunctions, progenitor cells (cells that tend to differentiate into a specific type of cell and can be pushed to differentiate into a ‘target’ cell) stop creating bone-producing cells, and instead create fat cells – making the bone weaker.

UAB researchers found that a protein called Cbf-beta plays a crucial role in supporting and maintaining the bone-producing cells. Studies of aged mice showed significantly reduced levels of Cbf-beta in stem cells, as compared to younger mice. Thus, they propose, maintaining Cbf-beta may be essential to preventing human age-associated osteoporosis.

The progenitor cells for osteoblasts are mesenchymal stem cells, the same cells that are found in teeth and that BioEden store. Besides osteoblasts, mesenchymal stem cells can also differentiate into the chondrocyte cells that make cartilage, the myocyte cells that help form muscles and adipocytes, or fat cells. Thus, the same progenitor cell has different possibilities of what it can turn into.

This knowledge of the mechanism driven by Cbf-beta can help explain the imbalance in bone maintenance seen in older people; one of the first steps to treating age-related osteoporosis.