You are hereMarch 22, 2016
Study Shows How Stem Cells Might Restore Bones Damaged by Osteoporosis
Durham, NC – A study recently published in STEM CELLS Translational Medicine points the way to a new, potentially restorative treatment for age-related or type II osteoporosis. When a single dose of a certain type of stem cell, called mesenchymal stromal cells (MSCs), was injected into mice with the disease, long-term bone engraftment and quality bone growth resulted. As an added benefit, the cells protected existing bone from damage.
Type II osteoporosis, which affects both men and women and can lead to hip fractures, occurs when there is a decline due to aging of MSCs, the type of stem cell that forms new bone cells. This decline reduces bone mass and can cause bones to become so weak and brittle that a fall or even mild stress like coughing can cause a fracture. A stooped posture and back pain are also common symptoms.
To date more than 500 clinical trials using MSCs have been registered with clinicaltrials.gov. Some are showing significant benefit in treating bone-related conditions. However, while many researchers believe osteoporosis could benefit from MSC therapy — particularly because their depletion drives the disease’s progression — no clinical trials are currently underway or recruiting to test this hypothesis.
As a first step toward what they hope leads to clinical trials, a team of researchers led by William Stanford, Ph.D., of the Ottawa Hospital Research Institute, Regenerative Medicine & Sprott Centre for Stem Cell Research, investigated whether minimally expanded (grown) MSCs can engraft long-term within mice bred specifically to exhibit human age-related osteoporosis and prevent the disease’s onset. The animals typically show signs of osteoporosis around 6 months old.
“Due to the poor homing abilities of culture-expanded MSCs to bone, previous animal studies testing MSCs’ ability to increase bone formation relied on administering the cells either locally, through genetic manipulation or by surface modification,” Dr. Stanford said. “We wanted to see whether minimally expanded MSCs made a difference.”
The MSC transplantation took place when the mice were 10 weeks old, with the cells injected directly into the animals’ bloodstream via a tail vein. Twenty-four weeks later the results were analyzed and did indeed show improved bone quality, turnover and, importantly, sustained skeletal competence over a control group of untreated animals.
“Our findings suggest that such MSC therapy may lead to broad and long-term regenerative consequences that address both the form and function of bone,” said co-investigator John E. Davies, Ph.D., D.Sc., of the University of Toronto’s Institute of Biomaterials and Biomedical Engineering and a member of the dental school faculty. “Further, this work demonstrates the therapeutic promise of minimally expanded MSC populations.”
“Given the numerous ongoing clinical trials utilizing MSCs, we suggest that ancillary studies should be added to these clinical trials to determine whether transplantation of MSCs increase bone remodeling and improve bone health in the MSC treated patients,” Dr. Stanford added.
“This disease can have debilitating effects in older adults and new treatment and prevention options are needed as the population ages,” said Anthony Atala, M.D., Editor-in-chief of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine. “This proof of concept study suggests that MSC transplantation may one day be a viable strategy for preventing osteoporosis.”
The full article, “Systemic MSC transplantation prevents functional bone loss in a mouse model of age-related osteoporosis,” can be accessed at www.StemCellsTM.com.