New research has discovered a cell type that governs the way bones form and maintain themselves, opening up a potential target for future therapies for bone disorders like osteoporosis. Led by faculty from the Perelman School of Medicine, a study shows that bone marrow adipogenic lineage precursors (MALPs) play a distinct role in the way bones remodel themselves. Defects in this process are the key issue at play in osteoporosis, so a therapy using these MALP cells to better regulate bone remodeling could result in better treatments. This research is published in the Journal of Clinical Investigation.
“Discovering new cellular and molecular mechanisms to control bone turnover will enable fine-tuning of existing therapies or design of novel therapeutics,” says the study’s senior author, Ling Qin, an associate professor of orthopaedic surgery. “For example, with the advance of gene-editing technology and novel cell-specific delivery approaches, in the future it would be possible to regulate MALP behavior as a therapy for bone disorders like osteoporosis.”
Healthy bone maintenance is a balance between osteoblasts, which secrete the materials necessary to form new bone, and osteoclasts, which absorb old bone material to make way for the new. A disruption in this balance one way or the other can result in unhealthy bone. In the case of osteoporosis, overactive osteoclasts eat away at bone faster than it can be reformed, resulting in bones that are less dense and more susceptible to fracture.
“By identifying what appears to be the full function of MALP cells, we believe that we have uncovered an extremely promising target that would never have been considered before,” Qin says. “If their RANKL secretions [a protein essential for forming osteoclasts] can be reliably disabled, it could rebalance bone remodeling in people with osteoporosis and allow for osteoblasts and osteocytes to ‘catch up.’”
This story is by Frank Otto. Read more at Penn Medicine News.