Scientists in the US have identified a gene involved in the fracture healing process. It´s thought that the discovery, reported in the journal Bone, could one day lead to new treatments for difficult-to-heal injuries.
Fracture healing involves communication between bone, muscle, vasculature and the thin membrane covering the outer surface of bones (periosteum), explained Lawrence Livermore National Laboratory (LLNL), reporting on the study. The periosteum contains stem cells that migrate to the fracture site and differentiate into chondrocytes (cartilage-forming cells) and/or osteoblasts (bone-forming cells).
Until now, little was known about the interaction between the periosteum stem cells and bone cells during fracture healing.
The team of scientists from LLNL; the University of California, Merced and Davis; Indiana University; and Regeneron Pharmaceuticals identified the ‘Sostdc1´ gene, which is expressed in the periosteum, as a regulator of periosteum stem cell activity during fracture repair.
The researchers believe that Sostdc1 may play an important role during stem cell self-renewal and differentiation, which may be useful for developing novel therapeutics for difficult-to-heal fractures.
“This work describes Sostdc1 activity in a new context, highlighting its potential role in the metabolism and repair of the skeleton,” commented Gaby Loots, an LLNL biologist and senior author of the study. “For the first time, we have linked Sostdc1 to the behaviour of stem cells, which is consistent with, and mechanistically may explain, Sostdc1-related characteristics as noted by other studies, such as in cancer prognosis, tooth development, kidney injury resistance and diet-induced obesity resistance.”
There are two general types of bone material: cortical bone, which is the dense, hard, outer shell of most bones; and trabecular bone, which is the “spongy” form of bone found at the ends of long bones, near joints and inside vertebrae. The study shows that Sostdc1 is important for trabecular bone maintenance, bone formation and early fracture repair, and the lack of Sostdc1 influences stem cell behaviour in response to injury.
“Future studies may allow us to harness the behaviour of these stem cells in other parts of the body where they may do even more good,” added Nicole Collette, an LLNL biologist and first author of the study. “This regulator is expressed all over the body, including in other tissues where stem cells are found.”