Newly discovered gene, new fracture treatment? Maybe, say scientists from Lawrence Livermore National Laboratory, University of California, Merced and Davis, Indiana University and Regeneron Pharmaceuticals, Inc.
Newfound Gene May Lead to Fracture Treatment
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To fill in the knowledge gap regarding the periosteum stem cells and the bone cells during fracture healing, researchers got to work and identified the “Sostdc1” gene as a regulator of periosteum stem cells activity during fracture repair.
According to the June 1, 2016 news release, “The study suggests that Sostdc1 has an important role during stem cell self-renewal and differentiation, which may be useful for developing novel therapeutics for difficult-to-heal fractures. The study showed that mutant mice lacking the Sostdc1 gene, despite having a lower trabecular bone density, had thicker, denser, cortical bone, which healed at an accelerated rate relative to their genetically normal counterparts when fractured. Furthermore, the team was able to show that suppression of the Sostdc1 gene induces a population of stem cells to rapidly expand and invade the fracture to contribute to the repair process.”
“This work describes Sostdc1 activity in a new context, highlighting its potential role in the metabolism and repair of the skeleton, ” said Gaby Loots, Ph.D., an LLNL biologist and senior author of the article. “For the first time, we have linked Sostdc1 to the behavior 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.”
“Future studies may allow us to harness the behavior of these stem cells in other parts of the body where they may do even more good, ” said 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.”
Dr. Loots told OTW, “Sostdc1 null mice have a more complex skeletal phenotype than the generalized sclerosteosis caused by Sost mutations, suggesting that Sostdc1 affects skeletal development and remodeling by different mechanisms. It remains to be determined whether genetic variants of Sostdc1, in humans, may contribute to both increased cortical bone mass, as well as increased porosity of trabecular bone, affecting the bone health of these patients.
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This is a fascinating development. In my practice we've seen similar outcomes with the revised protocol. The key differentiator seems to be patient selection criteria. Has anyone else noticed the correlation with BMI thresholds?
Great point. I'd push back slightly on the conclusion, the sample size in the cited study is too small to draw population-level inferences. That said, the directional signal is compelling and worth a larger RCT.
We implemented a similar approach last year. Early results are promising but we're still gathering 12-month follow-up data. Happy to share our protocol if anyone is interested.
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