Craniosynostosis, the premature fusion of the top of the skull in infants, is caused by an abnormal excess of a previously unknown type of bone-forming stem cell, according to a preclinical study led by researchers at Weill Cornell Medicine.
Craniosynostosis arises from one of several possible gene mutations, and occurs in about one in 2,500 babies. By constricting brain growth, it can lead to abnormal brain development if not corrected surgically. In complex cases, multiple surgeries are needed., the researchers examined in detail what happens in the skull of mice with one of the most common mutations found in human craniosynostosis.
"We can now start to think about treating craniosynostosis not just with surgery but also by blocking this abnormal stem cell activity," said study co-senior author Dr. Matt Greenblatt, an associate professor of pathology and laboratory medicine at Weill Cornell Medicine and a pathologist at NewYork-Presbyterian/Weill Cornell Medical Center.
The other co-senior author of the study was Dr. Shawon Debnath, a research associate in the Greenblatt laboratory.in 2018, Drs. Debnath and Greenblatt and their colleagues, described the discovery of a type of bone-forming stem cell they called the CTSK+ stem cell. Because this type of cell is present in the top of the skull, or"calvarium," in mice, they suspected that it has a role in causing craniosynostosis.lack one of the genes whose loss of function causes craniosynostosis.
"We were surprised to find that, instead of the mutation in CTSK+ stem cells leading to these stem cells being activated to fuse the bony plates in the skull as we expected, mutations in the CTSK+ stem cells instead led to the depletion of these stem cells at the sutures—and the greater the depletion, the more complete the fusion of the sutures," Dr. Debnath said.
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