Dental researchers hold aspirations for aspirin in bone regrowth
Los Angeles—Someday aspirin may play a major role in the development of treatments for bone conditions in the body, including in the oral cavity.
|Dr. Shi: Aspirin deactivated the cytokines, making bone regrowth possible.|
Dr. Songtao Shi, a professor at the University of Southern California Ostrow School of Dentistry’s Center for Craniofacial Molecular Biology, and a team of researchers have been investigating how aspirin works in manipulating a pair of cytokines, which are protein molecules that act as regulators and communicators between cells. Aspirin deactivated the cytokines, making bone regrowth possible.
In initial phases of study, Dr. Shi’s team sought to regenerate bone by exogenously applying bone marrow mesenchymal stem cells to scaffolding in experimental skull wounds in mice, but cell death by apoptosis ultimately occurred, inhibiting the stem cells from regenerating bone. These results led the team to question the role of the immune system in bone growth.
“There are a lot of immune components, a lot of cytokines,” Dr. Shi said. “We dissected one type of cell called TH1 cells. They produce very important inflammatory factors we call interferon gamma (IFN-g) and tumor necrosis factor-alpha (TNF-a). These two factors basically block the donor cells from bone regeneration.”
The team turned its attention to drug treatments that might thwart the work of IFN-g and TNF-a —which are cytokines.
“We asked, ‘Which drug can block IFN-g and TNF-a?’ We can put this drug in locally to prevent cells from being attacked by IFN-g and TNF-a.”
Aspirin ultimately did the trick in deactivating the cytokines. “It inhibited them,” Dr. Shi said.
Dr. Shi’s study, which is supported by a National Institute of Dental and Craniofacial Research grant, also explores how mesenchymal stem cells play a role in osteoporosis and in osteonecrosis of the jaw.
Dr. Shi and his team reported on their work in a Nature Medicine article, “Mesenchymal stem cell-based tissue regeneration is governed by recipient T lymphocytes via IFN-g and TNF-a,” which was published online Nov. 20, 2011.