A research team from UCLA has identified a combination of proteins that could considerably enhance clinical bone restoration. The results may be a big move toward developing effective therapies for bone skeletal problems, bone loss and osteoporosis.
The research, lead by Dr. Kang Ting, Dr. Chia Soo and Dr. Aaron James, a fellow in surgical pathology, will appear as the lead article in the month of February print edition of the American Journal of Pathology.
Present therapies for bone skeletal problems utilize bone morphogenetic protein-2, or BMP2, an FDA accepted bone healing protein. But the high concentrations required to stimulate human bone formation may have severe side effects, which includes deadly cervical swelling and irregular and inconsistent bone development.
The same study team has performed other research on bone development, which includes one that utilized a protein known as NELL-1, which successfully enhanced bone development and induced key factors for bone development in multiple animal models.
In the new research, the team combined the NELL-1 protein, which Ting discovered, with BMP2. They identified that the combination of the two proteins enhanced bone development while suppressing the development of fat cells — a negative side effect of BMP2, which motivates stem cells to form both bone and fat cells. By contrast, NELL-1 motivates stem cells to form bone cells instead of fat cells. Used jointly, the two proteins activate bone production more considerably than either does by itself.
Dr. Ting said says.
Prior to this research, large bone problems in sufferers were hard to treat with BMP2 or other current products available to surgeons. The combo of NELL-1 and BMP2 lead to enhanced safety and efficacy of bone regrowth in preclinical models and may, one day, provide patients considerably better bone healing.”
The research demonstrated that NELL-1 functions by triggering the cellular signaling pathway that regulates whether a stem cell differentiates into a bone cell or a fat cell. It also demonstrated that BMP2 can stimulate non-bone cells to form bone, with the possible risk for ectopic bone development (bone development in unwanted places).
The two proteins complement each other in that BMP2 allows to turn non-bone cells into bone developing cells, and NELL-1 then raises the bone-forming capability of bone cells.
“In comparison to BMP2, the novel capability of NELL-1 to induce bone development and repress the development of fat may highlight new therapy methods for osteoporosis and other treatments for bone loss,” Soo said.
Earlier and current research proved a strong rationale for combining NELL-1 with BMP2 to considerably enhance the safety and efficacy of present bone regeneration choices. The combo of NELL-1 and BMP2 may be especially useful for healing local bone problems in individuals who have osteoporosis or for those taking medicines, like as steroids that can restrict bone development.
NELL-1 is also presently in development as a single therapy for systemic therapy of osteoporosis. NELL-1, when given systemically, does not appear to cause ectopic bone. In contrast, because of its well-known capability to stimulate unwanted bone, BMP2 may not be as suitable for systemic administration.
Dr. No-Hee Park, dean of the UCLA School of Dentistry said,
Dr. Ting and his study team have made a extremely useful discovery for the field of bone regeneration. The investigators’ results have potential to assist large number of people who suffer from osteoporosis and other bone problems.