“Mice had an acceptable amount of bone at birth, but as they got older, they lost more and more bone,” said Dr. Brendan Lee, senior author of the report. Researchers found that the osteoblasts, which promote bone formation, worked fine when they abolished Notch function in bone forming cells. However, the animals lacked the ability to regulate activity of osteoclasts, whose primary function is to resorb or remove bone. Many women who have osteoporosis actually have a similar problem, an imbalance of bone formation versus bone resorption.
In the laboratory, Lee and his colleagues found that when animals were bred to lack Notch, they lost also the ability to suppress bone resorption. That balance between bone formation and resorption allows organisms to maintain a healthy skeleton. Future studies may look at the possiblity that loss of Notch interferes with the natural signal between osteoblasts and osteoclasts and prevents the homeostasis or natural balance between the two. That means the protein Notch and the cellular pathways that express and control it might be targets for drugs to treat bone disorders, said Lee.
This study began with patients who suffer from a problem called spondylocostal dysplasia. These children and adults have problems with the pattern of their spine. Several years ago, other scientists showed that a mutation of the pathway for Notch causes some of these problems. “Our care of these patients suggested to us that Notch may have important function even after the establishment of this initial pattern of the skeleton.”
“This is a complex system and it is why personalized medicine is important,” said Lee. “By identifying all of the cellular pathways that contribute to a specific trait or feature like bone mass in each person, we could one day develop therapies specific for that person.”
MEDICA.de; Source: Baylor College of Medicine