Karsenty and colleagues developed a genetically engineered mouse in which the osteoblasts could be deleted. They discovered that the absence of bone-forming cells had no effect on the osteoclasts, which continued to scoop out old bone tissue. As a result, this mouse model developed a disease that closely mimicks osteoporosis. Nevertheless, the fact that osteoblasts do not regulate osteoclast function in this model challenges scientists to find other ways to explain why bone mass remains constant. The ability to induce osteoporosis of variable severity should enable researchers to test new drugs against the disease, he said.
Osteoporosis affects millions of people, mostly women.
The disease causes loss of bone mass, especially in the spine, hips and wrists. The weakened bones result in more frequent fractures, which can be fatal in elderly people. Karsenty hopes his study will help scientists learn more about the mechanisms underlying bone remodeling in healthy animals as well as the cellular and molecular basis of diseases characterized by low bone mass. Conn. Hoechst Marlon Roussel, a German drug company, the March of Dimes Foundation and the National Institutes of Health supported the study. Copyright 1998 Baylor College of Medicine.