There is an increasing body of analytical and experimental evidence that demonstrates that fluid flow may be an important mediator of bone cell activity. It has been a century old mystery as to how osteocytes, the cells that live in bone, are able to sense mechanical strain and communicate this to the bone lining cells, or osteoblasts that produce new bone. Astronauts in long-term weightless space flight and patients in long-term bed rest can lose a significant fraction of their bone mass in the absence of mechanical loading. Since bone is such a stiff tissue and its strains are so small, researchers have long wondered how the osteocytes, which dwell in the lacunar-canalicular system of bone, are able to detect these tiny strains which are typically less that 0.1 percent.
In 1994 two Distinguished Professors at The Graduate Center and City College, Sheldon Weinbaum and Stephen Cowin, published a landmark paper which showed that these small deformations could produce fluid shear stresses on the long slender osteocyte processes which were of the same order of magnitude as the fluid shear stresses in the vascular system. This remarkable prediction is possible since the fluid space surrounding the cell processes in their canaliculi is two orders of magnitude smaller than our capillaries and they occupy only one percent of the bone volume. Subsequently many investigators experimentally demonstrated in cell culture studies that these fluid shear stresses could initiate intracellular signaling in fluid flow chambers when bone cells were subject to fluid shear in the theoretically predicted range. This was the catalyst for a new field of research in bone fluid flow.
More recently, Professors Weinbaum and Cowin and their Ph.D. students have tried to answer whether it is the fluid shear on the cell process membrane or the fluid drag on the tethering elements that connect the cell processes to the canalicular walls that are responsible for the initiating the intracellular signaling. They have proposed a new model to explain a fundamental dilemma. Bone cells when stretched on elastic substrates will elucidate biochemical responses for strains that are at least one percent. Such large whole tissue strains would cause bone fracture. The new model shows how the fluid drag on the tethering elements can produce hoop strains in the cell processes that are one to two orders of magnitude larger than bone tissue strains, and thus it provides a fundamental mechanism for resolving this basic paradox.
Professors Weinbaum and Cowin have formed a collaborative team with Dr. Mitchell Schaffler, Director of Orthopedic Research at Mt. Sinai School of Medicine, to verify the ultrastructural basis for and refine the new model. The project is funded through $1.7 million research grant from the NIH. Professor Sheldon Weinbaum is the principal investigator. The new grant supports two CUNY Ph.D. students and a post doc at Mt. Sinai. Two recent Ph.D.s involved in this research are Dr. Dajun Zhang, who is now an Assistant Professor at Rutgers, and Dr. Lidan You, who is doing a post doc at Stanford University.
Professor Weinbaum is one of eight living individuals who have been elected to all three National Academies, engineering, science, and medicine, and the first person since 1992 to have received this distinction. In 2001 he became the first engineer to receive a Guggenheim Fellowship in molecular and cellular biology. Both he and Professor Cowin are self taught and have no formal training in biology. The field of biomedical engineering did not exist when they received their education. In 1999 they jointly initiated the proposal for Biomedical Engineering in the CUNY Ph.D. Program in Engineering. In 2002 they established the new Department of Biomedical Engineering at City College, which accepted its first freshman class that fall.
http://www.ccny.cuny.edu/nycbe/index.html