Drugs to save a trip to the gym
Posted on 1 March 1997
The most important function of our skeletons is to support loads, so active individuals need stronger skeletons than couch potatoes. As it is a waste of energy to grow, maintain and move more bone than is absolutely necessary, our skeletons respond to the amount we use them in the same way as muscles. Weightlifters and astronauts are good examples of those with high and low bone mass respectively, as a result of their lifestyles. A more normal example is seen in tennis players, where bone in the serving arm is 30 per cent thicker than in the less exercised opposite arm.
This response to exercise works well for most of the time, but in later life, particularly in post-menopausal women with osteoporosis, there is an alteration in the effectiveness of exercise in maintaining bone mass, as though some form of mechanical thermostat has been turned down.
Many people with osteoporosis are diagnosed only when they have a fracture - after they have lost a lot of essential bone. Since current treatments are most effective only in stopping further bone loss, what is needed is a way to increase bone mass which has been lost.
The most potent influence in stimulating bone formation is mechanical loading, so research is aimed at identifying the early signalling which happens in bone cells after loading. Understanding this process will enable scientists to 'eavesdrop' on the chemical conversations between bone cells which dictate whether bones should be degraded or improved.
Researchers at the universities of York and Harvard have made some remarkable discoveries about how bones respond to loading. They will open the way to the development of drugs which can control bone development to the benefit of all. The research is led at York by Professor Tim Skerry.
Professor Skerry is the Smith and Nephew Professor of Cellular and Molecular Biology of Hard Tissue Repair at the University of York.