Orthopaedic surgeons would have felt temporarily secure with Heaney’s(Omaha) opening plea to replace the endocrine model of the skeleton with a biomechanical one. We are all familiar with the world-wide importance of osteoporosis and fractures, though the reasons for the recent increase in the age-adjusted fracture rate still elude us. Lau (Hong Kong) related it to physical inactivity andlow calcium intake. In Europe fracture rates varied, the highest being in France and the lowest in Turkey where more men than women were affected(Kanis, Sheffield). From the Gambia, Lo described delayed menarche and bone age, and reduced peak bone mass (by American standards), possibly related to low dietary calcium. On the prevention of osteoporotic fractures, Cummings (San Francisco) posed important questions-how to persuade more of the at-risk population to begin effective treatment such as hormone replacement therapy (HRT) and, once started, how to stay on it; and how to minimise the impact of falls. Most ‘fallers’ land on hard surfaces, so the effect of cushioning surfaces in the homes of old people could be dramatic. The skeleton depends on the osteoblasts, osteoclasts and osteocytes for its constant removal, replacement, and repair; and we have a good idea where these cells come from. However, we have little idea how they communicate with each other (Martin, Melbourne). Innumerable intercellular messengers (cytokines) and growth factors have been identified in the laboratory, but their overall function in the animal is obscure. The homozygous microphthalmic osteopetrotic mouse provided one example. The mutated gene for macrophage-colony stimulating factor(M-CSF) in this animal prevents bone resorption, accounts for its dense bones, and can be corrected by recombinant M-CSF (Fleisch, Berne).