ABSTRACT

It has been known for many years that oral sodium fluoride can produce a progressive and sustained increase in bone mass and hence in measured vertebral BMD. At cellular level it selectively stimulates the activity of the osteoblasts which, however, produce a woven type of bone that is structurally unsound. This change may differ from one part of the skeleton to another. Thus, there is no decrease in spinal fracture rate and possibly an increase in peripheral fractures in subjects on fluoride. Side effects include gastrointestinal problems and lower extremity pain syndrome. These conclusions have been drawn from some studies in America (fluoride dose 75 mg/day). Experience from France (where a smaller dose is used) is more encouraging. Likewise, a slow-release preparation of 25 mg twice daily increased spinal and femoral neck bone mass and reduced the frequency of new vertebral fractures. Currently, sodium fluoride is not used in the UK to treat osteoporosis but it has received a licence in the United States8,9,10

Other agents Parathyroid hormone in low doses can increase BMD, because of its anabolic effect on bone, but this has been demonstrated only in a research setting11. As with fluoride, there is some evidence of a redistribution of bone throughout the skeleton. Growth factors such as insulin-like growth factors, bone morphogenetic proteins and transforming growth factor-ß could be useful in the future, provided that they could be easily administered and targeted to the skeleton so that any increase in bone and mineralization would be restricted to the normal skeleton, and provided that they were free from side effects (Chapter 7).