For the risk getting osteoporosis as well as for diagnosis of osteoporosis 3 facts are highly important: bone-mass, the amount of bone-loss and bone-structures (microarchitecture of bone). All three parameters can be validated today with high precision but the amount of bone-loss seems to be the most important one, even for the decision of either antiresorptive or bone-stimulating therapy. But to calculate the amount of bone-loss until now at least two measurements of bone mineral density (BMD) are necessary which have to be performed within a certain period of time, depending on the reproducibility of the method to be used. If on the other hand the amount of bone-loss would be dependent on actual base-line bone-mass the right therapy could be started already after only one measurement of BMD. The aim of this study was therefore to investigate if there is any relation between the amount of bone-loss and base-line volumetric BMD. For this we separately measured trabecular and cortical bone densities of 135 women in three independent centres of osteoporosis in Zurich and Munich using the method of high resolution quantitative computed tomography - pQCT - with the Densiscan 1000, Scanco Medical, Zurich. We did this at least twice and then compared absolute volumetric BMD in the first step before we calculated trabecular and cortical bone loss per year for each woman. We could not only confirm again that bone loss in trabecular bone was significantly higher than in cortical bone and that the non-weight-bearing trabecular bone as could be found in the distal radius seems to be the skeletal site of maximum bone-loss, but moreover - and this is the more important finding - we could show that the amount of relative bone-loss was the higher the lower trabecular base-line volumetric BMD was. According to this the rate of fast-loser (more than 3.5% per year) increased the lower trabecular base-line volumetric BMD was. These results may lead to a new screening-test for the assessment of the individual risk of osteoporosis and for the individual risk of fast bone-loss which now can be evaluated with only one single measurement of BMD, to treat the so classified patients not only earlier but even more rational, dependent if either antiresorptive therapy or stimulation of bone-formation seems to be more important.

The importance of serial examinations over time with peripheral quantitative computed tomography (pQCT) is that they enable the detection of patients at high risk of osteoporosis, and the individualisation of prophylaxis and treatment. We have shown that postmenopausal patients with high bone turnover evaluated by biochemical markers are identical to fast bone losers as determined by pQCT. As a consequence, we use agents that inhibit bone resorption in patients who are fast bone losers and agents that stimulate bone formation in patients who are slow bone losers. To visualise bone microarchitecture, and to evaluate bone density and the rate of bone loss, we used a highly sensitive pQCT system (DENSISCAN 1000, reproducibility of 0.3% in a mixed population of normal individuals and patients with osteopenia or osteoporosis). This system enabled us to separately assess trabecular and cortical bone density in the radius and tibia, and to differentiate between fast and slow bone losers within a few months (threshold: 3% loss of trabecular bone density in the radius per year). We have shown that the lower the trabecular bone density in the distal radius, the higher the relative bone loss. To classify patients as slow and fast losers in the future, we may need only one measurement. With this highly precise measurement method, we have shown that calcitonin and etidronate are more effective in fast than in slow bone losers, and that vitamin D metabolites (calcitriol or 1 alpha-calcidol) and estrogens can halt fast bone loss. In conclusion, highly sensitive pQCT enables us to adapt the treatment to different forms of osteoporosis and bone turnover, resulting in an increase in the number of patients successfully treated and also in patient compliance. Because our treatment is based on precise, objective measurements, treatment modifications--especially in those who change from a slow to a fast bone-loser state--can be easily justified.

The European Parliament presented June 10th in Brussels the 'Osteoporosis Report in EU--Means for Prevention'. It was emphasized that in the EU more than 3500 million Ecu have to be spent for hospitalization and that more than 500,000 hospitals beds are being used by osteoporotic patients. According to some calculations this number will double within the next 50 years. The EU has set up eight steps to be considered, e.g. have densitometric measurements available for persons with high risk and have these measurement paid by the insurances to further finance and support research for the very important areas of prevention and treatment. One distinguishes between primary, secondary and tertiary prevention of osteoporosis. Primary prevention aims at reaching at adolescent age a peak bone mass as high as possible. Secondary prevention aims at reducing bone loss peri- and postmenopausal. The tertiary prevention with manifest osteoporosis aims at preventing fractures. Emphasis of the primary prevention is, besides a sufficient calcium intake, to omit risk factors; with secondary prevention the use of medical treatments such as estrogens/gestagens, bisphosphonates, and recently also SERMs is applied. The tertiary prevention tries mostly to reduce the femur fractures. In addition to drugs such as vitamin D/calcium, vitamin D metabolites and bisphosphonates it is very important to create 'a fall-proof home'. Also very useful are hip protectors.