In the past decade, we observed progress in the differential diagnosis of osteoporosis, mainly because of advanced radiological and laboratory procedures, including new bone markers. Loss of bone can also be related to primary and secondary forms of osteoporosis. Consequently, secondary osteoporosis (and osteomalacia) should be treated primarily according to the original disease. Although etiopathology of primary osteoporosis is still unclean differential therapy should be applied to the different subgroups (juvenile, postmenopausal, and senile osteoporosis). Furthermore, even patients of the same age and sex can be at risk for osteoporosis or have definite osteoporosis. This can be differentiated in "low or high turnover osteoporosis" and should be diagnosed and treated as described. Conjugated estrogens in combination with progesterone decrease the rate of endometrial carcinoma and have been established to be very effective in the treatment of high turnover osteoporosis and patients at high risk of developing manifest osteoporosis. In combination with calcium (1 g/day) total doses of estrogen can be reduced to 0.3 g/day. The same applies for the treatment of low turnover (mostly manifest) osteoporosis with fluoride. Daily doses of fluoride can be decreased from 80 mg sodium fluoride to 50g in combination with calcium. These reductions of daily fluoride doses decreases the rate of side effects and allows longer control periods, provided that bone measurements demonstrate a beneficial long-term effect. The control periods depend on the sensitivity of the bone density measurements. Special indications, modifications, alterations and additions of further drugs are discussed for the individual patient.

Combined Modality Therapy↗

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[Osteocalcin and bone metabolism in rheumatoid arthritis and osteoarthritis].

Osteocalcin is the most abundant noncollagenous protein of bone and is regarded as the best biochemical marker for bone formation. The synthesis of this protein in osteoblasts is stimulated by 1.25-Dihydroxyvitamin D3 (1.25(OH)2D3). The aim of this study was to examine the rate of bone formation measured by osteocalcin in patients (pts) with rheumatoid arthritis (RA) (n = 58) and osteoarthrosis (OA) (n = 14) and its dependence on various parameters of calcium and phosphate metabolism, especially vitamin D metabolites. Furthermore we compared the significance of alkaline phosphatase and osteocalcin as a parameter for bone turnover in these patients. According to treatment pts with RA were divided into four groups: one receiving gold salts (n = 14), one glucocorticoids (n = 13), one chloroquine (n = 14), and one nonsteroidal antiinflammatory drugs (NSAID) (n = 17). Pts with OA and RA treated with NSAID showed significantly lower values of osteocalcin than pts with RA treated with glucocorticoids or gold. In contrast to osteocalcin, alkaline phosphatase was significantly higher in all pts with RA than in pts with OA. 1.25(OH)2D, which was significantly (p less than 0.05) elevated in pts with RA treated with glucocorticoids, correlated significantly with parathyroid hormone (PTH). These data indicate that bone metabolism, at least in pts with OA and RA treated with NSAID is characterized by a decreased bone formation which is probably compensated in part in pts treated with glucocorticoids, as 1.25(OH)2D and PTH are significantly (p less than 0.05) elevated. Furthermore, the osteocalcin values were closely correlated with 1.25(OH)2D in pts with OA.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Inflammatory Agents, Non-Steroidal↗

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