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Regarding orthopaedic implant loosening it has been hypothesized that particle-activated macrophages release interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α). This in turn stimulates osteoblasts to release interleukin-6 (IL-6) and prostaglandin E2 (PGE2). These mediators recruit and activate osteoclasts and may therefore lead to bone resorption and loss of implant fixation. In this study we compared the ability of different materials to induce the release of IL-6 and PGE2 from primary isolated, human osteoblasts without preceding activation by macrophages. We tested stainless steel, cobalt–chromium alloy (CoCrMo), commercially pure titanium (cpTi), Ti–6Al–7Nb and Ti–6Al–4V processed in the same manner as corresponding clinical implants. After 12 and 24 h the cells had actively secreted IL-6 and PGE2. There were no clear differences among the implant materials or with the plastic control. The amount of factors the cells released in our study compare well with the findings of other authors who investigated osteoblasts on plastic. In comparison with the literature these amounts are lower than secretion levels of osteoblasts stimulated with implant particles, IL-1 or TNF-α. Moreover, other authors found that osteoclasts require higher concentrations of PGE2 to become activated than the concentrations measured in our experiments. Therefore, the amount of PGE2 released from the osteoblasts in our study is probably not sufficient to induce osteolytic activity. Because of contradictory statements in the literature it is unclear if the measured IL-6 concentrations promote osteolytic activity. Differences in material composition does not significantly influence the release of these factors if the materials have similar surface roughnesses. [Copyright &y& Elsevier]

Use of calcium supplements has increased dramatically in recent years yet little is known about the effect of calcium supplementation on colon physiology. We supplemented 22 individuals with a history of resected adenocarcinoma of the colon, but currently free of cancer, with 2000 or 3000 mg calcium for 16 wk. The effects of supplementation on duodenal bile acids and important fecal characteristics including total fecal output, wet and dry weight, pH, bile acids (in solids and in fecal water), and concentrations and total excretion of calcium, magnesium, phosphates (organic and inorganic), unesterified fatty acids and total fat were determined. Calcium supplementation significantly decreased the proportion of water in the stool (P = 0.03), doubled fecal excretion of calcium (P = 0.006), and increased excretion of organic phosphate (P = 0.035) but not magnesium. Calcium supplementation significantly decreased the proportion of chenodeoxycholic acid in bile (P = 0.007) and decreased the ratio of lithocholate to deoxycholate in feces (P = 0.06). The concentration of primary bile acids in fecal water decreased after 16 wk Ca supplementation. Together with other reports of a "healthier" bile acid profile with respect to colon cancer when changes such as those observed in this study were achieved, these results suggest a protective effect of calcium supplementation against this disease. [ABSTRACT FROM AUTHOR]

Presents a report from the periodical `Gastroenterology' on the beneficial effect of calcium carbonate supplementation on rectal proliferation associated with intestinal bypass.