Possible role of calcium in periodontal disease.
The uptake of Ca2+ by endotoxin-challenged 3T6 fibroblasts, in vitro, was studied. In recent years, the role of calcium in cell injury ultimately leading to cell death has attracted a fair amount of interest. The purpose of the study was to determine whether the direct toxic action of endotoxin is related to a disturbance in Ca2+ homeostasis. Increased calcium uptake in endotoxin-challenged cells was found to be directly related to the bacterial source and method of extraction of endotoxin, the cell density of the culture and the pH of the medium. The effect of endotoxin on calcium uptake was completely reversed by polymyxin B which is known to neutralize the endotoxicity of lipopolysaccharides. These results imply that the increased calcium uptake may be one of the mechanisms by which endotoxin causes direct tissue damage. The potential significance of these data to periodontal disease is discussed.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D002478:Cells, Cultured; D004731:Endotoxins / Q000633:toxicity; D004926:Escherichia coli; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D051379:Mice; D010510:Periodontal Diseases / Q000209:etiology* / Q000378:metabolism; D011112:Polymyxin B / Q000494:pharmacology; D013997:Time Factors
D004731:Endotoxins; D011112:Polymyxin B; D002118:Calcium