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Interactions between bacterial endotoxin and other stimulators of bone resorption in organ culture
Author(s) -
Raisz Lawrence G.,
Nukj Klaus,
Alander Cynthia B.,
Craig Ronald G.
Publication year - 1981
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1981.tb00943.x
Subject(s) - bone resorption , pathogenesis , resorption , endocrinology , medicine , parathyroid hormone , prostaglandin e2 , osteoclast , prostaglandin e , prostaglandin , osteolysis , chemistry , hormone , calcium , receptor , dentistry
Four agents which have been implicated in the pathogenesis of alveolar bone loss. In periodontaI disease, endotoxin, prostagandin E 2 (PGE 2 ), parathyroid hormone (PTH) and osteoclast activating factor (OAF), were studied for their effects on bone resorption as measured by the release of previously incorporated 45 Ca from long bone shafts of 19 day fetal rats. Endotoxin at concentrations of 4 to 25 ng/ml caused little increase in 45 Ca release but was able to enhance the response to submaximal concentrations of PGE 2 , PTH, and OAF. The response appeared synergistic, that is, it was greater than the sum of the individual responses when the agents were added singly. PTH and PGE 2 do not show such apparent synergism when added together. The effects of endotoxin were not inhibited by three structurally unrelated inhibitors of prostaglandin synthesis, indomethacin, flufenamic acid and RO 20–5720, and synergistic responses were similar when PGE 2 and endotoxin were added in the presence of indomethacin. We conclude that interactions between endotoxin and other bone resorbers can produce unexpectedly large resorptive responses and suggest that these interactions may be important in the pathogenesis of bone loss in periodontaJ disease and other forms of pathologic osteolysis.