title: Inhibition of prostaglandin synthesis leads to a change in adherence of mouse osteoclasts from bone to periosteum.
abstract: When mouse parietal bones were incubated for 1 day in medium containing indomethacin (Ind), the number of tartrate-resistant acid phosphatase-positive osteoclasts (TRAP+OC) counted on the bone surface was drastically reduced. This reduction did not occur with calcitonin or if the endocranial membrane (periosteum) was removed prior to incubation with Ind. The aim of this work was to determine the mechanism involved. TRAP+OC were found to be increased on the endocranial membrane adjacent to the resorbing surface after Ind treatment, compared with cultures supplemented with parathyroid hormone (PTH) or prostaglandin E2 (PGE2). However, this increase accounted for only half of those lost from the bone surface. TRAP negative osteoclasts were also seen on the membrane and, to a lesser extent, on the bone. Increased TRAP specific activity could be extracted from the endocranial membranes of bones incubated with Ind compared with PGE2 controls. When bones that had been exposed to Ind were then cultured for 1 day in PGE2, an increase in TRAP+OC occurred. This increase was blocked by the removal of the endocranial membrane prior to incubation with PGE2. We conclude that when prostaglandin production ceases, TRAP+OC become less adherent to bone and more adherent to the endocranial membrane. Stimulators of bone resorption appear to reverse this process.
authors.affiliation: Charles Salt Research Centre, Robert Jones and Agnes Hunt Orthopaedic and District Hospital NHS Trust, Oswestry, Shropshire, SY10 7AG, United Kingdom.
authors.forename: M J
authors.initials: MJ
authors.lastname: Marshall
authors.forename: I
authors.initials: I
authors.lastname: Holt
authors.forename: M W
authors.initials: MW
authors.lastname: Davie
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D002448:Cell Adhesion / Q000502:physiology; D002454:Cell Differentiation / Q000187:drug effects; D002729:Chloromercuribenzoates / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000494:pharmacology; D015536:Down-Regulation; D007213:Indomethacin / Q000494:pharmacology; D007527:Isoenzymes / Q000378:metabolism; D051379:Mice; D008808:Mice, Inbred CBA; D009924:Organ Culture Techniques; D010010:Osteoclasts / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D010281:Parathyroid Hormone / Q000494:pharmacology; D010294:Parietal Bone / Q000166:cytology / Q000201:enzymology / Q000378:metabolism; D010521:Periosteum / Q000378:metabolism; D000071681:Tartrate-Resistant Acid Phosphatase; D020245:p-Chloromercuribenzoic Acid
chemical_list: D002729:Chloromercuribenzoates; D016861:Cyclooxygenase Inhibitors; D015853:Cysteine Proteinase Inhibitors; D007527:Isoenzymes; D010281:Parathyroid Hormone; D020245:p-Chloromercuribenzoic Acid; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D015232:Dinoprostone; D007213:Indomethacin