A local pathophysiologic mechanism of the resorption of residual ridges: prostaglandin as a mediator of bone resorption.
The role of PG as a bone resorption mediator in RRR was investigated in the rat model and the following may be concluded from the data. 1. PG is suggested to be a mediator of the RRR. 2. The continuous and localized bone resorption in RRR may be caused by continuous synthesis of local PG. 3. PG producing cells and specific stimuli responsible for RRR are still unknown.
Nishimura
I
I
Harvard School of Dental Medicine, Boston, Mass.
Szabo
G
G
Flynn
E
E
Atwood
D A
DA
D000539:Alveolar Process / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001862:Bone Resorption / Q000473:pathology / Q000503:physiopathology*; D002452:Cell Count; D002508:Cephalometry; D003430:Cross-Sectional Studies; D015232:Dinoprostone / Q000494:pharmacology; D007213:Indomethacin / Q000493:pharmacokinetics / Q000494:pharmacology; D008137:Longitudinal Studies; D008297:Male; D010010:Osteoclasts / Q000187:drug effects / Q000473:pathology; D011453:Prostaglandins / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains
D011453:Prostaglandins; D015232:Dinoprostone; D007213:Indomethacin