Suppression of prostaglandin E2 synthesis in the membrane surrounding particulate polymethylmethacrylate in the rabbit tibia.
Fifteen mature, New Zealand, female rabbits were divided into two groups. Using sterile technique, a 6-mm drill hole was made in the tibia 1 cm distal to the knee joint bilaterally. The marrow was scooped out underneath the hole. The right tibia received Simplex particulate cement polymer and the left leg functioned as a prepared, but nonimplanted, control. All animals were fed a standard diet. Whereas the six animals in Group 1 received regular water, the nine animals in Group 2 drank water in which sodium naproxen was dissolved (1.375 mg per ml). The animals were killed after 16 weeks. The implant area was harvested under sterile conditions and maintained in tissue culture. The cumulative collection of tissue culture supernatants over a three-day period was assayed for Prostaglandin E2 (PGE2) via radioimmunoassay. Specimens from Group 1 produced an average of 106.0 +/- 10.9 ng PGE2 on the right side, and 35.3 +/- 6.0 ng PGE2 on the left side. Specimens from Group 2 produced an average of 31.1 +/- 6.1 ng PGE2 on the right experimental side and 26.0 +/- 5.1 ng PGE2 on the left control side. The ratio of PGE2 values for the right divided by the left side yielded higher values in Group 1, compared to Group 2. Cement polymer particles have been shown to produce a florid foreign body histologic reaction similar to that associated with prosthetic loosening in man. This experiment has demonstrated that the increased PGE2 production by the membrane surrounding particulate cement polymer can be suppressed by the administration of an oral cyclo-oxygenase inhibitor. PGE2 has been previously shown to induce bone resorption in vivo and in vitro. The use of nonsteroidal antiinflammatory drugs may be indicated in retarding the bone loss associated with early prosthetic loosening.
Stanford University Medical Center, Division of Orthopaedic Surgery, CA 94305-5326.
S B
SB
Goodman
R C
RC
Chin
S S
SS
Chiou
J S
JS
Lee
D000818:Animals; D001843:Bone Cements / Q000494:pharmacology*; D001862:Bone Resorption / Q000188:drug therapy; D015232:Dinoprostone / Q000032:analysis / Q000096:biosynthesis*; D005260:Female; D005549:Foreign-Body Reaction / Q000188:drug therapy*; D007595:Joint Prosthesis; D008566:Membranes / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D020366:Methylmethacrylate; D008768:Methylmethacrylates / Q000494:pharmacology*; D009288:Naproxen / Q000494:pharmacology* / Q000627:therapeutic use; D011475:Prosthesis Failure; D011817:Rabbits; D013977:Tibia / Q000737:chemistry / Q000187:drug effects*
D001843:Bone Cements; D008768:Methylmethacrylates; D020366:Methylmethacrylate; D009288:Naproxen; D015232:Dinoprostone