Evaluating suppression of PGE2, PAF, and histamine synthesis and histopathological changes of bones in the membrane surrounding particulate polymethylmethacrylate in the rat tibia

  Abstract   Introduction: Inflammation and wear debris may be responsible for bone lysis   and subsequent lost in aseptic arthroplasty. Prostaglandin E2, platelet activating factor,   and histamine are important mediators of inflammatory cells. We studied   histopathological changes of cement-bone interface after using specific antagonists   of these mediators.   Methods: Left and right tibiae of 120 rats in ten groups were drilled. The left side   was filled with polymethylmethacrylate and the right side was used as control. The   first three groups respectively received 1mg/kg, 10mg/kg, and 25mg/kg of terfenadine,   the second three groups respectively received 0.08mg/kg, 0.32mg/kg, and   0.64mg/kg of alprazolam, and the third three groups respectively received 1mg/kg,   5mg/kg, and 25mg/kg of naproxen. The tenth group received no drug and served as   the control group. The animals were killed after 16 weeks and studied by one pathologist.   Results: Cellular reaction in the left side was significantly more than the right side   in all cases. Medium and high doses of terfenadine and naproxen and high doses of   alprazolam could also significantly decrease giant cells and histiocytes.   Conclusion: Increased cellular reaction in the cement-bone interface was suppressed   by administration of PGE2, PAF, and histamine specific inhibitors. The use   of these agents may induce retardation of the bone loss associated with early prosthetic   loosening.