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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Aged, Aged, 80 and over, Alendronate, Arthroplasty, Replacement, Hip, Bone Density Conservation Agents, Cell Culture Techniques, Female, Fibroblasts, Hip Prosthesis, Humans, Male, Middle Aged, Osteolysis, Osteoprotegerin, Prosthesis Failure, RANK Ligand, RNA, Messenger.
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Does alendronate stimulate osteoprotegerin expression in fibroblasts from periprosthetic membrane? Context: Aseptic loosening of an implant after total joint arthroplasty is still a major complication that results from periprosthetic osteolysis. Fibroblasts in the interface membrane express receptor activator of nuclear factor kappa B ligand (RANKL) and stimulate osteoclast formation. Studies demonstrate that through the control of osteoclastic bone loss bisphosphonates inhibit wear particle-induced bone resorption around total hip arthroplasty. The majority of bisphosphonates studies have focused on their effects on osteoblasts and osteoclasts. Little attention has been paid to their action on fibroblasts. We isolated fibroblasts from the interface membrane that was obtained when revision hip arthroplasty was performed because of aseptic loosening. Fibroblasts were stimulated with alendronate. RANKL and osteoprotegerin (OPG) assays were performed using enzyme-linked immunosorbent assay kit and real time Reverse Transcription- Polymerase Chain Reaction (RT-PCR). We found that alendronate stimulated OPG mRNA and protein expression in a time and dose dependent manner. By contrast, alendronate did not affect RANKL expression.
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The results indicate that alendronate modulated OPG production by fibroblasts from periprosthetic membrane, which may prove helpful for the inhibition of bone loss during aseptic loosening following total joint arthroplasty. Final Decision: yes