Wear particles generated from a total joint prosthesis induce periprosthetic osteolysis chiefly by which cellular mechanism?
- A Macrophage phagocytosis of submicron particles triggering release of cytokines such as RANKL, TNF-alpha and IL-1 that stimulate osteoclast differentiation ✓
- B Direct activation of osteoclast precursors by particle phagocytosis in osteoblasts
- C Complement-mediated lysis of bone lining cells adjacent to the implant
- D T lymphocyte mediated type IV hypersensitivity destroying trabecular bone directly
Explanation
Submicron polyethylene and metal debris are phagocytosed by macrophages, which release inflammatory mediators including RANKL, TNF-alpha, IL-1 and IL-6. These drive osteoclastogenesis and resorption at the bone-implant interface, producing granulomatous pseudotumours and loosening. Osteoblasts are not the phagocytic cell, and although metal hypersensitivity exists it is not the principal pathway of wear-induced osteolysis.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.