A patient with a well-functioning total hip replacement presents 12 years later with progressive thigh pain and expanding cortical lysis on serial radiographs. An aggressive polyethylene wear pattern with dark-staining bone is found. The mechanism of osteolysis is best explained by:

• A Fatigue fracture of cement mantle generating third-body particles
• B Direct chemical cytotoxicity of polyethylene monomers on osteoblasts
• C Stress shielding causing disuse osteoporosis around the stem
• D Macrophage-mediated cytokine release (TNF-α, IL-1β, IL-6) in response to polyethylene wear debris ✓

Explanation

Polyethylene wear particles (particularly submicron-sized) are phagocytosed by macrophages and foreign-body giant cells at the implant–bone interface, triggering secretion of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, RANKL). This cytokine milieu activates osteoclastogenesis and inhibits osteoblasts, leading to aseptic osteolysis. Stress shielding produces proximal bone loss, not focal lytic lesions; monomer cytotoxicity is not a recognised mechanism for late osteolysis.

Reference: Maheshwari Essential Orthopaedics, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.