Microplastics and Wear-Particle Biology in Joint Arthroplasty: Converging Mechanisms, Clinical Relevance, and Future Biomaterials
- 1Department of Orthopaedic Surgery, King Fahad Hospital, Al Baha, SAU
Abstract
Total joint arthroplasty effectively restores function in end-stage joint disease, yet particle-induced periprosthetic osteolysis and aseptic loosening remain major causes of implant failure. Emerging evidence shows that environmental microplastics can accumulate in human bone marrow and synovial tissues, and their physicochemical similarities to prosthetic wear particles suggest potentially shared mechanisms of peri-implant inflammation. This review examines potentially shared mechanisms underlying innate immune activation, macrophage polarization, inflammasome signaling, and osteoclastogenesis and evaluates their translational relevance to arthroplasty failure and future biomaterial development. The pathogenic cascade induced by prosthetic debris involves inflammasome activation, pyroptosis, and receptor activator of nuclear factor kappa-B ligand (RANKL)-mediated osteoclastogenesis, ultimately contributing to periprosthetic osteolysis. Concurrently, translational evidence demonstrates the presence and bioaccumulation of environmental microplastics within human musculoskeletal tissues. These environmental polymers may induce cellular stress responses, oxidative stress, and activation of inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, that overlap with mechanisms implicated in particle-induced osteolysis. However, there is insufficient evidence to establish that environmental microplastics independently increase the clinical incidence of aseptic loosening. Current preventive strategies focus on improving implant material properties and reducing the generation and biological activity of wear particles, including the use of highly cross-linked and antioxidant-stabilized polyethylene. Environmental microplastics and prosthetic wear debris may therefore share converging inflammatory and osteolytic mechanisms that compromise the peri-implant bone microenvironment. While direct clinical causality between environmental microplastics and arthroplasty failure remains unproven, this intersection represents an emerging area of investigation in orthopedic biomaterials, periprosthetic immunology, and osteolysis prevention.
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BibTeX
@article{hassan2026microplastics,
title = {{Microplastics and Wear-Particle Biology in Joint Arthroplasty: Converging Mechanisms, Clinical Relevance, and Future Biomaterials}},
author = {Mohamed Elsayed Abdelhalim Hassan},
journal = {Cureus},
year = {2026},
month = oct,
doi = {10.7759/cureus.117529},
url = {https://doi.org/10.7759/cureus.117529},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Microplastics and Wear-Particle Biology in Joint Arthroplasty: Converging Mechanisms, Clinical Relevance, and Future Biomaterials
AU - Mohamed Elsayed Abdelhalim Hassan
PY - 2026
DA - 2026/10/06
JO - Cureus
DO - 10.7759/cureus.117529
UR - https://doi.org/10.7759/cureus.117529
AB - Total joint arthroplasty effectively restores function in end-stage joint disease, yet particle-induced periprosthetic osteolysis and aseptic loosening remain major causes of implant failure. Emerging evidence shows that environmental microplastics can accumulate in human bone marrow and synovial tissues, and their physicochemical similarities to prosthetic wear particles suggest potentially shared mechanisms of peri-implant inflammation. This review examines potentially shared mechanisms underlying innate immune activation, macrophage polarization, inflammasome signaling, and osteoclastogenesis and evaluates their translational relevance to arthroplasty failure and future biomaterial development. The pathogenic cascade induced by prosthetic debris involves inflammasome activation, pyroptosis, and receptor activator of nuclear factor kappa-B ligand (RANKL)-mediated osteoclastogenesis, ultimately contributing to periprosthetic osteolysis. Concurrently, translational evidence demonstrates the presence and bioaccumulation of environmental microplastics within human musculoskeletal tissues. These environmental polymers may induce cellular stress responses, oxidative stress, and activation of inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, that overlap with mechanisms implicated in particle-induced osteolysis. However, there is insufficient evidence to establish that environmental microplastics independently increase the clinical incidence of aseptic loosening. Current preventive strategies focus on improving implant material properties and reducing the generation and biological activity of wear particles, including the use of highly cross-linked and antioxidant-stabilized polyethylene. Environmental microplastics and prosthetic wear debris may therefore share converging inflammatory and osteolytic mechanisms that compromise the peri-implant bone microenvironment. While direct clinical causality between environmental microplastics and arthroplasty failure remains unproven, this intersection represents an emerging area of investigation in orthopedic biomaterials, periprosthetic immunology, and osteolysis prevention.
SN - 2168-8184
ER -