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Exploration of potential targets and toxicological mechanisms of microplastic exposure-induced osteoarthritis based on network toxicology, molecular docking and experimental validation
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Scientists found that tiny plastic particles (microplastics), which we regularly ingest through food and air, may damage joint cartilage and contribute to osteoarthritis by disrupting specific genes involved in inflammation and cell damage. Using computer modeling and lab experiments on cartilage cells, researchers also found that quercetin—a natural compound found in fruits and vegetables—may help protect against this damage, though more research is needed before it could be recommended as a treatment. This study adds to growing concerns about how everyday plastic exposure might affect joint health, while pointing toward a possible natural way to help defend against it.
Abstract Microplastics (MPs), ubiquitous environmental pollutants, enter the human body via dietary and respiratory pathways and impair bone and joint tissues, but their toxicological mechanisms in the onset and progression of osteoarthritis (OA) remain elusive. Herein, four common MPs—polyethylene (PE), polyethylene terephthalate (PET), polypropylene (PP), and polystyrene (PS)—were selected as research subjects. Core OA-related targets responsive to MPs exposure were screened using the Gene Expression Omnibus (GEO), SwissTargetPrediction, and Comparative Toxicogenomics Database (CTD), followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Weighted gene co-expression network analysis (WGCNA) combined with three machine learning algorithms (random forest, SVM-RFE, LASSO) was employed for cross-validation to identify key targets, whose diagnostic efficacy was validated via nomograms and receiver operating characteristic (ROC) curves. Molecular docking assays assessed the binding affinity between quercetin and the identified targets, while in vitro experiments preliminarily verified the chondrocyte toxicity of PS-MPs and the protective effects of quercetin. A total of 95 core targets were identified, primarily involved in oxidative stress, inflammatory responses, cartilage matrix metabolism, and cell proliferation/apoptosis. DDIT4 and CDKN1A (area under the curve [AUC] > 0.7) were identified as key diagnostic targets for OA. Quercetin stably bound to DDIT4 (binding energy: −7.8 kcal/mol) and CDKN1A (binding energy: −6.1 kcal/mol), preliminarily mitigating PS-MPs-induced chondrocyte damage. This study clarifies the role of MPs in OA progression, identifies DDIT4 and CDKN1A as core regulatory targets, and provides preliminary evidence that quercetin is a potential natural agent against MPs-induced OA.
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Scientists found that PET microplastics — tiny plastic particles from common plastic bottles and packaging — may worsen osteoarthritis by triggering inflammation and damaging cartilage cells at the molecular level. Using computer modeling and lab tests on cartilage cells, they pinpointed six specific genes that get switched on or off when exposed to these plastic particles, offering early clues about how everyday plastic pollution might contribute to joint disease. While this is still early-stage lab research (not yet tested in humans), it adds to growing evidence that microplastics in our environment could have real effects on joint health.
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A translational synthesis of clinical and experimental data examined the role of microplastic exposure in osteoarthritis (OA) development, finding evidence that MPs bioaccumulate in joint tissues and may promote inflammation and oxidative damage that disrupts cartilage homeostasis. The review identified MP exposure as a plausible but underexplored contributor to OA progression.
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Scientists found that tiny plastic particles called microplastics—already known to accumulate in human joints—can trigger a chain reaction that damages cartilage cells, worsening a protein called NFKB1 that drives inflammation and cell death. This research, done in cells rather than in people, suggests microplastic pollution could be a hidden contributor to osteoarthritis, the joint disease that causes pain and stiffness in millions of people, and it points to a possible drug target to block this damage in the future.
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This review synthesized mechanistic and epidemiological evidence linking environmental pollutants — including microplastics — to osteoarthritis pathogenesis. The authors found accumulating in vitro, animal, and human data suggesting that chemical exposures accelerate cartilage degradation and joint inflammation through multiple pathways.
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Researchers used computational analysis to investigate how PET microplastics might contribute to joint diseases like osteoarthritis and rheumatoid arthritis. They identified the PTGS2 gene, involved in inflammation, as a central hub connecting microplastic exposure to joint disease pathways. The study suggests that microplastics may worsen joint inflammation through specific molecular mechanisms, though further laboratory and clinical research is needed to confirm these computational findings.
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