Molecular signaling pathways in osteoarthritis and biomaterials for cartilage regeneration: a review

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Osteoarthritis is a prevalent degenerative joint disease characterized by cartilage degradation, synovial inflammation, and subchondral bone alterations, leading to chronic pain and joint dysfunction. Conventional treatments provide symptomatic relief but fail to halt disease progression. Recent advancements in biomaterials, molecular signaling modulation, and gene-editing technologies offer promising therapeutic strategies. This review explores key molecular pathways implicated in osteoarthritis, including fibroblast growth factor, phosphoinositide 3-kinase/Akt, and bone morphogenetic protein signaling, highlighting their roles in chondrocyte survival, extracellular matrix remodeling, and inflammation. Biomaterial-based interventions such as hydrogels, nanoparticles, and chitosan-based scaffolds have demonstrated potential in enhancing cartilage regeneration and targeted drug delivery. Furthermore, CRISPR/Cas9 gene editing holds promise in modifying osteoarthritis-related genes to restore cartilage integrity. The integration of regenerative biomaterials with precision medicine and molecular therapies represents a novel approach for mitigating osteoarthritis progression. Future research should focus on optimizing biomaterial properties, refining gene-editing efficiency, and developing personalized therapeutic strategies. The convergence of bioengineering and molecular science o

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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