Medications
Drugs and biologics targeting the chondrocyte or its matrix: DMOADs, hyaluronic acid injections, MACI, senolytics, and what the trials actually showed.
Reviews 11 DMOAD candidates including lorecivivint, sprifermin, UBX0101, TPX-100, GLPG1972, lutikizumab; none approved as of 2024.
Reviews anabolic, anti-catabolic, and anti-inflammatory DMOAD strategies; identifies cartilage matrix as the correct therapeutic target.
Intra-articular DMOAD trials 2025 update; sprifermin (FGF-18) showed cartilage thickness increase but not pain reduction; lorecivivint (Wnt/CLK2 inhibitor) in phase 3.
ACI showed sustained clinical improvement at long-term follow-up for focal chondral defects; MACI is the current US-approved product (Carticel phased out 2017).
Hyaluronic acid injections improve pain and function in knee OA; effect size modest and duration variable; works best in early OA with preserved cartilage.
MACI at minimum 10-year follow-up: significant durable improvement in patient-reported outcomes, satisfactory defect fill on MRI, low reoperation rate.
Senolytics (dasatinib plus quercetin, navitoclax) and senomorphics (rapamycin) under review as pharmacological interventions for OA via chondrocyte senescence clearance.
Editorial assessment: no approved DMOAD as of 2025; structural endpoints and patient-reported outcomes remain misaligned across trials.
Vosoritide, a C-type natriuretic peptide analogue, approved for achondroplasia in children; increases annual height velocity.
Preclinical: vestitol reduces ferroptosis features and OA progression via GSK3B/Nrf2/GPX4.
In vitro: hydroxysafflor yellow A limits oxidative lipid damage and calcification changes in endplate chondrocytes.
Preclinical hydrogel releasing hydrogen from magnesium, proposed as an OA therapy.
Review of why intra-articular carriers fail the translation step: clearance, penetration, and retention are the three unsolved problems.
Preclinical: dietary polyphenol chlorogenic acid limits OA progression by activating Nrf2/HO-1 and suppressing ferroptotic cartilage loss.
Review of how metformin protects chondrocytes through AMPK/SIRT1-driven autophagy and NF-kB suppression; positions a widely available drug as a candidate for OA intervention.
Nanoparticles delivering Salvianolic acid B restore mitochondrial function in chondrocytes by activating PINK1/Parkin-mediated mitophagy; preclinical OA model.
Gut microbial fermentation transforms epimedium polysaccharides into short-chain fatty acids that deliver substantially enhanced chondroprotective activity; links the gut-joint axis to a traditional herbal compound.
Nanoparticles coated with chondrocyte membrane homing peptide deliver tetrahedral framework nucleic acid (tFNA) to OA joints, polarising macrophages and protecting chondrocytes by rebalancing the cartilage-synovium inflammatory axis. Biomimetic targeting using the cell's own surface as camouflage.
Systematic review of pharmacological and biological strategies to extend cartilage graft viability, covering growth factors, cryoprotectants, anti-apoptotic agents, and immunomodulators; translational synthesis relevant to reconstructive and repair applications.
Review of OA drug delivery: exosomes, microparticles, nanoparticles, and hydrogels as carriers targeting articular chondrocytes and joint tissue; synthesis of nanoscale approaches to reducing cartilage degeneration.