Cell-free fat extract attenuates temporomandibular joint osteoarthritis via repressing ATF3-binding chromatin accessibility.

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)

Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease characterized by cartilage degradation and synovial inflammation with limited therapeutic options. In our study, cell-free fat extract (CEFFE), a bioactive fraction derived from adipose tissue, is evaluated as a therapeutic strategy for TMJOA. In chondrocytes, CEFFE enhances proliferation and viability, attenuates inflammatory apoptosis, and preserves extracellular matrix homeostasis by upregulating Col2a1 and Sox9 while suppressing matrix metalloproteinases. Integrated transcriptomic and epigenomic analyses demonstrate that CEFFE reduces the activating transcription factor 3 (ATF3) binding at the promoter of actin binding LIM protein 1 (ABLIM1) via repressing ATF3-binding chromatin accessibility, thereby inhibiting nuclear factor kappa-B (NF-κB) signaling. In a rat model of TMJOA, intra-articular administration of CEFFE alleviates cartilage degeneration, subchondral bone loss, and synovitis, without systemic toxicity. CEFFE also suppresses pro-inflammatory M1 macrophage polarization and decreases interleukin-1β and tumor necrosis factor-α expression in synovial tissue. These findings identify CEFFE as a dual-target therapeutic agent that modulates both chondrocytes and macrophages through epigenetic regulation of ATF3/ABLIM1/NF-κB signaling. Our study highlights CEFFE as a safe and accessible biomaterial

Evidence level

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

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