Smoking quitting promotes neuromuscular and cartilage recovery in knee osteoarthritis

Smoking is known to exacerbate systemic inflammation and musculoskeletal decline, however, its reversible effects in osteoarthritis (OA) remain poorly understood. We evaluated whether smoking cessation improves disease severity, physical and respiratory function, and biochemical markers of neuromuscular junction (NMJ) integrity (C-terminal agrin-fragment-22; CAF22) and cartilage degradation (C-telopeptide of type II collagen; CTX-II) in patients with knee OA.

This one-year longitudinal study included 57 quitters and 61 active smokers with OA. Disease severity was classified using the Oxford Knee Score (OKS). Additional outcomes included WOMAC, handgrip strength (HGS), gait speed, maximal inspiratory and expiratory pressures (MIP and MEP, respectively), and plasma biomarkers of cartilage degradation (CTX-II) and NMJ disruption (CAF22). Standardized protocols and validated instruments were applied throughout.

Quitters demonstrated significant improvements in OKS and WOMAC, along with increases in gait speed, HGS, and MIP compared to smokers (all p < 0.05). Disease severity distribution shifted favorably in quitters, with more patients moving from the severe to mild categories. In contrast, smokers showed worsening severity. In contrast to active smokers, quitters exhibited reduced CAF22 and CTX-II levels, suggesting an improved NMJ and cartilage integrity. Regression analyses confirmed strong associations between biomarker levels, disease severity, and functional outcomes.

Smoking cessation was associated with improvements in disease severity, musculoskeletal and respiratory function, and biomarker profiles over one year. These findings suggest that cessation may contribute to a more favorable clinical trajectory in knee OA, although further studies are needed to confirm underlying mechanisms.