1. Exposure to second-hand cigarette smoke exacerbates the progression of osteoarthritis in a surgical induced murine model.
- Author
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Rose BJ, Weyand JA, Liu B, Smith JF, Perez BR, Clark JC, Goodman M, Hirschi Budge KM, Eggett DL, Arroyo JA, Reynolds PR, and Kooyman DL
- Subjects
- Animals, Cartilage, Articular metabolism, Disease Progression, Female, Inflammation Mediators metabolism, Joints metabolism, Matrix Metalloproteinase 13 metabolism, Menisci, Tibial surgery, Mice, Inbred C57BL, NF-kappa B metabolism, Osteoarthritis metabolism, Osteoarthritis pathology, Transforming Growth Factor beta1 metabolism, Mice, Cartilage, Articular pathology, Joints pathology, Osteoarthritis etiology, Tobacco Smoke Pollution adverse effects
- Abstract
Osteoarthritis (OA), formerly understood to be a result of passive wear, is now known to be associated with chronic inflammation. Cigarette smoking promotes systemic inflammation and has been implicated in increased joint OA incidence in some studies, though the recent observational data on the association are contradictory. We hypothesize that second-hand smoke (SHS) treatment will increase the incidence of OA in a mouse model that has been subjected to a surgical destabilization of the medial meniscus (DMM). To test this hypothesis, we applied either SHS treatment or room air (RA) to mice for 28 days post-DMM surgery. Histopathology findings indicated that the knees of SHS mice exhibited more severe OA than their control counterparts. Increased expression of matrix metalloprotease-13 (MMP-13), an important extracellular protease known to degrade articular cartilage, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), an intracellular effector of inflammatory pathways, were observed in the SHS group. These findings provide greater understanding and evidence for a detrimental role of cigarette smoke on OA progression and systemic inflammation.
- Published
- 2021
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