OBJECTIVE: To determine whether smoking is related to change in tibial and patella cartilage, and the development or persistence of bone marrow lesions (BMLs) over 2 years in a cohort of middle-aged adults. METHODS: Two hundred and seventy-one adult subjects recruited from the Melbourne Collaborative Cohort Study underwent an MRI of their dominant knee at baseline and approximately 2 years later. Cartilage volume and BMLs were determined for both time points. At baseline, subjects also completed a questionnaire about current and past cigarette smoking. RESULTS: Being a 'smoker' (former or current) was associated with increased annual loss of medial but not lateral or patella cartilage volume (medial: difference = 13.4 microl, P = 0.03; lateral difference = 4.86 microl, P = 0.45, patella difference = -2.57 microl, P = 0.79). A relationship between increasing pack-years smoked and increased medial cartilage volume loss was also observed (P = 0.04). Amongst people who had a BML at baseline, BMLs present in 'ever smokers' were 11.4 [95% confidence interval (CI) 1.54, 89.9; P = 0.02] times more likely to persist over 2 years than those present in 'never smokers'. In addition, the relationship between smoking and increased medial cartilage loss for subjects with a BML present at baseline was partially mediated by the persistence of the BMLs over 2 years. CONCLUSION: This study contributes to the evidence of a detrimental effect of smoking on joint cartilage. Furthermore, it provides a possible mechanism that the association smoking shares with increased cartilage loss may be mediated via smoking impairing the ability for BMLs to resolve.
OBJECTIVE: To determine whether smoking is related to change in tibial and patella cartilage, and the development or persistence of bone marrow lesions (BMLs) over 2 years in a cohort of middle-aged adults. METHODS: Two hundred and seventy-one adult subjects recruited from the Melbourne Collaborative Cohort Study underwent an MRI of their dominant knee at baseline and approximately 2 years later. Cartilage volume and BMLs were determined for both time points. At baseline, subjects also completed a questionnaire about current and past cigarette smoking. RESULTS: Being a 'smoker' (former or current) was associated with increased annual loss of medial but not lateral or patella cartilage volume (medial: difference = 13.4 microl, P = 0.03; lateral difference = 4.86 microl, P = 0.45, patella difference = -2.57 microl, P = 0.79). A relationship between increasing pack-years smoked and increased medial cartilage volume loss was also observed (P = 0.04). Amongst people who had a BML at baseline, BMLs present in 'ever smokers' were 11.4 [95% confidence interval (CI) 1.54, 89.9; P = 0.02] times more likely to persist over 2 years than those present in 'never smokers'. In addition, the relationship between smoking and increased medial cartilage loss for subjects with a BML present at baseline was partially mediated by the persistence of the BMLs over 2 years. CONCLUSION: This study contributes to the evidence of a detrimental effect of smoking on joint cartilage. Furthermore, it provides a possible mechanism that the association smoking shares with increased cartilage loss may be mediated via smoking impairing the ability for BMLs to resolve.
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