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Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development

Citation

Ding, C and Cicuttini, F and Blizzard, CL and Jones, G, Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development, Arthritis & Rheumatism, 56, (5) pp. 1521-1528. ISSN 0004-3591 (2007) [Refereed Article]

DOI: doi:10.1002/art.22591

Abstract

Objective. To describe the effects of smoking on change in knee cartilage volume and increases in knee cartilage defects, and to test for interaction between smoldng and family history of osteoarthritis (OA). Methods. Subjects with at least 1 parent having severe primary knee OA (offspring) and randomly selected controls without this history (a total of 325 subjects with a mean age of 45 years) were measured at baseline and 2.3 years later. Knee cartilage volume and defect score (on a 0-4 scale) were determined using T1-weighted fat-saturated magnetic resonance imaging. Smoldng status and duration and number of cigarettes were recorded by questionnaire. Results. In offspring, smoldng was associated with annual change in medial and lateral tibial cartilage volume (β = -2.20% and β = -1.45%, respectively, for current smokers versus former smokers and those who had never smoked; β = -0.07%/pack-year at both tibial sites, for smoking severity) in multivariate analysis. Smoldng was also associated with increases (change ≥1) in medial and lateral tibiofemoral cartilage defect scores (odds ratio [OR] 4.91 and OR 2.98, respectively, for current smokers versus those who had never smoked; OR 9.90 and OR 12.98, respectively, for heavy smoldng [total of >20 pack-years] versus never smoking) (all P < 0.05). In contrast, smoking was not associated with any of the above in controls except for change in lateral tibial cartilage volume. There was significant interaction between smoldng and offspring-control status for change in medial tibial cartilage volume (P = 0.047) and increases in medial (P = 0.03) and lateral (P = 0.049) tibiofemoral cartilage defects. Conclusion. Smoking leads to knee cartilage loss and defect development primarily in individuals with a family history of knee OA. This provides evidence for a gene-environment interaction in the etiology of knee OA. © 2007, American College of Rheumatology.

Item Details

Item Type:Refereed Article
Research Division:Medical and Health Sciences
Research Group:Public Health and Health Services
Research Field:Epidemiology
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Skeletal System and Disorders (incl. Arthritis)
Author:Ding, C (Professor Chang-Hai Ding)
Author:Blizzard, CL (Professor Leigh Blizzard)
Author:Jones, G (Professor Graeme Jones)
ID Code:47147
Year Published:2007
Web of Science® Times Cited:57
Deposited By:Menzies Institute for Medical Research
Deposited On:2007-08-01
Last Modified:2008-05-14
Downloads:0

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