"[T]he results of this longitudinal study suggest that smoking leads to knee cartilage loss and defect development primarily in persons with a family history of knee OA. This provides evidence for a gene-environment interaction in the etiology of knee OA," writes lead author Changhai Ding, MD, senior research fellow with the Menzies Research Institute, University of Tasmania, in Hobart, Australia.
Longitudinal MRI study followed subjects for 2.3 years
Dr. Ding and colleagues used magnetic resonance imaging (MRI) at baseline and after 2.3 years of follow-up to measure knee cartilage volume and cartilage defects in 325 comprising 163 subjects who had at least one parent with a knee replacement for primary knee OA, and 162 controls who had no parent with either a history of symptomatic knee OA or a knee replacement for OA. Subjects had a mean age of 45 years
"[T]he aim of this longitudinal MRI-based study was to describe the association between smoking and changes in knee cartilage volume and/or defects and, when results were not consistent in the whole sample, to further test for interaction between smoking and family history of OA," Dr. Ding says.
Smoking status and duration were assessed by questionnaire. Knee pain was also assessed by questionnaire and defined as pain during the last 12 months for >24 hours or daily pain for >30 days. Knee cartilage volume and defects were measured by MRI scans of the right knee.
Of the total sample, the researchers found that current smokers had a higher prevalence of pain than former smokers or nonsmokers, but smoking status was not associated with baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects. Similarly, associations between smoking and rate of change in cartilage volume or defects were not significant. Overall, current smokers and heavy smokers with >20 pack-years had significantly greater loss of lateral cartilage volume and increases in lateral tibiofemoral cartilage defects compared with nonsmokers.
"The associations between pack-years of smoking and change in lateral tibial cartilage volume were of similar significance in both offspring and controls, suggesting that heavy smoking may be associated with more lateral tibial cartilage loss regardless of a family history of OA," the researchers report.
According to Dr. Ding, the investigators' primary aim was to examine the total sample group for the association between smoking and loss of knee cartilage volume and increases in knee cartilage defects. When the results were inconsistent, the investigators tested the effect of smoking on knee cartilage separately in the offspring and controls.
More smoking, less cartilage
"Somewhat unexpectedly, we found evidence of a gene-environment interaction between smoking and family history of OA with cartilage damage, in which the effect of smoking was much stronger and more consistent in those with at least one parent with severe knee OA. Offspring who smoked had greater tibial cartilage volume change and greater increases in tibiofemoral cartilage defects than did nonsmoking offspring. There was also a dose-response association," Dr. Ding reports.
In the control subjects with no family history of OA, smoking status was not associated with baseline tibial cartilage volume, tibiofemoral cartilage defects, changes in tibiofemoral cartilage volume, or increases in defects over the 2.3 years of follow-up. In addition, smoking status was not related to change in lateral tibial cartilage volume, but smoking pack-years was significantly related to changes in lateral tibial cartilage volume (P = .04).
Stopping smoking appears to benefit the knees, as well as the lungs and heart; loss of knee cartilage was less in former smokers than in current smokers.
"This study is the first to demonstrate harmful effects of smoking on both cartilage volume loss and cartilage defect development mainly in persons with a family history of severe knee OA," Dr. Ding concludes.
Table. Smoking and Annual Loss of Knee Cartilage Volume in Offspring of OA Patients
|
Smoking Status |
% Volume Change/Year, Medial Tibiofemoral Cartilage |
|
Ever smoking |
-1.34 |
|
Current smoking |
-2.20 |
|
Cartilage loss per pack-year |
-0.07 |
Source: Adapted from Ding et al.1
Reference
1. Ding C, Cicuttini F, Blizzard L, et al. Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development. Arthritis Rheum. 2007;56:1521-1528.