New findings from a study led by a Mayo Clinic rheumatologist indicate that men with knee osteoarthritis who smoke experience greater cartilage loss and more severe pain than men who do not smoke. Results will be published online this week in the Annals of the Rheumatic Diseases.
Knee osteoarthritis is one of the leading causes of disability in elders.
"This is a novel finding," says Shreyasee Amin, M.D., Mayo Clinic rheumatologist and lead study researcher. "Previous studies showed no association between cigarette smoking and knee osteoarthritis or even a protective effect of smoking."
The finding that cigarette smoking plays a role in the worsening of knee osteoarthritis is important, says Dr. Amin, as it is a potentially modifiable risk factor.
To conduct this study, the researchers examined 159 men with symptomatic knee osteoarthritis who participated in a prospective study on the natural history of the condition, the Boston Osteoarthritis of the Knee Study. The current study focused on men, as there were too few women in the original group studied who smoked (4 percent). The researchers took MRIs (magnetic resonance images) of the more symptomatic knee of each patient at the study beginning, and also 15 and 30 months later. Cartilage loss over follow-up, based on knee MRIs, was determined at the tibiofemoral joint (the connection between the thighbone and shinbone) and the patellofemoral joint (the junction of the knee cap and the thigh bone) in the knees, and a scoring tool was used to assess knee pain severity.
Nineteen, or 12 percent, of the men were current smokers at the study's start. These men also were leaner and younger than other study participants, so the researchers adjusted for these factors. The investigators found current smokers had a 2.3 fold increased risk of cartilage loss at the medial tibiofemoral joint and a 2.5 fold increased risk of cartilage loss at the patellofemoral joint compared to the men who had quit smoking or never smoked. Current smokers also had higher pain scores than men who were not current smokers, at the beginning of the study (60.5 vs. 45.0, with 100 as the highest possible pain score) and at follow up (59.4 vs. 44.3).
The association between smoking and cartilage loss in knee osteoarthritis could be explained by one or more of the following theories, according to the researchers:
- Smoking may disorder the cells and inhibit cell proliferation in the knee cartilage
- Smoking may increase oxidant stress, which contributes to cartilage loss
- Smoking may raise carbon monoxide levels in arterial blood, contributing to tissue hypoxia (insufficient blood oxygenation), which could impair cartilage repair
Dr. Amin and colleagues believe that the increased pain experienced by smokers with knee osteoarthritis may not be due to the effect of smoking on cartilage loss, as cartilage does not have pain fibers. They have several theories for the link:
- Smoking may affect other knee joint structures mediating knee pain
- Smoking may affect one's pain threshold for knee or other musculoskeletal pain
Dr. Amin says these findings are provocative and deserve further study, especially given the number of potential ways in which cigarette smoking could have a negative effect on knee joint cartilage.
Osteoarthritis, sometimes called degenerative joint disease or osteoarthrosis, is the most common form of arthritis. Osteoarthritis is characterized by the breakdown of joint cartilage and may affect any bodily joint, including those in the fingers, hips, knees, lower back and feet, though weight-bearing joints such as the knees are most susceptible. As cartilage slowly deteriorates over the years, chronic pain or varying amounts of discomfort can arise when standing and walking, and swelling also may occur with knee osteoarthritis. Over time, the cartilage deteriorates, and its smooth surface roughens. Eventually, if the cartilage wears down completely, bone may rub on bone, causing the ends of the bones to become damaged and the joints to become more painful. There is no known cause or cure for osteoarthritis, but available treatments can relieve pain and help patients remain active.
This study was funded by an Osteoarthritis Biomarkers Grant from the Arthritis Foundation, National Institutes of Health Grant AR47785 and a grant from Bayer Corporation. Study authors, in addition to Dr. Amin, include Jingbo Niu, M.D.; David Hunter, M.B.B.S., Ph.D.; Margaret Clancy; Michael LaValley, Ph.D.; and David Felson, M.D.; all from Boston University School of Medicine. Study authors from University of California at San Francisco include Ali Guermazi, M.D.; Mikayel Grigoryan, M.D.; and Harry Genant, M.D.
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