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Smoking seems to contribute to the development of knee cartilage loss and defects in those with a family history of knee osteoarthritis (OA), according to results reported by Dr. Changhai Ding and associates of the University of Tasmania in Australia.
In this study, 345 relatively young individuals (average age, 45 years) were measured at baseline and again 2.3 years later. Of the 162 persons with at least one parent with severe primary knee OA, 40 current smokers had greater loss in medial and lateral tibial cartilage volumes (beta = −2.20% and −1.45%. respectively) than did 47 former smokers and 75 never-smokers, after adjusting for confounding factors in a logistic regression analysis. Pack-years of smoking were also significantly associated with changes in cartilage volume (Arthritis Rheum. 2007;56:1521-8).
The authors did not find a similar relationship between smoking status and knee OA measures in 163 individuals with no family history of knee OA. The only factor significantly associated with smoking status in control individuals was change in lateral tibiofemoral cartilage volume, providing evidence for a “gene-environment interaction in the etiology of knee OA.”
Among those with a family history of knee OA, being a current smoker increased the risk of developing medial tibiofemoral cartilage defects by nearly fivefold during the study period and increased the risk of lateral tibiofemoral cartilage defects by threefold. The risk increases in heavy smokers (at least 20 pack-years) versus never-smokers were 10-fold and 13-fold, respectively.
The interaction in smoking status, family history of knee OA, and cartilage effects remained significant in regards to change in medial tibial cartilage volume and increases in cartilage defects, both medial and lateral, after adjusting for confounding factors. In the overall group, the prevalence of knee pain was higher in current smokers (41%) than in former smokers or never-smokers (33%), regardless of family history. However, there was no overall association between smoking status and baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects.
Smoking seems to contribute to the development of knee cartilage loss and defects in those with a family history of knee osteoarthritis (OA), according to results reported by Dr. Changhai Ding and associates of the University of Tasmania in Australia.
In this study, 345 relatively young individuals (average age, 45 years) were measured at baseline and again 2.3 years later. Of the 162 persons with at least one parent with severe primary knee OA, 40 current smokers had greater loss in medial and lateral tibial cartilage volumes (beta = −2.20% and −1.45%. respectively) than did 47 former smokers and 75 never-smokers, after adjusting for confounding factors in a logistic regression analysis. Pack-years of smoking were also significantly associated with changes in cartilage volume (Arthritis Rheum. 2007;56:1521-8).
The authors did not find a similar relationship between smoking status and knee OA measures in 163 individuals with no family history of knee OA. The only factor significantly associated with smoking status in control individuals was change in lateral tibiofemoral cartilage volume, providing evidence for a “gene-environment interaction in the etiology of knee OA.”
Among those with a family history of knee OA, being a current smoker increased the risk of developing medial tibiofemoral cartilage defects by nearly fivefold during the study period and increased the risk of lateral tibiofemoral cartilage defects by threefold. The risk increases in heavy smokers (at least 20 pack-years) versus never-smokers were 10-fold and 13-fold, respectively.
The interaction in smoking status, family history of knee OA, and cartilage effects remained significant in regards to change in medial tibial cartilage volume and increases in cartilage defects, both medial and lateral, after adjusting for confounding factors. In the overall group, the prevalence of knee pain was higher in current smokers (41%) than in former smokers or never-smokers (33%), regardless of family history. However, there was no overall association between smoking status and baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects.
Smoking seems to contribute to the development of knee cartilage loss and defects in those with a family history of knee osteoarthritis (OA), according to results reported by Dr. Changhai Ding and associates of the University of Tasmania in Australia.
In this study, 345 relatively young individuals (average age, 45 years) were measured at baseline and again 2.3 years later. Of the 162 persons with at least one parent with severe primary knee OA, 40 current smokers had greater loss in medial and lateral tibial cartilage volumes (beta = −2.20% and −1.45%. respectively) than did 47 former smokers and 75 never-smokers, after adjusting for confounding factors in a logistic regression analysis. Pack-years of smoking were also significantly associated with changes in cartilage volume (Arthritis Rheum. 2007;56:1521-8).
The authors did not find a similar relationship between smoking status and knee OA measures in 163 individuals with no family history of knee OA. The only factor significantly associated with smoking status in control individuals was change in lateral tibiofemoral cartilage volume, providing evidence for a “gene-environment interaction in the etiology of knee OA.”
Among those with a family history of knee OA, being a current smoker increased the risk of developing medial tibiofemoral cartilage defects by nearly fivefold during the study period and increased the risk of lateral tibiofemoral cartilage defects by threefold. The risk increases in heavy smokers (at least 20 pack-years) versus never-smokers were 10-fold and 13-fold, respectively.
The interaction in smoking status, family history of knee OA, and cartilage effects remained significant in regards to change in medial tibial cartilage volume and increases in cartilage defects, both medial and lateral, after adjusting for confounding factors. In the overall group, the prevalence of knee pain was higher in current smokers (41%) than in former smokers or never-smokers (33%), regardless of family history. However, there was no overall association between smoking status and baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects.