Cartilage Damage in Knee OA Is Not a Given

Smoking appears to contribute to the development of knee cartilage loss and defects in individuals with a family history of knee osteoarthritis (OA), according to the results reported by Dr. Changhai Ding and associates of the University of Tasmania in Australia.

In this study the knee cartilage of 345 relatively young individuals (the average age was 45 years) were measured at baseline and again 2.3 years later, and their risk factors were assessed.

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).

Dr. Ding and associates 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.

“This provides evidence for a gene-environment interaction in the etiology of knee OA,” the investigators wrote.

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. Similarly, a positive family history increased the risk of lateral tibiofemoral cartilage defects threefold.

The risk increases among heavy smokers (at least 20 pack-years) versus never-smokers were 10-fold and 13-fold, respectively.

The interaction among 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, even after adjusting for potentially confounding factors.

In the overall group, the prevalence of knee pain was higher among current smokers (41%) than it was among former smokers or never-smokers (33%), regardless of family history.

There was no overall association between smoking status and baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects.

Smoking appears to contribute to the development of knee cartilage loss and defects in individuals with a family history of knee osteoarthritis (OA), according to the results reported by Dr. Changhai Ding and associates of the University of Tasmania in Australia.

In this study the knee cartilage of 345 relatively young individuals (the average age was 45 years) were measured at baseline and again 2.3 years later, and their risk factors were assessed.

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).

Dr. Ding and associates 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.

“This provides evidence for a gene-environment interaction in the etiology of knee OA,” the investigators wrote.

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. Similarly, a positive family history increased the risk of lateral tibiofemoral cartilage defects threefold.

The risk increases among heavy smokers (at least 20 pack-years) versus never-smokers were 10-fold and 13-fold, respectively.

The interaction among 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, even after adjusting for potentially confounding factors.

In the overall group, the prevalence of knee pain was higher among current smokers (41%) than it was among former smokers or never-smokers (33%), regardless of family history.

There was no overall association between smoking status and baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects.

Smoking appears to contribute to the development of knee cartilage loss and defects in individuals with a family history of knee osteoarthritis (OA), according to the results reported by Dr. Changhai Ding and associates of the University of Tasmania in Australia.

In this study the knee cartilage of 345 relatively young individuals (the average age was 45 years) were measured at baseline and again 2.3 years later, and their risk factors were assessed.

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).

Dr. Ding and associates 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.

“This provides evidence for a gene-environment interaction in the etiology of knee OA,” the investigators wrote.

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. Similarly, a positive family history increased the risk of lateral tibiofemoral cartilage defects threefold.

The risk increases among heavy smokers (at least 20 pack-years) versus never-smokers were 10-fold and 13-fold, respectively.

The interaction among 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, even after adjusting for potentially confounding factors.

In the overall group, the prevalence of knee pain was higher among current smokers (41%) than it was among former smokers or never-smokers (33%), regardless of family history.

There was no overall association between smoking status and baseline tibial cartilage volume or prevalent tibiofemoral cartilage defects.