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Statin Use Linked to 57% Reduction in Knee OA Incidence

BRUSSELS — Statin therapy may exert yet another beneficial clinical effect – preventing development of knee osteoarthritis and slowing its progression – based on an analysis of more than 3,000 people who were enrolled in a prospective cohort study.

In an analysis of people in the Rotterdam Study, statin use was significantly linked with a more-than-50% reduced rate of knee osteoarthritis (OA) incidence, and a more-than-50% reduced rate of knee OA progression after adjustment for several baseline risk factors, Dr. Stefan Clockaerts said at the congress. In contrast, statin use had no significant impact on the incidence or progression of hip OA.

The findings suggest that knee OA may be at least partly a metabolic disease, said Dr. Clockaerts of Erasmus University, Rotterdam, the Netherlands, and the University of Antwerp (Belgium).

“We think that there is a difference in the pathogenesis of hip and knee osteoarthritis, and that several systemic factors – such as cholesterol, body mass index, and diabetes – appear to influence knee osteoarthritis” but not deterioration of the hip, Dr. Clockaerts said in an interview.

“Our idea is that metabolic alterations are more important for knee osteoarthritis than for hip osteoarthritis.”

For example, Dr. Clockaerts cited prior reports that cholesterol may have a damaging effect on cartilage, and it may increase the formation and activity of bone marrow lesions. “Cholesterol is probably not good for knee osteoarthritis,” he said. Synovial fluid contains cholesterol, and statin treatment would reduce the level.

An additional hypothesis is that vascular pathology may contribute to the OA disease process, and that the beneficial effects of statin treatment on atherosclerosis and vascular function may also link statins and knee OA. The anti-inflammatory effect of statins most likely also plays a role.

“The systemic and intra-articular anti-inflammatory effects of statins are the most plausible explanations for the effect,” Dr. Clockaerts said.

The Rotterdam Study began in 1990 and enrolled 7,983 men and women aged 55 years or older into a longitudinal cohort study.

The analysis by Dr. Clockaerts and his associates focused on participants with knee and hip x-rays that were available from baseline and follow-up and were evaluable for scoring on the Kellgren-Lawrence (KL) scale. They excluded study participants with a history of rheumatoid arthritis, gout, ankylosing spondylitis, or a leg fracture that was treated with a prosthesis.

Information on statin use came from computerized pharmacy records for the Rotterdam suburb where participants lived. The analysis considered to be a statin user anyone who received a statin prescription for at least 100 days for at least 50% of the drug's recommended daily dosage.

They identified incident OA of the knee or hip in people with a baseline KL score of 0 or 1 that subsequently became 2 or greater.

They defined a case of OA progression to be a person with a baseline KL score of 1, 2, or 3 whose score later increased by at least 1 point. Average follow-up was 6 years.

The analysis showed that among 3,056 people who were evaluable for incident knee OA, statin users had a statistically significant, 57% reduced rate of knee OA, compared with nonusers, after adjustment for baseline age, diabetes, BMI, total cholesterol:HDL cholesterol ratio, and bone mineral density, said Dr. Clockaerts at the congress, which was presented by the Osteoarthritis Research Society International. (See box.)

Progression of knee osteoarthritis among 1,412 people with a baseline KL score of 1–3 occurred 53% less often in the statin users, compared with nonusers after adjustment for age, BMI, and BMD, which was a statistically significant difference.

The analysis did not look at the impact of specific statin types.

A similar analysis showed no significant interaction of statin use and the incidence of new-onset or progressing hip OA in more than 4,000 people who were evaluable for one of these end points, according to Dr. Clockaerts.

Further studies should directly test a statin's effect in an animal model for OA, such as the STR/ort mouse, which also shows metabolic derangements, he said.

Dr. Clockaerts said that he had no disclosures.

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BRUSSELS — Statin therapy may exert yet another beneficial clinical effect – preventing development of knee osteoarthritis and slowing its progression – based on an analysis of more than 3,000 people who were enrolled in a prospective cohort study.

In an analysis of people in the Rotterdam Study, statin use was significantly linked with a more-than-50% reduced rate of knee osteoarthritis (OA) incidence, and a more-than-50% reduced rate of knee OA progression after adjustment for several baseline risk factors, Dr. Stefan Clockaerts said at the congress. In contrast, statin use had no significant impact on the incidence or progression of hip OA.

The findings suggest that knee OA may be at least partly a metabolic disease, said Dr. Clockaerts of Erasmus University, Rotterdam, the Netherlands, and the University of Antwerp (Belgium).

“We think that there is a difference in the pathogenesis of hip and knee osteoarthritis, and that several systemic factors – such as cholesterol, body mass index, and diabetes – appear to influence knee osteoarthritis” but not deterioration of the hip, Dr. Clockaerts said in an interview.

“Our idea is that metabolic alterations are more important for knee osteoarthritis than for hip osteoarthritis.”

For example, Dr. Clockaerts cited prior reports that cholesterol may have a damaging effect on cartilage, and it may increase the formation and activity of bone marrow lesions. “Cholesterol is probably not good for knee osteoarthritis,” he said. Synovial fluid contains cholesterol, and statin treatment would reduce the level.

An additional hypothesis is that vascular pathology may contribute to the OA disease process, and that the beneficial effects of statin treatment on atherosclerosis and vascular function may also link statins and knee OA. The anti-inflammatory effect of statins most likely also plays a role.

“The systemic and intra-articular anti-inflammatory effects of statins are the most plausible explanations for the effect,” Dr. Clockaerts said.

The Rotterdam Study began in 1990 and enrolled 7,983 men and women aged 55 years or older into a longitudinal cohort study.

The analysis by Dr. Clockaerts and his associates focused on participants with knee and hip x-rays that were available from baseline and follow-up and were evaluable for scoring on the Kellgren-Lawrence (KL) scale. They excluded study participants with a history of rheumatoid arthritis, gout, ankylosing spondylitis, or a leg fracture that was treated with a prosthesis.

Information on statin use came from computerized pharmacy records for the Rotterdam suburb where participants lived. The analysis considered to be a statin user anyone who received a statin prescription for at least 100 days for at least 50% of the drug's recommended daily dosage.

They identified incident OA of the knee or hip in people with a baseline KL score of 0 or 1 that subsequently became 2 or greater.

They defined a case of OA progression to be a person with a baseline KL score of 1, 2, or 3 whose score later increased by at least 1 point. Average follow-up was 6 years.

The analysis showed that among 3,056 people who were evaluable for incident knee OA, statin users had a statistically significant, 57% reduced rate of knee OA, compared with nonusers, after adjustment for baseline age, diabetes, BMI, total cholesterol:HDL cholesterol ratio, and bone mineral density, said Dr. Clockaerts at the congress, which was presented by the Osteoarthritis Research Society International. (See box.)

Progression of knee osteoarthritis among 1,412 people with a baseline KL score of 1–3 occurred 53% less often in the statin users, compared with nonusers after adjustment for age, BMI, and BMD, which was a statistically significant difference.

The analysis did not look at the impact of specific statin types.

A similar analysis showed no significant interaction of statin use and the incidence of new-onset or progressing hip OA in more than 4,000 people who were evaluable for one of these end points, according to Dr. Clockaerts.

Further studies should directly test a statin's effect in an animal model for OA, such as the STR/ort mouse, which also shows metabolic derangements, he said.

Dr. Clockaerts said that he had no disclosures.

Vitals

Source Elsevier Global Medical News

BRUSSELS — Statin therapy may exert yet another beneficial clinical effect – preventing development of knee osteoarthritis and slowing its progression – based on an analysis of more than 3,000 people who were enrolled in a prospective cohort study.

In an analysis of people in the Rotterdam Study, statin use was significantly linked with a more-than-50% reduced rate of knee osteoarthritis (OA) incidence, and a more-than-50% reduced rate of knee OA progression after adjustment for several baseline risk factors, Dr. Stefan Clockaerts said at the congress. In contrast, statin use had no significant impact on the incidence or progression of hip OA.

The findings suggest that knee OA may be at least partly a metabolic disease, said Dr. Clockaerts of Erasmus University, Rotterdam, the Netherlands, and the University of Antwerp (Belgium).

“We think that there is a difference in the pathogenesis of hip and knee osteoarthritis, and that several systemic factors – such as cholesterol, body mass index, and diabetes – appear to influence knee osteoarthritis” but not deterioration of the hip, Dr. Clockaerts said in an interview.

“Our idea is that metabolic alterations are more important for knee osteoarthritis than for hip osteoarthritis.”

For example, Dr. Clockaerts cited prior reports that cholesterol may have a damaging effect on cartilage, and it may increase the formation and activity of bone marrow lesions. “Cholesterol is probably not good for knee osteoarthritis,” he said. Synovial fluid contains cholesterol, and statin treatment would reduce the level.

An additional hypothesis is that vascular pathology may contribute to the OA disease process, and that the beneficial effects of statin treatment on atherosclerosis and vascular function may also link statins and knee OA. The anti-inflammatory effect of statins most likely also plays a role.

“The systemic and intra-articular anti-inflammatory effects of statins are the most plausible explanations for the effect,” Dr. Clockaerts said.

The Rotterdam Study began in 1990 and enrolled 7,983 men and women aged 55 years or older into a longitudinal cohort study.

The analysis by Dr. Clockaerts and his associates focused on participants with knee and hip x-rays that were available from baseline and follow-up and were evaluable for scoring on the Kellgren-Lawrence (KL) scale. They excluded study participants with a history of rheumatoid arthritis, gout, ankylosing spondylitis, or a leg fracture that was treated with a prosthesis.

Information on statin use came from computerized pharmacy records for the Rotterdam suburb where participants lived. The analysis considered to be a statin user anyone who received a statin prescription for at least 100 days for at least 50% of the drug's recommended daily dosage.

They identified incident OA of the knee or hip in people with a baseline KL score of 0 or 1 that subsequently became 2 or greater.

They defined a case of OA progression to be a person with a baseline KL score of 1, 2, or 3 whose score later increased by at least 1 point. Average follow-up was 6 years.

The analysis showed that among 3,056 people who were evaluable for incident knee OA, statin users had a statistically significant, 57% reduced rate of knee OA, compared with nonusers, after adjustment for baseline age, diabetes, BMI, total cholesterol:HDL cholesterol ratio, and bone mineral density, said Dr. Clockaerts at the congress, which was presented by the Osteoarthritis Research Society International. (See box.)

Progression of knee osteoarthritis among 1,412 people with a baseline KL score of 1–3 occurred 53% less often in the statin users, compared with nonusers after adjustment for age, BMI, and BMD, which was a statistically significant difference.

The analysis did not look at the impact of specific statin types.

A similar analysis showed no significant interaction of statin use and the incidence of new-onset or progressing hip OA in more than 4,000 people who were evaluable for one of these end points, according to Dr. Clockaerts.

Further studies should directly test a statin's effect in an animal model for OA, such as the STR/ort mouse, which also shows metabolic derangements, he said.

Dr. Clockaerts said that he had no disclosures.

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Statin Use Linked to 57% Reduction in Knee OA Incidence
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