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Further evidence supporting a genetic contribution to common OA derives from studies looking at aggregation of OA within families [ 4- 10] and within ethnic/geographic groups [ 11- 14], and in twins [ 15- 17].
Many variants have been suggested as risk factors for common OA based on association studies [ 18- 25].
In addition, the results of our trial are of high clinical interest regarding the low risk of side effects of the treatment compared to common OA treatments, for example, intra-articular injections of glucocorticosteroids [ 1].
Genetic studies provided evidence that genes orchestrating growth plate endochondral ossification play a underlying role in common OA susceptibility, 2 hence functional follow-up approaches require focus on both the early developmental and late-acting effects of these OA genes.
In light of the evidence supporting a genetic contribution to common OA, investigators have sought to identify genetic variants, or chromosomal regions predicted to contain variants, that contribute to common forms of OA.
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Bone marrow lesions (BMLs), common OA-related magnetic resonance (MR) imaging findings, are associated with OA progression and pain [ 2- 13].
The most common OA-affected joints were knee and hand.
We are arguing, however, that the low level of research funding in the US is likely to have a direct and negative effect on social scientists' ability to pay the article processing charges associated with the most common Gold OA business model.
Calcium deposition is common in OA menisci.
Synovial inflammation determined by MRI has been shown to be common in OA [ 27].
A condition as common as OA is in urgent need of disease-modifying treatment (DMOAD).
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