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Strontium ranelate: ready for clinical use as disease-modifying osteoarthritis drug?
  1. Floris P J G Lafeber1,
  2. Jacob M van Laar2
  1. 1Rheumatology & Clinical Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands
  2. 2Musculoskeletal Research Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
  1. Correspondence to Professor Floris P J G Lafeber, UMC Utrecht, Rheumatology & Clinical Immunology, Utrecht 3508 GA, The Netherlands; f.lafeber{at}umcutrecht.nlFPJGL and JMvL contributed equally.

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In the past decade, clinical practice in rheumatology has been transformed by the advent of ‘biologicals’. The use of these new drugs has significantly improved the outcome of patients with rheumatoid arthritis especially for those refractory to (patient-tailored) conventional disease-modifying antirheumatic drug (DMARD) therapy. The question is, is it now time for a gap-bridging, large step forward in the treatment of an even more commonly seen rheumatic disease, osteoarthritis? Has the era of the disease-modifying osteoarthritis drug (DMOAD) begun? Is ‘OA the new RA’ (quote from Professor P Conaghan, 2012 annual meeting of the British Society of Rheumatology (BSR)), or is this still wishful thinking?

It no longer needs proclamation of worldwide numbers of patients who suffer from non-attendance and decreased productivity at work and unemployment, or costs of medical and paramedical care, medication use, and surgical treatments with joint replacement in the end, to recognise that osteoarthritis is a huge socioeconomic problem.1 Osteoarthritis is the most common disabling joint disease worldwide. Moreover, its incidence and prevalence are increasing because of ageing, higher life expectancy, and lifestyle changes, leading to a growing population of patients with osteoarthritis.2

Osteoarthritis is clinically characterised primarily by joint pain and consequently functional limitations. Cartilage degradation is still considered pivotal in its pathology. This might be considered surprising, since cartilage is not innervated, so osteoarthritic pain must arise from other tissues involved. Changes in periarticular bone, synovial tissue and other periarticular soft tissue structures such as ligaments and muscles are inextricably related to the osteoarthritic process. Obviously, all these structural changes are part of a cascade that eventually leads to overt osteoarthritis, and they need to be considered in unison when related to clinical symptoms. The sequence and relative importance of each of these processes may differ between individuals, between joints, between disease …

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