Nicola Veronese1, Cyrus Cooper2, Jean-Yves Reginster3, Marc Hochberg4, Jaime Branco5, Olivier Bruyère6, Roland Chapurlat7, Nasser Al-Daghri8, Elaine Dennison9, Gabriel Herrero-Beaumont10, Jean-François Kaux11, Emmanuel Maheu12, René Rizzoli13, Roland Roth14, Lucio C Rovati15, Daniel Uebelhart16, Mila Vlaskovska17, André Scheen18. 1. National Research Council, Neuroscience Institute, Aging Branch, Padova, Italy. Electronic address: ilmannato@gmail.com. 2. MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK; NIHR Musculoskeletal Biomedical Research Unit, University of Oxford, Oxford, UK; WHO Collaborating Centre for Public Health Aspects of Musculoskeletal Health and Aging, Liège, Belgium. 3. WHO Collaborating Centre for Public Health Aspects of Musculoskeletal Health and Aging, Liège, Belgium; Department of Public Health, Epidemiology and Health Economics, University of Liège, CHU Sart Tilman B23, 4000 Liège, Belgium; Chair for Biomarkers of Chronic Diseases, Biochemistry Department, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia. 4. Division of Rheumatology & Clinical Immunology, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Geriatric Research, Education and Clinical Center, Baltimore, MD, USA; Medical Care Clinical Center, VA Maryland Health Care System, Baltimore, MD, USA. 5. CEDOC, NOVA Medical School, Universidade Nova de Lisboa, Department of Rheumatology, CHLO, Hospital Egas Moniz, Lisbon, Portugal. 6. WHO Collaborating Centre for Public Health Aspects of Musculoskeletal Health and Aging, Liège, Belgium; Department of Public Health, Epidemiology and Health Economics, University of Liège, CHU Sart Tilman B23, 4000 Liège, Belgium. 7. INSERM UMR 1033, Université de Lyon, Hôpital E Herriot, 69437 Lyon cedex 03, France. 8. Chair for Biomarkers of Chronic Diseases, Biochemistry Department, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia. 9. MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK. 10. Department of Rheumatology, Bone and Joint Research Unit, Fundación Jiménez Diaz, Universidad Autonoma, Madrid, Spain. 11. Department of Physical & Rehabilitation Medicine and Sports Traumatology, SportS(2), FIFA Medical Centre of Excellence, University and University Hospital of Liège, 4000 Liège, Belgium. 12. Rheumatology Department, AP-HP, Saint-Antoine Hospital, 4 Blvd. Beaumarchais, 75011 Paris, France. 13. WHO Collaborating Centre for Public Health Aspects of Musculoskeletal Health and Aging, Liège, Belgium; Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva, Switzerland. 14. Max-Reger-Strasse 17-19, 45128 Essen-Suedviertel, Germany. 15. School of Medicine and Surgery, University of Milano - Bicocca, Milan, Italy; Department of Clinical Research, Rottapharm Biotech, Monza, Italy. 16. Division of Musculoskeletal, Internal Medicine and Oncological Rehabilitation, Department of Orthopaedics and Traumatology, Hôpital du Valais (HVS), Centre Hospitalier du Valais Romand (CHVR), CVP, Crans-Montana, Switzerland. 17. Medical University Sofia, Medical Faculty, Department of Pharmacology, 2, Zdrave str., 1431 Sofia, Bulgaria. 18. Division of Diabetes, Nutrition and Metabolic Disorders and Clinical Pharmacology Unit, Department of Medicine, University of Liège, CHU Liège, Sart Tilman B35, B-4000 Liège, Belgium.
Abstract
OBJECTIVES: Type 2 diabetes mellitus (T2DM) and osteoarthritis (OA) are common diseases that frequently co-exist, along with overweight/obesity. While the mechanical impact of excess body weight on joints may explain lower limb OA, we sought to explore whether T2DM is linked to OA outside of excess weight and whether T2DM may play a role in OA pathophysiology. The consequence of T2DM on OA outcomes is a question of research interest. METHODS: We conducted a critical review of the literature to explore the association between T2DM and OA, whether any association is site-specific for OA, and whether the presence of T2DM impacts on OA outcomes. We also reviewed the literature to assess the safety of anti-OA treatments in patients with T2DM. RESULTS: T2DM has a pathogenic effect on OA through 2 major pathways involving oxidative stress and low-grade chronic inflammation resulting from chronic hyperglycemia and insulin resistance. T2DM is a risk factor for OA progression and has a negative impact on arthroplasty outcomes. Evidence is mounting for safety concerns with some of the most frequently prescribed anti-OA medications, including paracetamol, non-steroidal anti-inflammatory drugs, and corticosteroid injections, while other anti-OA medications may be safely prescribed in OA patients with T2DM, such as glucosamine and intra-articular hyaluronic acid. CONCLUSIONS: Future research is needed to better understand whether diabetes control and prevention can modulate OA occurrence and progression. The selection of therapy to treat OA symptoms in patients with T2DM may require careful consideration of the evidence based to avoid untoward safety issues.
OBJECTIVES:Type 2 diabetes mellitus (T2DM) and osteoarthritis (OA) are common diseases that frequently co-exist, along with overweight/obesity. While the mechanical impact of excess body weight on joints may explain lower limb OA, we sought to explore whether T2DM is linked to OA outside of excess weight and whether T2DM may play a role in OA pathophysiology. The consequence of T2DM on OA outcomes is a question of research interest. METHODS: We conducted a critical review of the literature to explore the association between T2DM and OA, whether any association is site-specific for OA, and whether the presence of T2DM impacts on OA outcomes. We also reviewed the literature to assess the safety of anti-OA treatments in patients with T2DM. RESULTS:T2DM has a pathogenic effect on OA through 2 major pathways involving oxidative stress and low-grade chronic inflammation resulting from chronic hyperglycemia and insulin resistance. T2DM is a risk factor for OA progression and has a negative impact on arthroplasty outcomes. Evidence is mounting for safety concerns with some of the most frequently prescribed anti-OA medications, including paracetamol, non-steroidal anti-inflammatory drugs, and corticosteroid injections, while other anti-OA medications may be safely prescribed in OApatients with T2DM, such as glucosamine and intra-articular hyaluronic acid. CONCLUSIONS: Future research is needed to better understand whether diabetes control and prevention can modulate OA occurrence and progression. The selection of therapy to treat OA symptoms in patients with T2DM may require careful consideration of the evidence based to avoid untoward safety issues.
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