Type 2 diabetes mellitus and osteoarthritis
- PMID: 30712918
- PMCID: PMC6642878
- DOI: 10.1016/j.semarthrit.2019.01.005
Type 2 diabetes mellitus and osteoarthritis
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.
Keywords: Obesity; Osteoarthritis; Pathophysiology; Safety; Type 2 diabetes mellitus.
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
O. Bruyere reports grants from Biophytis, IBSA, MEDA, Servier, SMB, and Theramex, outside of the submitted work.
C. Cooper reports personal fees from Alliance for Better Bone Health, Amgen, Eli Lilly, GSK, Medtronic, Merck, Novartis, Pfizer, Roche, Servier, Takeda and UCB, outside of the submitted work.
R. Rizzoli reports personal fees for lecture or advisory boards from Radius Health, Labatec, Nestlé and Danone, outside of the submitted work.
A. J. Scheen declares no conflict of interest with the content of this paper. He has received lecturer/scientific advisor/clinical investigator fees from AstraZeneca, Boehringer Ingelheim, Eli Lilly, Janssen, Merck Sharp & Dohme, Novartis, NovoNordisk, Sanofi and Servier.
J. Branco declares no conflict of interest with the content of this paper. He has received scientific advisor and/or speaker and/or clinical investigator fees from AstraZeneca, BIAL, Biogen, Eli Lilly, Novartis and Pfizer.
L.C. Rovati is a former employee of Rottapharm, the company that developed and commercialized prescription crystalline glucosamine sulfate, now commercialized by Mylan. He is currently Chief Scientific Officer of Rottapharm Biotech, which has no commercial interests in glucosamine or any other drugs for OA discussed here.
E. Dennison reports personal fees for lectures or advisory boards from UCB and Pfizer, outside of the submitted work.
J.F. Kaux reports a grant from Eli Lilly, outside of the submitted work.
E. Maheu reports personal fees from Expanscience, FIDIA, IBSA - GENEVRIER, LCA (France), TRB Chemedica, Rottapharm - Meda, outside of the submitted work.
N. Al-Daghri, J-Y. Reginster, G. Herrero-Beaumont, D. Uebelhart, N. Veronese, M. Hochberg, R. Roth, R. Chapurlat, and M. Vlaskovska report nothing to disclose.
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