Abstract

Osteoarthritis (OA) is one of the most prevalent degenerative joint diseases, which results in the inevitable destruction of joints leading to pain and joint immobility. Some studies have reported a potential link between diabetes mellitus (DM) and the worsening symptoms and severity of OA. Based on our literature review, the microcellular environment of patients with DM showed accelerated joint destruction and increased inflammation in every anatomical aspect of the joint including the bones, tendons, ligaments, cartilage, and synovium. Additionally, the biomechanical and biochemical properties of these tissues were more severely impacted in patients with DM and OA compared to those without DM, suggesting that DM plays an important role in the pathogenesis of OA. Specifically, we found that advanced glycation end products (AGEs) are the key to inducing the acceleration of joint destruction; however, their role in the pathogenesis has yet to be fully mapped out. In this narrative review, we aim to explore the role that DM plays in the acceleration of OA leading to increased reports of joint pain in those with both diseases. We believe this topic of discussion to be important due to the increased prevalence of both diseases over the last several decades, potentially leading to an increased medical burden on both patients and the community at large.

Highlights

  • BackgroundOsteoarthritis (OA) is one of the most prevalent joint disorders, and it leads to diarthrodial articular cartilage deterioration with eventual disability in adults [1,2]

  • The biomechanical and biochemical properties of these tissues were more severely impacted in patients with diabetes mellitus (DM) and OA compared to those without DM, suggesting that DM plays an important role in the pathogenesis of OA

  • Based on the literature review, we report on DM influencing the musculoskeletal system, the bones, tendons, ligaments, and cartilage of joints most frequently affected in OA

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Summary

Introduction

BackgroundOsteoarthritis (OA) is one of the most prevalent joint disorders, and it leads to diarthrodial articular cartilage deterioration with eventual disability in adults [1,2]. Recent studies have suggested phenotypically subcategorizing OA to better understand the pathogenesis and causes related to OA. These subtypes entail age-related, post-traumatic event-related, and metabolic syndrome-related categories [1]. By breaking OA down into categories, we can further evaluate how other preexisting conditions and differences in lifestyle can affect the progression of OA. This issue is especially relevant given the rise in the prevalence of metabolic syndrome-related OA [1]. Even hyperglycemia alone was reported to be associated with a separate mechanism on the pathogenesis and advancement of OA through the accumulation of advanced glycation end products (AGEs), oxidative stress, and dysregulation of articular cartilage metabolism [1,2]

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