The impact of type 2 diabetes on the development of tendinopathy

Abstract

Tendinopathy is a chronic and often painful condition affecting both professional athletes and sedentary subjects. It is a multi‐etiological disorder caused by the interplay among overload, ageing, smoking, obesity (OB) and type 2 diabetes (T2D). Several studies have identified a strong association between tendinopathy and T2D, with increased risk of tendon pain, rupture and worse outcomes after tendon repair in patients with T2D. Moreover, consequent immobilization due to tendon disorder has a strong impact on diabetes management by reducing physical activity and worsening the quality of life. Multiple investigations have been performed to analyse the causal role of the individual metabolic factors occurring in T2D on the development of tendinopathy. Chronic hyperglycaemia, advanced glycation end‐products, OB and insulin resistance have been shown to contribute to the development of diabetic tendinopathy. This review aims to explore the relationship between tendinopathy and T2D, in order to define the contribution of metabolic factors involved in the degenerative process and to discuss possible strategies for the clinical management of diabetic tendinopathy.

Irisin inhibits tenocyte response to inflammation in vitro: New insights into tendon‐muscle cross‐talk

“…Tendinopathy is a chronic disorder characterized by pain and loss of function with a significant burden on daily activities and tolerance to physical exercise (PE) in both athletic and sedentary populations 1 . The development of tendinopathy has been traditionally imputed to tendon overuse and overload, but may also occur in association with other risk factors including sex, aging, obesity, type 2 diabetes, smoking, etc 2 . From a pathophysiological perspective, tendinopathy is characterized by the progressive accumulation of extracellular matrix (ECM) damage along with increased release of proinflammatory cytokines (e.g., interleukin [IL]‐1β, IL‐17, tumor necrosis factor‐α [TNF‐α], interferon γ), chemokines (e.g., C‐C Motif Chemokine Ligand [CCL]−2 and 13), and matrix‐degrading enzymes (e.g., matrix metalloproteinases) 3 .…”

“…1 The development of tendinopathy has been traditionally imputed to tendon overuse and overload, but may also occur in association with other risk factors including sex, aging, obesity, type 2 diabetes, smoking, etc. 2 From a pathophysiological perspective, tendinopathy is characterized by the progressive accumulation of extracellular matrix (ECM) damage along with increased release of proinflammatory cytokines (e.g., interleukin [IL]-1β, IL-17, tumor necrosis factor-α [TNF-α], interferon γ), chemokines (e.g., C-C Motif Chemokine Ligand…”

Why Use Adipose-Derived Mesenchymal Stem Cells in Tendinopathic Patients: A Systematic Review

“…Among them, tendon overload in sports or in specific work activities has been reported to be a crucial factor promoting 2 of 14 tendinopathies [11,12]. Similarly, some metabolic and hormonal imbalances, including diabetes, thyroid hormones, estrogens, testosterone, growth hormone, cortisol, cholesterol and glutamatergic changes, occur [13][14][15][16][17][18][19]. Inflammation also seems to play a critical role in tendon degeneration [6].…”

Effect of Diabetes on Tendon Structure and Function: Not Limited to Collagen Crosslinking

“…The effect of DM on tendons is evidenced by an increased incidence of tendon disorders and a higher prevalence of tendinopathy in patients with DM compared to their age-and sex-matched peers without DM. 9,10 The etiology of Achilles tendon dysfunction includes a spectrum of pathologic changes associated with an overuse injury, training errors, inflammatory disorders, and intrinsic disease or degeneration. Tendon disorders in DM are characterized by impaired tendon structure, function, and healing capacity that lead to tendon-limited joint range of motion and three times higher risk of tendon injury relative to individuals without DM.…”