Does glucocorticoid exposure explain the association between metabolic dysfunction and tendinopathy?

Abstract

Background: While metabolic health is acknowledged to affect connective tis sue structure and function, the mechanisms are unclear. Glucocorticoids are present in almost every cell type throughout the body and control key physiological processes such as energy homeostasis, stress response, inflammatory and immune processes, and cardiovascular function. Glucocorticoid excess manifests as visceral adiposity, dyslipidemia, insulin resistance, and type 2 diabetes. As these metabolic states are also associated with tendinopathy and tendon rupture, it may be that glucocorticoids excess is the link between metabolic health and tendinopathy. Objective: To synthesise current knowledge linking glucocorticoid exposure to tendon structure and function. Methods: Narrative literature review. Results: We provide an overview of endogenous glucocorticoid production, regulation, and signalling. Next we review the impact that oral glucocorticoid has on risk of tendon rupture and the effect that injected glucocorticoid has on resol ution of symptoms. Then we highlight the clinical and mechanistic overlap between tendinopathy and glucocorticoid excess in the areas of visceral adiposity, dyslipidemia, insulin resistance and type 2 diabetes. In these areas, we highlight the role of glucocorticoids and how these hormones might underpin the connection between metabolic health and tendon dysfunction. Conclusions: There are several plausible pathways through which glucocorticoids might mediate the connection between metabolic health and tendinopathy.

Keywords

• tendinopathy
• glucocorticoids
• cortisol
• hypothalamic-pituitaryadrenal axis
• metabolic health
• type 2 diabetes mellitus
• visceral adipose tissue