Diabetic Fasciopathy Linking Chronic Hyperglycemia and Advanced Glycation End Products to Musculoskeletal Dysfunction

Abstract

Diabetes-related injury to fascia had received less attention than vascular and neurological complications despite its potential contribution to musculoskeletal dysfunction. This narrative review examined the relationship between chronic hyperglycemia, advanced glycation end products (AGEs), fascial remodeling, and clinical impairment. A targeted literature search emphasized human imaging and tissue studies, mechanistic reviews, and clinical guidelines. Evidence was synthesized thematically, with established associations distinguished from proposed mechanisms. Human studies consistently reported increased plantar fascia thickness and associations with glycemic exposure, neuropathy, microvascular disease, and altered plantar loading. Direct tissue analysis demonstrated site-specific nanoscale stiffening, whereas some ultrasound elastography studies reported lower macroscopic stiffness. These differences suggested that anatomical location, measurement scale, and tissue organization influenced mechanical findings. AGE-related collagen modification, oxidative stress, inflammation, and extracellular matrix remodeling provided a plausible biological framework, but direct evidence for diabetes-specific impairment of hyaluronan-mediated gliding remained limited. No validated diagnostic criteria or fascia-specific treatment pathway were identified in the reviewed literature. The review supported diabetic fasciopathy as an emerging explanatory framework rather than an established independent diagnosis. Clinical implications favored comprehensive metabolic care, preservation of mobility, management of regional disorders, and guideline-directed diabetic foot protection. Prospective studies were needed to establish diagnostic thresholds, incremental prognostic value, and treatment responsiveness.