Diabetes: a silent player in musculoskeletal interventional radiology response

Abstract

Diabetes has an important role in the development of several musculoskeletal disorders, such as adhesive capsulitis of the shoulder (ACs) and stenosing flexor tenosynovitis of the finger (SfTf). The etiopathophysiology of ACs and SfTf in diabetic patients is associated with both chronic hyperglycemia, increased amounts of visceral adiposity and chronic inflammation. Chronic hyperglycemia stimulates the creation of cross-links between collagen molecules, impairing degradation and resulting in the build-up of excessive collagen deposits in the cartilage, ligaments, tendon sheaths and tendons. Increased adipocytes in diabetic patients secrete proteins and cytocines such as TNF-α, IL-6 and IL-13 which result in overproduction of pro-inflammatory factors, destruction of normal tissue architecture and fibrosis. Both hyperglycemia and adipocytes inhibit efferocytosis, limiting natural resolution. Recently, multiple image-guided interventional radiology musculoskeletal treatment options have been developed, such as ultrasound-guided glenohumeral capsule hydrodistension for ACs and ultrasound-guided percutaneous pulley release for trigger finger. Diabetes can negatively influence outcomes in patients with ACs and SfTf and may impact the decision of which specific procedure technique should be employed. Further studies are necessary to define how diabetes influences response to interventional radiology treatments of these disorders, as well as the extent to which control of blood sugar levels can contribute towards the personalization and optimization of patient follow up.

Influence of diabetes on response to ultrasound guided hydrodistension treatment of adhesive capsulitis: a retrospective study

“…Several mechanisms may explain the association of AC with diabetes. Chronic hyperglycemia, increased visceral adiposity and chronic inflammation of diabetes may have central roles in this association [ 23 ]. Chronic hyperglycemia stimulates the development of cross-links between collagen molecules.…”

“…Due to these cross-links, the breakdown of collagen molecules is impaired, eventually accumulating in cartilage, ligaments, tendon sheaths and in the tendons. Patients with diabetes have an increase in visceral adipocytes, which secrete cytokines, such as tumor necrosis factor alpha (TNF-a) and interleukin-6 (IL-6), resulting in the overproduction of other pro-inflammatory cytokines [ 23 ]. This pro-inflammatory environment will exacerbate inflammation and insulin resistance.…”

“…This pro-inflammatory environment will exacerbate inflammation and insulin resistance. In turn, fatty acids secreted by adipocytes promote neutrophil survival and decrease the removal of apoptotic cells by phagocytic cells, increasing collagen deposition in the glenohumeral capsule, giving rise to a stiff and painful shoulder [ 23 ]. Finally, chronic inflammation results in excessive accumulation of collagen and other extracellular matrix components, with destruction of the normal tissue architecture in the joints.…”

“…Finally, chronic inflammation results in excessive accumulation of collagen and other extracellular matrix components, with destruction of the normal tissue architecture in the joints. Thus, these 3 factors perpetuate the disease [23][24][25][26][27].…”

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.…”