Occurrence of tendon pathologies in metabolic disorders

Abstract

This article reviews the pathogenetic role of metabolic disorders, which are of paramount relevance to the progression of tendon damage. In diabetes, the prevalence of rheumatological diseases is high, mainly because of the deleterious effects of advanced glycation end products that deteriorate the biological and mechanical functions of tendons and ligaments. In heterozygous familial hypercholesterolaemia, most patients develop Achilles xanthomatosis, a marker of high risk for cardiovascular disease caused by cholesterol deposition in the tendons. Tendon degeneration has also been observed in non-familial hypercholesterolaemia. Monosodium urate crystal deposition in soft tissues is a hallmark of chronic gouty arthritis. In this group of diseases, the mobilization of cholesterol and uric acid crystals is presumably followed by low-grade inflammation, which is responsible for tendon degeneration. Adiposity may contribute to tendon disorders via two different mechanisms: increased weight on the load-bearing tendons and systemic dysmetabolic factors that trigger subclinical persistent inflammation. Finally, tendon abnormalities have been observed in some rare congenital metabolism disorders such as alkaptonuria.

Histopathological study of the Achilles tendon after exposure to bisphenol-A and its subsequent treatment with platelet growth factors

“…this produced an anchoring area, which reduced their sliding movement, and also because the type III formed by the scarring lacked the capacity to organize itself into thick longitudinal fasciculi, and it was usually arranged as fibrous areas within the tendon, thus losing its traction ability. Normally, type III collagen fibres show a striated morphology, but when they are formed inside fibrous tissues they are abnormally synthesized and some atypical thickenings, known as microkeloids, are produced, and they turn into rupture-sensitive areas (aBate et al, 2013;rOCheSter, 2013). at present, there are no references regarding direct BPa action in the tendon, and very few related to its action in the muscle (MOrtaVazI et al, 2013;WaNg et al, 2013;GIMéNez et al, 2016).…”

Are There Biologic Factors of Good Prognosis after a Platelet Rich Plasma (PRP) Injection for Tendinopathies ?

“…This study presents, to the best of the authors' knowledge, the first attempt to correlate biomarkers as factors of good prognosis to the evolution of the recovery. Hyperglycemia and especially type II diabetes, leads to a disorganization of collagen fibers, and an increase in tendons thickness and volume [20] ; hyperthyroidism increases collagen catabolism and hypothyroidism leads to a decreased collagen metabolism [21]; hypercholesterolemia impairs the tendon extra cell matrix and thus alters its biomechanical properties [22] and finally, hyperucemia could cause an inflammation provoking the degeneration of the tendon tissue [23]. It might then be surprising that no correlation was found between the values of the biological markers and the evolution of the tendons healing evaluated by the VAS and the algometer.…”

Systematic review of biochemical biomarkers for neck and upper-extremity musculoskeletal disorders

“…First, lipids (xanthoma) may be deposited on tendons which may alter their biomechanical properties (43). Xanthoma may also initiate a low-grade inflammation in tendons, initiating chronic tendon degeneration (80,81). Lastly, lipids may alter the extracellular matrix and reduce circulation, both impairing tissue healing (43).…”