Occurrence of tendon pathologies in metabolic disorders (original) (raw)
Related papers
Metabolic Influences on Risk for Tendon Disorders
Advances in Experimental Medicine and Biology, 2016
Advances in Experimental Medicine and Biology presents multidisciplinary and dynamic findings in the broad fields of experimental medicine and biology. The wide variety in topics it presents offers readers multiple perspectives on a variety of disciplines including neuroscience, microbiology, immunology, biochemistry, biomedical engineering and cancer research. Advances in Experimental Medicine and Biology has been publishing exceptional works in the field for over 30 years and is indexed in Medline, Scopus, EMBASE, BIOSIS, Biological Abstracts, CSA, Biological Sciences and Living Resources (ASFA-1), and Biological Sciences. The series also provides scientists with up to date information on emerging topics and techniques.
Hyperglycemia and Degenerative Tendinopathy: A Role for Diet in Tendon Health
Tendinopathies are a common source of pain, poor mobility and decreased performance. The cause of tendinopathy is multi-factorial and systemic inputs play an underappreciated role. Metabolic syndrome is a growing problem in the developed world and usually involves varying degrees of insulin resistance and central obesity. Chronic hyperglycemia and central obesity are independent risk factors for degenerative tendon disease and the underlying mechanisms involve an accelerated accumulation of advanced glycation end-products (AGE’s), collagen cross-linking, oxidative damage, and aberrant remodeling of the extracellular matrix. Consuming a diet that results in consistently optimal blood glucose levels and improvements in body composition may improve tendon health in the general population. Lifestyle interventions for preventing and treating tendinopathies should be considered given that evidence based treatment options are limited.
Lipids, adiposity and tendinopathy: is there a mechanistic link? Critical review
British journal of sports medicine, 2014
Being overweight or obese is associated with an elevated risk of tendon pathology. However, for sportspeople the epidemiological data linking weight or adiposity on one hand, and risk of tendon pathology on the other, are less consistent. Indeed, the mechanistic links between diet, adiposity and tendon pathology remain largely unexamined. Recent studies have begun to examine the effects of dietary interventions on outcomes such as tendon biomechanics or pain. Oxidised low-density lipoprotein has been shown to (A) accumulate in the tendon tissues of mice that eat a fatty diet and (B) induce a pathological phenotype in human tendon cells. This paper addresses the current debate: is excessive body mass index (causing increased load and strain on tendon tissue) per se the underlying mechanism? Or do local or systemic influences of fat on tendons predispose to tendon pathology? This narrative review argues that excessive blood lipids may be an important avenue for clinical investigations.
Insulin Resistance and Tendinopathy
Critical Reviews in Physical and Rehabilitation Medicine, 2015
Tendinopathy is most prevalent among males suffering from insulin resistance secondary to metabolic syndrome and type II diabetes mellitus. The mechanistic relationship between insulin resistance and the development of tendinopathy is not fully understood. Tendon tissue changes associated with insulin resistance include disruption of collagen crosslinking, alterations in proteoglycan synthesis, and the presence of advanced glycosylation end products. In this review we focus on the epidemiology of tendinopathy among insulin resistant populations and the potential mechanisms underlying tendon degeneration related to insulin resistance and related diseases.
ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo), 2016
Introduction: Tendinopathies and tendon tears account for over 30% of all musculoskeletal consultations. Obesity, which is becoming one of the world´s most prevalent public health issues, may be associated with this condition. Objective: To review the literature about tendinopathies and obesity association. Methods: This is a descriptive exploratory study using the portal Medline. Literature in English language from 2006 to 2014 were reviewed. Results: The pathogenesis of tendinopathies includes inflammatory, regenerative and degenerative processes that happen simultaneously from early to late phases of the disease. Mechanical stress upon tendons seems to be one of the most important factors to initiate the inflammatory response, but it´s not the only one that can deflagrate it: there are other extrinsic, genetic and metabolic factors that may be involved. Therefore, tendinopathies in obese patients can be due to tendon overload because of the excess of weight, but also because of i...
Disability & Rehabilitation, 2008
Purpose. Tendon injuries (tendinopathy) are prevalent across the population, affecting active and inactive individuals and manual workers. The aetiology of tendinopathy is not known. However, extrinsic factors such as load are known to affect the prevalence. More recently, intrinsic factors have been shown to also affect tendons; genes, biomechanics, and strength have been shown to influence tendon disease. One intrinsic factor that appears to have an association with tendinopathy is body composition; more specifically central adiposity. Several studies have reported this association, and several studies have found the association when reporting other aspects of tendinopathy. Method. This paper will detail what is known about the association between tendinopathy and body composition, examine the strength of the association by evaluating studies in the area and speculate on potential mechanisms for the association. Results. The association between tendon health and adiposity, especially central adiposity, warrants further investigation. Conclusion. There may be an interaction between adiposity and tendon pathology. Adiposity may be a key intrinsic risk factor that is translated into tendon disease in the presence of additional intrinsic (e.g., diabetes) and extrinsic factors (e.g., load).
Cumulative effects of hypercholesterolemia on tendon biomechanics in a mouse model
Journal of Orthopaedic Research, 2011
High cholesterol represents a significant healthcare problem. Clinical studies have linked hypercholesterolemia to Achilles tendon xanthomas and rotator cuff tears, and research in other systems indicates detrimental effects of high cholesterol; however, understanding of its impact on tendon properties and healing is limited. We hypothesized that tendons from aging hypercholesterolemic (APOE) mice would exhibit inferior baseline and healing mechanical properties compared to controls, while younger, but mature mice would be no different. Surprisingly, tensile testing of patellar tendons from 14-week-old APOE mice receiving a unilateral full-thickness central defect resulted in normalized (injured:sham) cross-sectional areas closer to baseline (p ¼ 0.02) compared to controls. Uninjured data from 10month-old APOE mice showed a decrease in elastic modulus (p ¼ 0.02), indicating a detrimental effect of hypercholesterolemia on tendon properties in this model. These results could benefit patients through knowledge that high cholesterol could increase the likelihood of tendon tears. Furthermore, knowledge that tendon tears are indicative of high cholesterol could provide orthopedic clinicians with an additional preventive treatment opportunity for patients with undiagnosed hypercholesterolemia. ß
Journal of Applied Physiology, 2014
Eriksen C, Svensson RB, Scheijen J, Hag AM, Schalkwijk C, Praet SF, Schjerling P, Kjaer M, Magnusson SP, Couppé C. Systemic stiffening of mouse tail tendon is related to dietary advanced glycation end products but not high-fat diet or cholesterol. Tendon pathology is related to metabolic disease and mechanical overloading, but the effect of metabolic disease on tendon mechanics is unknown. This study investigated the effect of diet and apolipoprotein E deficiency (ApoE Ϫ/Ϫ ) on mechanical properties and advanced glycation end product (AGE) cross-linking of non-weight-bearing mouse tail tendons. Twenty ApoE Ϫ/Ϫ male mice were used as a model for hypercholesterolemia along with 26 wild-type (WT) mice. One-half of the mice from each group was fed a normal diet (ND) and the other half was fed a high-fat diet (HFD) to induce obesity. All were killed at 40 wk, and tail tendon fascicles were mechanically tested to failure and analyzed for AGEs. Diets were also analyzed for AGEs. ApoE Ϫ/Ϫ mice displayed a 14% increase in plateau modulus compared with WT mice (P Ͻ 0.05), whereas HFD mice displayed a 13% decrease in plateau modulus (P Ͻ 0.05) and a 12% decrease in total modulus (P Ͻ 0.05) compared with ND mice. Tail tendons of HFD mice had significantly lower concentrations of AGEs [carboxymethyllysine (CML): 26%, P Ͻ 0.0001; methylglyoxal-derived hydroimidazolone 1 (MG-H1): 15%, P Ͻ 0.005; pentosidine: 13%, P Ͻ 0.0005]. The HFD had ϳ44-fold lower content of CML (P Ͻ 0.01), ϳ29-fold lower content of carboxyethyllysine (P Ͻ 0.005), and ϳ16-fold lower content of MG-H1 (P Ͻ 0.05) compared with ND. ApoE Ϫ/Ϫ increased, whereas HFD decreased mouse tail tendon stiffness. Dietary AGE content may be a crucial determinant for accumulation of AGE cross-links in tendons and for tissue compliance. The results demonstrate how systemic metabolic factors may influence tendon health. advanced glycation end products; tendon biomechanics; cholesterol
Electron microscopic investigation of the effects of diabetes mellitus on the Achilles tendon
The Journal of Foot and Ankle Surgery, 1997
Fine structural changes in the Achilles tendons of patients with long-term diabetes mellitus were investigated. All patients had clinical and electrophysiological evidence of diabetic neuropathy and had ulceration and/or Charcot neuroarthropathy. Several differences between tendons of diabetic (n = 12) and nondiabetic (n = 5) individuals were observed by electron microscopy. In diabetics, these differences included increased packing density of collagen fibrils, decreases in fibrillar diameter, and abnormal fibril morphology. In one diabetic patient, individual collagen fibrils were tightly apposed so that many areas of tendon appeared as a single mass of closely adhering fibrillae. In addition, foci in which collagen fibrils appeared twisted, curved, overlapping and otherwise highly disorganized were common in specimens from most patients (11 of 12). These morphologic abnormalities in the Achilles tendons of diabetics appear to reflect a poorly known process of structural reorganization that may be the result of nonenzymatic glycation expressed over many years. Such structural changes could contribute to the tightening of the Achilles tendor a phenomenon consistent with clinical observations of extreme shortening of the Achilles tendon-gastrocnemius-soleus complex common in advanced diabetic neuropaths. In patients with diabetic neuropathy, tendon shortening causes severe equinus that may precipitate serious ulceration, stress fractures, and Charcot collapse of the foot. However, in nondiabetics, the fine structure of the Achilles tendon appears normal, consistent with the finding that the ultrastructural changes result from diabetes rather than neuropathy.