Lipids, adiposity and tendinopathy: is there a mechanistic link?

NewsBot · Dec 9, 2014

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Lipids, adiposity and tendinopathy: is there a mechanistic link? Critical review
Alex Scott, Johannes Zwerver, Navi Grewal, Agnetha de Sa, Thuraya Alktebi, David J Granville, David A Hart
Br J Sports Med doi:10.1136/bjsports-2014-093989

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.
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Admin2 · Dec 9, 2014

Related Thread:
Statins and tendon complications

NewsBot · Oct 16, 2015

Is higher serum cholesterol associated with altered tendon structure or tendon pain? A systematic review
Benjamin J Tilley, Jill L Cook, Sean I Docking, James E Gaida
Br J Sports Med doi:10.1136/bjsports-2015-095100

Background Tendon pain occurs in individuals with extreme cholesterol levels (familial hypercholesterolaemia). It is unclear whether the association with tendon pain is strong with less extreme elevations of cholesterol.

Objective To determine whether lipid levels are associated with abnormal tendon structure or the presence of tendon pain.

Methods We conducted a systematic review and meta-analysis. Relevant articles were found through an electronic search of 6 medical databases—MEDLINE, Cochrane, AMED, EMBASE, Web of Science and Scopus. We included all case–control or cross-sectional studies with data describing (1) lipid levels or use of lipid-lowering drugs and (2) tendon structure or tendon pain.

Results 17 studies (2612 participants) were eligible for inclusion in the review. People with altered tendon structure or tendon pain had significantly higher total cholesterol, low-density lipoprotein cholesterol and triglycerides, as well as lower high-density lipoprotein cholesterol; with mean difference values of 0.66, 1.00, 0.33, and −0.19 mmol/L, respectively.

Conclusions The results of this review indicate that a relationship exists between an individual’s lipid profile and tendon health. However, further longitudinal studies are required to determine whether a cause and effect relationship exists between tendon structure and lipid levels. This could lead to advancement in the understanding of the pathoaetiology and thus treatment of tendinopathy.
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NewsBot · Dec 11, 2015

Bad for your heart = bad for your tendons, potential for early detection of high cholesterol?

NewsBot · Jul 15, 2016

Influence of Hyperlipidemia on the Treatment of Supraspinatus Tendinopathy With or Without Tear
Jae-Min Kim, MD, Min-Wook Kim, MD, PhD and Hyun-Jung Do, MD
Ann Rehabil Med. 2016 Jun;40(3):463-469

Objective
To investigate the influence of hyperlipidemia on the treatment of supraspinatus tendinopathy, with or without tear.

Methods
We retrospectively reviewed the data of patients with shoulder pain and patients with supraspinatus tendinopathy, with or without tear, were included in the study. Exclusion criteria were prior shoulder surgery, prior steroid injection, neurological diseases that could lead to shoulder pain, and use of lipid-lowering medication. According to the serum lipid profiles, patients were assigned to either the hyperlipidemia or non-hyperlipidemia group. By analyzing the numeric rating scale (NRS) before treatment, and at 2 weeks and 8 weeks after treatment, we compared the difference in treatment effect between the two groups.

Results
No significant baseline difference was found among the two groups for age, gender, body mass index, duration of pain, side of pain, range of motion of affected shoulder, or physical examination. On the repeated-measures analysis of variance, NRS scores significantly decreased with time for both groups (p<0.001). When analyzing the effect of time between the subjects factor, there was significant difference in the treatment effect between the two groups (p<0.001), namely NRS was less decreased in the hyperlipidemia group.

Conclusion
We found that hyperlipidemia may be an adversely affecting factor in the treatment of supraspinatus tendinopathy with or without tear.
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NewsBot · Dec 6, 2016

How lipids hurt tendons: Current understanding
Manit Arora, Esha Aror
Journal of Arthroscopy and Joint Surgery; 29 November 2016

Hyperlipidemia has profound effects on tendon substance and mechanical properties. The common misconception is that hyperlipidemia manifests only as tendon xanthomas. Fatty streaks and signal changes are much more common than xanthomas, which may be considered as the end product of organized hyperlipidemic changes. The composition of xanthomas and the cause of lipid-mediated damage to tendons are discussed.
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NewsBot · Apr 11, 2017

old review:

Is adiposity an under-recognized risk factor for tendinopathy? A systematic review.
Gaida JE, Ashe MC, Bass SL, Cook JL.
Arthritis Rheum. 2009 Jun 15;61(6):840-9. doi: 10.1002/art.24518.

OBJECTIVE:
Tendon injuries have been reported to occur more frequently in individuals with increased adiposity. Treatment also appears to have poorer outcomes among these individuals. Our objective was to examine the extent and consistency of associations between adiposity and tendinopathy.
METHODS:
A systematic review of observational studies was conducted. Eight electronic databases were searched (Allied and Complementary Medicine, Biological Abstracts, CINAHL, Current Contents, EMBase, Medline, SPORTDiscus, and Web of Science) and citation tracking was performed on included reports. Studies were included if they compared adiposity between subjects with and without tendon injury or examined adiposity as a predictor of conservative treatment success.
RESULTS:
Four longitudinal cohorts, 14 cross-sectional studies, 8 case-control studies, and 2 interventional studies (28 in total) met the inclusion criteria, providing a total of 19,949 individuals. Forty-two subpopulations were identified, 18 of which showed elevated adiposity to be associated with tendon injury (43%). Sensitivity analyses indicated a clustering of positive findings among studies that included clinical patients (81% positive) and among case-control studies (77% positive).
CONCLUSION:
Elevated adiposity is frequently associated with tendon injury. Published reports suggest that elevated adiposity is a risk factor for tendon injury, although this association appears to vary depending on aspects of study design and measurement. Adiposity is of particular interest in tendon research because, unlike a number of other reported risk factors for tendon injury, it is somewhat preventable and modifiable. Further research is required to determine if reducing adiposity will reduce the risk of tendon injury or improve the results of treatment.
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NewsBot · Aug 12, 2018

Tendon pathology in hypercholesterolaemia patients: Epidemiology, pathogenesis and management
YangYangaHongbinLubJinQub
Journal of Orthopaedic Translation; 6 August 2018

Tendon pathology is a general term used to describe a group of musculoskeletal conditions related to tendons and surrounding structures. There is only limited evidence available regarding the exact aetiology and natural history of tendon pathology. In hypercholesterolaemia environments, lipids could accumulate within the extracellular matrix of the tendon and thus affect the mechanical properties of the tendon. Current evidence suggested that hypercholesterolaemia was an important risk factor in the development and progression of tendon pathology. The severity of hypercholesterolaemia was correlated with the severity of tendon pathology.

The translational potential of this article: Hypercholesterolaemia lead to the structural, inflammatory and mechanical changes in tendons, which predispose hypercholesterolaemia patients to a greater risk of tendon pathology. Measurements of serum cholesterol are suggested to be performed in patients presenting with tendon pathology. The strict control of hypercholesterolaemia would mitigate the development and progression of tendon pathology.
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NewsBot · Apr 7, 2020

High cholesterol induces apoptosis and autophagy through the ROS-activated AKT/FOXO1 pathway in tendon-derived stem cells
Kaiqun Li, Ye Deng, Ganming Deng, Pengyu Chen, Yutian Wang, Hangtian Wu, Zhiguo Ji, Zilong Yao, Xianrong Zhang, Bin Yu & Kairui Zhang
Stem Cell Research & Therapy volume 11, Article number: 131 (2020)

Background
Hypercholesterolemia increases the risk of tendon pain and tendon rupture. Tendon-derived stem cells (TDSCs) play a vital role in the development of tendinopathy. Our previous research found that high cholesterol inhibits tendon-related gene expression in TDSCs. Whether high cholesterol has other biological effects on TDSCs remains unknown.

Methods
TDSCs isolated from female SD rats were exposed to 10 mg/dL cholesterol for 24 h. Then, cell apoptosis was assessed using flow cytometry and fluorescence microscope. RFP-GFP-LC3 adenovirus transfection was used for measuring autophagy. Signaling transduction was measured by immunofluorescence and immunoblotting. In addition, Achilles tendons from ApoE −/− mice fed with a high-fat diet were histologically assessed using HE staining and immunohistochemistry.

Results
In this work, we verified that 10 mg/dL cholesterol suppressed cell proliferation and migration and induced G0/G1 phase arrest. Additionally, cholesterol induced apoptosis and autophagy simultaneously in TDSCs. Apoptosis induction was related to increased expression of cleaved caspase-3 and BAX and decreased expression of Bcl-xL. The occurrence of autophagic flux and accumulation of LC3-II demonstrated the induction of autophagy by cholesterol. Compared with the effects of cholesterol treatment alone, the autophagy inhibitor 3-methyladenine (3-MA) enhanced apoptosis, while the apoptosis inhibitor Z-VAD-FMK diminished cholesterol-induced autophagy. Moreover, cholesterol triggered reactive oxygen species (ROS) generation and activated the AKT/FOXO1 pathway, while the ROS scavenger NAC blocked cholesterol-induced activation of the AKT/FOXO1 pathway. NAC and the FOXO1 inhibitor AS1842856 rescued the apoptosis and autophagy induced by cholesterol. Finally, high cholesterol elevated the expression of cleaved caspase-3, Bax, LC3-II, and FOXO1 in vivo.

Conclusion
The present study indicated that high cholesterol induced apoptosis and autophagy through ROS-activated AKT/FOXO1 signaling in TDSCs, providing new insights into the mechanism of hypercholesterolemia-induced tendinopathy.
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NewsBot · Dec 24, 2021

Evaluation of Therapeutic Effects of Quercetin Against Achilles Tendinopathy in Rats via Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Metalloproteinases
Halil Sezgin Semis, MD, Cihan Gur, PhD, Mustafa Ileriturk, PhD, ...
The American Journal of Sports Medicine December 15, 2021

Background:
Achilles tendinopathy, seen in athletes and manual labor workers, is an inflammatory condition characterized by chronic tendon pain. Owing to the toxicity that develops in various organs attributed to the use of anti–inflammatory drugs, there is a need for new therapeutic agents.

Purpose:
In the present study, the effects of quercetin (Que), the one that attracted the most attention of researchers studying this group of flavonoids, were investigated against collagenase–induced tendinopathy.

Study Design:
Controlled laboratory study.

Methods:
A total of 35 Sprague-Dawley rats were used in the study. Tendinopathy was created by injecting a single dose of collagenase (10 μL; 10 mg/mL) into the tendons of rats. Thirty minutes after the injection, Que was administered at doses of 25 or 50 mg/kg. Que administration was carried out for 7 days. Animals underwent a motility test at the end of the study. In addition, markers of oxidative stress, inflammation, apoptosis, and autophagy, as well as the expression levels of matrix metalloproteinases (MMPs 2, 3, 9, and 13), ICAM-1, and STAT3, were measured in tendon tissues with biochemical, molecular, and Western blot techniques.

Results:
The results showed that oxidative stress, inflammation, apoptosis, and autophagy were triggered by the injection of collagenase. In addition, MMPs, ICAM-1, and STAT3 were activated to participate in the development of tendinopathy. Que was found to reduce ICAM-1 levels in tendon tissue. Moreover, Que showed antioxidant, anti–inflammatory, antiapoptotic, and antiautophagic effects on tendons against tendinopathy. More important, Que suppressed the expression of MMPs in the tendon tissues.

Conclusion:
Que has protective properties against collagenase–induced tendon damage in rats.

Clinical Relevance:
We believe that with further study, Que may be shown to be an alternative treatment option for athletes or others who experience tendon injuries
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