Risk Factors For Tendinopathy Research Articles

Associations of normal fasting glucose levels and of insulin resistance with degenerative rotator cuff tear

BackgroundThe upper normoglycemic range has been proposed as a risk factor for degenerative rotator cuff tendon tear (RCT), and insulin resistance has been suggested as a risk factor for tendinopathy. However, no research has established their association with degenerative RCT in the general population. This study aimed to determine whether fasting glucose levels and insulin resistance are risk factors for degenerative RCT in the normoglycemic population and identify the risk range for fasting glucose.MethodsThis study included 418 normoglycemic participants from a rural cohort. Participants completed questionnaires, physical exams, blood tests, and MRI evaluations of both shoulders. Insulin resistance was assessed using a triglyceride/high-density-lipoprotein (TG/HDL) ≥ 3.5. Logistic regression analysis was used to determine the association between fasting glucose level, TG/HDL ≥ 3.5, and other factors and degenerative RCT. The study calculated the areas under the receiver operating characteristic curve (AUC) to determine the more appropriate predicting value between the scale and categorical values of fasting glucose levels, and compared the AUCs using the DeLong method.ResultsIn the multivariable analyses, both scale and categorical values of fasting glucose levels, and TG/HDL ≥ 3.5 were significantly associated with degenerative RCT. Fasting glucose levels ≥ 90.5 mg/dL (OR: 3.87, 95% CI: 2.10–7.06) in scale value and 90–99 mg/dL (OR: 4.13, 95% CI: 2.87–8.12) in categorical value were significantly associated with degenerative RCT (P < .001). The AUC of the scale value of fasting glucose levels ≥ 90.5 mg/dL was 0.68. The AUC of the categorical value of fasting glucose levels of 90–99 mg/dL was 0.70. Because of the significantly larger AUC of the categorical value of fasting glucose levels of 90–99 mg/dL, those fasting glucose levels were determined to be independently associated with degenerative RCT (P < .001).ConclusionsHigh fasting glucose levels within the normal range may link to increase insulin resistance and risk of degenerative RCT. Normoglycemic levels of 90–99 mg/dL and insulin resistance may be risk factors for degenerative RCT.Level of evidenceLevel III, prognostic study.

Longitudinal Evidence for High-Level Patellar Tendon Strain as a Risk Factor for Tendinopathy in Adolescent Athletes

BackgroundHigh tendon strain leads to sub-rupture fatigue damage and net-catabolic signaling upon repetitive loading. While high levels of tendon strain occur in adolescent athletes at risk for tendinopathy, a direct association has not yet been established. Therefore, in this prospective longitudinal study, we examined the hypothesis that adolescent athletes who develop patellar tendon pain have shown increased levels of strain in advance.MethodsIn 44 adolescent athletes (12–17 years old), patellar tendon mechanical properties were measured using ultrasonography and inverse dynamics at four time points during a season. Fourteen athletes developed clinically relevant tendon pain (SYM; i.e., reduction of the VISA-P score of at least 13 points), while 23 remained asymptomatic (ASYM; VISA-P score of > 87 points). Seven cases did not fall into one of these categories and were excluded. Tendon mechanical properties of SYM in the session before the development of symptoms were compared to a randomly selected session in ASYM.ResultsTendon strain was significantly higher in SYM compared to ASYM (p = 0.03). The risk ratio for developing symptoms was 2.3-fold higher in athletes with tendon strain ≥9% (p = 0.026). While there was no clear evidence for systematic differences of the force applied to the tendon or tendon stiffness between SYM and ASYM (p > 0.05), subgroup analysis indicated that tendon force increased prior to the development of symptoms only in SYM (p = 0.034).DiscussioThe study provides novel longitudinal evidence that high tendon strain could be an important risk factor for patellar tendinopathy in adolescent athletes. We suggest that inadequate adaptation of tendon stiffness to increases in muscle strength may occur if adolescent athletes are subject to mechanical loading which does not provide effective tendon stimulation.

Is there a critical stage during puberty when basketball players develop abnormal structure in their patellar tendon?

Introduction: Approximately 20% of physically active adolescents have an abnormal patellar tendon observed on greyscale ultrasound, a known risk factor for tendinopathy. Most tendon pathology develops over life, but patellar tendon pathology appears to affect adolescents. It is unclear at what stage of skeletal maturity tendon abnormalities develop. Tendinopathy impacts a player’s ability to participate in sport, is persistent and recurrent. Identifying a critical time when the patellar tendon is vulnerable to developing abnormality may aid injury prevention strategies.

The Effect of Age and Intrinsic Aerobic Exercise Capacity on the Expression of Inflammation and Remodeling Markers in Rat Achilles Tendons.

Old age, adiposity, and metabolic disorders are known as risk factors for chronic tendinopathy, which is a common problem in both athletes and the general population. However, the importance of these influencing factors has not yet been well understood. This study investigated alterations in gene expression and histology of Achilles tendons of young (10 weeks) and old (100 weeks) rats bred for low (low capacity runners, LCR) and high (high capacity runners, HCR) intrinsic aerobic exercise capacity. In this rat model, LCR displayed a phenotype of reduced exercise capacity, higher body weight, and metabolic dysfunctions compared to HCR. We hypothesized that the risk factors for tendinopathy in old LCR could lead to more pronounced impairments in Achilles tendon tissue. In quantitative real-time PCR (qPCR), age-related downregulation of tenocyte markers e.g., tenomodulin, genes related to matrix modeling and remodeling (e.g., collagens, elastin, biglycan, fibronectin, tenascin C) as well as transforming growth factor beta 3 (Tgfb3) have been detected. Inflammation marker cyclooxygenase 2 (Cox2) was downregulated in old rats, while microsomal prostaglandin E synthase 2 (Ptges2) was upregulated in old HCR and old LCR. In all groups, interleukin 6 (Il6), interleukin 1 beta (Il1b), and tumor necrosis factor alpha (Tnfa) showed no significant alteration. In histological evaluation, tendons of old rats had fewer and more elongated tenocyte nuclei than young rats. Even though a higher content of glycosaminoglycans, a sign of degeneration, was found in old HCR and LCR, no further signs of tendinopathy were detectable in tendons of old rats by histological evaluation. Low intrinsic aerobic exercise capacity and the associated phenotype did not show significant effects on gene expression and tendon histology. These findings indicate that aging seems to play a prominent role in molecular and structural alterations of Achilles tendon tissue and suggests that other risk factors associated with intrinsic aerobic exercise capacity are less influential in this rat model.

Lifestyle Factors as Risk Factors and Treatment Options in Tendinopathy

Physical therapists and other therapists often treat patients with tendinopathy, which is a condition that occurs frequently and has poor prognosis and long recovery time. Multiple lifestyle factors have found to be risk factors for tendinopathy. Lifestyle factors such as exercise and movement, nutrition, sleep and psychosocial factors are often interrelated and can create a vicious spiral for patients with tendinopathy. Unhealthy lifestyle factors can cause chronic pain, low-grade inflammation, elevated adiposity, higher waist-to-rib ratio, greater body mass index, overweight, obesity, high cholesterol, metabolic syndrome, diabetes type II, rheumatoid arthritis and inflammatory-related diseases, which are the main factors explaining the association between lifestyle factors and tendinopathy. Single or multiple lifestyle interventions are available for the treatment of patients with tendinopathy. Both exercise and movement and nutritional interventions tend to improve tendon health and recovery of tendinopathy indirectly by decreasing adiposity, weight, diabetic symptoms, low-grade inflammation and pain. They are also likely to improve blood levels, bone and muscle health, and collagen synthesis of tendons, tendon function and tendon-related pain. Sleep, psychological factors, smoking behaviour and alcohol use also affect tendon pain and tissue healing. Physical therapists and other therapists may incorporate interventions as part of the treatment of tendinopathy targeted at improving sleep and psychosocial factors. Smoking behaviour and alcohol use should be discouraged, for which multiple interventions are available. The purpose of this commentary article is to inform physical therapists and other therapists about lifestyle factors as risk factors and treatment options in tendinopathy.

Influence of genetic factors in elbow tendon pathology: a case-control study

Elbow tendinopathy is a common pathology of the upper extremity that impacts both athletes and workers. Some research has examined the genetic component as a risk factor for tendinopathy, mainly in the lower limbs. A case-control study was designed to test for a relationship between certain collagen gene single nucleotide polymorphisms (SNPs) and elbow tendon pathology. A sample of 137 young adult athletes whose sports participation involves loading of the upper limb were examined for the presence of structural abnormalities indicative of pathology in the tendons of the lateral and medial elbow using ultrasound imaging and genotyped for the following SNPs: COL5A1 rs12722, COL11A1 rs3753841, COL11A1 rs1676486, and COL11A2 rs1799907. Anthropometric measurements and data on participants’ elbow pain and dysfunction were collected using the Disabilities of the Arm, Shoulder and Hand and the Mayo Clinic Performance Index for the Elbow questionnaires. Results showed that participants in the structural abnormality group had significantly higher scores in pain and dysfunction. A significant relationship between COL11A1 rs3753841 genotype and elbow tendon pathology was found (p = 0.024), with the CT variant associated with increased risk of pathology.

Vascular Endothelial Growth Factor Receptor-2 Polymorphisms Have Protective Effect against the Development of Tendinopathy in Volleyball Athletes.

The aim of the study was to investigate whether genetic variants in VEGF and KDR genes can be correlated with susceptibility of tendinopathy in volleyball athletes. This study was conducted at the Brazilian Volleyball Federation, and comprised 179 volleyball athletes: 88 had a confirmed diagnosis of tendinopathy (cases), whereas 91 had no evidence of the disease (controls). The VEGF (-2578C>A, -460T>C and +936C>T) and KDR (-604C>T, 1192G>A and 1719T>A) polymorphisms were determined by TaqMan real-time polymerase chain reaction. The odds ratio (OR) with their 95% confidence intervals (CI) were calculated using an unconditional logistic regression model. The evaluation of demographic and clinical characteristics revealed the athlete age (P < 0.001), years of practice in volleyball (P < 0.001) and presence of pain (P = 0.001) were risk factors for tendinopathy. KDR 1192 GA and GA + AA genotypes were associated with lower risk of tendinopathy (OR: 0.41, 95% CI: 0.19–0.88 and OR: 0.47, 95% CI: 0.23–0.98, respectively). The KDR (-604C>T, 1192G>A and 1719T>A) haplotypes CGA and CAT were associated with decreased tendinopathy risk (OR: 0.46, 95% CI: 0.21–0.99 and OR: 0.23, 95% CI: 0.07–0.76, respectively). With regards to pain, traumatic lesion and away from training due to injury, VEGF and KDR polymorphisms were not associated with clinical symptoms complaints. The present results provide evidence that the KDR polymorphisms were associated with development of tendinopathy, and can contribute to identify new therapeutic targets or personalized training programs to avoid tendinopathy development in athletes.

Achilles tendons in people with type 2 diabetes show mildly compromised structure: an ultrasound tissue characterisation study

BackgroundMusculotendinous overuse injuries are prevalent in people with type 2 diabetes. Non-enzymatic glycosylation of collagen resulting in tendon stiffening may play a role. In this case–control study we determined whether...

BMP4 and FGF3 haplotypes increase the risk of tendinopathy in volleyball athletes

To investigate whether genetic variants can be correlated with tendinopathy in elite male volleyball athletes. Case-control study. Fifteen single nucleotide polymorphisms within BMP4, FGF3, FGF10, FGFR1 genes were investigated in 138 elite volleyball athletes, aged between 18 and 35 years, who undergo 4-5h of training per day: 52 with tendinopathy and 86 with no history of pain suggestive of tendinopathy in patellar, Achilles, shoulder, and hip abductors tendons. The clinical diagnostic criterion was progressive pain during training, confirmed by magnetic resonance image. Genomic DNA was obtained from saliva samples. Genetic markers were genotyped using TaqMan real-time PCR. Chi-square test compared genotypes and haplotype differences between groups. Multivariate logistic regression analyzed the significance of covariates and incidence of tendinopathy. Statistical analysis revealed participant age (p=0.005) and years of practice (p=0.004) were risk factors for tendinopathy. A significant association between BMP4 rs2761884 (p=0.03) and tendinopathy was observed. Athletes with a polymorphic genotype have 2.4 times more susceptibility to tendinopathy (OR=2.39; 95%CI=1.10-5.19). Also, association between disease and haplotype TTGGA in BMP4 (p=0.01) was observed. The FGF3 TGGTA haplotype showed a tendency of association with tendinopathy (p=0.05), and so did FGF10 rs900379. FGFR1 showed no association with disease. These findings indicate that haplotypes in BMP4 and FGF3 genes may contribute to the tendon disease process in elite volleyball athletes.

Obesity as a risk factor for tendinopathy: a systematic review.

Purpose. In the last few years, evidence has emerged to support the possible association between increased BMI and susceptibility to some musculoskeletal diseases. We systematically review the literature to clarify whether obesity is a risk factor for the onset of tendinopathy. Methods. We searched PubMed, Cochrane Central, and Embase Biomedical databases using the keywords “obesity,” “overweight,” and “body mass index” linked in different combinations with the terms “tendinopathy,” “tendinitis,” “tendinosis,” “rotator cuff,” “epicondylitis,” “wrist,” “patellar,” “quadriceps,” “Achilles,” “Plantar Fascia,” and “tendon.” Results. Fifteen studies were included. No level I study on this subject was available, and the results provided are ambiguous. However, all the 5 level II studies report the association between obesity measured in terms of BMI and tendon conditions, with OR ranging between 1.9 (95% CI: 1.1–2.2) and 5.6 (1.9–16.6). Conclusions. The best evidence available to date indicates that obesity is a risk factor for tendinopathy. Nevertheless, further studies should be performed to establish the real strength of the association for each type of tendinopathy, especially because the design of the published studies does not allow identifying a precise cause-effect relationship and the specific role of obesity independently of other metabolic conditions.

Is adiposity an under‐recognized risk factor for tendinopathy? A systematic review

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. 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. 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). 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.