Background: This article systematically reviews the current evidence regarding inflammation in Tendinopathy with the aim to increase understanding of a potential common pathophysiology. Methods: Following the PRISMA statements, the terms: (tendinopathy OR (tendons AND rupture)) AND (inflammation OR (inflammation AND cells) OR immune system OR inflammation mediators OR bacteria) were used. One thousand four hundred thirty-one articles were identified which was screened down to 53. Results: 39/53 studies mentioned inflammatory cells but had contradicting conclusions. Macrophages were the most common cell type and inflammatory markers were detectable in all the articles which measure them. Conclusions: The included studies show different conclusions, but this heterogeneity is not unexpected since the clinical criteria of 'tendinopathy' encompass a huge clinical spectrum. Different 'tendinopathy' conditions may have different pathophysiology, and even the same clinical condition may be at different disease stages during sampling, which can alter the histological and biochemical picture. Control specimen sampling was suboptimal since the healthy areas of the pathological-tendon may actually be subclinically diseased, as could the contralateral tendon in the same subject. Detection of inflammatory cells is most sensitive using immunohistochemistry targeting the cluster of differentiation markers, especially when compared to the conventional haematoxylin and eosin staining methods. The identified inflammatory cell types favour a chronic inflammatory process; which suggests a persistent stimulus. This means NSAID and glucocorticoids may be useful since they suppress inflammation, but it is noted that they may hinder tendon healing and cause long term problems. This systematic review demonstrates a diversity of data and conclusions in regard to inflammation as part of the pathogenesis of Tendinopathy, ranging from ongoing or chronic inflammation to non-inflammatory degeneration and chronic infection. Whilst various inflammatory markers are present in two thirds of the reviewed articles, the heterogenicity of data and lack of comparable studies means we cannot conclude a common pathophysiology from this systematic review.

BackgroundTendinopathy is a chronic disorder that affects a huge population, and is causing high socioeconomical impacts worldwide. Tendinopathy was reported to be more prevalent in diabetic patients, and chronic inflammation was proposed to play an important role in its development. It was also known that diabetic patients present in a pro-inflammatory state. There is a possibility that the high glucose environment in diabetic patients lead to chronic inflammation in the tendon, and eventually the development of tendinopathy. In this study, we would simulate the diabetic environment in an in vitro setup, to assess the effect of a high glucose level on cultured tendinopathic and healthy tendon derived stem cells (TDSCs) under inflammatory stress. We would first like to assess whether there are differences between the inflammatory response in tendinopathic and healthy TDSCs. We would then investigate whether a high glucose level may lead to changes in the inflammatory response in healthy tendon cells.MethodsTendinopathic TDSCs were cultured from 2 torn rotator cuff tendons and 1 ruptured patellar tendon. Healthy TDSCs were cultured from 3 gender matched healthy hamstring tendons. Cells were stimulated by either 2ng/ml IL-1B for 24 hours, 11.1 mmol/L glucose for 24 hours, or both. mRNA was collected and processed for qPCR targeting B-actin, ALOX12, ALOX15, FPR1, FPR2, ChemR23, and COX2.ResultsUpregulation of FPR1 (p=0.050) ChemR23 (p=0.050), ALOX15 (p=0.050) was significantly weakened when comparing tendinopathic and healthy TDSCs stimulated with IL-1b. The upregulation of ALOX15 (p=0.050), was significantly lower in stimulated healthy TDSCs in a high glucose environment when comparing with those stimulated under a regular glucose level. A high glucose level also induced upregulation of COX2 (p=0.046) in healthy TDSCs and tendinopathic TDSCs (p=0.050).ConclusionThe results of this study provide a possible explanation to the increased risk to develop tendinopathy in diabetic patients. Chronic inflammation observed in tendinopathy may be due to the weakening of pro-resolving responses in tendinopathic TDSCs, and a high glucose environment may lead to chronic inflammation and ultimately tendinopathy by persistent stimulation and weakening of pro-resolving response in healthy TDSCs.

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BackgroundUnderlying muscle weakness may explain the inconsistency in the development of rotator cuff tendinopathy in population with similar activity levels. This systematic review aims to assess existing prospective studies to evaluate whether muscle weakness is a risk factor to the development of rotator cuff tendinopathy. MethodsA systematic search was performed using the PRISMA guidelines. Prospective studies measuring muscle strength or stiffness and the incidence of rotator cuff tendinopathy will be included. Quality assessment was performed with the Newcastle-Ottawa Quality Assessment Scale. ResultsThe search yielded 6 studies, with a total of 523 trained overhead athletes followed up for 1 season. External and internal rotation strength was described as protective factors for the development of rotator cuff tendinopathy, with an odds ratio of 0.940 (p < 0.05) and 0.946 (p < 0.01) respectively for each N/m increased in force generated. Limited range of motion of <106o for shoulder external rotation was also described as a risk factor with an odds ratio of 1.12 (p < 0.001).Imbalance between external and internal rotation strength was reported as a risk factor for shoulder injuries in 2 studies, with a relative risk of 2.57 (p < 0.05) reported in 1 of them. Supraspinatus weakness was also reported as a risk factor for shoulder injuries in 1 study, with no odds ratio or relative risk provided. Due to insufficient data, combination into a meta-analysis was not possible. ConclusionsLimited evidence support that weakness of the external rotators, weakness in the internal rotators, and limited range of motion in external rotation are risk factors to the development of rotator cuff tendinopathy. Very limited evidence support that imbalance in external rotator and internal rotator strength, and supraspinatus weakness are risk factors for rotator cuff tendinopathies. Future cohort studies may improve on existing evidence with investigations on more muscle groups, a longer follow-up time, clearly documented injury history, and a stringent diagnosis to rotator cuff tendinopathy.