Stereological Quantification of Immune-Competent Cells in Baseline Biopsy Specimens From Achilles Tendons

Kragsnæs, Maja Skov; Fredberg, Ulrich; Stribolt, Katrine; Kjær, Susanne K.; Bendix, Knud; Ellingsen, Torkell

doi:10.1177/0363546514542329

Cited by 66 publications

(56 citation statements)

References 58 publications

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“…Presence of neovascularization is well documented in advanced tendinopathies and can be demonstrated using Doppler Ultrasound examination [20,22,23,24,25,26]. Similarly, in our study the presence of neovascularization of the LHBT was confirmed in 78% of specimens.…”

Section: Discussionsupporting

confidence: 82%

“…The assessment of neovascularization was based on the criteria from the Bonar scale [18,19,20]. The scores 0, 1, 2, 3 contribute to the following stages of neovascularization seen in ten high-power fields (HPFs): 0 -modest and average occurrence of the blood vessels, 1 -incidental cluster of capillaries less than one per 10 HPFs, 2 -indicates 1-2 clusters per 10 HPFs, 3 -indicates more than 2 clusters per 10 high-power fields.…”

Section: Methodsmentioning

confidence: 99%

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Process of neovascularisation compared with pain intensity in tendinopathy of the long head of the biceps brachii tendon associated with concomitant shoulder disorders, after arthroscopic treatment. Microscopic evaluation supported by immunohistochemical

Zabrzyński¹,

Paczesny²,

Łapaj

et al. 2018

Folia Morphol

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Section: Discussionsupporting

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Process of neovascularisation compared with pain intensity in tendinopathy of the long head of the biceps brachii tendon associated with concomitant shoulder disorders, after arthroscopic treatment. Microscopic evaluation supported by immunohistochemical

Zabrzyński¹,

Paczesny²,

Łapaj

et al. 2018

Folia Morphol

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“…Interleukin-1ß has been proposed as an initiator of tendinopathy [30] and may be an acceptable model of tendon cell inflammation; however, the issue remains controversial. In any event, persistent presence of macrophages (important sources of IL-1ß) is supported by recent data in patients with chronic tendinopathy who had been followed up for more than 4 years [19]. Ethical issues limit harvesting healthy tendon, and thus we had to use two different anatomical sources for tendon specimen, ie, semitendinosus (healthy tendon) and rotator cuff (tendinopathic tissue).…”

Section: Discussionmentioning

confidence: 92%

Platelet-rich Plasma Modulates the Secretion of Inflammatory/Angiogenic Proteins by Inflamed Tenocytes

Andı́a

Rubio‐Azpeitia

Maffulli

2015

Clinical Orthopaedics &Amp; Related Research

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Background Platelet-rich plasma therapies for tendinopathy appear to provide moderate pain reduction. However, the biological mechanisms behind the observed clinical effects remain poorly characterized. Questions/purposes The purpose of this study was to explore whether platelet-rich plasma modifies the inflammatory/angiogenic status of already inflamed tenocytes by examining (1) gene expression; (2) modulation of chemokine and interleukin secretion; and (3) differences between healthy and tendinopathic tenocytes. Methods Cells from both healthy and tendinopathic tendons were exposed to interleukin (IL)-1ß and after treated with platelet-rich plasma. Modifications in the expression of selected genes were assessed by real-time reverse transcription-polymerase chain reaction and changes in secretion of angiogenic/inflammatory molecules by enzyme-linked immunosorbent assay. Platelet-rich plasmainduced changes in tendinopathic cells were compared with normal after normalizing platelet-rich plasma data against IL-1ß status in each specific sample. Results In IL-1ß-exposed cells, platelet-rich plasma downregulates expression of IL-6/CXCL-6 (mean, 0.015; 95% confidence interval [CI], 0.005-0.025; p = 0.026), IL-6R (mean, 0.61; 95% CI, 0.27-0.95; p = 0.029), and IL-8/CXCL-8 (mean, 0.02; 95% CI, 0.007-0.023; p = 0.026). Secretion of IL-6/CXCL6, 0.35 (95% CI, 0.3-0.4; p = 0.002), IL-8/CXCL8, 0.55 (95% CI, 0.5-0.7; p = 0.01), and monocyte chemoattractant protein-1/CCL2, 0.40 (95% CI, 0.2-0.6; p = 0.001) was reduced by platelet-rich plasma, whereas vascular endothelial growth factor increased by twofold, (95% CI, 1.7-2.3; p \ 0.001). RANTES/CCL5 increased by10-fold (95% CI, 4-17) and hepatocyte growth factor by 21-fold (95% CI, 0.2-42) in tendinopathic and by 2.3-fold (95% CI, 2-3) and threefold (95% CI, 1-5) in normal cells (p = 0.005 for both). Conclusions Platelet-rich plasma induces an immunomodulatory and proangiogenic phenotype consistent with healing mechanisms with few differences between tendinopathic and normal cells. Clinical Relevance Platelet-rich plasma injections in pathological and nearby tissue might help to recover tendon homeostasis.

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“…Growing evidence supports the contribution of inflammation to the development of tendinopathy (16)(17)(18)(19)(20)(21). Whilst animal models of induced tendinopathy have improved our understanding of acute inflammatory processes (22), the phenotypes of the key cells orchestrating inflammation and fibrosis in human soft tissue pathologies such as tendinopathy and enthesopathy have not been fully characterized.…”

Section: Introductionmentioning

confidence: 99%

Inflammation activation and resolution in human tendon disease

et al. 2015

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Improved understanding of the role of inflammation in tendon disease is required to facilitate therapeutic target discovery. We studied supraspinatus tendons from patients experiencing pain before and after surgical subacromial decompression treatment. Tendons were classified as having early, intermediate or advanced disease and inflammation was characterized through activation of pathways mediated by Interferon, NF-κB, glucocorticoid receptor and STAT-6. Inflammation signatures revealed expression of genes and proteins induced by Interferon and NF-κB in early stage disease and genes and proteins induced by STAT-6 and glucocorticoid receptor activation in advanced stage disease. The pro-resolving proteins FPR2/ALX and ChemR23 were increased in early stage disease compared to intermediate-advanced stage disease. Patients who were pain-free post-treatment had tendons with increased expression of CD206 and ALOX15 mRNA compared to tendons from patients who continued to experience pain post-treatment, suggesting that these genes and their pathways may moderate tendon pain. Stromal cells from diseased tendons cultured in vitro showed increased expression of NF-κB and Interferon target genes after treatment with lipopolysaccharide or IFNγ compared to stromal cells derived from healthy tendons. We identified 15-epi Lipoxin A 4 , a stable lipoxin metabolite derived from aspirin treatment, as potentially beneficial in the resolution of tendon inflammation. *Corresponding author Stephanie G Dakin, stephanie.dakin@ndorms.ox.ac.uk Corresponding author telephone +44 (0)1865 227374. Author contributions: SGD performed all experiments and wrote the manuscript with input from all co-authors. SGD, AJC and FOM designed the study. FOM, UO and GW provided qPCR reagents and FOM and UO performed array analysis. FOM and GW provided human macrophages for co-culture experiments. CY facilitated confocal image acquisition. BD, KW, BW, LR and AJC facilitated procurement and collection of healthy and diseased shoulder tendons from patients.

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Stereological Quantification of Immune-Competent Cells in Baseline Biopsy Specimens From Achilles Tendons

Abstract: New insight into the role of immune-competent cells in chronic Achilles tendinopathy.

Cited by 66 publications

References 58 publications

Process of neovascularisation compared with pain intensity in tendinopathy of the long head of the biceps brachii tendon associated with concomitant shoulder disorders, after arthroscopic treatment. Microscopic evaluation supported by immunohistochemical

Process of neovascularisation compared with pain intensity in tendinopathy of the long head of the biceps brachii tendon associated with concomitant shoulder disorders, after arthroscopic treatment. Microscopic evaluation supported by immunohistochemical

Platelet-rich Plasma Modulates the Secretion of Inflammatory/Angiogenic Proteins by Inflamed Tenocytes

Inflammation activation and resolution in human tendon disease

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