Inflammation is present in early human tendinopathy.
BACKGROUND
The cellular mechanisms of tendinopathy remain unclear particularly with respect to the role of inflammation in early disease. The authors previously identified increased levels of inflammatory cytokines in an early human model of tendinopathy and sought to extend these studies to the cellular analysis of tissue.


OBJECTIVE
To characterize inflammatory cell subtypes in early human tendinopathy, the authors explored the phenotype and quantification of inflammatory cells in torn and control tendon samples.


METHODS
Controlled laboratory study.


METHODS
Torn supraspinatus tendon and matched intact subscapularis tendon samples were collected from 20 patients undergoing arthroscopic shoulder surgery. Control samples of subscapularis tendon were collected from 10 patients undergoing arthroscopic stabilization surgery. Tendon biopsy samples were evaluated immunohistochemically by quantifying the presence of macrophages (CD68 and CD206), T cells (CD3), mast cells (mast cell tryptase), and vascular endothelium (CD34).


RESULTS
Subscapularis tendon samples obtained from patients with a torn supraspinatus tendon exhibited significantly greater macrophage, mast cell, and T-cell expression compared with either torn supraspinatus samples or control subscapularis-derived tissue (P < .01). Inflammatory cell infiltrate correlated inversely (r = .5; P < .01) with rotator cuff tear size, with larger tears correlating with a marked reduction in all cell lineages. There was a modest but significant correlation between mast cells and CD34 expression (r = .4; P < .01) in matched subscapularis tendons from shoulders with supraspinatus ruptures.


CONCLUSIONS
This study provides evidence for an inflammatory cell infiltrate in early mild/moderate human tendinopathy. In particular, the authors demonstrate significant infiltration of mast cells and macrophages, suggesting a role for innate immune pathways in the events that mediate early tendinopathy. Clinical Relevance Further mechanistic studies to evaluate the net contribution and hence therapeutic utility of these cellular lineages and their downstream processes may reveal novel therapeutic approaches to the management of early tendinopathy.
Millar
Neal L
NL
Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, Scotland, United Kingdom. n.millar@clinmed.gla.ac.uk
Hueber
Axel J
AJ
Reilly
James H
JH
Xu
Yinghua
Y
Fazzi
Umberto G
UG
Murrell
George A C
GA
McInnes
Iain B
IB
D000328:Adult; D000368:Aged; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis / Q000378:metabolism*; D008875:Middle Aged; D008954:Models, Biological; D012782:Shoulder; D052256:Tendinopathy / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D055815:Young Adult
D018836:Inflammation Mediators