Search tips
Search criteria 


Logo of bmcmudisBioMed Centralsearchsubmit a manuscriptregisterthis articleBMC Musculoskeletal Disorders
BMC Musculoskelet Disord. 2012; 13: 53.
Published online Apr 5, 2012. doi:  10.1186/1471-2474-13-53
PMCID: PMC3341204
Local biochemical and morphological differences in human Achilles tendinopathy: a case control study
Pingel J,corresponding author1 Fredberg U,2 Qvortrup K,3 Larsen JO,4 Schjerling P,1 Heinemeier K,1 Kjaer M,1 and Langberg H5
1Institute of Sports Medicine, Department of Orthopedic Surgery M. Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
2Department of Rheumatology, Silkeborg Hospital, Silkeborg, Denmark
3Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark
4Department of Neuroscience and Pharmacology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
5Department of Public Health, University of Copenhagen, Copenhagen, Denmark
corresponding authorCorresponding author.
Pingel J: jessica.pingel/at/; Fredberg U: ulrifred/at/; Qvortrup K: QVORTRUP/at/; Larsen JO: JYO/at/; Schjerling P: peter/at/; Heinemeier K: katjaheinemeier/at/; Kjaer M: michaelkjaer/at/; Langberg H: henninglangberg/at/
Received December 5, 2011; Accepted April 5, 2012.
The incidence of Achilles tendinopathy is high and underlying etiology as well as biochemical and morphological pathology associated with the disease is largely unknown. The aim of the present study was to describe biochemical and morphological differences in chronic Achilles tendinopathy. The expressions of growth factors, inflammatory mediators and tendon morphology were determined in both chronically diseased and healthy tendon parts.
Thirty Achilles tendinopathy patients were randomized to an expression-study (n = 16) or a structural-study (n = 14). Biopsies from two areas in the Achilles tendon were taken and structural parameters: fibril density, fibril size, volume fraction of cells and the nucleus/cytoplasm ratio of cells were determined. Further gene expressions of various genes were analyzed.
Significantly smaller collagen fibrils and a higher volume fraction of cells were observed in the tendinopathic region of the tendon. Markers for collagen and its synthesis collagen 1, collagen 3, fibronectin, tenascin-c, transforming growth factor-β fibromodulin, and markers of collagen breakdown matrix metalloproteinase-2, matrix metalloproteinase-9 and metallopeptidase inhibitor-2 were significantly increased in the tendinopathic region. No altered expressions of markers for fibrillogenesis, inflammation or wound healing were observed.
The present study indicates that an increased expression of factors stimulating the turnover of connective tissue is present in the diseased part of tendinopathic tendons, associated with an increased number of cells in the injured area as well as an increased number of smaller and thinner fibrils in the diseased tendon region. As no fibrillogenesis, inflammation or wound healing could be detected, the present data supports the notion that tendinopathy is an ongoing degenerative process.
Trial registration
Current Controlled Trials ISRCTN20896880
Keywords: Collagen, Gene expression, Patients, Growth factors, Tissue turnover
Articles from BMC Musculoskeletal Disorders are provided here courtesy of
BioMed Central