Premium
Early development of tendinopathy in humans: Sequence of pathological changes in structure and tissue turnover signaling
Author(s) -
Tran Peter H. T.,
MalmgaardClausen Nikolaj M.,
Puggaard Rikke S.,
Svensson René B.,
Nybing Janus D.,
Hansen Philip,
Schjerling Peter,
Zinglersen Amanda H.,
Couppé Christian,
Boesen Mikael,
Magnusson S. Peter,
Kjaer Michael
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201901309r
Subject(s) - tendinopathy , medicine , achilles tendon , tendon , asymptomatic , pathogenesis , tendinitis , pathological , surgery
Abstract Overloading of tendon tissue with resulting chronic pain (tendinopathy) is a common disorder in occupational‐, leisure‐ and sports‐activity, but its pathogenesis remains poorly understood. To investigate the very early phase of tendinopathy, Achilles and patellar tendons were investigated in 200 physically active patients and 50 healthy control persons. Patients were divided into three groups: symptoms for 0‐1 months (T1), 1‐2 months (T2) or 2‐3 months (T3). Tendinopathic Achilles tendon cross‐sectional area determined by ultrasonography (US) was ~25% larger than in healthy control persons. Both Achilles and patellar anterior‐posterior diameter were elevated in tendinopathy, and only later in Achilles was the width increased. Increased tendon size was accompanied by an increase in hypervascularization (US Doppler flow) without any change in mRNA for angiogenic factors. From patellar biopsies taken bilaterally, mRNA for most growth factors and tendon components remained unchanged (except for TGF‐beta1 and substance‐P) in early tendinopathy. Tendon stiffness remained unaltered over the first three months of tendinopathy and was similar to the asymptomatic contra‐lateral tendon. In conclusion, this suggests that tendinopathy pathogenesis represents a disturbed tissue homeostasis with fluid accumulation. The disturbance is likely induced by repeated mechanical overloading rather than a partial rupture of the tendon.