Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Low tendon stiffness and abnormal ultrastructure distinguish classic Ehlers-Danlos syndrome from benign joint hypermobility syndrome in patients

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Influence of FGF23 and Klotho on male reproduction: Systemic vs direct effects

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Early development of tendinopathy in humans: Sequence of pathological changes in structure and tissue turnover signaling

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Maintenance of muscle strength following a one-year resistance training program in older adults

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. The influence of prolonged strength training upon muscle and fat in healthy and chronically diseased older adults

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Associations between shoulder symptoms and concomitant pathology in patients with traumatic supraspinatus tears

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. The effect of 4 months exercise training on systemic biomarkers of cartilage and bone turnover in hip osteoarthritis patients

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. Early development of tendinopathy in humans: Sequence of pathological changes in structure and tissue turnover signaling

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

There is a clinical overlap between classic Ehlers-Danlos syndrome (cEDS) and benign joint hypermobility syndrome (BJHS), with hypermobility as the main symptom. The purpose of this study was to investigate the role of type V collagen mutations and tendon pathology in these 2 syndromes. In patients (cEDS, n=7; BJHS, n=8) and controls (Ctrl, n=8), we measured patellar tendon ultrastructure (transmission electron microscopy), dimensions (magnetic resonance imaging), and biomechanical properties (force and ultrasonographic measurements during a ramped isometric knee extension). Mutation analyses (COL5A1 and COL5A2) were performed in the patients. COL5A1 mutations were found in 3 of 4 of the patients with cEDS. Patellar tendon dimensions were similar between the groups, but large, irregular collagen fibrils were in 4 of 5 patients with cEDS. In the cEDS group, tendon stiffness and Young's modulus were reduced to ∼50% of that in BJHS and Ctrl groups (P<0.05). The nonhypermobile, healthy controls were matched with the patients in age, sex, body weight, and physical activity, to compare outcomes. COL5A1 mutations led to structural tendon pathology and low tendon stiffness in cEDS, explaining the patients' hypermobility, whereas no tendon pathology was found that explained the hypermobility in BJHS.

OriginalsprogEngelsk
TidsskriftF A S E B Journal
Vol/bind28
Udgave nummer11
Sider (fra-til)4668-76
Antal sider9
ISSN0892-6638
DOI
StatusUdgivet - nov. 2014

ID: 44828102