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Trigger finger, tendinosis, and intratendinous gene expression
Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Orthopaedics in Linköping.
Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences.
2014 (English)In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 24, no 2, 363-368 p.Article in journal (Refereed) Published
Abstract [en]

The pathogenesis of trigger finger has generally been ascribed to primary changes in the first annular ligament. In contrast, we recently found histological changes in the tendons, similar to the findings in Achilles tendinosis or tendinopathy. We therefore hypothesized that trigger finger tendons would show differences in gene expression in comparison to normal tendons in a pattern similar to what is published for Achilles tendinosis. We performed quantitative real-time polymerase chain reaction on biopsies from finger flexor tendons, 13 trigger fingers and 13 apparently healthy control tendons, to assess the expression of 10 genes which have been described to be differently expressed in tendinosis (collagen type 1a1, collagen 3a1, MMP-2, MMP-3, ADAMTS-5, TIMP-3, aggrecan, biglycan, decorin, and versican). In trigger finger tendons, collagen types 1a1 and 3a1, aggrecan and biglycan were all up-regulated, and MMP-3and TIMP-3 were down-regulated. These changes were statistically significant and have been previously described for Achilles tendinosis. The remaining four genes were not significantly altered. The changes in gene expression support the hypothesis that trigger finger is a form of tendinosis. Because trigger finger is a common condition, often treated surgically, it could provide opportunities for clinical research on tendinosis.

Place, publisher, year, edition, pages
Wiley , 2014. Vol. 24, no 2, 363-368 p.
Keyword [en]
tendinopathy; tendinosis; stenosing tendovaginitis; tendovaginitis stenosans; quantitative real-time PCR; qPCR
National Category
Orthopedics Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-106131DOI: 10.1111/j.1600-0838.2012.01514.xISI: 000332982700018OAI: oai:DiVA.org:liu-106131DiVA: diva2:714034
Available from: 2014-04-25 Created: 2014-04-24 Last updated: 2017-12-05
In thesis
1. Tendinosis in Trigger Finger
Open this publication in new window or tab >>Tendinosis in Trigger Finger
2017 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Trigger finger is one of the most common hand conditions, with a prevalence of almost 3%. The aetiology remains unclear even though many causes have been suggested. The prevailing paradigm is that the pathogenesis of trigger finger is ascribed to primary changes in the first fibrous condensation of the tendon sheath (A1-pulley). Several studies have investigated pathology in the pulley, but few have investigated the tendon. The general aim of this thesis was to find out if there is pathology in the trigger finger tendon and to define it.

We first looked at trigger finger tendon biopsies in a light microscope, and found that they were histologically different from healthy tendons. They showed signs of micro-ruptures, collagen degradation, increased amounts of ground substance, both hyper- and hypo-cellular areas, round active cell nuclei and absence of inflammatory cells, all similar to tendinosis. The histological picture was further assessed by using a scoring system for Achilles tendinosis. The trigger finger tendons scored high, suggesting a similar histopathology.

Next, we performed a quantitative real-time polymerase chain reaction (qPCR) on trigger finger tendons. We assessed the mRNA expression of 10 genes, which have been described to be differently expressed in Achilles tendinosis (collagen 1 and 3, versican, decorin, biglycan, aggrecan, MMP-2, MMP-3, ADAMTS-5, and TIMP-3). The overall expression pattern agreed with previous studies on Achilles tendinosis, suggesting that the cellular function in trigger finger tendons is disturbed in a similar way as in Achilles tendinosis.

Recent experimental and observational research has suggested potential side effects of statin treatment on tendons, but firm evidence was lacking. We performed an epidemiological study on two large population-based cohorts. Statin use was found to increase the risk of both trigger finger and tendinosis in the shoulder and Achilles tendons, especially among men. This suggests a similar pathology in trigger finger and tendinosis.

We have also studied the time to treatment effect after a single injection of glucocorticoid in trigger finger. Our results suggest that 60-80% of patients can expect resolution of the triggering within 14 days, and half of them within seven days. This result allows correct information to be given to the patient and proper planning of follow-ups.

In conclusion, the pathology in trigger finger tendons is similar to tendinosis in other tendons.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2017. 61 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1573
National Category
Gastroenterology and Hepatology Neurology Hematology Other Clinical Medicine Clinical Laboratory Medicine
Identifiers
urn:nbn:se:liu:diva-136784 (URN)10.3384/diss.diva-136784 (DOI)9789176855355 (ISBN)
Public defence
2017-06-07, Granitsalen, Universitetssjukhuset, Linköping, 13:00 (English)
Opponent
Supervisors
Available from: 2017-04-25 Created: 2017-04-25 Last updated: 2017-05-09Bibliographically approved

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Lundin, Anna-CarinAspenberg, PerEliasson, Pernilla T.

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Scandinavian Journal of Medicine and Science in Sports
OrthopedicsCell and Molecular Biology

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