Glucocorticoids suppress proteoglycan production by human tenocytes
Background The role of glucocortiocid injection therapy in spontaneous tendon rupture is controversial. We hypothesized that glucocorticoids suppress proteoglycan production in tendon and studied the in vitro effects of dexamethasone and triamcinolone on proteoglycan production by cultured human ten...
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Published in | Acta orthopaedica Vol. 76; no. 6; pp. 927 - 931 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Basingstoke
Taylor & Francis
01.12.2005
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Subjects | |
Online Access | Get full text |
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Summary: | Background The role of glucocortiocid injection therapy in spontaneous tendon rupture is controversial. We hypothesized that glucocorticoids suppress proteoglycan production in tendon and studied the in vitro effects of dexamethasone and triamcinolone on proteoglycan production by cultured human tenocytes.
Material and methods We obtained primary cultures of human tenocytes from explants of healthy human patellar tendon. The human tenocytes were treated with 1 μM dexamethasone or 1 μM triamcinolone. The amount of proteoglycan production was measured by
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S-sulfate incorporation assay and compared with control cultures. The reversibility of the effect of dexamethasone by co-incubation with 10 ng platelet-derived growth factor (PDGFBB) was also tested.
Results Treatment with 1 μM triamcinolone reduced the amount of
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S-sulfate incorporation to 80% of control cultures (p = 0.007), whereas 1 μM dexamethasone reduced it to 72% (p = 0.01). Co-incubation of 10 ng/mL PDGFBB with 1 μM dexamethasone returned the
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S-sulfate incorporation to a level thatwas significantly higher than for dexamethasone treatment alone (108%; p = 0.01).
Interpretation Glucocorticoids suppressed proteoglycan production in cultured human tenocytes. The suppression by dexamethasone was reversed by simultaneous addition of PDGFBB. Suppressed proteoglycan production may affect the viscoelastic properties of tendon and increase the risk of spontaneous rupture.
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ISSN: | 1745-3674 1745-3682 |
DOI: | 10.1080/17453670610046118 |