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 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 ³⁵S-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 ³⁵S-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 ³⁵S-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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