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 microM dexamethasone or 1 microM 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 microM triamcinolone reduced the amount of 35S-sulfate incorporation to 80% of control cultures (p = 0.007), whereas 1 microM dexamethasone reduced it to 72% (p = 0.01). Co-incubation of 10 ng/mL PDGFBB with 1 microM dexamethasone returned the 35S-sulfate incorporation to a level that was 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.
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 microM dexamethasone or 1 microM 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 microM triamcinolone reduced the amount of 35S-sulfate incorporation to 80% of control cultures (p = 0.007), whereas 1 microM dexamethasone reduced it to 72% (p = 0.01). Co-incubation of 10 ng/mL PDGFBB with 1 microM dexamethasone returned the 35S-sulfate incorporation to a level that was 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.