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Glucocorticoids Differentially Inhibit Viability, Proliferation and Differentiation of Human Tenocytes
Rich Hillesheim, BS1; A. Lee Osterman, MD2; Rowena McBeath, MD, PhD2
1School of Medicine/Orthopaedic Surgery, Thomas Jefferson University, Philadelphia, PA; 2The Philadelphia Hand Center, Thomas Jefferson University, Philadelphia, PA

Purpose: Glucocorticoid injections (GCI) are widely used to treat upper extremity tendinosis, including trigger finger, DeQuervain's tendinosis, and lateral epicondylosis. Despite such widespread use of GCI as a therapeutic treatment modality, the cellular and molecular response of human tendon to glucocorticoid injection is unclear. Although effective in ameliorating the pain response at low dose-frequency intervals1, several case reports have noted tendon rupture after triamcinolone injection2,3,4. We hypothesized that the mechanism of action of GCI on tendinopathy may, in actuality, be due to effects of glucocorticoids on the viability, proliferation and differentiation of tendon cells.

Materials & Methods: Human tenocytes were isolated from patients (ages 20-55) undergoing revision amputation for traumatic hand injury using IRB-approved protocols. Tenocytes were plated onto fibronectin-coated coverslips and treated with betamethasone (10-7 to 10-3 mol/L), triamcinolone (10-7 to 10-3 mol/L) or dexamethasone (10-7 to 10-3 mol/L) and harvested after one week. Viability was assessed using live/dead cell assay, proliferation assessed by cell counting, and differentiation assessed by immunofluorescence and RT-PCR of tenocyte molecular markers collagen I, tenomodulin and scleraxis.

Results: Treatment of human tenocytes with glucocorticoids at therapeutic doses (>1mM) resulted in decreased tenocyte viability and proliferation (Figure 1). Also, treatment of human tenocytes with triamcinolone resulted in decreased proliferation as compared to betamethasone and dexamethasone at all doses tested. Furthermore, treatment of human tenocytes with all glucocorticoids resulted in decreased expression of collagen I by immunofluorescence and RT-PCR.

Conclusions:

  1. Treatment of human tenocytes with glucocorticoids at therapeutic levels results in decreased cell viability, proliferation and differentiation.
  2. Glucocorticoids do not have a uniform effect on tenocyte proliferation: triamcinolone causes decreased tenocyte viability, proliferation and differentiation in comparison to betamethasone and dexamethasone.
  3. All steroids tested cause decreased tenocyte differentiation.
  4. These results suggest that, in therapeutic doses at frequent intervals, glucocorticoid injections may cause tendon injury due to effects on cell viability, proliferation and differentiation.
References Cited
1Schubert et al. 2013 Hand 8: 439-444 2Taras et al. (1995) JHS 20A: 276-277 3Fitzgerald et al. (2005) JHS 30A: 479-482 4Yamada et al. (2011) JHSEur 6: 77-78

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