ABSTRACT
Stenosing tenosynovitis of the first dorsal compartment of the wrist (a.k.a. de Quervain's disease) is common but how estrogen is involved is still unknown. We previously reported that inflammation was involved in the pathogenesis of this ailment. In the present study, we extended our investigation of estrogen receptor (ER)-ß expression to determine whether estrogen is involved in the pathogenesis of de Quervain's. Intraoperative retinaculum samples were collected from 16 patients with the ailment. Specimens were histologically graded by collagen structure and immunohistochemically evaluated by quantifying the expression of ER-ß, interleukin (IL)-1ß and IL-6 (inflammatory cytokines), cyclooxygenase (COX)-2 (an inflammatory enzyme), and vascular endothelial growth factor (VEGF), and Von Willebrand's factor (vWF). De Quervain's occurs primarily in women. The female:male ratio in our study was 7:1. We found that ER-ß expression in the retinaculum was positively correlated with disease grade and patient age. Additionally, disease severity was associated with inflammatory factors--IL-1ß and IL-6, COX-2, and VEGF and vWF in tenosynovial tissue. The greater the levels of ER-ß expression, tissue inflammation, and angiogenesis are, the more severe de Quervain's disease is. ER-ß might be a useful target for novel de Quervain's disease therapy.
Subject(s)
De Quervain Disease/genetics , De Quervain Disease/metabolism , Estrogen Receptor beta/metabolism , Adult , Age Factors , Aged , Angiogenesis Inducing Agents/metabolism , Case-Control Studies , De Quervain Disease/diagnosis , De Quervain Disease/therapy , Estrogen Receptor beta/genetics , Female , Gene Expression Regulation , Humans , Immunohistochemistry , Inflammation/genetics , Inflammation/metabolism , Inflammation/pathology , Inflammation Mediators/metabolism , Male , Middle Aged , Neovascularization, Pathologic/genetics , Neovascularization, Pathologic/metabolism , Risk Factors , Severity of Illness IndexABSTRACT
BACKGROUND: De Quervain disease is a stenosing condition of the sheath of the abductor pollicis longus and extensor pollicis brevis tendons at the radial styloid process. Previous studies consistently reported that the pathological change of this condition is thought to be primarily an extensor retinaculum thickened by fibrosis and angiogenesis instead of inflammation. Contradictorily, the conservative treatment for de Quervain disease is anti-inflammatory medication. The inflammatory response may be involved in this disease; however, there is no present study directly evidencing whether the inflammatory responses exist in de Quervain disease or not. The histopathology of de Quervain disease is yet to be elucidated clearly. PURPOSE: To grade all specimens in the different stages and characterize specific inflammatory cell and factors to examine whether inflammatory response is involved in de Quervain disease. METHODS: Retinaculum samples were collected from 13 patients with de Quervain disease after surgery. The specimens were evaluated histologically by collagen structure grading and immunohistochemically by quantifying the presence of neutrophil elastase, macrophages, cyclooxygenase, and vascular endothelium. RESULTS: Neutrophil elastase and cyclooxygenase occur in the de Quervain disease retinaculum and increased with the grade of collagen structure. After angiogenesis, macrophage infiltration occurs in the grade II matrix worse than grade III matrix. CONCLUSIONS: Inflammation is present in de Quervain disease. This study provides direct evidence for inflammatory cell and infiltration factors and offer valuable clues for specific pharmacological therapies for de Quervain disease.
