Job N Doornberg1, Tjalling Bosse2, Mark S Cohen3, Jesse B Jupiter4, David Ring4, Peter Kloen1. 1. Department of Orthopaedic Surgery, Academic Medical Center & University of Amsterdam, Secretariaat G4-Noord, Meibergdreef 9, 1100 DD Amsterdam, The Netherlands. 2. Leids Universitair Medisch Centrum, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. 3. Section of Hand and Elbow Surgery, Rush University Medical Center, 1611 West Harrison Street, Chicago, IL 60612. 4. Orthopaedic Hand and Upper Extremity Service, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114.
Abstract
BACKGROUND: Elbow stiffness is a common complication after elbow trauma. The elbow capsule is often thickened, fibrotic, and contracted at the time of surgical release. The limited studies available suggest that the capsule is contracted because of fibroblast-to-myofibroblast differentiation. We hypothesize that myofibroblasts are absent in normal elbow capsules and in acute trauma and that they are subsequently elevated in patients with posttraumatic elbow contracture. METHODS: We obtained twenty-one human elbow joint capsules within fourteen days after an elbow fracture and/or dislocation and thirty-four elbow joint capsules in thirty-four patients who had undergone operative release of posttraumatic contractures more than five months after injury. Myofibroblasts in the joint capsules were quantified with use of immunohistochemistry. Alpha-smooth muscle actin was used as a marker for myofibroblasts. Samples were characterized and were scored by an independent pathologist blinded for clinical data. RESULTS: Eleven capsules were associated with the acute phase after trauma (hours to less than seven days), and staining for alpha-smooth muscle actin was negative in all but one capsule. Ten capsules were associated with a later posttraumatic phase with myofibroblasts staining positive for alpha-smooth muscle actin in all but two capsules. Thirty-two long-standing contractures showed a histological pattern consistent with chronic stages of fibrosis, characterized by increased fibroblast-like cell proliferation and higher cellular density of fibroblast-like cells with highly unstructured collagen. Two joint capsules showed an earlier phase of fibrosis. Only two of the long-standing contractures had staining of alpha-smooth muscle actin in fibroblast-like cells; the lack of staining in the other contractures suggested an absence of myofibroblasts. CONCLUSIONS: This study presents negative results on the hypothesis that myofibroblast numbers are elevated in long-standing (more than five months) human posttraumatic elbow capsules. The absence of myofibroblasts in long-standing elbow contracture capsules is in contrast to most other studies on human tissue in the literature to date.
BACKGROUND: Elbow stiffness is a common complication after elbow trauma. The elbow capsule is often thickened, fibrotic, and contracted at the time of surgical release. The limited studies available suggest that the capsule is contracted because of fibroblast-to-myofibroblast differentiation. We hypothesize that myofibroblasts are absent in normal elbow capsules and in acute trauma and that they are subsequently elevated in patients with posttraumatic elbow contracture. METHODS: We obtained twenty-one human elbow joint capsules within fourteen days after an elbow fracture and/or dislocation and thirty-four elbow joint capsules in thirty-four patients who had undergone operative release of posttraumatic contractures more than five months after injury. Myofibroblasts in the joint capsules were quantified with use of immunohistochemistry. Alpha-smooth muscle actin was used as a marker for myofibroblasts. Samples were characterized and were scored by an independent pathologist blinded for clinical data. RESULTS: Eleven capsules were associated with the acute phase after trauma (hours to less than seven days), and staining for alpha-smooth muscle actin was negative in all but one capsule. Ten capsules were associated with a later posttraumatic phase with myofibroblasts staining positive for alpha-smooth muscle actin in all but two capsules. Thirty-two long-standing contractures showed a histological pattern consistent with chronic stages of fibrosis, characterized by increased fibroblast-like cell proliferation and higher cellular density of fibroblast-like cells with highly unstructured collagen. Two joint capsules showed an earlier phase of fibrosis. Only two of the long-standing contractures had staining of alpha-smooth muscle actin in fibroblast-like cells; the lack of staining in the other contractures suggested an absence of myofibroblasts. CONCLUSIONS: This study presents negative results on the hypothesis that myofibroblast numbers are elevated in long-standing (more than five months) humanposttraumatic elbow capsules. The absence of myofibroblasts in long-standing elbow contracture capsules is in contrast to most other studies on human tissue in the literature to date.
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