Hermann O Mayr1,2, Fanny F Fassbender3, Wolf C Prall4,5, Florian Haasters4,5, Anke Bernstein3, Amelie Stoehr4,6. 1. Department of Orthopaedics and Traumatology, Albert Ludwig University of Freiburg, Hugstetterstrasse 55, 79106, Freiburg, Germany. hermann.mayr@uniklinik-freiburg.de. 2. Department of Knee, Hip and Shoulder Surgery, Schön Clinik Munich-Harlaching, Academic Teaching Hospital of the Paracelsus Private Medical University Salzburg, Strubergasse 21, 5020, Salzburg, Austria. hermann.mayr@uniklinik-freiburg.de. 3. Department of Orthopaedics and Traumatology, Albert Ludwig University of Freiburg, Hugstetterstrasse 55, 79106, Freiburg, Germany. 4. Department of Knee, Hip and Shoulder Surgery, Schön Clinik Munich-Harlaching, Academic Teaching Hospital of the Paracelsus Private Medical University Salzburg, Strubergasse 21, 5020, Salzburg, Austria. 5. Department of General, Trauma and Reconstructive Surgery, Munich University Hospital LMU, Nussbaumstr. 20, 80336, Munich, Germany. 6. OCM Clinic Munich, Steinerstr. 6, 81369, Munich, Germany.
Abstract
INTRODUCTION: Arthrofibrosis (AF) is the result of increased cell proliferation and synthesis of matrix proteins (collagen I, III, and VI). Especially after invasive knee surgery, e.g., ligament reconstruction or knee replacement, abnormal fibroblast proliferation with pathological periarticular fibrosis can be observed leading to severely limited joint motion. The pathogenesis of AF is currently not fully understood. The present work aims to determine pathogenic factors. MATERIALS AND METHODS: A descriptive, histological and immunohistochemical comparative study was performed on tissue samples of 14 consecutive patients undergoing arthrolysis for joint stiffness due to AF. Seven human autopsy specimens served as control. Samples were stained for expression of relevant markers such as CD68, α-smooth muscle actin (ASMA), beta-catenin, BMP-2 and examined for the histological grade of AF (cell-rich versus cell-poor) and compared to a control. Furthermore, a microscopic evaluation of the samples for cell differentiation and number was performed. RESULTS: Tissue sections of cell-rich fibrosis showed a significantly higher expression of CD68 compared to the control with less than 10% of CD68 positive cells (p = 0.002). In cell-poor fibrosis no statistically significant difference was obvious (p = 0.228). Expression of ASMA in synovia, vessels, cell-rich and cell-poor fibrosis showed median values of 2.00 in the AF group and 1.75 in the control. Both groups differed significantly (p = 0.003). AF tissue showed a significantly difference in expression of β-catenin (p < 0.001) compared to the control. The overall difference between AF and control group in expression of BMP-2 was also statistically significant (p = 0.002). CONCLUSIONS: Expression of CD68, ASMA, beta-catenin and BMP-2 is significantly increased in AF tissue samples. Based on presented findings, histological evaluation and immunohistochemical assessment of CD68, ASMA, β-catenin and BMP-2 expression may proof useful to diagnose AF and to analyze AF activity.
INTRODUCTION: Arthrofibrosis (AF) is the result of increased cell proliferation and synthesis of matrix proteins (collagen I, III, and VI). Especially after invasive knee surgery, e.g., ligament reconstruction or knee replacement, abnormal fibroblast proliferation with pathological periarticular fibrosis can be observed leading to severely limited joint motion. The pathogenesis of AF is currently not fully understood. The present work aims to determine pathogenic factors. MATERIALS AND METHODS: A descriptive, histological and immunohistochemical comparative study was performed on tissue samples of 14 consecutive patients undergoing arthrolysis for joint stiffness due to AF. Seven human autopsy specimens served as control. Samples were stained for expression of relevant markers such as CD68, α-smooth muscle actin (ASMA), beta-catenin, BMP-2 and examined for the histological grade of AF (cell-rich versus cell-poor) and compared to a control. Furthermore, a microscopic evaluation of the samples for cell differentiation and number was performed. RESULTS: Tissue sections of cell-rich fibrosis showed a significantly higher expression of CD68 compared to the control with less than 10% of CD68 positive cells (p = 0.002). In cell-poor fibrosis no statistically significant difference was obvious (p = 0.228). Expression of ASMA in synovia, vessels, cell-rich and cell-poor fibrosis showed median values of 2.00 in the AF group and 1.75 in the control. Both groups differed significantly (p = 0.003). AF tissue showed a significantly difference in expression of β-catenin (p < 0.001) compared to the control. The overall difference between AF and control group in expression of BMP-2 was also statistically significant (p = 0.002). CONCLUSIONS: Expression of CD68, ASMA, beta-catenin and BMP-2 is significantly increased in AF tissue samples. Based on presented findings, histological evaluation and immunohistochemical assessment of CD68, ASMA, β-catenin and BMP-2 expression may proof useful to diagnose AF and to analyze AF activity.
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