Lokalisation von TGF-β und PDGF und deren Bedeutung für die Pathogenese der Arthrofibrose

Abstract

Arthrofibrosis is a disabling complication after knee trauma and surgery and is characterised clinically by joint stiffness. Due to an immune response, the proliferation of fibroblasts and synthesis of extracellular matrix proteins are increased. The cytokines transforming growth factor beta (TGF-beta) and platelet-derived growth factor (PDGF) are critical players in tissue fibrosis, stimulating cell proliferation and the production of various extracellular matrix proteins. Tissue samples from the infrapatellar fat pad and intercondylar synovia of seven patients (age 18-49 years) suffering from arthrofibrosis were taken at surgery. The mean interval between trauma and arthrolysis was 14.3 months. All samples were stained with haematoxylin and eosin, and monoclonal and polyclonal antibodies were applied for immunohistological localisation of TGF-beta and PDGF. The percentage of both cytokines was then analysed using an image analysis system. Tissue samples with no macroscopic pathology of the synovial tissue from eight patients for anterior cruciate ligament replacement served as controls. Immunostaining for TGF-beta and PDGF was found to be increased in arthrofibrotic tissue. Both cytokines could be detected subsynovially around inflammatory cells. The profibrotic cytokines TGF-beta and PDGF play an important role in the pathogenesis of arthrofibrosis. Both cytokines are key mediators of tissue fibrosis.

A potential mode of action for Anakinra in patients with arthrofibrosis following total knee arthroplasty

“…TGF-β1 is widely accepted as a key mediator of fibrosis in multiple organs and has been demonstrated to be elevated in arthrofibrotic tissue 14 . Treatment of infra-patellar fat pad ( Fig.…”

Human xylosyltransferases – mediators of arthrofibrosis? New pathomechanistic insights into arthrofibrotic remodeling after knee replacement therapy

“…We used the disease classification provided by the World Health Organization (ICD-10, version 2012). While secondary arthrofibrosis and implant malpositioning were excluded by X-ray examination, postoperative complications such as infection or deep vein thrombosis were excluded as described before 4 6 19 . Patients with actual or suspected arthrofibrosis were divided into three groups due to diagnostic confidence: arthrofibrosis score 1 (Afib1): suspected arthrofibrosis based on clinical findings, short Time diagnosis and incomplete differential diagnosis, Afib2: arthrofibrosis based on clinical findings, Afib3: arthrofibrosis based on strong clinical findings as well as histopathological findings reported by an external institution.…”

“…Although the predicted incidence of primary arthrofibrosis after knee replacement is 10%, its pathogenesis is mostly unclear and no diagnostic marker has been described 4 . Until today, the diagnosis is based on histopathological findings and clinical symptoms such as loss of motion 5 6 . Treatment of arthrofibrosis is challenging and several therapeutic strategies have been discussed 4 7 .…”

BMP-2 Dependent Increase of Soft Tissue Density in Arthrofibrotic TKA

“…In the pathogenesis of arthrofibrosis, the persistence of physiological inflammation leads to a transdifferentiation of fibroblasts [1, 7, 17, 24, 25], followed by fibrosis of the soft tissue [1, 18, 19, 26]. Within the context of this tissue transformation, further studies have demonstrated HO in arthrofibrosis [1, 16-19].…”