Synovialitis vom arthrofibrotischen Typ

Abstract

After rheumatologic conservative medical therapy has been exhausted in degenerative and inflammatory joint diseases, arthroplastic operations are an important option to restore quality of life. Endoprosthesis-associated arthrofibrosis is a severe fibrosing disease of the synovial membrane after endoprosthetic operations. Neither the morphological substrate nor histopathological criteria have been described. The aim was to describe the histopathological substrate of arthrofibrosis and to define histological and immunohistochemical criteria of arthrofibrosis on the basis of tissue samples derived from revision. In histopathological analyses arthrofibrosis revealed a synovialitis with varying fibrosis, without detectable ossification and without minimal wear particle reaction (so-called synovialitis of arthrofibrotic type, SAT). A 3-stage grading was determined based on the cellular density of the fibrous tissue (fibroblast cellularity). In 191 cases with SAT, grade 1 was found in 24.1 % (n = 46), grade 2 was found in 51.8 % (n = 99) and grade 3 was found in 24.1 % (n = 46). The control group consisted of 29 cases with synovialitis of indifferent type (type IV membrane). If SAT grades 2 and 3 are summed together, i.e. the distance between the fibroblasts was less than two cell lengths, the difference of the fibroblast cellularity compared with the type IV membrane was significant (p < 0.001). Above SAT grade 2 the diagnosis of arthrofibrosis could be made with a sensitivity 0.7592 and specificity 0.8276. The SM-alpha-actin cytoplasmic positivity of fibroblasts indicates a myofibroblast phenotype and the β-catenin positivity suggests a resemblance to fibromatosis or a keloid-like process. In the quantitative evaluation of the β-catenin positive fibroblasts, there was a significant difference (p < 0.001) between type IV membrane and SAT. A threshold value of 20 beta-catenin positive cells per microscopic high power field (HPF) was determined, which represents in conjunction with the clinical information a new histopathological diagnosis component (sensitivity 0.720, specificity 0.867).

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

“…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 .…”

Predominance of synovial sensory nerve fibers in arthrofibrosis following total knee arthroplasty compared to osteoarthritis of the knee

“…There are several important starting points in the etiology of AF. Activation of the fibroblast and myofibroblast is an important aspect with increased production of collagen type VI [ 11 ], alpha-smooth muscle protein [ 12 ], β-catenin [ 13 ], reactive oxygen and nitrogen species (also in macrophages and neutrophils) [ 14 ], and bone morphogenic protein type II [ 15 ]. The proinflammatory cytokine interleukin (IL)-1β might also play a role since injection of anakinra, the IL-1 receptor antagonist, was effective in an open study in AF patients [ 16 ].…”

“…In addition, sonographic studies in humans demonstrated increased neovascularization in the synovial tissue and infrapatellar fat pad (Hoffa) [ 4 ]. All these factors relevant for a profibrotic process demonstrate a continuous smoldering low-grade inflammation characterized as a new type of synovialitis [ 13 ].…”

“…Patients were characterized by classical instruments such as the Knee Society Clinical Rating System (KSS), the Knee Injury and Osteoarthritis Outcome Score (KOOS), and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC index) [ 22 – 24 ]. The proliferative process in articular tissue was estimated by cellular density, which was a perfect marker of synovialitis related to AF [ 13 ].…”