The synovial-like membrane at the bone-cement interface in loose total hip replacements and its proposed role in bone lysis.

The small ubiquitin‐like modifier mediates the resistance of prosthesis‐loosening fibroblast‐like synoviocytes against fas‐induced apoptosis

“…This is also of interest for aseptic prosthesis loosening, because it has been demonstrated that the inflamed synovial membrane in RA and the synovium-like interface membrane in aseptic prosthesis loosening share some important features (1,11), and several lines of evidence suggest that fibroblasts derived from this membrane exhibit an aggressive phenotype that is similar to that of RA FLS (12,13). Therefore, we set out to study the apoptotic response of prosthesis-loosening FLS in comparison with that of RA FLS and investigated whether posttranslational modifications by SUMO-1 (in a manner similar to that in RA FLS) contributes to the resistance of prosthesis-loosening FLS to programmed cell death.…”

“…It is characterized by the development and destructive growth of a synovium-like membrane at the interface between the implanted prosthesis and bone (1,2). Synovium-like membrane formation is widely considered a foreign body reaction initiated by wear debris particles from the prosthesis.…”

“…However, the cellular and molecular mechanisms that initiate development of this membrane and promote its growth remain incompletely understood. Multiple data suggest that in addition to macrophages, fibroblasts of the synovium-like membrane play an important role in aseptic loosening, and there is evidence that the synovial membrane in rheu-matoid arthritis (RA) and the synovium-like membrane share certain similarities in both their cellular properties and their destructive behavior (1)(2)(3). Specifically, it has been hypothesized that during their differentiation from bone marrow progenitors, prosthesis-loosening fibroblastlike synoviocytes (FLS) acquire features of cellular activation that are similar to those seen in RA FLS.…”

Emerging Ideas: Instability-induced Periprosthetic Osteolysis Is Not Dependent on the Fibrous Tissue Interface

“…With prosthetic aseptic loosening, a fibroblast-rich tissue forms at the bone-implant interface [4,6,9,10,16,24]. This fibrous layer may serve different roles in the periprosthetic zone: one mechanical, leading to component subsidence, and the other biologic, in which osteoclastogenic cytokines are expressed.…”

“…This fibrous layer may serve different roles in the periprosthetic zone: one mechanical, leading to component subsidence, and the other biologic, in which osteoclastogenic cytokines are expressed. At the time of revision surgery, the fibrous tissue has been shown in several studies to have the capacity to produce multiple proinflammatory cytokines such as prostaglandin E2, collagenase [8][9][10], and receptor activator of nuclear factor kappaB ligand (RANKL) [18]. This fibrous tissue was found to be heavily infiltrated with particulate cement and polyethylene debris [9], leading to the hypothesis that fibroblasts in the interface membrane respond to particulate wear debris, stimulating the release of osteoclastogenic cytokines [13].…”