Development and characteristics of a synovial‐like interface membrane around cemented tibial hemiarthroplasties in a novel rat model of aseptic prosthesis loosening

Pap, G.; Machner, A.; Rinnert, Torsten; Hörler, Dorothy; Gay, Renate E.; Schwarzberg, H; Neumann, Wolfram; Michel, Beat A.; Gay, Steffen; Pap, Thomas

doi:10.1002/1529-0131(200104)44:4<956::aid-anr153>3.3.co;2-v

Cited by 18 publications

(27 citation statements)

References 6 publications

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“…This shortcoming is also true in the animal models, as demonstrated by a modified rat model that incorporated a running wheel for 2 h/day for 5 days/week. 64 Despite…”

Section: Animal Modelsmentioning

confidence: 99%

Aseptic loosening

2004

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“…This shortcoming is also true in the animal models, as demonstrated by a modified rat model that incorporated a running wheel for 2 h/day for 5 days/week. 64 Despite…”

Section: Animal Modelsmentioning

confidence: 99%

Aseptic loosening

2004

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“…3 4 A major drawback of TJA is so called "aseptic loosening". 5 The aetiology of this condition is blamed on two major factors (a) particles of polyethylene (PE), bone cement, ceramics, or metal resulting from wear (wear particles) stimulate macrophages to produce resorption stimulating factors and thus lead to periprosthetic osteolysis; [6][7][8][9][10] or (b) lack of initial stability, which is considered essential for osseointegration. 11 12 Apart from aseptic loosening, loosening may be induced by periprosthetic infection (septic loosening), which originates from minimal bacterial contamination during surgery or from bacteria that reach the prosthesis via the bloodstream or lymphatic system.…”

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confidence: 99%

Proposal for a histopathological consensus classification of the periprosthetic interface membrane

2006

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Aims:The introduction of clearly defined histopathological criteria for a standardised evaluation of the periprosthetic membrane, which can appear in cases of total joint arthroplasty revision surgery.Methods:Based on histomorphological criteria, four types of periprosthetic membrane were defined: wear particle induced type (detection of foreign body particles; macrophages and multinucleated giant cells occupy at least 20% of the area; type I); infectious type (granulation tissue with neutrophilic granulocytes, plasma cells and few, if any, wear particles; type II); combined type (aspects of type I and type II occur simultaneously; type III); and indeterminate type (neither criteria for type I nor type II are fulfilled; type IV). The periprosthetic membranes of 370 patients (217 women, 153 men; mean age 67.6 years, mean period until revision surgery 7.4 years) were analysed according to the defined criteria.Results:Frequency of histopathological membrane types was: type I 54.3%, type II 19.7%, type III 5.4%, type IV 15.4%, and not assessable 5.1%. The mean period between primary arthroplasty and revision surgery was 10.1 years for type I, 3.2 years for type II, 4.5 years for type III and 5.4 years for type IV. The correlation between histopathological and microbiological diagnosis was high (89.7%), and the inter-observer reproducibility sufficient (85%).Conclusion:The classification proposed enables standardised typing of periprosthetic membranes and may serve as a tool for further research on the pathogenesis of the loosening of total joint replacement. The study highlights the importance of non-infectious, non-particle induced loosening of prosthetic devices in orthopaedic surgery (membrane type IV), which was observed in 15.4% of patients.

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Meinecke

Pap

Mendoza

et al. 2009

Arthritis & Rheumatism

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Objective. To study the expression of small ubiquitin-like modifier 1 (SUMO-1) in aseptic loosening of prosthesis implants and to investigate its role in regulating the susceptibility of prosthesis-loosening fibroblastlike synoviocytes (FLS) to Fas-induced apoptosis.Methods. Specimens of aseptically loosened tissue were obtained at revision surgery, and the expression of SUMO-1 was analyzed by in situ hybridization. SUMO-1 levels in FLS were determined by quantitative polymerase chain reaction and Western blot analysis. Immunohistochemistry and confocal microscopy were used to study the subcellular localization of SUMO-1. The functional role of SUMO-1 in Fas-induced apoptosis of prosthesis-loosening FLS was investigated by small interfering RNA-mediated knockdown of SUMO-1 and by gene transfer of the nuclear SUMO-specific protease SENP1.Results. SUMO-1 was expressed strongly in aseptically loosened tissue and was found prominently at sites adjacent to bone. Prosthesis-loosening FLS expressed levels of SUMO-1 similar to the levels expressed by rheumatoid arthritis (RA) FLS, with SUMO-1 being found mainly in promyelocytic leukemia protein nuclear bodies. Knockdown of SUMO-1 had no effect on spontaneous apoptosis but significantly increased the susceptibility of prosthesis-loosening FLS to Fas-induced apoptosis. Gene transfer of the nuclear SUMO-specific protease SENP1 reverted the apoptosis-inhibiting effects of SUMO-1. Conclusion. These data suggest that SUMO-1 is involved in the activation of both RA FLS and prosthesis-loosening FLS by preventing these cells from undergoing apoptosis. Modification of nuclear proteins by SUMO-1 contributes to the antiapoptotic effects of SUMO-1 in prosthesis-loosening FLS, providing evidence for the specific activation of sumoylation during their differentiation. Therefore, SUMO-1 may be an interesting target for novel strategies to prevent aseptic prosthesis loosening.Aseptic loosening of prosthetic implants is a major long-term complication of joint replacement surgery. 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 rheuSupported in part by the DFG (grants Pa689/2 and Pa689/3) and the Arbeitsgemeinschaft Rheumaorthopädie of the German Society of Rheumatology.

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Development and characteristics of a synovial‐like interface membrane around cemented tibial hemiarthroplasties in a novel rat model of aseptic prosthesis loosening

Cited by 18 publications

References 6 publications

Aseptic loosening

Aseptic loosening

Proposal for a histopathological consensus classification of the periprosthetic interface membrane

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

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