Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • Therefore the histomorphology and the

    2022-07-21

    Therefore, the histomorphology and the comprehensive analysis of TMJ-RA pathogenesis need to be completed although clinical findings in TMJ-RA are similar to RA in other joints [41]. Especially for the dentist, the difficulties associated with diagnosing TMJ-RA patients [49] posing challenges to diagnose and recover the effects of TMJ-RA.
    Fas-deficiency in RA pathogenesis Fas antigen is expressed in various tissues, including the thymus. Fas antigen also shares structural homology with many cell-surface receptors (e.g., tumor necrosis factor (TNF) receptors) and has been shown to mediate apoptosis [50]. In human RA, FLICE-inhibitory protein (FLIP) an antiapoptotic protein, has been detected in synovial tissues and fibroblast-like synoviocytes (FLS) culture. It has been reported that FLS of RA is sensitized to promote Fas mediated-apoptosis by the down-regulation of FLIP [51]. In mice, the Fas antigen gene maps to chromosome 19 and mice that carry a lymphoproliferation mutation (MRL/lpr mice) have been found to have defects in the Fas antigen gene [52], [53]. An aberrant transcription factor in MRL/lpr mice causes premature termination of Fas transcription, and this results in aberrant splicing of Fas mRNA (Fig. 2) [54]. The clinical symptoms exhibited by MRL/lpr mice include hypergammablobulinaemia, production of anti-DNA antibodies, rheumatoid factor (RF), arthritis, and glomerulonephritis. Moreover, the latter closely resembles human autoimmune systemic lupus erythematosus (SLE) [55]. MRL/lpr mice are suitable as a model to study an immune complex disease, to determine the etiology, and to evaluate the therapies. Several studies were done using MRL/lpr mice, such as the effect of the radiation therapy to ameliorate the autoimmune disease [56], the therapeutic effects of Artemisinin analog SM934 to ameliorate lupus syndromes [57], allergic PI-3065 in blepharitis [58], the analysis pathogenesis of Graft-versus-host disease (GVHD)-like wasting syndrome by defects in Fas-mediated lymphocyte apoptosis [59], and histopathological analysis of spontaneous arthritis [60], [61]. The pathogenesis of RA in MRL/lpr mice particularly involves interactions between osteoclast cells and immune cells (e.g., activated dendritic cells (DCs) with peripheral T cells) via RANKL activation. Thus, a possible therapeutic treatment for lymphoproliferative and autoimmune arthritis has been tested in MRL/lpr mice with induction of Fas-independent apoptosis of CD4+ T cells via TRAIL/TRAIL-R2 which was achieved by performing multiple transfers of activated and Fas-deficient DCs [62], [63]. It has been reported that osteoprotegerin (OPG) induces apoptosis in osteoclast and osteoclast precursor via Fas/FasL pathway. OPG has been shown to trigger the increase of Bax/Bcl-2 ratio and the level of activated cleaved-caspase 9 and caspase 3 in dose-dependent manner [64]. When staining for tartrate-resistant acid phosphatase (TRAP) was performed in long bones and the TMJs of MRL/lpr mice and control mice, the former contained a greater number of osteoclasts. This observation suggests that mutation of Fas leads to prolonged survival of osteoclasts (Fig. 2) [17], [65]. Correspondingly, defects in Fas have been associated with a greater number of osteoclasts and subsequent reductions in bone mineral density, bone volume, and trabecular thickness [17].
    S1P, a cell-derived lysophospholipid growth factor [66], is the final metabolite of the sphingolipid pathway and it is generated from Sphk and S1P lyase [67]. S1P binds G protein-coupled receptors (GPCRs) at the cell surface, particularly the S1P1–5 receptors (Fig. 3) [68], to mediate a wide variety of essential cellular processes: cell differentiation, survival, proliferation, migration, and invasion, as well as angiogenesis and trafficking of immune cells [69], [70], [71], [72]. While S1P1–3 are widely expressed in various tissues, expression of S1P4 and S1P5 is restricted to immune cells and cells of the central nervous system [73], [74].