2019
DOI: 10.1007/s00011-019-01274-4
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Immunoexpression of canonical Wnt and NF-κB signaling pathways in the temporomandibular joint of arthritic rats

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Cited by 18 publications
(24 citation statements)
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“…The Wnt/β-catenin signaling pathway is a classical Wnt signaling pathway, and it is also the most detailed and important Wnt signaling pathway currently studied. The Wnt/β-catenin pathway can affect the process and prognosis of RA by affecting the proliferation of fibroblast-like synoviocytes and regulating the secretion of inflammatory factors and bone metabolism/bone destruction [4][5][6][7].…”
Section: Introductionmentioning
confidence: 99%
“…The Wnt/β-catenin signaling pathway is a classical Wnt signaling pathway, and it is also the most detailed and important Wnt signaling pathway currently studied. The Wnt/β-catenin pathway can affect the process and prognosis of RA by affecting the proliferation of fibroblast-like synoviocytes and regulating the secretion of inflammatory factors and bone metabolism/bone destruction [4][5][6][7].…”
Section: Introductionmentioning
confidence: 99%
“…Related studies demonstrated that interaction of CRP with its receptor promoted proin ammatory cytokines (IL-1β, IL-6 and TNF-α) production, leading to ampli cation of in ammatory reaction [26,36]. And in CFA induced TMJ in ammation, IL-1β and TNF-α acted as the speci c up-regulated proin ammatory factors [11,12,37]. By PCR analysis and IHC staining in synovial membrane, we found lower level of IL-1β and IL-6 in CFA + CRP group compared to CFA group (Fig.…”
Section: Discussionmentioning
confidence: 99%
“…In ammation is believed to be the vital factor for this pathological process, since pro-in ammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukins IL-1β and IL-6 are elevated in synovial uid of TMD patients [6,10]. While up-regulated in ammation factors aggravate TMJ-OA development, medical treatments targeted on in ammatory cytokines and signaling pathways show bene t effects on in ammation absorption and TMJ-OA recovery [11,12]. TNF-α inhibitors and IL-1 receptor antagonist are the well-established therapeutic approaches for RA treatment [13][14][15], and antibodies to TNF-α, IL-1β and IL-6 show positive effects during RA therapy investigation [16,17].…”
Section: Introductionmentioning
confidence: 99%
“…The OA symptoms are subchondral bone sclerosis; synovial inflammation includes synovial hyperplasia, fibrosis, and thickening of the synovial capsule, activated synoviocytes, and in some cases, lymphocytic infiltrate (B- and T-cells as well as plasma cells), cartilage degradation, ligament calcification, and osteophyte formation [ 3 ]. The pathogenesis of OA involves the interaction between mechanical, genetic, metabolic, and inflammatory mechanisms [ 4 , 5 ]. Traditional pharmacological therapies and nonpharmacological treatments such as surgical procedures can only provide symptomatic relief; however, damaged cartilage cannot be restored effectively [ 6 ].…”
Section: Introductionmentioning
confidence: 99%