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    • Receptor activator of NF B ligand RANKL and

    2022-06-30

    Receptor activator of NF-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) stimulate the generation of osteoclast Azithromycin Dihydrate [10], [11], [12], [13]. In response to sphingosine 1-phosphate (S1P) signaling, osteoclasts then attach to regions of bone undergoing resorption [14]. In RA when S1P is expressed at higher levels, sphingosine kinase (Sphk) 1 is also present at higher levels and this leads to resistance to Fas-mediated death signaling (Fig. 2) [15], [16]. The activity and number of osteoclasts are modulated by rates of cell death and cell differentiation [17]. Communication between osteoclasts and osteoblasts or T cells is also mediated by RANKL and S1P receptor 1 (S1P1), and this signaling promotes cell regulation, proliferation, migration, apoptosis, expression of inflammatory genes [18], [19], [20], chemotaxis [21], and differentiation [22], [23]. Events downstream of RANKL binding to osteoclasts involves the activation of various signaling pathways, including nuclear factor of activated T cells cytoplasmic 1 (NFATc1), Akt/PKB, NF-κB, JNK, p38, and ERK, to induce the differentiation, activity, and survival of osteoclasts [14], [24]. In addition, RANKL binding of osteoclast progenitor cells leads to upregulation of Fas expression via NF-κB, thereby resulting in osteoclast cells being targets of Fas-stimulated apoptosis [25]. To promote cell death, Fas-stimulated apoptosis in osteoclasts involving the release of cytochrome c from mitochondria and activation of both caspase 3 and caspase 9 [17]. To date, the predominant strategies for decreasing bone resorption include the addition of estrogen, tamoxifen, or certain bisphosphonates to accelerate the death rate of osteoclasts or decrease osteoclast formation [17], [26], [27], [28], [29], [30]. In this review, we discuss our findings that osteoclast activity-dependent Fas/S1P1 signaling via activation of NF-κB mediates the development of RA and bone resorption in the TMJ. In addition, a prospective therapeutic intervention involving administration of SN50 to block signaling by p50 NF-κB to attenuate osteoclastogenesis in the pathogenesis of temporomandibular joint rheumatoid arthritis (TMJ-RA) is discussed.
    TMJ-RA The TMJ is needed for sliding and hinge movements of the jaw. Consequently, it is the most frequently used joint in the body [31]. The TMJ is composed of an articular disc and the mandibular condyle which provide upper and lower articular cavities between the condyle and the glenoid fossa [32]. Unlike other synovial joints, the condyle of the mandible of the TMJ produces less type I collagen [33], its superficial layer does not produce type II collagen, and its articular surfaces consist of fibrous tissue rather than hyaline cartilage [34]. In addition, mandibular condyle cartilage originates from cranial neural crest cells and is considered a secondary cartilage of the chondroskeleton [35]. Clinically, the TMJ is involved in 4–80% of RA cases [36], [37], [38]. This wide range is due on the different examinations performed, the different selection of the patient populations and age distribution, the duration of the RA occurs, the different diagnostic criteria for classifying joint involvement, and the imaging techniques used [5], [37], [38], [39], [40], [41], [42], [43]. However, more than 50% of patients with RA complaints about TMJ discomfort [36], [44], [45]. Manifestation of RA in the TMJ can include swelling, pain, impaired movement, and crepitation. These characteristics are similar to the manifestations of RA in other joints, and these symptoms usually correlate well with radiographic change observed in joints. Specifically in the TMJ, radiographic changes can include erosion, the presence of a subcortical cyst, and a gradual decrease in joint space due to granulation, deossification, pencil head, or spiked deformity of the condylar head [41], [44]. Several studies were found in TMJ-RA. Proteoglycan-induced arthritis mice showed a degradation of cartilage matrix in TMJ due to the effects of the cytokines from the inflamed joints [46]. The ratio of RANKL and OPG was significantly increased in TMJ of collagen-induced acetate rats [47]. The pathway of TMJ involvement in human RA was found to be the same as in other joints based on the analysis of histological findings [48]. However, it should be emphasized that due to the originates difference of the cartilage of TMJ and other joints [35], the pathogenesis of RA in TMJ may differ from the other joints.