Collectively, we show that RTA-408 inhibits NF-κB signaling by suppressing the recruitment of TRAF6 to STING, in addition to attenuating osteoclastogenesis and OVX-induced bone loss in vivo, suggesting that it could be a promising candidate for treating osteoporosis in the future.
Taken together, our results show that circulating miR-19b plays an important role in enhancing osteoblastogenesis, possibly through regulation of the PTEN/pAKT/Runx2 pathway, and may be a useful therapeutic target in bone loss disorders, such as osteoporosis.
These findings suggest that Snx10 and PIKfyve are involved in the regulation of endosome/lysosome homeostasis via the synthesis of PI(3,5)P2 and may point to a new strategy to prevent bone loss.
Collectively, we show that RTA-408 inhibits NF-κB signaling by suppressing the recruitment of TRAF6 to STING, in addition to attenuating osteoclastogenesis and OVX-induced bone loss in vivo, suggesting that it could be a promising candidate for treating osteoporosis in the future.
This is a retrospective study of 77 rTHA cases with severe acetabular bone loss (Paprosky ≥ 2C) treated exclusively with a DM cup (NOVAE STICK; Serf, Décines-Charpieu, France) cemented into a cage (Kerboull cross, Burch-Schneider, or ARM rings).
In order to demonstrating the ICAM-1 might possess a dual effects on osteoclastognesis by directly affecting the adhesion of mature osteoclast and indirectly participates the RANKL/RANK induced osteoclastic precursors differentiation, however, these results still should be conducted by a series study for further demonstrating, but the further exploring on the role of ICAM-1 in osteoclastogenesis will definitely provide a promising therapeutic targets for treating bone loss diseases.
Accordingly, our finding suggests a critical role of miR-325-3p in linking inflammation to impaired cementum regeneration and provides a potential possibility for applying miR-325-3p inhibitors in the treatment of periodontitis-related bone loss.
In summary, miR-181b-5p/OSM axis could be a viable therapeutic target for patients with surgically removed primary tumors to reduce bone metastasis and prevent bone loss.
Collectively, we show that RTA-408 inhibits NF-κB signaling by suppressing the recruitment of TRAF6 to STING, in addition to attenuating osteoclastogenesis and OVX-induced bone loss in vivo, suggesting that it could be a promising candidate for treating osteoporosis in the future.
These findings suggest that Snx10 and PIKfyve are involved in the regulation of endosome/lysosome homeostasis via the synthesis of PI(3,5)P2 and may point to a new strategy to prevent bone loss.
In this study, we established experimental periodontitis (EP) on transgenic mice overexpressing miR-335-5p (335-Tg) to investigate the novel effects of miR-335-5p on periodontal inflammation and bone loss.
This is a retrospective study of 77 rTHA cases with severe acetabular bone loss (Paprosky ≥ 2C) treated exclusively with a DM cup (NOVAE STICK; Serf, Décines-Charpieu, France) cemented into a cage (Kerboull cross, Burch-Schneider, or ARM rings).
TNF-α in gingival crevicular fluid was significantly higher in bone loss group (p < 0.01); MMP-8 (p = 0.34) by MMP-9 (p < 0.05) in bone loss group obtained lower values than in control group.
The cancellous bone osteopenia was no longer observed after the intraperitoneal administration of antibodies directed to the negative regulatory region (NRR) of Notch3.
We discovered that PIP5k1β deletion in mice resulted in obvious bone loss and that PIP5K1β was highly expressed during both osteoclast and osteoblast differentiation.
Conditional knockout of SH3BP2 and SYK in myeloid lineage cells with LysM-Cre mice recapitulated the reduced bone loss without affecting both inflammatory cytokine expression and osteoclast induction, suggesting that the SH3BP2-SYK axis plays a key role in regulating alveolar bone loss by mechanisms that regulate the bone-resorbing function of osteoclasts rather than differentiation.
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, block inflammatory mediators, upregulate antioxidant enzymes and bone formation markers.
• Standard ACR QCT-cutoff values for osteoporosis (< 80 mg/cm <sup>3</sup> ) and osteopenia (≤ 120 mg/cm <sup>3</sup> ) can also be applied scanner independently in calibrated opportunistic QCT.
We previously demonstrated that Rgs12 is essential for osteoclast differentiation and its deletion in vivo protected mice against pathological bone loss.
Patients with CP and uncontrolled T2D presented severe periodontal disease and inflammation (PPD, p = 0.0072; CAL, p = 0.0480; bone loss, p = 0.0088), higher levels of CASP1 mRNA expression (p = 0.0026), a stronger pattern of staining for NLRP3 and ASC proteins in the epithelium and connective tissues, and significantly higher production of IL-18 (p = 0.0063) and IL-1β (p = 0.0018) in comparison with healthy or CP subjects.
Low bone turnover osteopenia has been reported in mice with conditional deletion of the PKD1 and PKD2 genes in osteoblasts, and preliminary clinical data also suggest suppressed bone turnover in patients with ADPKD.
Bone loss and endocrine dysfunction are potential late complications of allogeneic stem cell transplant (allo-SCT); however, scant information concerning the long-term effects in SCT adult patients is available.