Here, we show that deleting Pinch1 in osteocytes and mature osteoblasts using the 10-kb mouse Dmp1-Cre and Pinch2 globally (double KO; dKO) results in severe osteopenia throughout life, while ablating either gene does not cause bone loss, suggesting a functional redundancy of both factors in bone.
Here, we show that deleting Pinch1 in osteocytes and mature osteoblasts using the 10-kb mouse Dmp1-Cre and Pinch2 globally (double KO; dKO) results in severe osteopenia throughout life, while ablating either gene does not cause bone loss, suggesting a functional redundancy of both factors in bone.
Here, we show that deleting Pinch1 in osteocytes and mature osteoblasts using the 10-kb mouse Dmp1-Cre and Pinch2 globally (double KO; dKO) results in severe osteopenia throughout life, while ablating either gene does not cause bone loss, suggesting a functional redundancy of both factors in bone.
To compare associations of current and past self-reported bone-specific physical activity, and current accelerometer-determined physical activity (PA), with bone structure (bone mineral density [BMD] and microarchitecture) in postmenopausal women with osteopenia or osteoporosis.
To compare associations of current and past self-reported bone-specific physical activity, and current accelerometer-determined physical activity (PA), with bone structure (bone mineral density [BMD] and microarchitecture) in postmenopausal women with osteopenia or osteoporosis.
There are no studies that have evaluated the correlation between self-rated pain, peri-implant clinical and radiographic parameters (plaque index [PI], bleeding on probing [BOP], probing depth [PD], and crestal bone loss [CBL]) and whole salivary interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) levels among patients with and without peri-implantitis.
There are no studies that have evaluated the correlation between self-rated pain, peri-implant clinical and radiographic parameters (plaque index [PI], bleeding on probing [BOP], probing depth [PD], and crestal bone loss [CBL]) and whole salivary interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) levels among patients with and without peri-implantitis.
There are no studies that have evaluated the correlation between self-rated pain, peri-implant clinical and radiographic parameters (plaque index [PI], bleeding on probing [BOP], probing depth [PD], and crestal bone loss [CBL]) and whole salivary interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) levels among patients with and without peri-implantitis.
The hypothesis is that self-rated peri-implant oral symptoms (OS) and clinical (plaque index [PI] and probing depth [PD]) and radiographic (crestal bone loss [CBL]) are higher in (cigarette-smokers [CS]) and (waterpipe-users) than (nonsmokers [NS]).
In conclusion, PAAE activates the BMP-2/Smad1, 5/Runx2 pathway to induce osteoblastic differentiation and mineralization in BMSCs and can inhibit OVX-induced bone loss.
In conclusion, PAAE activates the BMP-2/Smad1, 5/Runx2 pathway to induce osteoblastic differentiation and mineralization in BMSCs and can inhibit OVX-induced bone loss.
CONCLUSIONS The SIRT6-TRPV1-CGRP signal axis is the key to regulating OD in hMSCs, which could be a potential therapeutic target for osteoporosis and bone loss-related diseases.
CONCLUSIONS The SIRT6-TRPV1-CGRP signal axis is the key to regulating OD in hMSCs, which could be a potential therapeutic target for osteoporosis and bone loss-related diseases.
The clinical parameters, radiographic bone loss and the levels of SLIT3, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in GCF were measured.
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.
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.
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.
Moreover, although a previous study has demonstrated moderate osteopenia in 12 week-old Pls3-deficient mice based on μCT scanning, there is no reported analysis of such a model on the basis of undecalcified histology and bone-specific histomorphometry.
In addition, administration of an anti-S100A4 monoclonal antibody (mAb) that we developed attenuated the stimulation of osteoclastogenesis and bone loss by mtMDA in mice.