Results 61 to 70 of about 182,622 (382)

Use of Denosumab in Children With Osteoclast Bone Dysplasias: Report of Three Cases. [PDF]

open access: yes, 2019
Denosumab has been used successfully to treat disease-associated osteoclast overactivity, including giant cell tumor of bone. Given its mechanism of action, denosumab is a potent potential treatment of other osteoclast bone dysplasias including central ...
Bernthal, Nicholas M   +8 more
core   +2 more sources

Vav1 inhibits RANKL-induced osteoclast differentiation and bone resorption [PDF]

open access: yes, 2019
Vav1 is a Rho/Rac guanine nucleotide exchange factor primarily expressed in hematopoietic cells. In this study, we investigated the potential role of Vav1 in osteoclast (OC) differentiation by comparing the ability of bone marrow mononuclear cells (BMMCs)
Cha, Young-Nam   +6 more
core   +2 more sources

Impact of Janus Kinase Inhibition with Tofacitinib on Fundamental Processes of Bone Healing [PDF]

open access: yes, 2020
Both inflammatory diseases like rheumatoid arthritis (RA) and anti-inflammatory treatment of RA with glucocorticoids (GCs) or non-steroidal anti-inflammatory drugs (NSAIDs) negatively influence bone metabolism and fracture healing.
Brinkman, Antonia Clara Katharina   +10 more
core   +1 more source

Diabetes Medication Metformin Inhibits Osteoclast Formation and Activity in In Vitro Models for Periodontitis

open access: yesFrontiers in Cell and Developmental Biology, 2022
Diabetes and periodontitis are comorbidities and may share common pathways. Several reports indicate that diabetes medication metformin may be beneficial for the periodontal status of periodontitis patients.
Lucy Y. Tao   +8 more
doaj   +1 more source

METTL3 Modulates Osteoclast Differentiation and Function by Controlling RNA Stability and Nuclear Export

open access: yesInternational Journal of Molecular Sciences, 2020
Osteoclast differentiation and function are crucial for maintaining bone homeostasis and preserving skeletal integrity. N6-methyladenosine (m6A) is an abundant mRNA modification that has recently been shown to be important in regulating cell lineage ...
Di Li   +4 more
semanticscholar   +1 more source

The Origin of Osteoclasts

open access: yesImmunobiology, 1982
We are satisfied from studies with mi mi osteopetrotic mutant mice that osteoclasts arise from the myeloid tissue of bone marrow and not as formerly proposed from osteoprogenitor cells. Grafts of compatible normal myeloid cells cure the osteopetrosis by the substitution of the qualitatively defective osteoclasts with normal ones.
J.F. Loutit, N.W. Nisbet
openaire   +3 more sources

Brucella and Osteoarticular Cell Activation: Partners in Crime [PDF]

open access: yes, 2017
Osteoarticular brucellosis is the most common presentation of human active disease although its prevalence varies widely. The three most common forms of osteoarticular involvement are sacroiliitis, spondylitis, and peripheral arthritis.
Adamopoulos   +95 more
core   +1 more source

Hormone-stimulated modulation of endocytic trafficking in osteoclasts [PDF]

open access: yes, 2012
Copyright @ 2012 Stenbeck, Lawrence and Albert. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and ...
Albert, AP, Lawrence, KM, Stenbeck, G
core   +2 more sources

Osteoprotegerin reduces osteoclast resorption activity without affecting osteogenesis on nanoparticulate mineralized collagen scaffolds. [PDF]

open access: yes, 2019
The instructive capabilities of extracellular matrix-inspired materials for osteoprogenitor differentiation have sparked interest in understanding modulation of other cell types within the bone regenerative microenvironment.
Bischoff, David   +11 more
core  

Calcium‐sensing receptor induces the apoptosis of chondrocytes in cooperation with phosphate transporter

open access: yesFEBS Open Bio, EarlyView.
Excess Ca2+ ions activate the Calcium‐Sensing Receptor (CaSR), which subsequently drives the uptake of excess inorganic phosphate (Pi) via the Pi transporter (Pit−1) in chondrocytes. This mechanism causes a toxic increase in intracellular Pi concentration, ultimately leading to chondrocyte apoptosis and pathological mineralization. Excess extracellular
Sachie Nakatani   +7 more
wiley   +1 more source

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