Docosahexaenoic Acid Inhibits Osteoclastogenesis via FFAR4-Mediated Regulation of Inflammatory Cytokines.

Osteoclastogenesis-the activation and differentiation of osteoclasts-is one of the pivotal processes of bone remodeling and is regulated by RANKL/RANK signaling, the decoy function of osteoprotegerin (OPG), and a cascade of pro- and anti-inflammatory cytokines. The disruption of this balance leads to pathological bone loss in diseases such as osteoporosis and rheumatoid arthritis. FFAR4 (Free Fatty Acid Receptor 4), a G protein-coupled receptor for long-chain omega-3 fatty acids, has been confirmed as a key mediator of metabolic and anti-inflammatory effects.

The Role of Cytokines in Orthodontic Tooth Movement.

A challenge in orthodontic treatment is the long time taken to move teeth, which extends the long treatment period. Accordingly, various treatment protocols and orthodontic materials have been developed to shorten the orthodontic treatment period. However, controlling biological reactions is considered necessary to further shorten this treatment period.

Evaluation of the effects for root resorption in orthodontic tooth movement with micro-osteoperforations in mice.

Background/purpose: Orthodontic treatment is one of the most demanding procedures available for both patients and clinicians. The challenges stem from the extended duration to achieve desired results, often necessitating surgical interventions, such as micro-osteoperforations (MOPs). This study aimed to investigate the biological effects and extent of changes resulting from these interventions.

Ultra-broadband ptychography for dispersive samples.

X-ray ptychography has emerged as a powerful imaging tool on X-ray synchrotron facilities. Implementation of ptychography on laboratory-scale X-ray sources has largely been hindered by their poor temporal coherence and low flux. Here we propose an ultra-broadband method incorporating structured illumination to enhance the robustness of ptychography to broadband sources.

Osteocyte necroptosis drives osteoclastogenesis and alveolar bone resorption during orthodontic tooth movement.

Orthodontic tooth movement (OTM) has been described as a bone remodeling process mediated by the expression of various inflammatory cytokines, including tumor necrosis factor-α (TNF-α). Necroptosis is a form of regulated cell death that is mainly induced by TNF-α, leading to the release of damage-associated molecular patterns (DAMPs) that cause inflammation. However, the role of osteocyte necroptosis in regulating osteoclastogenesis during OTM remains unclear.

Exacerbating orthodontic tooth movement in mice with salt-sensitive hypertension.

Background/purpose: Orthodontic tooth movement (OTM) is a critical aspect of dental treatment that requires the precise control of bone remodeling processes. Hypertension (HTN) can affect the effectiveness of OTM. Salt-sensitive hypertension (SSHTN) is of particular concern due to its detrimental effects on bone health, potentially altering orthodontic outcomes.

Angiotensin II Promotes Osteocyte RANKL Expression via AT1R Activation.

Osteocytes are the most abundant cell type in the skeleton, with key endocrine functions, particularly in regulating osteoblast and osteoclast activity to maintain bone quality. Angiotensin II (Ang II), a critical component of the renin-angiotensin-aldosterone system, is well-known for its role in vasoconstriction during hypertension. Beyond its cardiovascular functions, Ang II participates in various biological processes, including bone metabolism.

Role of CXCL10 released from osteocytes in response to TNF-α stimulation on osteoclasts.

Tumor necrosis factor-alpha (TNF-α) is a significant cytokine that regulates bone resorption under inflammatory conditions. However, its mechanism of action in osteocytes remains unclear. In this study, highly purified osteocytes were isolated from dentin matrix protein 1 (DMP1)-Topaz mice using cell sorter.

(D-Ala)GIP Inhibits Inflammatory Bone Resorption by Suppressing TNF-α and RANKL Expression and Directly Impeding Osteoclast Formation.

Glucose-insulinotropic polypeptide (GIP) is an incretin hormone that induces insulin secretion and decreases blood glucose levels. In addition, it has been reported to suppress osteoclast formation. Native GIP is rapidly degraded by dipeptidyl peptidase-4 (DPP-4).

Rotational position error correction in ptychography.

Accurate determination of scan positions is essential for achieving high-quality reconstructions in ptychographic imaging. This study presents and demonstrates a method for determining the rotation angle of the scan pattern relative to the detector pixel array using diffraction data. The method is based on the Fourier-Mellin transform and cross-correlation calculation.

Azilsartan inhibits inflammation-triggered bone resorption and osteoclastogenesis via suppression of TNF-α expression in macrophages.

Introduction: Hypertension is a major risk factor for cardiovascular disease (CVD) and is associated with increased bone loss due to excessive activity of the local renin-angiotensin system (RAS). Angiotensinogen/Angiotensin (ANG) II/Angiotensin II type 1 receptor (AT1R) axis is considered as the core axis regulating RAS activity. Azilsartan is an FDA-approved selective AT1R antagonist that is used to treat hypertension.