Local administration of high-dose diabetes medicine exendin-4 inhibits orthodontic tooth movement in mice.

Objectives: To investigate the effects of exendin-4 on orthodontic tooth movement distance, root resorption, and expression levels of osteoclast-related cytokines in a mouse model.

Materials And Methods: A 10-g NiTi coil spring was placed between the anterior alveolar bone and upper left first molar of 8-week-old male C57BL/6 mice. Twenty microliters of exendin-4 solution (containing 0.

Effect of a DPP-4 Inhibitor on Orthodontic Tooth Movement and Associated Root Resorption.

Objectives: Dipeptidyl peptidase-4 (DPP-4) inhibitors are used as a treatment for type 2 diabetes mellitus and have also recently been applied to enhance bone quality and density, and increase the expression of bone markers. This study aimed to investigate the effect of a DPP-4 inhibitor on orthodontic tooth movement (OTM) and related root resorption in a mouse model.

Materials And Methods: Mice were randomly divided into three groups: those undergoing OTM with the addition of a DPP-4 inhibitor (30 g), those undergoing OTM and receiving phosphate-buffered saline (PBS), and those without force loading (control group).

Anti-c-fms Antibody Prevents Osteoclast Formation and Bone Resorption in Co-Culture of Osteoblasts and Osteoclast Precursors In Vitro and in Ovariectomized Mice.

Osteoporosis morphology is characterized by bone resorption and decreases in micro-architecture parameters. Anti-osteoporosis therapy targets osteoclasts because bone resorption is a unique function of osteoclasts. Anti-c-fms antibodies against the receptor for macrophage colony-stimulating factor (M-CSF) inhibit osteoclast formation and bone resorption in vitro and in vivo.

Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption.

The process of bone remodeling is the result of the regulated balance between bone cell populations, namely bone-forming osteoblasts, bone-resorbing osteoclasts, and the osteocyte, the mechanosensory cell type. Osteoclasts derived from the hematopoietic stem cell lineage are the principal cells involved in bone resorption. In osteolytic diseases such as rheumatoid arthritis, periodontitis, and osteoporosis, the balance is lost and changes in favor of bone resorption.

Obtaining Primary Osteocytes through Murine Calvarial Fractionation of GFP-Expressing Osteocytes.

The osteocyte, once thought to be a passive resident of the bone given the backstage function of sensing mechanical loading, is now brought to the spotlight and has been shown to have multiple major functions like actively modifying the extracellular matrix and forming an endocrine organ with the lacunocanalicular system that encloses it sending messages to distant sites. Owing to the methods that made it possible to test the osteocyte in vitro from isolating primary osteocytes to osteocyte-like cell lines, osteocytes are now experiencing a resounding interest and a surge of knowledge on structure and function. Many aspects of the osteocyte biology and interaction with other molecular components are yet to be discovered.

TNF-α stimulates the expression of RANK during orthodontic tooth movement.

Objective: This study aimed to evaluate the effects of tumor necrosis factor (TNF)-α on receptor activator of nuclear factor-κB (RANK) expression in osteoclast precursors in vitro and during orthodontic tooth movement (OTM) in vivo.

Design: We assessed whether TNF-α influenced RANK expression levels in osteoclast precursors in vitro by real-time PCR and western blotting. For in vivo experiments, TNF-α was subcutaneously injected into mouse calvariae daily for 5 days.

IL-33 Inhibits TNF-α-Induced Osteoclastogenesis and Bone Resorption.

Interleukin (IL)-33 is a member of the IL-1 family, which acts as an alarmin. Several studies suggested that IL-33 inhibited osteoclastogenesis and bone resorption. Tumor necrosis factor-α (TNF-α) is considered a direct inducer of osteoclastogenesis.

TNF-α Directly Enhances Osteocyte RANKL Expression and Promotes Osteoclast Formation.

Osteoimmunology peeks into the interaction of bone and the immune system, which has largely proved to be a multiplex reaction. Osteocytes have been shown to regulate bone resorption through the expression of RANKL in physiologic and pathologic conditions. TNF-α, a product of the immune system, is an important cytokine regulating bone resorption in inflammatory conditions either directly or by increasing RANKL and M-CSF expressions by osteoblasts and stromal cells.

TNF-α is responsible for the contribution of stromal cells to osteoclast and odontoclast formation during orthodontic tooth movement.

Compressive force during orthodontic tooth movement induces osteoclast formation in vivo. TNF-α plays an important role in mouse osteoclast formation and bone resorption induced by compressive force during orthodontic tooth movement. Stromal cells, macrophages and T cells take part in TNF-α-induced osteoclast formation in vitro.

Effect of TNF--Induced Sclerostin on Osteocytes during Orthodontic Tooth Movement.

Osteocytes are abundant cells in bone, which contribute to bone maintenance. Osteocytes express receptor activator of nuclear factor kappa-B ligand (RANKL) and regulate osteoclast formation. Orthodontic tooth movement (OTM) occurs by osteoclast resorption of alveolar bone.

Establishment of an orthodontic retention mouse model and the effect of anti-c-Fms antibody on orthodontic relapse.

Orthodontic relapse after orthodontic treatment is a major clinical issue in the dental field. However, the biological mechanism of orthodontic relapse is still unclear. This study aimed to establish a mouse model of orthodontic retention to examine how retention affects the rate and the amount of orthodontic relapse.

Docosahexaenoic Acid Inhibits Inflammation-Induced Osteoclast Formation and Bone Resorption Through GPR120 by Inhibiting TNF-α Production in Macrophages and Directly Inhibiting Osteoclast Formation.

Docosahexaenoic acid (DHA) is an n-3 fatty acid that is an important structural component of the cell membrane. DHA exerts potent anti-inflammatory effects through G protein-coupled receptor 120 (GPR120), which is a functional receptor for n-3 fatty acids. DHA also regulates osteoclast formation and function.

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro.

Bone remodeling is a complex process and it involves periods of deposition and resorption. Bone resorption is a process by which bone is broken down by osteoclasts in response to different stimuli. Osteoclast precursors differentiate into multinuclear osteoclasts in response to macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor Kappa-B ligand (RANKL).

DPP-4 inhibitor impedes lipopolysaccharide-induced osteoclast formation and bone resorption in vivo.

Objectives: Dipeptidyl peptidase 4 (DPP-4) inhibition is a new therapeutic strategy for type 2 diabetic patients. DPP-4 has been reported to enhance inflammation. However, the effect of DPP-4 inhibition on inflammation remains unknown.

C-X-C Motif Chemokine 12 Enhances Lipopolysaccharide-Induced Osteoclastogenesis and Bone Resorption In Vivo.

C-X-C motif chemokine 12 (CXCL12) belongs to the family of CXC chemokines. Lipopolysaccharide (LPS) induces inflammation-induced osteoclastogenesis and bone resorption, and in recent years, stimulatory effects of CXCL12 on bone resorption have also been reported. In the present study, we investigated the effects of CXCL12 on LPS-induced osteoclastogenesis and bone resorption.

The Glucagon-Like Peptide-1 Receptor Agonist Exendin-4 Inhibits Lipopolysaccharide-Induced Osteoclast Formation and Bone Resorption via Inhibition of TNF- Expression in Macrophages.

Glucagon-like peptide-1 (GLP-1) receptor agonists are an effective treatment approach for type 2 diabetes. Recently, anti-inflammatory effects of GLP-1 receptor agonists have also been reported. Lipopolysaccharide (LPS) induces inflammation and osteoclast formation.

Role of Muramyl Dipeptide in Lipopolysaccharide-Mediated Biological Activity and Osteoclast Activity.

Lipopolysaccharide (LPS) is an endotoxin and bacterial cell wall component that is capable of inducing inflammation and immunological activity. Muramyl dipeptide (MDP), the minimal essential structural unit responsible for the immunological activity of peptidoglycans, is another inflammation-inducing molecule that is ubiquitously expressed by bacteria. Several studies have shown that inflammation-related biological activities were synergistically induced by interactions between LPS and MDP.

Perineural invasion and expression of nerve growth factor can predict the progression and prognosis of oral tongue squamous cell carcinoma.

Background: Perineural invasion (PNI) and nerve growth factor (NGF) expression are found to be significantly associated with the progression and/or prognosis of several human cancers.

Methods: Immunohistochemical staining for S-100 and NGF proteins was performed to assess the PNI and NGF expression level in 116 oral tongue squamous cell carcinoma (OTSCC) specimens, respectively.

Results: The PNI rate increased from 22% of the original pathological report, through 39% after reevaluation of hematoxylin and eosin-stained tissue sections, to 51% with the help of anti-S-100 immunostaining.

Oral traumatic ulcerative granuloma with stromal eosinophilia: A clinicopathological study of 34 cases.

Background/purpose: Traumatic ulcerative granuloma with stromal eosinophilia (TUGSE) is a special oral ulcerative lesion that shares many clinical features of an oral squamous cell carcinoma. This study reports the clinicopathological features of 34 oral TUGSE lesions in Taiwanese patients.

Methods: Thirty-four TUGSE cases were retrieved from the files of the Department of Oral Pathology and Oral Diagnosis, National Taiwan University Hospital from 2003 to 2009.

Increased expression of MCM5 is significantly associated with aggressive progression and poor prognosis of oral squamous cell carcinoma.

Background: Overexpression of MCM5 protein has been found to be significantly associated with the progression and prognosis of several human cancers.

Methods: This study used immunohistochemistry to examine the expression of MCM5 protein in 97 specimens of oral squamous cell carcinomas (OSCC), 80 specimens of oral epithelial dysplasia (OED, including 31 mild, 29 moderate, and 20 severe OED samples), and 20 specimens of normal oral mucosa (NOM).

Results: We found that the mean nuclear MCM5 labeling indices (LIs) increased significantly from NOM (15 ± 6%), through mild (25 ± 10%), moderate (34 ± 9%), and severe OED (43 ± 12%), to OSCC samples (61 ± 16%, P < 0.