Elucidating the mechano-molecular dynamics of TRAP activity using CRISPR/Cas9 mediated fluorescent reporter mice.

Osteoclasts are essential for bone remodeling by adapting their resorptive activity in response to their mechanical environment. However, the molecular mechanisms underlying this process remain unclear. Here, we demonstrated the role of tartrate-resistant acid phosphatase (TRAP, Acp5), a key enzyme secreted by osteoclasts, in bone remodeling and mechanosensitivity.

Toll-like receptor-2 induced inflammation causes local bone formation and activates canonical Wnt signaling.

It is well established that inflammatory processes in the vicinity of bone often induce osteoclast formation and bone resorption. Effects of inflammatory processes on bone formation are less studied. Therefore, we investigated the effect of locally induced inflammation on bone formation.

Laser-Modified Ti Surface Improves Paracrine Osteogenesis by Modulating the Expression of DKK1 in Osteoblasts.

Titanium surface modifications are widely used to modulate cellular behavior by recognition of topographical cues. However, how those modifications affect the expression of mediators that will influence neighboring cells is still elusive. This study aimed to evaluate the effects of conditioned media from osteoblasts cultured on laser-modified titanium surfaces on the differentiation of bone marrow cells in a paracrine manner and to analyze the expression of Wnt pathway inhibitors.

Stimulation of Osteoclast Formation by Oncostatin M and the Role of WNT16 as a Negative Feedback Regulator.

Oncostatin M (OSM), which belongs to the IL-6 family of cytokines, is the most potent and effective stimulator of osteoclast formation in this family, as assessed by different in vitro assays. Osteoclastogenesis induced by the IL-6 type of cytokines is mediated by the induction and paracrine stimulation of the osteoclastogenic cytokine receptor activator of nuclear factor κ-B ligand (RANKL), expressed on osteoblast cell membranes and targeting the receptor activator of nuclear factor κ-B (RANK) on osteoclast progenitor cells. The potent effect of OSM on osteoclastogenesis is due to an unusually robust induction of RANKL in osteoblasts through the OSM receptor (OSMR), mediated by a JAK-STAT/MAPK signaling pathway and by unique recruitment of the adapter protein Shc1 to the OSMR.

Biocompatibility of new calcium aluminate cement: tissue reaction and expression of inflammatory mediators and cytokines.

Introduction: The aim of this study was to evaluate the biocompatibility of a new calcium aluminate cement (EndoBinder) in subcutaneous tissue of rats in comparison with mineral trioxide aggregate and calcium hydroxide hard-setting cement.

Methods: Polyethylene tubes (1.5 × 10 mm) containing the dental cements were implanted into dorsal subcutaneous tissue of 30 rats.

Osteogenesis-inducing calcium phosphate nanoparticle precursors applied to titanium surfaces.

This study investigated the effects of the morphology and physicochemical properties of calcium phosphate (CaP) nanoparticles on osteogenesis. Two types of CaP nanoparticles were compared, namely amorphous calcium phosphate (ACP) nano-spheres (diameter: 9-13 nm) and poorly crystalline apatite (PCA) nano-needles (30-50 nm × 2-4 nm) that closely resemble bone apatite. CaP particles were spin-coated onto titanium discs and implants; they were evaluated in cultured mouse calvarial osteoblasts, as well as after implantation in rabbit femurs.

The expression of chemokines CCL19, CCL21 and their receptor CCR7 in oral squamous cell carcinoma and its relevance to cervical lymph node metastasis.

The purpose of this study is to determine the expression of CCL19, CCL21, and CCR7 in samples of oral squamous cell carcinoma (OSCC) and their relationship with clinical and microscopic parameters. A comparative analysis was made of the mRNA expression of these chemokines and receptor in OSCC and normal oral mucosa. The immunoexpression of CCR7, CCL19, and CCL21 was also verified in OSCC and lymph nodes.

Expression of suppressor of cytokine signaling 1 and 3 in ligature-induced periodontitis in rats.

Objective: Evaluate expression of inducible negative regulators of JAK/STAT pathway and their target proteins during the course of ligature-induced experimental periodontal disease in rats.

Design: Rats were sacrificed 07, 15 and 30 days after disease induction for histological evaluation of periodontal inflammation and macroscopic analysis of alveolar bone loss. SOCS expression and the activation status of STAT1 and STAT3 were evaluated in gingival biopsies by real time PCR and Western blot.

Effects of intrapulpal temperature change induced by visible light units on the metabolism of odontoblast-like cells.

Purpose: To investigate the effects of intrapulpal temperature changes induced by a quartz tungsten halogen (QTH) and a light emitting diode (LED) curing units on the metabolism of odontoblast-like cells.

Methods: Thirty-six 0.5 mm-thick dentin discs obtained from sound human teeth were randomly assigned into three groups: QTH, LED and no light (control).

Cytotoxic effects and pulpal response caused by a mineral trioxide aggregate formulation and calcium hydroxide.

Purpose: To evaluate the in vivo pulpal response after pulpotomy with different capping agents. In addition, the in vitro cytotoxic effects of both materials were assessed by applying them on culture of pulp cells.

Methods: For the in vivo test, the coronal pulp of 28 teeth of dogs was mechanically removed and the root pulps were capped with the following dental materials: Group 1: Pro-Root MTA (PRMTA); and Group 2 (control): calcium hydroxide saline paste (CH).

Cytotoxic effects of different concentrations of chlorhexidine.

Purpose: To evaluate the cytotoxic effects of different concentrations of Chlorhexidine (Chx) to the odontoblast cell line MDPC-23.

Methods: The odontoblast-like cells were seeded (30,000 cells/cm2) in 60 wells of 24-well dishes and then incubated in contact with the following experimental and control solutions: Group 1: 0.0024% Chx; Group 2: 0.