Low-intensity laser irradiation stimulates mineralization via increased BMPs in MC3T3-E1 cells.

Background: Previously, we reported that low-intensity laser irradiation accelerated bone formation, and that this mechanism deeply involved insulin-like growth factor I expression. However, as bone formation is supported by many local factors, the mechanism involved in laser irradiation remains incompletely understood. Therefore, the purpose of this study was to determine the effects of laser irradiation on the osteogenic response in vitro.

Low-level laser therapy stimulates mineralization via increased Runx2 expression and ERK phosphorylation in osteoblasts.

Objective: This study examined the effects of low-level laser therapy (LLLT) on osteoblasts via insulin-like growth factor I (IGF-I) signal transduction.

Background: Because orthodontic treatment is usually accompanied by bone formation, if bone formation can be promoted, the treatment and retention periods will be shorter. Recently, we reported the stimulatory effects of LLLT on bone formation.

IL-17A stimulates the expression of inflammatory cytokines via celecoxib-blocked prostaglandin in MC3T3-E1 cells.

Objective: The prostaglandins (PGs) released from osteoblasts can alter the process of bone remodelling. Recently, we showed that compressive force induced the expression of pro-inflammatory cytokine interleukin (IL)-17s and their receptors in osteoblastic MC3T3-E1 cells and that IL-17A was expressed most highly. Consequently, in the current study we examined the effect of IL-17A and/or celecoxib on PGE(2) production and the expression of cyclooxygenases (COXs) and inflammatory cytokines in MC3T3-E1 cells.

Compressive force stimulates the gene expression of IL-17s and their receptors in MC3T3-E1 cells.

During orthodontic tooth movement, cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts can alter the process of bone remodeling. Recently, interleukin-17 (IL-17) was found to stimulate osteoclastic resorption through osteoblasts by inducing receptor activator of nuclear factor κB ligand (RANKL) expression. However, the relationship between mechanical stress and IL-17 production by osteoblasts is not clear.

Compressive force induces osteoclast differentiation via prostaglandin E(2) production in MC3T3-E1 cells.

In orthodontic tooth movement, prostaglandin E(2) (PGE(2)) released from osteoblasts can alter the normal process of bone remodeling. We previously showed that compressive force (CF) controls bone formation by stimulating the production of PGE(2) and Ep2 and/or Ep4 receptors in osteoblasts. The present study was undertaken to examine the effect of CF on the production of PGE(2), cyclooxygenase-2 (COX-2), macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) using osteoblastic MC3T3-E1 cells and to examine the indirect effect of CF on osteoclast differentiation using RAW264.

Effect of compressive force on the expression of inflammatory cytokines and their receptors in osteoblastic Saos-2 cells.

Objective: In orthodontic tooth movement, some cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts on the pressure side can alter the normal processes of bone remodelling, resulting in physiological bone resorption. We examined the effect of compressive force and interleukin (IL)-1 type I receptor antagonist (IL-1ra) on the expression of inflammatory cytokines that promote osteoclast formation, as well as on their receptors, in osteoblastic Saos-2 cells.

Design: The cells were cultured in Dulbecco's modified Eagle medium containing 10% fetal bovine serum with or without continuous compressive force (0.

Compressive force stimulates the expression of osteogenesis-related transcription factors in ROS 17/2.8 cells.

Objective: To determine how compressive force affects the expression of osteogenesis-related transcription factors in osteoblasts.

Design: Cells of ROS 17/2.8, a typical osteoblastic cell line, were cultured with or without continuous compressive force (0.

Effect of compressive force on the production of prostaglandin E(2) and its receptors in osteoblastic Saos-2 cells.

In orthodontic tooth movement, prostaglandin E(2) (PGE(2)) released from osteoblasts can alter the normal process of bone remodeling. We examined the effect of compressive force (CF) on PGE(2) production, PGE receptors (Ep1-4) expression, phosphorylation of protein kinase A (p-PKA), and calcium content in Saos-2 cells. PGE(2) production increased as CF strength.

Effects of compressive force on the differentiation of pluripotent mesenchymal cells.

The purpose of this study was to determine the effect of mechanical stress on the differentiation of the pluripotent mesenchymal cell line C2C12. C2C12 cells were cultured continuously under compressive force (0.25-2.

Lipopolysaccharide enhances the production of nicotine-induced prostaglandin E2 by an increase in cyclooxygenase-2 expression in osteoblasts.

Previous studies have indicated that lipopolysaccharide (LPS) from Gram-negative bacteria in plaque induces the release of prostaglandin E(2) (PGE(2)), which promotes alveolar bone resorption in periodontitis, and that tobacco smoking might be an important risk factor for the development and severity of periodontitis. We determined the effect of nicotine and LPS on alkaline phosphatase (ALPase) activity, PGE(2) production, and the expression of cyclooxygenase (COX-1, COX-2), PGE(2) receptors Ep1>4, and macrophage colony stimulating factor (M-CSF) in human osteoblastic Saos-2 cells. The cells were cultured with 10(-3) M nicotine in the presence of 0, 1, or 10 mug/ml LPS, or with LPS alone.

Functional role of transforming growth factor-beta type III receptor during palatal fusion.

The molecular regulation of palatogenesis continues to be an active area of investigation to provide a foundation for understanding the molecular etiology of cleft palate. Transforming growth factor (TGF) -beta type III receptor (TbetaR-III) has been shown to be specifically expressed in the medial edge epithelium at critical stages of palatal shelf adherence during palatogenesis. The aim of this study was to examine TbetaR-III mRNA localization and expression levels in vivo and to determine the requirement for TbetaR-III expression during palatal fusion in vitro.

Aging stimulates cyclooxygenase-2 expression and prostaglandin E2 production in human periodontal ligament cells after the application of compressive force.

Background And Objectives: Some clinical studies show that alveolar crestal bone loss is higher in adults than in young patients during orthodontic treatment, but the causes of such a phenomenon have not been elucidated. It is known that prostaglandin E2 (PGE2) is a proinflammatory agent and one of the potent osteoclast-inducing factors, and is produced by human periodontal ligament cells in response to orthodontic force. The aim of this study was to investigate age-related change in the biosynthetic capacity of PGE2 and its regulatory gene, cyclooxygenase 2 (COX-2) from periodontal ligament cells in response to mechanical stress.

Inclination of the occlusal plane is associated with the direction of the masticatory movement path.

Using lateral cephalograms and a jaw movement-recording system, the relationship between the masticatory movement path and dentofacial morphology was investigated in 17 subjects (9 males and 8 females, mean age 23.5 years) without a history of orthodontic treatment. The masticatory movement path was measured at the right and left lower first molar while the subjects chewed gum.

Effect of compressive force on the expression of MMPs, PAs, and their inhibitors in osteoblastic Saos-2 cells.

Bone matrix turnover is regulated by matrix metalloproteinases (MMPs), tissue inhibitors of matrix metalloproteinases (TIMPs), and the plasminogen activation system, including tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), and plasminogen activator inhibitor type-1 (PAI-1). We previously demonstrated that 1.0g/cm(2) of compressive force was an optimal condition for inducing bone formation by osteoblastic Saos-2 cells.

Optimal compressive force induces bone formation via increasing bone morphogenetic proteins production and decreasing their antagonists production by Saos-2 cells.

Orthodontic tooth movement induced alveolar bone resorption and formation around the teeth applied mechanical force. Although mechanical force can promote bone formation, the molecular mechanism that underlies this phenomenon is not fully understood. The purposes of this study were to determine how mechanical stress affects the osteogenic response of human osteoblastic cells (Saos-2), and also to examine the optimal compressive force for osteogenesis in vitro.

The effect of IL-1alpha on the expression of matrix metalloproteinases, plasminogen activators, and their inhibitors in osteoblastic ROS 17/2.8 cells.

Interleukin-1 (IL-1) plays key roles in altering bone matrix turnover. This turnover is regulated by matrix metalloproteinases (MMPs), tissue inhibitor of matrix metalloproteinases (TIMPs), and the plasminogen activation system, including tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA) , and plasminogen activator inhibitor type-1 (PAI-1). In this study, we examined the effect of IL-1alpha on the expression of the MMPs, TIMPs, tPA, uPA, and PAI-1 genes in osteoblasts derived from the rat osteosarcoma cell line ROS 17/2.

Lipopolysaccharide stimulates the production of prostaglandin E2 and the receptor Ep4 in osteoblasts.

Previous studies have indicated that one of the causes of alveolar bone destruction with periodontitis is lipopolysaccharide (LPS) from the cell wall of gram-negative bacteria in plaque, and that prostaglandin E(2) (PGE(2)) is one of the bone resorption factors that stimulate osteoclast formation through an intercellular interaction between osteoblasts and osteoclast precursors. The present study was undertaken to determine the effect of LPS on cell growth, alkaline phosphatase (ALPase) activity, the production of PGE(2), and the expression of receptors by PGE(2), cyclooxygenase (COX)-1, and COX-2, using human osteosarcoma cell line Saos-2 as osteoblasts. The cells were cultured with 0, 1, or 10 microg mL(-1) of LPS for up to 14 days.

Optimal compressive force induces bone formation via increasing bone sialoprotein and prostaglandin E(2) production appropriately.

Although orthodontic tooth movement can promote bone formation, the molecular mechanism that underlies this phenomenon is not fully understood. The purposes of this study were to determine how mechanical stress affects the osteogenic response of human osteoblastic cells (Saos-2), and also examine the optimal compression for osteogenesis in vitro. Saos-2 cells cultured with or without continuously compressive force (0.