Bone remodelling induced by physical stress is prostaglandin E2 mediated

Sömjen, Dalia; Binderman, Itzhak; Berger, Esther; Harell, A

doi:10.1016/0304-4165(80)90126-9

Cited by 320 publications

(84 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Both molecules have been demonstrated to mediate a mechanical signal by leading to the activation of phosphorylation of cellular proteins by protein kinases. Furthermore, the role of local chemical mediators, such as prostaglandins (Somjen et al, 1980) and cytokines (Saito et al, 1991), in mechanotransduction has been documented in cultured cells. However, only a few studies have investigated the mechanical response in bone cells at the gene level.…”

Section: (I) Introductionmentioning

confidence: 99%

Effect of Mechanical Loading On Periodontal Cells

Pavlin

Gluhak-Heinrich²

2001

Critical Reviews in Oral Biology & Medicine

View full text Add to dashboard Cite

Mechanical loading is an important regulatory factor in alveolar bone homeostasis, and plays an essential role in maintaining the structure and mass of the alveolar processes throughout lifetime. A better understanding of the cellular and molecular responses of periodontal cells is a prerequisite for further improvements of therapeutic approaches in orthodontics, periodontal and alveolar bone repair and regeneration, implantology, and post-surgical wound healing. The purpose of this review is to provide an insight into some cell culture and animal models used for studying the effects of mechanical loading on periodontal cells, and into the recent developments and utilization of new in vivo animal models. There has been an increased awareness about the need for improvement and development of in vivo models to supplement the widely used cell culture models, and for biological validation of in vitro results, especially in the light of evidence that developmental models may not always reflect bone homeostasis in an adult organism. Due to the limitations of in vivo models, previous studies on mechanical regulation of alveolar bone osteoblasts and cementoblasts mostly focused on proliferative responses, rather than on the stimulation of cell differentiation. To address this problem, we have recently characterized and implemented a mouse osteoinductive tooth movement model for studying mechanically induced regulation of osteoblast-and cementoblast-associated genes. In this model, a defined and reproducible mechanical osteogenic loading is applied during a time course of up to two weeks. Regulation of gene expression in either wild-type or transgenic animals is assessed by a relative quantitative measurement of the level of target mRNAs directly within the subpopulations of periodontal cells. To date, results demonstrate a defined temporal pattern of cellspecific gene regulation in periodontal osteoblasts mechanically stimulated to differentiate and deposit bone matrix. The responses of osteoblast-associated genes to mechanical loading were 10-to 20-fold greater than the increase in the numbers of these cells, indicating that the induction of differentiation and an increase of cell function are the primary responses to osteogenic loading. The progression of the osteoblast phenotype in the intact mouse periodontium was several-fold faster compared with that in cultured cells, suggesting that the mechanical signal may be targeting osteoblast precursors in the state of readiness to respond to an environmental challenge, without the initial proliferative response. An early response of alkaline phosphatase and bone sialoprotein genes was detected after 24 hrs of treatment, followed by a concomitant stimulation of osteocalcin and collagen I between 24 and 48 hrs, and deposition of osteoid after 72 hrs. Although cementoblasts constitutively express biochemical markers similar to those of osteoblasts, distinct responses of osteocalcin, collagen I, and bone sialoprotein genes to mechanical loading were observed in the ...

show abstract

Section: (I) Introductionmentioning

confidence: 99%

Effect of Mechanical Loading On Periodontal Cells

Pavlin

Gluhak-Heinrich²

2001

Critical Reviews in Oral Biology & Medicine

View full text Add to dashboard Cite

show abstract

“…Assays were performed at 30°C in a Gilford 250 automatic recording spectrophotometer using an assay, as described previously [17,181, in [27]. In all cases, the changes in uptake of [3H]thymidine into the cells were much too small to account for the changes in [3H]thymidine incorporation into DNA.…”

Section: Materials and Methods Biochemicalsmentioning

confidence: 99%

Stimulation by defined parathyroid hormone fragments of cell proliferation in skeletal-derived cell cultures

Sömjen¹,

Binderman

Schlüter

et al. 1990

Biochemical Journal

View full text Add to dashboard Cite

We have reported previously that parathyroid hormone (PTH) acts on cultured bone cells to stimulate creatine kinase (CK) activity and [3H]thymidine incorporation into DNA via phosphoinositide turnover, in addition to its other actions via increased cyclic AMP production. We also found that mid-region fragments of PTH stimulate [3H]thymidine incorporation into avian chondrocytes. In the present study of mammalian systems, we demonstrate differential effects of defined synthetic PTH fragments on CK activity and DNA synthesis, as compared with cyclic AMP production, in osteoblast-enriched embryonic rat calvaria cell cultures, in an osteoblast-like clone of rat osteosarcoma cells (ROS 17/2.8) and in chondroblasts from rat epiphysial cartilage cell cultures. Unlike full-length bovine (b)PTH-(1-84) or the fully effective shorter fragment human (h)PTH-(1-34), fragments lacking the N-terminal region of the hormone did not increase cyclic AMP formation, whereas they did stimulate increases in both DNA synthesis and CK activity. Moreover, the PTH fragment hPTH-(28-48) at 10 /M inhibited the increase in cyclic AMP caused by 10 nm-bPTH-(1-84). The increase of CK activity in ROS 17/2.8 cells caused by bPTH-(1-84) or hPTH-(28-48) was completely inhibited by either cycloheximide or actinomycin D, as was shown previously for rat calvaria cell cultures. These results indicated the presence of a functional domain of PTH in the central part of the molecule which exerts its mitogenic-related effects on osteoblast-and chondroblast-like cells in a cyclic AMP-independent manner. Since cyclic AMP formation by PTH leads to bone resorption, specific mid-region fragments of PTH might prove suitable for use in vivo to induce bone formation without concomitant resorption. INTRODUCTIONIn conjunction with its regulation of calcium homeostasis, parathyroid hormone (PTH) can stimulate both net bone formation and resorption, depending on the conditions of application. Increased levels of cyclic AMP [1] are considered to mediate the action of PTH in causing bone resorption [2] and stimulation of ornithine decarboxylase activity [3,4]. On the other hand, PTH has also been shown to exert proliferative and anabolic effects,

show abstract

“…Such (re)-modeling requires bone resorption and deposition by the concerted efforts of osteoblasts and osteoclasts. Several studies have demonstrated that, in the absence of the systemic and local factors, mechanical loading on osteoblasts in vitro is able to increase prostaglandin release (4), stimulate cell division (5), alter collagen synthesis (6), and promote collagenase activity (7). Other induced proteins such as insulin-like growth factors I and II, transforming growth factor-␤, osteocalcin, osteopontin, nitric-oxide synthase, and cyclooxygease-2 have also been reported (8).…”

mentioning

confidence: 99%

Protein Kinase C-δ Transactivates Platelet-derived Growth Factor Receptor-α in Mechanical Strain-induced Collagenase 3 (Matrix Metalloproteinase-13) Expression by Osteoblast-like Cells

Yang

Hsieh

Yao

et al. 2009

Journal of Biological Chemistry

View full text Add to dashboard Cite

Mechanical strain to bone is considered to be important for the maintenance of bone integrity and architecture. The process of bone (re)modeling under mechanical loading may repair fatigue damage and improve bone strength (1-3). Such (re)-modeling requires bone resorption and deposition by the concerted efforts of osteoblasts and osteoclasts. Several studies have demonstrated that, in the absence of the systemic and local factors, mechanical loading on osteoblasts in vitro is able to increase prostaglandin release (4), stimulate cell division (5), alter collagen synthesis (6), and promote collagenase activity (7). Other induced proteins such as insulin-like growth factors I and II, transforming growth factor-␤, osteocalcin, osteopontin, nitric-oxide synthase, and cyclooxygease-2 have also been reported (8).Previously, we reported that mechanical strain induces collagenase 3 (MMP-13) 2 expression by MC3T3-E1 osteoblastlike cells (9). The MMP-13 mRNA induction is transient, stable, and does not require de novo protein synthesis, suggesting that an immediate action be taken by strained osteoblasts to participate in the resorption phase of matrix (re)modeling. MMP-13 is a neutral proteinase capable of degrading native fibrillar collagens in the extracellular space (10, 11). It may be involved in situations where rapid and effective remodeling of collagenous extracellular matrix is required. Hence, MMP-13 can be detected in primary fetal ossification during bone morphogenesis, and in remodeling of the mature skeletal tissue (12,13).Mechanical strain induction of MMP-13 may be mediated through a process of mechanotransduction, converting physical forces into biochemical signals and integrating these signals into cellular responses. In our stretch chamber system, we showed that the mechanotransduction utilizes the MEK/ERK signaling pathway to implement MMP-13 expression (9). However, the transduction mechanism involved remains unclear and awaits further investigation. Three lines of studies have prompted us to investigate the receptor of platelet-derived growth factor receptor (PDGFR) as a potential mechanoreceptor in the MMP-13 induction. PDGF-BB induces MMP-13 expression in osteoblasts (14, 15), whereas in vascular smooth

show abstract

Bone remodelling induced by physical stress is prostaglandin E2 mediated

Cited by 320 publications

References 21 publications

Effect of Mechanical Loading On Periodontal Cells

Effect of Mechanical Loading On Periodontal Cells

Stimulation by defined parathyroid hormone fragments of cell proliferation in skeletal-derived cell cultures

Protein Kinase C-δ Transactivates Platelet-derived Growth Factor Receptor-α in Mechanical Strain-induced Collagenase 3 (Matrix Metalloproteinase-13) Expression by Osteoblast-like Cells

Contact Info

Product

Resources

About