Mechanical Compressive Force Research Articles

Theoretical and Experimental Advances in High-Pressure Behaviors of Nanoparticles.

Using compressive mechanical forces, such as pressure, to induce crystallographic phase transitions and mesostructural changes while modulating material properties in nanoparticles (NPs) is a unique way to discover new phase behaviors, create novel nanostructures, and study emerging properties that are difficult to achieve under conventional conditions. In recent decades, NPs of a plethora of chemical compositions, sizes, shapes, surface ligands, and self-assembled mesostructures have been studied under pressure by in-situ scattering and/or spectroscopy techniques. As a result, the fundamental knowledge of pressure-structure-property relationships has been significantly improved, leading to a better understanding of the design guidelines for nanomaterial synthesis. In the present review, we discuss experimental progress in NP high-pressure research conducted primarily over roughly the past four years on semiconductor NPs, metal and metal oxide NPs, and perovskite NPs. We focus on the pressure-induced behaviors of NPs at both the atomic- and mesoscales, inorganic NP property changes upon compression, and the structural and property transitions of perovskite NPs under pressure. We further discuss in depth progress on molecular modeling, including simulations of ligand behavior, phase-change chalcogenides, layered transition metal dichalcogenides, boron nitride, and inorganic and hybrid organic-inorganic perovskites NPs. These models now provide both mechanistic explanations of experimental observations and predictive guidelines for future experimental design. We conclude with a summary and our insights on future directions for exploration of nanomaterial phase transition, coupling, growth, and nanoelectronic and photonic properties.

The effect of light compressive and tensile mechanical forces on SOST and POSTN expressions in human periodontal ligament cells: an in vitro study.

Periodontal ligament (PDL) cells play an important role in mechanosensing and secretion of signaling molecules during bone remodeling. However, the regulatory mechanism is unknown. The aim of the present study is to investigate the expression pattern of periostin and sclerostin in response to orthodontic forces in periodontal ligament cells in vitro. PDL cells were isolated from extracted teeth and treated with compressive forces of 25gr/cm2 or equiaxial tension forces at frequency 1Hz for 0, 24, 48, and 72h. qRT-PCR was applied to evaluate the gene expressions. The secretion of sclerostin and periostin was assessed using ELISA. DAPI staining was used to evaluate apoptosis. The expression of sclerostin elevated significantly at protein and gene levels under compression forces after 24h, while the application of tensile forces induced the expression of periostin and its upstream regulator RUNX2 (p < 0.05). Gene expression up-regulation was significant for POSTN and RUNX2 after 48 and 72h tensile forces. Also, the gene expression of sclerostin reduced in a time-dependent manner after application of tensile force. The compression forces enhanced apoptosis to 7.5 ± 3.5% and induced gene expression of apoptotic markers of CASP9, and BCL2 within 72h of exposure. Periostin and sclerostin play an important role in orthodontic loads and their expressions are affected oppositely by compressive and tensile forces that might be suggested as a biomarkerfor assessment of bone remodeling during orthodontic treatment.

Osteoclast-like activity of U937 cells, peripheral blood mononuclear cells, and periodontal ligament fibroblasts subjected to mechanical stress by centrifugal force

Several in vitro models have investigated the consequences of mechanical stimuli on osteoclasts (OCs). However, the mechanisms whereby mechanical forces trigger osteoclast responses remain poorly understood, and the generation of reactive oxygen species (ROS) and their relationship with bone resorption in OCs under the influence of mechanical forces require investigation. The present work examined the role of centrifugal force application on ROS production and its effect on osteoclast activity and differentiation. Human U937 macrophage cells, peripheral blood mononuclear cells (PBMCs), and periodontal ligament (PDL) fibroblasts treated with polyethylene glycol (PEG) or N-acetylcysteine (NAC) were subject to centrifugal force. Osteoclast markers such as tartrate-resistant acid phosphatase (TRAP) and bone resorption activities were measured. ROS levels and actin ring formation were determined. Also, U937 cell responses to centrifugal force and PEG-induced fusion were studied. Individual cells subjected to centrifugal exertion increased their ROS levels, formed actin-like rings, revealed TRAP expression and bone resorption activities, and expressed typical osteoclast markers. Control PEG-fused U937 cells also showed these effects, and cell treatment with NAC stopped all these responses. Centrifugal force, as well as PEG-induced cell fusion, can promote osteoclast-like features, including oxidative stress. The present experimental model allowed us to understand the mechanisms underlying the osteoclast differentiation associated with ROS production stimulated by mechanical compressive force, where NAC can contribute to reducing this oxidative stress condition.

Effects of compressive stress combined with mechanical vibration on osteoclastogenesis in RAW 264.7 cells.

To investigate the effects of compressive force and/or mechanical vibration on NFATc1, DCSTAMP, and CTSK (cathepsin K) gene expression and the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells in RAW 264.7 cells, a murine osteoclastic-like cell line. RAW 264.7 cells were subjected to mechanical vibration, compressive force, or compressive force combined with vibration. Cell viability and the numbers of TRAP-positive multinucleated cells were evaluated. NFATc1, DCSTAMP, and CTSK gene expressions were analyzed using real-time quantitative reverse transcription polymerase chain reaction. Compressive force combined with mechanical vibration significantly increased the numbers of TRAP-positive multinucleated cells but did not significantly affect cell viability. In addition, compressive force combined with mechanical vibration significantly increased NFATc1, DCSTAMP, and CTSK mRNA expression compared with compressive force or vibration alone. Compressive force combined with mechanical vibration induces osteoclastogenesis and upregulates NFATc1, DCSTAMP, and CTSK gene expression in RAW 264.7 cells. These results provide more insight into the mechanisms by which vibratory force accelerates orthodontic tooth movement.

LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling

Temporomandibular joint OA (TMJOA) is a common degenerative joint disease, leads to structural damage and ultimately loss of function. Matrix degradation is one of the first pathogenesis during the progression of OA, it was effective to inhibit matrix degradation to block the development of OA. In this study, an in vivo model (compressive mechanical force) and an in vitro model (IL-1β) were used to induce OA-like changes in TMJ cartilage and chondrocytes. We revealed lysyl oxidase like-2 (LOXL2) play a critical role in TMJOA. LOXL2 expression decreased in mechanical stress/IL-β induced TMJOA-like lesions in both in vivo models and in vitro models. Furthermore, recombinant LOXL2 (rhLOXL2) treatment ameliorated the degenerative changes induced by mechanical stress in vivo, including the thinning cartilage, down-expression of collagen II and proteoglycan, and over-expression of TNF-a, while LOXL2 antibody (anti-LOXL2) treatment exacerbated these changes. Mechanistically, the protection of LOXL2 in chondrocytes was induced partly through activation of the Integrin/FAK pathway. The inhibition of the Integrin/FAK pathway could neutralized the effects caused by rhLOXL2. Collectively, our study suggests that the LOXL2 plays a protective role in mechanical stress induced TMJOA-like changes, and the Integrin/FAK pathway may be a key downstream pathway in this process.

Modeling the effect of softening in magnetoactive elastomers

Magnetoactive elastomers (MAE) are composites in which a polymer matrix is filled with microparticles of an isotropic ferromagnet with a low coercive force. The functionality of such materials is due to their ability to change the structure under the influence of an external magnetic field and is determined by the interaction of particles and a matrix on mesoscopic (the order of particle size) scales. In MAE, the effect of softening has been experimentally observed. This effect consists in the fact that in the range of deformations from 0,1 to 1%, the effective modulus of elasticity of the material drops sharply. This work looks into the development of a simple numerical model that qualitatively describes this softening effect. The formation of a chain of particles in an applied magnetic field and its destruction under the action of tensile and compressive mechanical forces are considered. The obtained results clarified the mechanisms of softening in MAE.

Effect of high fat diet and excessive compressive mechanical force on pathologic changes of temporomandibular joint

The aim of this study was to investigate the effect of high fat diet and excessive compressive mechanical force on temporomandibular joint. In vivo, a mouse model of temporomandibular joint compressive loading device was used. A high fat diet mouse model and a combined mouse model intraperitoneally treated with or without simvastatin were used in the study. The pathological changes of mandibular condylar cartilage were assessed by Safranin-O staining. The IL-1β, MMP-3, leptin expression changes in the cartilage were detected by immunohistochemistry. In vitro, the mandibular condylar chondrocytes were treated with or without L-1β and simvastatin. The mRNA expression level of matrix MMPs and leptin were assessed. Both excessive compressive mechanical force and high fat diet induced obesity caused TMJ osteoarthritis-like changes and increased expression of IL-1β, MMP-3, and leptin. These pathological changes were much more serious when the two interventions were exerted together, while simvastatin could obviously alleviate these changes. The mRNA expression of MMP-3, MMP-13, and leptin increased in the IL-1β treated chondrocytes treated with IL-1β, and decreased with simvastatin treatment. The development of temporomandibular joint pathological changes could be caused by the excessive compressive mechanical force and high fat diet induced obesity.

Osteocytes promote osteoclastogenesis via autophagy-mediated RANKL secretion under mechanical compressive force

Osteocytes sense extracellular mechanical stimuli and transduce them into biochemical signals to regulate bone remodeling. The function is also evidenced in orthodontic tooth movement. But the underlying mechanisms haven't been clarified. Autophagy is an evolutionarily conserved cellular catabolic process which affects cellular secretory capabilities. We hypothesized that mechanical force activated osteocyte autophagy through TFE3-related signaling and further promoted osteocyte-mediated osteoclastogenesis. In the present study, we demonstrated that osteocyte autophagy was activated under mechanical compressive force using murine orthodontic tooth movement model since the number of LC3B-positive osteocytes increased by 3-fold in the compression side. In addition, both in vitro mechanical compression and chemical autophagy agonist increased the secretion of RANKL in osteocytes by 3-fold and 4-fold respectively, which is a crucial cytokine for osteoclastogenesis. Lastly, conditioned medium collected from compressed osteocytes promoted the development of osteoclasts. These results suggest that osteocytes could promote osteoclastogenesis via autophagy-mediated RANKL secretion under mechanical compressive force. Our research might provide evidence for exploring methods to accelerate tooth movement in clinic.

Synergistic alveolar bone resorption by diabetic advanced glycation end products and mechanical forces.

The association between diabetes mellitus (DM) and bone diseases is acknowledged. However, the mechanistic pathways leading to the alveolar bone (AB) destruction remain unclear. This study aims to elucidate the mechanical forces (MF)-induced AB destruction in DM and its underlying mechanism. In vivo periodontal tissue responses to MF were evaluated in rats with diabetes. In vitro human periodontal ligament (PDL) cells were either treated with advanced glycation end products (AGEs) alone or with AGEs and MF. In vivo, the transcription of VEGF-A, colony stimulating factor-1 (CSF-1), and Ager was upregulated in diabetes, whereas changes in DDOST and Glo1 mRNAs were negligible. DM induced VEGF-A protein in the vascular cells of the PDL and subsequent angiogenesis, but DM itself did not induce osteoclastogenesis. MF-induced AB resorption was augmented in DM, and such augmentation was morphologically substantiated by the occasional undermining resorption as well as the frontal resorption of the AB by osteoclasts. The mRNA levels of CSF-1 and vascular endothelial growth factor (VEGF) during MF application were highly elevated in diabetes, compared with those of the normal counterparts. In vitro, AGEs treatment elevated Glut-1 and CSF-1 mRNA levels via the p38 and JNK pathways, whereas OGT and VEGF levels remained unchanged. Compressive MF especially caused upregulation of VEGF, CSF-1, and Glut-1 levels, and such upregulation was further enhanced by AGEs treatment. Overloaded MF and AGEs metabolites may synergistically aggravate AB destruction by upregulating CSF-1 and VEGF. Therefore, regulating the compressive overloading of teeth, as well as the levels of diabetic AGEs, may prove to be an effective therapeutic modality for managing DM-induced AB destruction.

Vibration enhances PGE2 , IL-6, and IL-8 expression in compressed hPDL cells via cyclooxygenase pathway.

Although vibration combined with orthodontic force may accelerate orthodontic tooth movement, little is known about the mechanisms that regulate the associated cellular responses. The goal of this study was to investigate whether mechanical vibration combined with compressive force regulates cyclooxygenase (COX)-2/prostaglandin E2 (PGE2 ) and interleukin (IL)-6 and IL-8 messenger RNA (mRNA) and protein expression in human periodontal ligament (hPDL) cells via the COX pathway. The primary cultured hPDL cells were exposed to mechanical vibration, compressive force or a combination of both mechanical vibration and compressive force at 24, 48, and 72hours. The COX-2, IL-6, IL-8, receptor activator of nuclear factor kappa-Β ligand (RANKL), and osteoprotegrin (OPG) mRNA expressions were determined using quantitative real-time polymerase chain reaction (qPCR). The PGE2 , IL-6, and IL-8 protein expressions were quantified by enzyme-linked immunosorbent assay (ELISA). To demonstrate whether the expression of PGE2 , IL-6, and IL-8 was in the COX-dependent pathway, the hPDL cells were treated with indomethacin. To determine whether PGE2 stimulated the hPDL cells to express IL-6 and IL-8, exogenous PGE2 was added to the culture media. The combination of mechanical vibration and compressive force synergistically upregulated RANKL/OPG, COX-2/PGE2 , IL-6 and IL-8 mRNA, and protein expression. The indomethacin significantly attenuated the increases of PGE2 , IL-6, and IL-8 expression in cells stimulated with compressive force or mechanical vibration combined with compressive force. In addition, exogenous PGE2 increased IL-6 and IL-8 mRNA and protein expressions in hPDL cells. Mechanical vibration may enhance alveolar bone resorption at the compression side during orthodontic tooth movement via a mechanism involving the cyclooxygenase pathway.

BIO alleviated compressive mechanical force-mediated mandibular cartilage pathological changes through Wnt/β-catenin signaling activation.

Osteoarthritis induced by compressive mechanical force is characterized by decreased chondrocyte proliferation and degradation of the ECM. To examine underlying mechanisms of the pathological changes of mandibular cartilage induced by compressive mechanical force, an established animal model was used to examine Wnt signaling activation by glycogen synthase kinase-3 beta (GSK3β) inhibitor 6-Bromoindirubin-3'-oxime (BIO) injection in vivo. Histological changes in mandibular cartilage were assessed via hematoxylin & eosin (HE), masson, and alcian blue staining. Immunohistochemistry and real-time PCR were performed to evaluate activation of the Wnt signaling pathway and chondrocytes proliferation markers. Chondrocytes apoptosis was examined by TUNEL staining. During the compressive mechanical force loading-mediated process, Wnt signaling was largely inhibited, which showed the inhibited expression of β-catenin and the increased expression of GSK-3β. The expression of chondrocytes proliferation markers Ki67, and proliferating cell nuclear antigen (PCNA) also decreased. With BIO injection, the Wnt signaling was restored and the proliferation of mandibular chondrocytes was also increased in the late stage (7 days) of compressive mechanical force loading. Finally, the decreasing mandibular cartilage thickness, the degradation of extracellular matrix, and the erosion of bone trabecula were subsequently restored. Also, the changes of extracellular matrix markers such as collagen II and collagen X, matrix metalloproteases, and inflammatory cytokines were reversed followed by the injection of BIO. In summary, compressive mechanical force decreased endogenously Wnt signaling, leading to impaired proliferation in chondrocytes and degradation in cartilage matrix. Restoration of Wnt signaling largely recovered the proliferation defects and alleviated the pathological changes of mandibular cartilage. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1228-1237, 2018.

Influence of Some Physical Properties of Cassava Tubers on Mechanical Compressive Cracking force of TMS 30572 and TMS 4(2)1425 Cassava Varieties

The influence of some physical properties of cassava tubers on the mechanical compressive cracking force of TMS 30572 and TMS 4(2)1425 cassava varieties were investigated. 1200 tubers were freshly harvested from the Teaching and Research Farm of the Obafemi Awolowo University, Ile-Ife, Nigeria. Each of the cassava cultivars was about 1.5 years old. The tubers were cleaned and sliced into different lengths ranging from 25 – 150 mm in steps of 25 mm. Slices of a particular length were sorted into 8 diameter groups: 21 – 30, 31 – 40, 41 – 50, 51 – 60, 61 – 70, 71 – 80, 81 – 90, and 91 – 100 mm, for each variety. The compressive cracking force of the sliced tubers was determined using an adapted Tensometer. The mechanical compressive cracking force required to break the tubers of the two cassava varieties (TMS 30572 and TMS 4(2)1425) increases with increase in length and peel thickness of tubers while it decreases with increase in diameter of tubers. Thus, these physical properties must be given a serious attention in the design and development of cassava peeling machine.

Buckling delamination of a PZT/Metal/PZT sandwich rectangular thick plate containing interface inner band cracks

This work studies the 3D buckling delamination problem around the interface band cracks which are in the PZT/Metal/PZT sandwich rectangular thick plate within the scope of the piecewise homogeneous body model by utilizing the so-called 3D linearized theory of stability loss for piezoelectric materials. It is assumed that the plate is simply supported with respect to mechanical quantities and short-circuit conditions with respect to the electric potential along all its lateral edge-surfaces. On the face planes of the PZT layers, the open-circuit condition with respect to the electrical displacement is satisfied. It is also assumed that on the opposite two ends of the plate which are parallel to the band cracks’ front, uniformly distributed normal compressive mechanical forces act. The critical values of these forces under are determined by employing an initial imperfection criterion. For solution of the corresponding boundary value problems the 3D FEM is utilized and numerical results on the critical forces and on the influence of the problem parameters on these forces are presented and discussed. In particular, it is established that the piezoelectricity of the face layers and the three dimensionality of the problem cause to increase the values of the critical forces.

Cementogenesis is inhibited under a mechanical static compressive force via Piezo1.

To investigate whether Piezo1, a mechanotransduction gene mediates the cementogenic activity of cementoblasts under a static mechanical compressive force. Murine cementoblasts (OCCM-30) were exposed to a 2.0 g/cm2 static compressive force for 3, 6, 12, and 24 hours. Then the expression profile of Piezo1 and the cementogenic activity markers osteoprotegerin (Opg), osteopontin (Opn), osteocalcin (Oc), and protein tyrosine phosphataselike member A (Ptpla) were analyzed. Opg, Opn, Oc, and Ptpla expression was further measured after using siRNA to knock down Piezo1. Real-time PCR, Western blot, and cell proliferation assays were performed according to standard procedures. After mechanical stimulation, cell morphology and proliferation did not change significantly. The expression of Piezo1, Opg, Opn, Oc, and Ptpla was significantly decreased, with a high positive correlation between Opg and Piezo1 expression. After Piezo1 knockdown, the expression of Opg, Opn, Oc, and Ptpla was further decreased under mechanical stimulation. Cementogenic activity was inhibited in OCCM-30 cells under static mechanical force, a process that was partially mediated by the decrease of Piezo1. This study provides a new viewpoint of the pathogenesis mechanism of orthodontically induced root resorption and repair.

Mechanical force-mediated pathological cartilage thinning is regulated by necroptosis and apoptosis.

This study aimed to identify the mechanisms underlying mandibular chondrocyte cell death and cartilage thinning in response to mechanical force. An invivo model (compressive mechanical force) and an invitro model (TNF-α+cycloheximide) were used to induce mandibular chondrocyte necroptosis. Hematoxylin and eosin staining and transmission electron microscopy were used to assess histological and subcellular changes in mandibular chondrocyte. Immunohistochemistry, western blotting, and real-time PCR were performed to evaluate changes in necroptotic protein markers. Cell activity, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were examined invitro. The expression of RIP1, RIP3 and Caspase-8 in mandibular chondrocytes significantly increased after 4 days of compressive mechanical force. Furthermore, the inhibition of necroptosis by Necrostatin-1 (Nec-1) or the inhibition of apoptosis by N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD) partially restored mechanical force-mediated mandibular cartilage thinning and chondrocyte death. Moreover, a synergistic effect on cell death inhibition and mandibular cartilage thickness restoration were found when treated with Nec-1+Z-VAD. The results of the invitro model were in line with the invivo ones, indicating that the changes in MMP and ROS generation contributed to mandibular chondrocyte apoptosis and necroptosis. In addition to apoptosis, necroptosis also plays critical roles in pathological changes in mandibular cartilage after compressive mechanical force stimulation, implying RIP1, a master protein that mediates both necroptosis and apoptosis, as a potential therapeutic target in temporal mandibular osteoarthritis.

Abstract A60: Hyaluronan and cancer cell derived swelling of solid tumors and implications for cancer therapy

Abstract A solid tumor is an aberrant tissue made of cancer cells and a variety of host cells—all embedded in an extracellular matrix—nourished by blood vessels and drained by lymphatic vessels. Rapid tumor growth in the confined space of the host tissue results in the accumulation of mechanical forces within structural components of the tumor, and between the tumor and the host. These forces can shape the tumor microenvironment and determine in large part tumor progression and response to treatment. Despite the important role that mechanical forces play in tumor growth, the contribution of swelling to tumor mechanics remains unexplored. Tumors rich in hyaluronan exhibit a highly negative fixed charge density. Repulsive forces among these negative charges cause swelling of the tumor and development of swelling solid stress. Additionally, fixed negative charges attract free cations from the tumor interstitial space creating an imbalance of ion distribution and a Donnan osmotic fluid pressure. Furthermore, it has been shown that tumor swelling can be produces not only by hyaluronan but also cancer cells swell due to osmotic regulation, which is required for their survival under compressive forces. In this study, we design an experimental set up to measure hyaluronan derived swelling solid stress in two orthotopic breast tumor models of different extracellular matrix composition. We also calculate the Donnan osmotic pressure and the solid stress owing to interactions with the host tissue, utilizing the experimental data and developing a triphasic biomechanical mathematical model. The mathematical model accounts for the fluid and the solid phase of a tumor and the transport of anions and cations. Furthermore, we measure the swelling of cancer cell spheroids under compressive mechanical forces in order to quantify cell derived tumor swelling. We will present data showing that swelling stress contributes significantly to tumor mechanics, whereas Donnan osmotic pressure is negligible. Interestingly, histological analysis revealed a linear correlation between swelling stress and the ratio of hyaluronan to collagen content. Our analysis further suggested an inverse relation of swelling stress to vessel diameter and tumor perfusion. These results provide guidelines for emerging therapeutic strategies that target the tumor microenvironment to alleviate swelling stress and improve perfusion and drug delivery. Citation Format: Chrysovalantis Voutouri, Christiana Polydorou, Panagiotis Papageorgis, Triantafyllos Stylianopoulos. Hyaluronan and cancer cell derived swelling of solid tumors and implications for cancer therapy. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr A60.

Ca2+-Dependent Endoplasmic Reticulum Stress Regulates Mechanical Stress–Mediated Cartilage Thinning

Our previous study identified that endoplasmic reticulum stress (ERS) plays a critical role in chondrocyte apoptosis and mandibular cartilage thinning in response to compressive mechanical force, although the underlying mechanisms remain elusive. Because the endoplasmic reticulum (ER) is a primary site of intracellular Ca2+ storage, we hypothesized that Ca2+-dependent ERS might be involved in mechanical stress–mediated mandibular cartilage thinning. In this study, we used in vitro and in vivo models to determine Ca2+ concentrations, histological changes, subcellular changes, apoptosis, and the expression of ERS markers in mandibular cartilage and chondrocytes. The results showed that in chondrocytes, cytosolic Ca2+ ([Ca2+]i) was dramatically increased by compressive mechanical force. Interestingly, the inhibition of Ca2+ channels by ryanodine and 2-aminoethoxydiphenyl borate, inhibitors of ryanodine receptors and inositol trisphosphate receptors, respectively, partially rescued mechanical force–mediated mandibular cartilage thinning. Furthermore, chondrocyte apoptosis was also compromised by inhibiting the increase in [Ca2+]i that occurred in response to compressive mechanical force. Mechanistically, the ERS induced by compressive mechanical force was also repressed by [Ca2+]i inhibition, as demonstrated by a decrease in the expression of the ER stress markers 78 kDa glucose-regulated protein (GRP78) and 94 kDa glucose-regulated protein (GRP94) at both the mRNA and protein levels. Collectively, these data identified [Ca2+]i as a critical mediator of the pathological changes that occur in mandibular cartilage under compressive mechanical force and shed light on the treatment of mechanical stress–mediated cartilage degradation.

Nanomaterials under stress: A new opportunity for nanomaterials synthesis and engineering

Abstract

Thermo-Electro-Mechanical Buckling of Shear Deformable Hybrid Circular Functionally Graded Material Plates

Buckling analysis of perfect circular functionally graded plates with surface-bounded piezoelectric layers based on the first-order shear deformation theory is presented in this article. The material properties of the functionally graded (FG) layer are assumed to vary continuously through the plate thickness by distribution of power law of the volume fraction of the constituents. The plate is assumed to be under constant electrical field and two types of thermal loadings, namely, the uniform temperature rise and nonlinear temperature gradient through the thickness. Also, the stability of a plate under radial mechanical compressive force is examined. The equilibrium and stability equations are derived based on the first-order shear deformation plate theory using a variational approach. The boundary condition of the plate as an immovable type of the clamped edge is considered. Resulting equations are employed to obtain the closed-form solution for the critical buckling temperature for each loading case. The effects of electric field, piezo-to-host thickness ratio, and power law index of functionally graded plates subjected to thermo-mechanical-electrical loads are investigated. The results are compared with the classical plate theory and verified with the available data in the open literature.

Force-induced Adrb2 in Periodontal Ligament Cells Promotes Tooth Movement

The sympathetic nervous system (SNS) regulates bone resorption through β-2 adrenergic receptor (Adrb2). In orthodontic tooth movement (OTM), mechanical force induces and regulates alveolar bone remodeling. Compressive force-associated osteoclast differentiation and alveolar bone resorption are the rate-limiting steps of tooth movement. However, whether mechanical force can activate Adrb2 and thus contribute to OTM remains unknown. In this study, orthodontic nickel-titanium springs were applied to the upper first molars of rats and Adrb1/2-/- mice to confirm the role of SNS and Adrb2 in OTM. The results showed that blockage of SNS activity in the jawbones of rats by means of superior cervical ganglion ectomy reduced OTM distance from 860 to 540 μm after 14 d of force application. In addition, the injection of nonselective Adrb2 agonist isoproterenol activated the downstream signaling of SNS to accelerate OTM from 300 to 540 μm after 7 d of force application. Adrb1/2-/- mice showed significantly reduced OTM distance (19.5 μm) compared with the wild-type mice (107.6 μm) after 7 d of force application. Histopathologic analysis showed that the number of Adrb2-positive cells increased in the compressive region of periodontal ligament after orthodontic force was applied on rats. Mechanistically, mechanical compressive force upregulated Adrb2 expression in primary-cultured human periodontal ligament cells (PDLCs) through the elevation of intracellular Ca2+ concentration. Activation of Adrb2 in PDLCs increased the RANKL/OPG ratio and promoted the peripheral blood mononuclear cell differentiation to osteoclasts in the cocultured system. Upregulation of Adrb2 in PDLCs promoted osteoclastogenesis, which accelerated OTM through Adrb2-enhanced bone resorption. In summary, this study suggests that mechanical force-induced Adrb2 activation in PDLCs contributes to SNS-regulated OTM.