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PubMed1991

Baboon fibrinogen adsorption and platelet adhesion to polymeric materials.

The role of fibrinogen in mediating platelet adhesion to polymers exposed to blood plasma was studied by comparison of the effect of plasma dilution on fibrinogen adsorption and platelet adhesion, and by the use of coagulation factor deficient plasmas. Polyetherurethane substrates were first preadsorbed with dilute plasma, then contacted with washed platelets suspended in a modified, apyrase containing Tyrode's buffer. Platelet adhesion was studied under static conditions in Multiwell dishes, and also under shearing conditions using a parallel plate perfusion chamber. Fibrinogen adsorption and platelet adhesion were measured using 125I radiolabeled baboon fibrinogen and 111In radiolabeled baboon platelets, respectively. Surfaces were characterized by electron spectroscopy for chemical analysis (ESCA). When fibrinogen adsorption to Biomer was measured after 2 h contact with a series of dilute plasma solutions under static conditions, a peak in adsorption was observed from 0.26% plasma, i.e., adsorption was greater from 0.26% plasma than from either more or less dilute plasma. A peak in subsequent platelet adhesion to the plasma preadsorbed surfaces, measured after 2 h static incubation with washed platelets, was also observed but occurred on Biomer preadsorbed with 1.0% plasma. When fibrinogen adsorption was measured after 5 min contact under shearing conditions, the fibrinogen adsorption peak occurred on surfaces that had been exposed to 1.0% plasma. A peak in platelet adhesion to these preadsorbed surfaces, measured after 5 min contact with the platelet suspensions under shearing conditions, was observed on Biomer preadsorbed with 0.1% plasma. Shifts between the positions of the peaks in protein adsorption and platelet adhesion occurred on other polymers tested as well. Platelet adhesion was almost completely inhibited when baboon and human plasmas lacking fibrinogen (i.e., serum, heat defibrinogenated plasma, and congenitally afibrinogenemic plasma) were used. Platelet adhesion was restored to near normal when exogenous fibrinogen was added to fibrinogen deficient plasmas. Adhesion was also inhibited completely when a monoclonal antibody directed against the glycoprotein IIb/IIIa complex was added to the platelet suspension. Platelet adhesion to surfaces preadsorbed to von Willebrand factor deficient plasma was the same as to surfaces preadsorbed with normal plasma. While it appears that surface bound fibrinogen does mediate the initial attachment of platelets to Biomer, the observation that the fibrinogen adsorption and platelet adhesion maxima do not coincide exactly also suggests that the degree of subsequent platelet adhesion is dictated not only by the amount of surface bound fibrinogen but also by its conformation.

Adsorption↗
PubMed1995

Expanded polytetrafluoroethylene (Gore-Tex Surgical Membrane) is superior to oxidized regenerated cellulose (Interceed TC7+) in preventing adhesions.

OBJECTIVE: To compare the impact of expanded polytetrafluoroethylene (PTFE; Gore-Tex Surgical Membrane; W. L. Gore & Associates, Inc., Flagstaff, AZ) and oxidized regenerated cellulose (Interceed TC7, Johnson & Johnson Medical, Inc., Arlington, TX) on the development of postsurgical adhesions. DESIGN: A multicenter, nonblinded, randomized clinical trial. SETTING: University medical centers. INTERVENTIONS: Each barrier was allocated randomly to the left or right sidewall of every patient. PATIENTS: Thirty-two women with bilateral pelvic sidewall adhesions undergoing reconstructive surgery and second-look laparoscopy. MAIN OUTCOME MEASURES: Adhesion score (on a 0- to 11-point scale), the area of adhesion (cm2), and the likelihood of no adhesions. RESULTS: The use of both barriers was associated with a lower adhesion score and area of adhesion postoperatively. However, those sidewalls covered with PTFE had a significantly lower adhesion score (0.97 +/- 0.30 versus 4.76 +/- 0.61 points, mean +/- SEM) and area of adhesion (0.95 +/- 0.35 versus 3.25 +/- 0.62 cm2). Overall, more sidewalls covered with PTFE had no adhesions (21 versus 7) and, when adhesions were present on the contralateral sidewall, the number of sidewalls covered with PTFE without adhesions was greater than those covered with oxidized regenerated cellulose (16 versus 2). CONCLUSION: Expanded polytetrafluoroethylene was associated with fewer postsurgical adhesions to the pelvic sidewall than oxidized regenerated cellulose.

Adolescent↗
PubMed1996

Integrins in cell adhesion and signaling.

Cell adhesive interactions play important roles during many normal physiological processes such as embryonic development and wound repair, and also during the progression of diseases such as cancer. Cell adhesion is mediated by the specific interactions of cell surface receptors with extracellular glycoproteins. The best characterized cell adhesion receptors are the integrins. Integrins comprise a family of more than 23 noncovalent, heterodimeric complexes consisting of an alpha and a beta subunit. Each subunit is a glycoprotein with a large, globular extracellular domain and a transmembrane domain. Most integrins have relatively small cytoplasmic domains consisting of fewer than 60 amino acids. Although many integrins can bind fibronectin, the alpha 5, beta 1, integrin is the major fibronectin receptor on most cells. This integrin mediates such cellular responses to fibronectin substrates as adhesion, migration, assembly of extracellular matrix, and signal transduction. Integrin ligands, such as fibronectin, are not passive adhesive molecules but are active participants in the cell adhesive process that leads to signal transduction. The best characterized integrin ligand is fibronectin. Fibronectin is a multifunctional glycoprotein comprised of three different types of homologous repeating units (termed type I, type II, and type III). Fibronectin has at least two independent cell adhesive regions: one located near the center of the polypeptide chain in the ninth and tenth type III modules binds to the alpha 5 beta 1 integrin. The biological function of the central cell adhesive region requires two critical amino acid sequences--an Arg-Gly-Asp (RGD) sequence and a Pro-His-Ser-Arg-Asn (PHSRN) sequence, which function in synergy--for optimal binding to the alpha 5 beta 1 integrin. Furthermore, the spacing between the crucial RGD and PHSRN sequences is also important for activity, suggesting the sequences themselves are necessary, but not sufficient, to account for the cell adhesive activity of fibronectin. One of the manifestations of integrin-mediated signal transduction including protein tyrosine phosphorylation. One cytoplasmic protein that is phosphorylated in response to cell adhesion is the focal adhesion kinase known as pp125FAK or FAK. The beta 1, beta 3, and beta 5 integrin intracellular domains are sufficient to initiate signal transduction pathways. Furthermore, alternative splicing can regulate the ability of beta integrin intracellular domains to participate in signal transduction. Other intracellular responses to cell adhesion include stimulation of migration, the assembly of an F-actin cytoskeleton and specialized structures called focal contacts, changes of cytoplasmic pH and calcium ion concentration, and modulation of proliferation and gene expression. Such varied modes of signal transduction are probably differentially controlled by a mechanism that requires either integrin receptor clustering alone, ligand occupancy in addition to clustering, or clustering and/or ligand occupancy plus tyrosine kinase activity for different responses. The examination of the fundamental mechanisms important for adhesion of cultured human cells and the resultant signaling processes has the potential of providing an understanding of molecular mechanisms involved in complex physiological processes and serving the basis for the development of novel therapeutic agents for the treatment of human disease.

Cell Adhesion↗
PubMed1997

Analysis of the involvement of the von Willebrand factor-glycoprotein Ib interaction in platelet adhesion to a collagen-coated surface under flow conditions.

The requisite initial reaction for in vivo thrombus formation in flowing blood is platelet adhesion to the exposed surface of the extracellular matrix. The contribution of von Willebrand factor (vWF ) in plasma and glycoprotein (GP) Ib on the platelet membrane to platelet adhesion has been well-documented. We have recently developed a procedure (the "flow adhesion assay") for measuring platelet adhesion under flow conditions that allowed us to characterize platelet adhesion to a collagen-coated surface. Here, we apply our method to analyze platelet adhesion to a vWF-coated surface to determine how this might differ from adhesion to a collagen-coated surface. Platelet adhesion to the vWF-coated surface was monitored as the linear increase in the area occupied by adherent platelets. The fluorescence image showed that platelets adhering to the vWF surface were mainly single platelets, and if any were present, the platelet aggregates were small, this being the primary difference from the adhesion to a collagen surface, where adherent platelets were mostly in aggregates. The flow adhesion assay detected the movement of platelets on the vWF surface, suggesting the reversible binding of vWF with platelets. The velocity of the platelets increased at higher shear rates or at lower vWF densities on the surface. Treatment of the vWF-coated surface with the aggregating agent botrocetin before initiation of blood flow increased platelet adhesion while dramatically decreasing the velocity of platelet movement. The present observations on the adhesion of platelets to the vWF-pretreated collagen surface and measurements of the velocity of platelets moving on the collagen surface suggest that the first interaction on the collagen-coated surface is the binding of vWF molecules to the collagen surface. This small number of vWF molecules would serve to attract and slow platelets flowing near the surface. This would facilitate the actual adhesion to the collagen surface that is mainly generated by the interaction between platelet collagen receptors, including GP Ia/IIa and GP VI, with collagen.

Adsorption↗
PubMed2004

Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-alpha, IL-1beta.

Nicotine, the major immunomodulatory components of cigarette smoking, is among the leading risk factors in atherosclerosis and various other diseases. The subject of this study is to observe how nicotine affects the function of macrophages and vascular endothelial cells. The changes of nicotine on releasing of cytokines from Ana-1 were detected by radio-immunoassay (RIA) or enzyme-link immunosorbent assay (ELISA). The adhesion of monocytes to human umbilical vein endothelial cells (HUVECs) with Ana-1 supernatant-activated was evaluated through adhesion experiments. ELISA and RT-PCR methods examined expression of soluble adhesion molecular protein and their mRNA. Which cytokines in Ana-1 supernatant affecting HUVECs ability to express adhesion molecular were tested by adhesion blockade analysis and ELISA. The results showed TNF-alpha, IL-1beta could reach the peak with 0.06mM nicotine treated for 24 and 12 h on Ana-1, respectively, but IL-8 and IFN-gamma had no significant alter. Adhesion experiments proved treatment of HUVECs with supernatant of Ana-1 for 24 h obviously augmented the adhesion of monocytes to HUVECs. ELISA and PCR demonstrated expression of soluble intracellular adhesion molecule-1 protein (sICAM-1) increased sharply at 24 h, while soluble vascular cell adhesion molecule-1 protein (sVCAM-1) and soluble endothelial selectin protein (sE-selectin) rose at 9 h; ICAM-1, VCAM-1 and E-selectin mRNA had a similar tendency. Treatment of HUVECs with anti-TNF-alpha, anti-IL-1beta antibodies pre-neutralized supernatant of Ana-1 could block monocytes adhesion. In conclusion, our findings suggest that nicotine could augment macrophages releasing TNF-alpha and IL-1beta, furthermore TNF-alpha and IL-1beta could up-regulate the expression of adhesion molecule and increase adhesion of monocytes to HUVECs. These might be one of the reasons that leaded to endothelial dysfunction.

Animals↗
PubMed2003

Analysis of the effect of disturbed flow on monocytic adhesion to endothelial cells.

The preferential adhesion of monocytes to vascular endothelial cells (ECs) at regions near branches and curvatures of the arterial tree, where flow is disturbed, suggests that hemodynamic conditions play significant roles in monocyte adhesion. The present study aims to elucidate the effects of disturbed flow on monocyte adhesion to ECs and the adhesive properties of ECs. We applied, for the first time, the micron-resolution particle image velocimetry (microPIV) technique to analyze the characteristics of the disturbed flow produced in our vertical-step flow (VSF) chamber. The results demonstrated the existence of a higher near-wall concentration and a longer residence time of the monocytic analog THP-1 cells near the step and the reattachment point. THP-1 cells showed prominent adhesion to ECs pretreated with TNFalpha in the regions near the step and the reattachment point, but they showed virtually no adhesion to un-stimulated ECs. Pre-incubation of the TNFalpha-treated ECs with antibodies against intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin inhibited the THP-1 adhesion; the maximal inhibition was observed with a combination of these antibodies. Pre-exposure of ECs to disturbed flow in VSF for 24 h led to significant increases in their surface expressions of ICAM-1 and E-selectin, but not VCAM-1, and in the adhesion of THP-1 cells. Our findings demonstrate the importance of complex flow environment in modulating the adhesive properties of vascular endothelium and consequently monocyte adhesion in regions of prevalence of atherosclerotic lesions.

Blood Flow Velocity↗
PubMed1996

Cyclosporine enhances leukocyte adhesion to vascular endothelium under physiologic flow conditions.

We investigated the effect of cyclosporine (CyA) on leukocyte adhesion to endothelium under flow conditions. Confluent human umbilical vein endothelial cells (HUVECs) were incubated for 24 hours with CyA (1, 5, and 10 micromol/L) and then exposed to a total human leukocyte suspension in a parallel plate flow chamber under laminar flow (1.5 dynes/cm2. Human umbilical vein endothelial cells stimulated with interleukin-1beta (20 U/mL) were used as a positive control. Adherent cells were measured by digital image analysis. Results showed that CyA dose-dependently increased the number of leukocytes adhering to HUVECs compared with control cells. Leukocyte adhesion markedly increased on HUVECs incubated with interleukin-lbeta, one of the most potent inducers of endothelial cell adhesiveness. Exposure of endothelial cells to CyA did not affect the number of rolling leukocytes, which was similar to control values. To examine the role of adhesion molecules in CyA-induced leukocyte adhesion, HUVECs were incubated with monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin before adhesion assay. Functional blocking of ICAM-1, VCAM-1, and E-selectin on endothelial cells significantly inhibited CyA (10 micromol/L)-induced leukocyte adhesion. Confocal fluorescence microscopy studies showed that CyA induced an increase in the endothelial surface expression of ICAM-1, VCAM-1, and E-selectin. Pretreatment of leukocytes with the platelet activating factor receptor antagonist L659,989 significantly reduced the number of leukocytes adhering to CyA-treated HUVECs. We suggest that CyA enhances leukocyte adhesion to endothelium by upregulating adhesive proteins on endothelial surface membrane. Blocking leukocyte receptor for platelet-activating factor partially prevents adhesion, suggesting a role for endothelial cell-associated platelet-activating factor in the interaction between leukocytes and CyA-treated endothelium.

Cell Adhesion↗
PubMed1998

Antioxidant regulation of phorbol ester-induced adhesion of human Jurkat T-cells to endothelial cells.

Regulation of adhesion molecule expression and function by reactive oxygen species via specific redox sensitive mechanisms have been reported. The effects of clinically safe antioxidants in the regulation of adhesion molecule expression in human endothelial cells (ECV), and adherence of human Jurkat T cells to ECV cells were investigated. The thiol antioxidant, alpha-lipoate, at clinically relevant doses down-regulated phorbol 12-myristate 13-acetate (PMA)-induced adhesion molecule expression and cell-cell adhesion. Inhibition of PMA-induced ICAM-1 and VCAM-1 expression as well as PMA-induced adhesion of Jurkat T-cells to ECV cells by alpha-lipoate was dose dependent (50-250 microM). The effect was significant for ICAM-1 (p < .01) and VCAM-1 (p < .01) expression in cells pretreated with 100 microM alpha-lipoate compared to PMA-activated untreated cells. Inhibition of PMA-induced adhesion molecule expression and cell-cell adhesion was more pronounced when a combination of antioxidants, alpha-lipoate and alpha-tocopherol, were used compared to the use of either of these antioxidant alone. The regulation of adhesion molecule expression and function by low concentration of antioxidants investigated does not appear to be NF-kappaB regulated or transcription dependent because no change in the mRNA response was observed. Protein kinase C (PKC) has been suggested to regulate PMA-induced adhesion molecule expression by post-transcriptional stabilization of adhesion molecule mRNA. Alpha-lipoate pretreatment did not influence the response of PKC activity to PMA. Oxidants are known to be involved in the regulation of cell adhesion processes. Treatment of ECV cells with PMA induced generation of intracellular oxidants. Alpha-lipoate (100 or 250 microM) treatment decreased PMA-induced generation of intracellular oxidants. The inhibitory effect of low concentration of alpha-lipaote alone or in combination with alpha-tocopherol on agonist-induced adhesion processes observed in this study may be of potential therapeutic value.

Antioxidants↗
PubMedDate not supplied

Cell adhesion: more than just glue (review).

The ability of cells to interact with each other and their surroundings in a co-ordinated manner depends on multiple adhesive interactions between neighbouring cells and their extracellular environment. These adhesive interactions are mediated by a family of cell surface proteins, termed cell adhesion molecules. Fortunately these adhesion molecules fall into distinct families with adhesive interactions varying in strength from strong binding involved in the maintenance of tissue architecture to more transient, less avid, dynamic interactions observed in leukocyte biology. Adhesion molecules are extremely versatile cell surface receptors which not only stick cells together but provide biochemical and physical signals that regulate a range of diverse functions, such as cell proliferation, gene expression, differentiation, apoptosis and migration. In addition, like many other cell surface molecules, they have been usurped as portals of entry for pathogens, including prions. How the mechanical and chemical messages generated from adhesion molecules are integrated with other signalling pathways (such as receptor tyrosine kinases and phosphatases) and the role that aberrant cell adhesion plays in developmental defects and disease pathology are currently very active areas of research. This review focuses on the biochemical features that define whether a cell surface molecule can act as an adhesion molecule, and discusses five specific examples of how cell adhesion molecules function as more than just 'sticky' receptors. The discussion is confined to the signalling events mediated by members of the integrin, cadherin and immunoglobulin gene superfamilies. It is suggested that, by controlling the membrane organization of signalling receptors, by imposing spatial organization, and by regulating the local concentration of cytosolic adapter proteins, intercellular and cell-matrix adhesion is more than just glue holding cells together. Rather dynamic 'conversations' and the formation of multi-protein complexes between adhesion molecules, growth factor receptors and matrix macromolecules can now provide a molecular explanation for the long-observed but poorly understood requirement for a number of seemingly distinct cell surface molecules to be engaged for efficient cell function to occur.

Animals↗
PubMed1984

Adhesion of Leptospira at a solid-liquid interface: a model.

Two strains of the saprophytic Leptospira biflexa serovar patoc display reversible and irreversible adhesion at a solid-liquid interface. Both forms of adhesion are enhanced in the presence of 20 microM carbonyl cyanide meta-chlorophenyl hydrazone (CCCP), an uncoupler which inhibits motility of the bacteria. Microscopic observations also indicated that motility may have a role in adhesion as only actively motile organisms were seen to detach from the substratum. A dynamic model is proposed for adhesion of these organisms at a solid-liquid interface. It is suggested that the level of reversible adhesion is determined by the comparative rates of attachment (ON phase) and detachment (OFF phase). As reversible adhesion is mediated by weak forces of attraction, bacterial motility or gentle washing could promote the OFF phase. When motility is inhibited, the OFF phase is reduced and the ON phase continues (as motility is not required for the ON phase) causing the level of reversible adhesion to increase. Since reversible adhesion is a prerequisite for irreversible adhesion, then increased reversible adhesion leads directly to increased irreversible adhesion. Reversible adhesion appears to be mediated by the weak attractive forces of the "secondary minimum" whereas the mechanism facilitating irreversible adhesion of leptospires is not known.

Leptospira↗
PubMed2005

Effect of fracture strength of primer-adhesive mixture on bonding effectiveness.

OBJECTIVE: The purpose of this study was to measure the micro-tensile bond strength (microTBS) of two adhesives to dentin and to correlate this microTBS with the micro-tensile fracture strength (microTFS) of primer-adhesive mixtures of the two adhesives. METHODS: The three-step etch&rinse adhesive OptiBond FL (Kerr) and the two-step self-etch adhesive Clearfil SE Bond (Kuraray) were used to bond Filtek Z100 (3M ESPE) to twenty mid-coronal dentin surfaces. The microTBS was determined at 1 and 24 h after light-curing. In addition, the microTFS of primer-adhesive mixtures (primer:adhesive=1:3 by weight) and of the pure adhesives (controls) were measured after the same time intervals. RESULTS: The microTBS to dentin of OptiBond FL at 24 h was significantly higher than at 1 h and than the microTBS of Clearfil SE Bond at 24 h. The mean microTFS of the primer-adhesive mixtures was always lower than the microTFS of the respective adhesives. The highest reduction in microTFS due to mixing primer with the adhesive resin was measured for Clearfil SE Bond. Both the microTFS of the primer-adhesive mixtures and the pure adhesives of OptiBond FL and Clearfil SE Bond increased with time. SIGNIFICANCE: The early 1 h microTBS to dentin was lower than the 24 h microTBS for OptiBond FL, but not for Clearfil SE Bond. Differences in polymerization efficiency as well as in the resulting interfacial strength may explain such varying early bond strengths to dentin.

Composite Resins↗
PubMed1979

Phospholipid composition of substrate adhesion sites of normal, virus-transformed, and revertant murine cells.

The phospholipid composition of cell-substratum adhesion sites, obtained after EGTA-mediated detachment of cells from the tissue-culture substratum, was determined for [32P]orthophosphate radiolabeled Balb/c 3T3, SV40-transformed (SVT2), and concanavalin A selected revertant variant cell lines. All of the major phospholipid classes were found in the substrate-attached material, but there was an enrichment for specific phospholipid species in this adhesive material as compared to whole-cell and surface-enriched membranes. The phospholipid composition was remarkable similar for the whole-cell and surface-enriched membrane fractions from the three cell lines. However, pronounced differences in the phospholipid composition of the adhesion sites were observed as a result of viral transformation--SVT2 sites were clearly enriched in phosphatidylethanolamine and depleted in phosphatidylcholine when compared to 3T3 sites. This alteration in adhesion site phospholipids of transformed cells reverted to 3T3-like values in the adhesive material of revertant cells. The composition of adhesive material of newly attaching cells was also examined to differentiate compositional differences between "footpad" adhesion sites and "footprints", adhesive material pinched off from the posterior of cells as they move across the substratum. Pulse and pulse-chase analyses of the [32P]phospholipids revealed some differences in synthesis and turnover rates in the three cell lines; in addition, altered rates of deposition of newly synthesized material into adhesion sites of transformed cells were observed. These data afford further evidence that the cell-substratum adhesion sites are highly specialized areas of the cell surface enriched in components which are intricately involved in the adhesive process. The transformation-dependent changes in adhesion site phospholipids may help to determine the basis for the altered adhesive properties of transformed cells.

Animals↗
PubMed2002

Demonstrating the clinical and cost effectiveness of adhesion reduction strategies.

OBJECTIVE: To examine the feasibility of conducting Randomized Controlled Trials (RCT) in lower abdominal surgery to demonstrate a reduction in adhesion-related admissions following use of an adhesion reduction product, and to model the cost effectiveness of such products. METHODS: The number of patients in each limb of a RCT comparing an adhesion reduction product to a control has been estimated based on 25% and 50% reductions in adhesion-related readmissions one year after surgery, for P = 0.05 at a power of 80% and P=0.01 at a power of 90%. A cost effectiveness model based on the Surgical and Clinical Adhesions Research Group (SCAR) database has been developed which calculates the percentage reduction in readmissions required of an adhesion reduction product to return the cost of investment. It also estimates the cumulative costs of adhesion-related readmissions for lower abdominal surgery and the cost savings associated with an adhesion reduction policy using a low or high cost product. RESULTS: 7.2% of patients undergoing lower abdominal surgery will readmit due to adhesions in the first year after surgery. To demonstrate a 25% reduction in readmissions one year after surgery, it is calculated that a RCT would require between 5686 (P = 0.05, power=80%) and 7766 (P = 0.01, power = 90%) lower abdominal surgery patients followed-up for one year. A cost effectiveness analysis demonstrates that routine use of adhesion reduction products costing pound 50 per patient will payback the cost of such investment if they reduce adhesion-related readmissions by 16% after 3 years. A product costing pound 200 will need to offer a 64.1% reduction in readmissions after 3 years. For the estimated 158 000 lower abdominal surgery operations conducted in the UK each year, the cumulative costs of adhesion-related readmissions over 10 years are estimated at pound 569 Million. CONCLUSION: Demonstrating the clinical effectiveness of adhesion reduction products in the RCT setting is unlikely to be feasible due to the large number of patients required. Products costing pound 200 or more are unlikely to payback their direct costs.

Journal Article↗
PubMed2002

The effect of repeated bonding on the shear bond strength of different orthodontic adhesives.

One problem clinicians face during treatment is bracket failure. In a busy orthodontic practice, a significant number of teeth will need to be rebonded. The purpose of this study was to evaluate the effect of repeated bonding with 2 different adhesives, a composite and a cyanoacrylate, on the shear bond strength of orthodontic brackets. Thirty-one freshly extracted human molars were collected. Brackets were bonded with 1 of the orthodontic adhesives according to the manufacturer's instructions. In group I, the teeth were etched with 37% phosphoric acid, a sealant was applied, and the brackets were bonded with Transbond XT (3M Unitek, Monrovia, Calif) and light cured for 20 seconds. In group II, the teeth were etched with 35% phosphoric acid, and the brackets were bonded with SmartBond (Gestenco International, Göthenburg, Sweden). In each group, the teeth were bonded and debonded 3 times with the same adhesive. At each sequence, the brackets were removed within 30 minutes after bonding to simulate the clinical condition at which a newly bonded bracket is tied to the archwire. Student t tests and the analysis of variance repeated measure were used to compare the shear bond strength between adhesives and within each adhesive at different debonding sequences. The results indicated that, at the first debonding sequence, the 2 adhesives did not have significantly different shear bond strengths. Between debonding sequence 1 and 2, there was a significant (P <or=.05) decrease in the shear bond strength of both adhesives. SmartBond decreased from x = 5.7 +/- 3.8 MPa to x = 2.2 +/- 2.6 MPa, and Transbond decreased from x = 6.1 +/- 3.4 to x = 4.1 +/- 2.3 MPa. When the 2 adhesives were compared at the second debonding sequence, the shear bond strength of Transbond was significantly greater than that of SmartBond (P =.046). Between debonding sequences 2 and 3, there were no significant differences either between the adhesives or in the change within each adhesive. The highest values for shear bond strength were obtained after the initial bonding. Rebonded teeth had significantly lower shear bond strength. The composite adhesive had a higher shear bond strength than the cyanoacrylate adhesive at the second bonding/debonding sequence but not at the third. The changes in bond strength after repeated bonding may be related to changes in the morphologic characteristics of the tooth surface caused by adhesive remnants.

Analysis of Variance↗
PubMedDate not supplied

Effect of water storage on the bonding effectiveness of 6 adhesives to Class I cavity dentin.

Adhesive-dentin interfaces degrade with time. This study determined the effect water storage may have on the bonding effectiveness of adhesives to occlusal Class I cavity-bottom dentin. Six adhesives, all representing contemporary classes of adhesives, were applied: a 3-step (OptiBond FL, Kerr) and 2-step (Scotchbond 1*, 3M ESPE) etch-and-rinse adhesive, a 2-step (Clearfil SE, Kuraray) and 1-step (Adper prompt, 3M ESPE) self-etch adhesive and a 2-step (FujiBond LC, GC) and 1-step (Reactmer, Shofu) resin-modified glass-ionomer adhesive. Bonding effectiveness was assessed by microtensile bond strength testing (MTBS) and electron microscopy (Feg-SEM and TEM). The MTBS was determined after 1 day and 1 year water storage of the entire restored cavity (indirect exposure of the adhesive-dentin interface to water) and prepared microTBS-beams (direct exposure of the adhesive-dentin interface to water). The hypotheses tested were: (1) resin-dentin bonds formed at the bottom of Class I cavities resist 1-year water storage and (2) an adjacent composite-enamel bond protects the composite-dentin bond against degradation. Non-parametric Kruskal-Wallis analysis statistically analyzed the microTBSs. The first hypothesis was rejected, as only the microTBS of OptiBond FL and Clearfil SE did not significantly decrease after 1-year direct and/or indirect water storage. The second hypothesis was corroborated, as the bonding effectiveness of most simplified adhesives (Scotchbond 1, Adper Prompt, FujiBond LC and Reactmer) approached 0 (because of the frequent pre-testing failures) after 1-year direct water exposure. The second hypothesis concluded that the 3-step etch-and-rinse adhesive must still be regarded the "gold standard." Though microTBS decreased significantly, Clearfil SE, as a 2-step self-etch adhesive, was the only simplified adhesive to perform reliably after 1-year direct water exposure.

Dental Bonding↗
PubMedDate not supplied

One-day bonding effectiveness of new self-etch adhesives to bur-cut enamel and dentin.

Self-etch adhesives try to solve difficulties commonly associated with the clinical application of etch-and-rinse adhesives. Their application procedure is considered less time-consuming and, more importantly, less technique-sensitive. The main objective of this study was to determine the bonding effectiveness to and the interaction with enamel/dentin of three contemporary one- and two-step self-etch adhesives by microtensile bond strength testing (microTBS), Fe-SEM and TEM when compared to a control two-step self-etch and a three-step etch-and-rinse adhesive. The one-step self-etch adhesive, Adper Prompt (3M ESPE), scored the lowest microTBS of all experimental and control adhesives tested. Conversely, the two-step self-etch adhesives Clearfil SE (Kuraray) and OptiBond Solo Plus Self-Etch (Kerr) approached the values obtained by the three-step etch-and-rinse control (OptiBond FL, Kerr) when bonded to enamel and dentin. Ultramorphological characterization showed that interfacial morphology and the pH of the self-etch primer/adhesive are strongly associated. The interaction with dentin varied from the formation of a submicron, hydroxyapatite-containing hybrid layer for the "mild" self-etch adhesive Clearfil SE to a 3-5 microm thick, hydroxyapatite-depleted hybrid layer for the "strong" self-etch adhesive Adper Prompt. The two-step self-etch adhesives AdheSE and OptiBond Solo Plus Self-Etch presented with a hybrid layer with a hydroxyapatite-depleted top part and a hydroxyapatite-containing base part and were therefore classified into a new group of self-etch adhesives, namely "intermediary strong" self-etch adhesives.

Acid Etching, Dental↗
PubMedDate not supplied

Enamel bond strengths of pairs of adhesives from the same manufacturer.

Most manufacturers of dental adhesives have both a total-etch adhesive and a simplified self-etching adhesive available on the market. This study measured the enamel microtensile bond strengths of five pairs of enamel adhesives as a function of enamel roughness. The proximal surfaces of 25 extracted mandibular molars were sectioned with a diamond saw to obtain 50 enamel rectangles with an area of 8x4 mm2. The enamel rectangles were divided in two equal parts via a groove to obtain 4x4 mm2 squared bonding surfaces. One half was roughened with a coarse diamond bur under water for five seconds, while the other half was kept intact. The enamel surfaces were randomly assigned to 10 enamel adhesives grouped into five pairs. Each pair included one self-etch adhesive and one total-etch adhesive from the same manufacturer: Adper Prompt and Adper Single Bond (PLP and SB, 3M ESPE); AdheSE and Excite (ADH and EXC, Ivoclar Vivadent); OptiBond Solo Plus SE and OptiBond Solo Plus (OPTSE and OPT, Kerr); Tyrian SPE/One-Step Plus and One-Step (TYR and OST, BISCO, Inc); Xeno III and Prime&Bond NT (XEN and PBNT, Dentsply). The adhesives were applied according to the manufacturers' instructions. Buildups were constructed with Filtek Z250 (3M ESPE). The specimens were sectioned in sticks with a cross section of 0.8+/-0.2 mm2 and tested to failure in tension at a crosshead speed of 1 mm/minute. Two-way ANOVA followed by Duncan's post-hoc test at p<0.05 was computed. The highest mean bond strengths were obtained with total-etch adhesives. For "roughened enamel," three pairs of materials had statistically different means in which the total-etch adhesive resulted in statistically higher bond strengths (MPa) than the corresponding self-etch adhesive: EXC (36.6) > ADH (23.0) at p<0.026; OPT (34.5) > OPTSE (25.3) at p<0.028; PBNT (36.6) > XEN (19.5) at p<0.0001. For "intact enamel," four pairs of materials resulted in statistically different means: SB (31.7) > PLP (20.9) at p<0.049; EXC (37.9) > ADH (16.3) at p<0.0001; OST (30.1) > TYR (18.0); PBNT (43.8) > XEN (16.0) at p<0.0001. When the same adhesive was compared on intact vs roughened enamel, all the self-etch materials resulted in lower bond strengths on intact enamel, but this difference was only significant for TYR (p<0.042) and ADH (p<0.050). For total-etch materials, only OPT resulted in statistically lower bond strengths when applied on intact enamel p<0.011).

Acrylic Resins↗
PubMed1990

[The influence of the adhesive resin for the deformation of the metallic plate].

From both vital and denture sides, the design of denture in dental clinic needs taking care of various viewpoints; alleviation of the adverse effect on the periodontium is necessary on the vital side, and prevention of possible rupture of the denture at its functioning and taking hygienic measures are necessary on the denture side. Utilization of the metal and adhesive, 4-META containing resin (hereinafter referred to as adhesive resin) in the design of denture has been reported to be not only hygienically advantageous because of difficult adhesiveness of bacterial flora due to solid union between the metal and the resin, but also less in danger of the denture rupture from its finishing line portion. However, a few reports have been made on the analysis of the correlation between the mechanical strength of the whole of denture and the use of adhesive resin and on the deformation of the metallic frame due to curing shrinkage of adhesive resin. In the present study, in terms of these problems, utilizing the modal analysis applying a vibrato-logical technique and the strain gauge device appropriate for the determination of the time-course, samples of chrome-cobalt alloy and of partial denture were examined for the influence of inserted adhesive and non-adhesive resins upon them. The following results were obtained: 1. The results of the determination by the strain gauge method revealed that the insertion of adhesive resin tended to have more displacement volume for more insertion volume and for thinner chrome-cobalt alloy sample and that of non-adhesive resin had practically no adhesive force, suggesting a small deformation of the sample due to curing shrinkage, with little interlocking force. 2. The results of modal analysis revealed that the insertion of the adhesive resin onto the denture sample led to an increase in mechanical strength and a rigid body modality of the activity at the finishing line portion compared with the non-adhesive resin. 3. From the results of the determination by the strain gauge method and of the modal analysis, the application of adhesive resin was suggested to increase the intensity of denture.

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