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PubMed2002

HIV-1-induced production of endothelin-1 in an in vitro model of the human blood-brain barrier.

Evidence suggests that the HIV-1 envelope glycoproteins play a role in the central nervous system (CNS) complications of AIDS. Endothelin-1 (ET-1) has also been implicated in brain injury and the progression of the AIDS dementia complex (ADC). Here, we used a real-time reverse transcription polymerase chain reaction assay and an immunometric assay to show that in vitro model of the blood-brain barrier (BBB) consisting of a monolayer co-culture of astrocytes and human brain microvascular endothelial cells (A-HBMEC) increased its expression of ET-1 mRNA and secretion of ET-1 peptide when infected with HIV-1. The enhanced expression of ET-1 occurred independently of viral replication as it was also induced by the viral glycoprotein coat HIV-1g120SF. These results show that one mechanism by which HIV-1 might affect the CNS is by inducing release of ET-1 by the BBB.

AIDS Dementia Complex↗
PubMed2002

An in vitro model of Parkinson's disease: linking mitochondrial impairment to altered alpha-synuclein metabolism and oxidative damage.

Chronic systemic complex I inhibition caused by rotenone exposure induces features of Parkinson's disease (PD) in rats, including selective nigrostriatal dopaminergic degeneration and formation of ubiquitin- and alpha-synuclein-positive inclusions (Betarbet et al., 2000). To determine underlying mechanisms of rotenone-induced cell death, we developed a chronic in vitro model based on treating human neuroblastoma cells with 5 nm rotenone for 1-4 weeks. For up to 4 weeks, cells grown in the presence of rotenone had normal morphology and growth kinetics, but at this time point, approximately 5% of cells began to undergo apoptosis. Short-term rotenone treatment (1 week) elevated soluble alpha-synuclein protein levels without changing message levels, suggesting that alpha-synuclein degradation was retarded. Chronic rotenone exposure (4 weeks) increased levels of SDS-insoluble alpha-synuclein and ubiquitin. After a latency of >2 weeks, rotenone-treated cells showed evidence of oxidative stress, including loss of glutathione and increased oxidative DNA and protein damage. Chronic rotenone treatment (4 weeks) caused a slight elevation in basal apoptosis and markedly sensitized cells to further oxidative challenge. In response to H2O2, there was cytochrome c release from mitochondria, caspase-3 activation, and apoptosis, all of which occurred earlier and to a much greater extent in rotenone-treated cells; caspase inhibition provided substantial protection. These studies indicate that chronic low-grade complex I inhibition caused by rotenone exposure induces accumulation and aggregation of alpha-synuclein and ubiquitin, progressive oxidative damage, and caspase-dependent death, mechanisms that may be central to PD pathogenesis.

Animals↗
PubMed1994

An in vitro model of thyroid neoplasia: permanently transfected FRTL-5 cells with thyroglobulin promoter-cholera toxin A1 subunit minigene.

BACKGROUND: Activating mutations of protein Gs alpha that stimulates adenylyl cyclase are present in a subset of thyroid adenomas. Cholera toxin A1 subunit (CT) mimics these mutations via adenosine diphosphate-ribosylation of Gs alpha. METHODS: To test the role of activated Gs alpha in thyroid neoplasia we developed an in vitro model. With molecular genetic techniques a transgene (TG-CT) in which the thyroglobulin gene (TG) promoter directs expression of CT was made. This transgene was transfected into rat thyroid follicular cells (FRTL-5). Integration of TG-CT transgene and its expression were examined. RESULTS: Polymerase chain reaction of DNA from transfected FRTL-5 cells identified the TG-CT transgene in six cell lines. The TG-CT transfected clones exhibited up to a 65-fold (1.29 +/- 0.37 pmols cyclic adenosine monophosphate (cAMP)/micrograms DNA) increase in cAMP over nontransfected FRTL-5 cells (0.02 +/- 0.001 pmols cAMP/micrograms DNA). Insulin, a known stimulator of the TG promoter, further induced CT gene expression and led to a 209-fold (10.43 +/- 0.10 pmols cAMP/micrograms DNA) increase in cAMP over nontransfected cells (0.05 +/- 0.00 pmols cAMP/microgram DNA). CONCLUSIONS: By mimicking a known mutation associated with thyroid neoplasms, these permanently transfected FRTL-5 cell lines will serve as a model to examine the long-term potential neoplastic effects of activated Gs alpha on thyroid follicular cells.

Animals↗
PubMed1999

In vitro models to predict the in vivo mechanism, rate, and extent of placental transfer of dideoxynucleoside drugs against human immunodeficiency virus.

OBJECTIVE: We tested the hypothesis that the mechanism, rate, and extent of in vivo placental transfer of dideoxynucleoside drugs against human immunodeficiency virus can be predicted by the in vitro perfused human placenta and the drug octanol-water partition coefficient. STUDY DESIGN: Near-term pregnant macaques (Macaca nemestrina ) underwent long-term catheterization for the administration of 4 dideoxynucleosides against human immunodeficiency virus: zidovudine, didanosine, zalcitabine, and stavudine. Maternal plasma, fetal plasma, and amniotic fluid concentrations were determined frequently after intravenous bolus and/or infusion of the drugs administered into the maternal or fetal circulation on separate occasions. Antipyrine was included in all experiments as a marker of placental blood flow. The mechanism, rate, and extent of placental transfer of the 4 dideoxynucleosides in perfused human placenta were determined and compared with the findings obtained by others. RESULTS: The mechanism and rate of the antipyrine-normalized placental transfer of the 4 dideoxynucleosides in perfused human placenta were highly correlated with those observed in vivo. The extent of placental transfer (fetal/maternal steady-state plasma concentration ratio) was also highly correlated with both the antipyrine-normalized placental transfer clearance (clearance index) determined in the in vitro perfused human placenta model (r 2 = 0.95, in vitro clearance-index model) and the drug octanol-water partition coefficient (r 2 = 0.99, in vitro partition-coefficient model). To determine the predictive capacity of these correlative models, we predicted the fetal/maternal steady-state plasma concentration ratio of each drug after excluding the data on that drug from the model fit. Both in vitro models to predict in vivo placental transfer of drug models resulted in good predictions of the observed fetal/maternal steady-state plasma concentration ratio (mean error: in vitro clearance-index model = -1. 2%; in vitro partition-coefficient model = 3.9%). CONCLUSIONS: We propose that our models will accurately predict the extent of placental transfer of dideoxynucleoside drugs against human immunodeficiency virus. The models may also be applicable to other classes of drugs, regardless of therapeutic category, provided that these drugs passively diffuse across the placenta. Such a result will expedite phase 1 clinical trials of drugs in pregnant women.

Animals↗
PubMed1992

Adaptive resistance following single doses of gentamicin in a dynamic in vitro model.

Adaptive resistance is a phenomenon recently described for Pseudomonas aeruginosa and other gram-negative bacilli following exposure to aminoglycoside antibiotics. It is a reversible form of resistance which develops within 1 to 2 h of initial exposure to an aminoglycoside and disappears several hours after removal of the antibiotic. We investigated adaptive resistance in P. aeruginosa ATCC 27853 following single doses of gentamicin by using a dynamic in vitro model which mimics in vivo pharmacokinetics. The initial peak gentamicin concentrations were 2.5, 8, and 25 mg/liter, and these were followed by an exponential decay in the concentration, with a half-life of 2.5 h. The degree of adaptive resistance was greater and the duration was longer with higher initial gentamicin concentrations. Maximal adaptive resistance occurred between 2 and 10 h following 8 mg/liter and between 2 and 16 h following 25 mg/liter. Full recovery of susceptibility occurred at approximately 36, 39, and 43 h following 2.5, 8, and 25 mg/liter, respectively, at which times the gentamicin concentrations were extremely low. Longer dosing intervals for aminoglycosides may improve efficacy by allowing time for adaptive resistance to resolve.

Drug Resistance, Microbial↗
PubMed1999

Cytoadherence of Babesia bovis-infected erythrocytes to bovine brain capillary endothelial cells provides an in vitro model for sequestration.

Babesia bovis, an intraerythrocytic parasite of cattle, is sequestered in the host microvasculature, a behavior associated with cerebral and vascular complications of this disease. Despite the importance of this behavior to disease etiology, the underlying mechanisms have not yet been investigated. To study the components involved in sequestration, B. bovis parasites that induce adhesion of the infected erythrocytes (IRBCs) to bovine brain capillary endothelial cells (BBEC) in vitro were isolated. Two clonal lines, CD7(A+I+) and CE11(A+I-), were derived from a cytoadherent, monoclonal antibody 4D9.1G1-reactive parasite population. This antibody recognizes a variant, surface-exposed epitope of the variant erythrocyte surface antigen 1 (VESA1) of B. bovis IRBCs. Both clonal lines were cytoadhesive to BBEC and two other bovine endothelial cell lines but not to COS7 cells, FBK-4 cells, C32 melanoma cells, or bovine brain pericytes. By transmission electron microscopy, IRBCs were observed to bind to BBEC via the knobby protrusions on the IRBC surface, indicating involvement of components associated with these structures. Inhibition of protein export in intact, trypsinized IRBCs ablated both erythrocyte surface reexpression of parasite protein and cytoadhesion. IRBCs allowed to recover surface antigen expression regained the ability to bind endothelial cells, demonstrating that parasite protein export is required for cytoadhesion. We propose the use of this assay as an in vitro model to study the components involved in B. bovis cytoadherence and sequestration.

Adhesiveness↗
PubMed2000

Adenosine triphosphate-dependent potassium channel modulation and cardioplegia-induced protection of human atrial muscle in an in vitro model of myocardial stunning.

OBJECTIVES: Although adenosine triphosphate-dependent potassium channel openers have been shown to enhance cardioplegic protection in animal myocardium, there is a lack of data on human cardiac tissues. We aimed at determining, on human atrial muscle, whether adenosine triphosphate- dependent potassium channels are involved in protection caused by high-potassium cardioplegia and whether adenosine triphosphate-dependent potassium channel activation might improve cardioplegic protection in an in vitro model of myocardial stunning. METHODS: Human atrial trabeculae were obtained from adult patients undergoing cardiac operations. In an organ bath at 37 degrees C, the preparations were subjected to 60 minutes of hypoxia at a high stimulation rate either in Tyrode solution (control, n = 17) or in St Thomas' Hospital solution without additives (n = 6) or associated with 100 nmol/L bimakalim (n = 7) or 1 micromol/L glibenclamide (n = 7), followed by 60 minutes of reoxygenation and 15 minutes of positive inotropic stimulation with 1 micromol/L dobutamine. RESULTS: Atrial developed tension was reduced by hypoxia to 27% +/- 5% of baseline and incompletely recovered after reoxygenation to 38% +/- 7%, whereas dobutamine restored contractility to 74% +/- 7% of basal values. St Thomas' Hospital solution with or without bimakalim improved developed tension after reoxygenation and dobutamine (P <.0001 vs control), whereas glibenclamide inhibited these protective effects of cardioplegic arrest (P =.001 vs St Thomas' Hospital solution). After reoxygenation, the protective effect of bimakalim disappeared at a high pacing rate (400- and 300-ms cycle length) but recovered during dobutamine superfusion. CONCLUSIONS: Adenosine triphosphate-dependent potassium channels are likely involved in the cardioprotective effects of cardioplegia in human atrial trabeculae and adenosine triphosphate-dependent potassium channel activation with bimakalim used as an additive to cardioplegia enhanced protection.

Adenosine Triphosphate↗
PubMed2001

Regulation of thyroid cell proliferation by TSH and other factors: a critical evaluation of in vitro models.

TSH via cAMP, and various growth factors, in cooperation with insulin or IGF-I stimulate cell cycle progression and proliferation in various thyrocyte culture systems, including rat thyroid cell lines (FRTL-5, WRT, PC Cl3) and primary cultures of rat, dog, sheep and human thyroid. The available data on cell signaling cascades, cell cycle kinetics, and cell cycle-regulatory proteins are thoroughly and critically reviewed in these experimental systems. In most FRTL-5 cells, TSH (cAMP) merely acts as a priming/competence factor amplifying PI3K and MAPK pathway activation and DNA synthesis elicited by insulin/IGF-I. In WRT cells, TSH and insulin/IGF-I can independently activate Ras and PI3K pathways and DNA synthesis. In dog thyroid primary cultures, TSH (cAMP) does not activate Ras and PI3K, and cAMP must be continuously elevated by TSH to directly control the progression through G(1) phase. This effect is exerted, at least in part, via the cAMP-dependent activation of the required cyclin D3, itself synthesized in response to insulin/IGF-I. This and other discrepancies show that the mechanistic logics of cell cycle stimulation by cAMP profoundly diverge in these different in vitro models of the same cell. Therefore, although these different thyrocyte systems constitute interesting models of the wide diversity of possible mechanisms of cAMP-dependent proliferation in various cell types, extrapolation of in vitro mechanistic data to TSH-dependent goitrogenesis in man can only be accepted in the cases where independent validation is provided.

Animals↗
PubMed2004

Screening for supra-additive effects of cytotoxic drugs and gamma irradiation in an in vitro model for hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world. A wide variety of treatment modalities is available for palliative therapy of HCC, although there is no strong evidence that these treatments can have a significant impact on survival. The aim of this work was to screen cytotoxic drugs relevant in the treatment of HCC for enhancement of the effect of irradiation in an in vitro model. As the majority of patients presenting with HCC suffer reduced liver function, attention was paid to low-dose effects of the cytotoxic drugs tested. To reflect this situation in vivo, multicellular tumor aggregates or "spheroids" of HepG2 cells were cultured and exposed to gamma irradiation alone or in combination with cisplatin for 4 h, gemcitabin for 4 or 24 h, or 5-fluorouracil for 4 h. In one experiment, the spheroids were cultured for 4 weeks in multiwell plates that allowed adhesion. Measurement of two-dimensional spheroid outgrowth was made every week for each spheroid. This kind of growth depends on the proliferation and motility of the cells that form the spheroid. In a second experiment, toxicity was evaluated by comparative growth curves by means of a three-dimensional growth assay and by histology. Supra-additive effects lasting for 4 weeks were observed for all drugs tested in combination with a gamma irradiation of 10 Gy.

Antineoplastic Agents↗
PubMed2002

Evidence of toxic side effects of perfluorohexyloctane after vitreoretinal surgery as well as in previously established in vitro models with ocular cell types.

BACKGROUND: Cases of ocular irritation have been observed after early clinical trials using perfluorohexyloctane (F6H8) as endotamponade. In our clinic two of three eyes developed severe inflammatory-like reactions after intermediate-term tamponade. These cases will be depicted, serving as background for the experimental study. To elucidate possible toxic effects of F6H8 on different ocular cell types and corneal tissue we applied our previously established in vitro models to investigate effects of F6H8 on cultured ocular cells in comparison with perfluorodecaline. METHODS: Vitality and proliferation of cultured human corneal endothelial cells (HCEC) and human retinal pigment epithelial cells (RPE) were measured after incubation with F6H8 or perfluorodecaline for up to 5 days. Vitality was evaluated using the Live/Dead assay, and proliferation was determined according to BrdU incorporation. Additionally the endothelium of donor corneas was incubated with F6H8 for 5 days and endothelial cell morphology was documented. RESULTS: After 5 days incubation with F6H8, cultures of RPE and HCEC showed significantly lower extinctions for vital cells as well as a non-significant decrease in proliferation compared with controls. Analysis by means of fluorescence microscopy after treatment with F6H8 or perfluorodecaline revealed decreased cell densities (F6H8 > perfluorodecaline) within contact areas. The endothelium of donor corneas incubated in presence of F6H8 developed circumscribed necrotic areas. CONCLUSIONS: Decreased amounts of vital cells cannot be explained solely by mechanical effects or nutritional deficit due to direct contact, since F6H8 has a lower specific weight than perfluorodecaline. The ability of the remaining cells to proliferate revealed that they were not irreversibly damaged. Due to the high lipophilicity of F6H8 interactions with cellular lipoprotein membranes as well as other toxic effects have to be considered and should further be investigated prior to clinical use.

Aged↗
PubMed1998

Isolated extracellular matrix-based three-dimensional in vitro models to study orthotopically cancer cell infiltration and invasion.

An initial event in colon cancer progression is the migration of epithelial cells through the basement membrane (BM) and the invasion of the colon submucosa, where tumour cells enter blood and lymph vessels to spread throughout the body. To interrupt this process would mean the prevention of metastasis. In order to investigate tumour cell invasion orthotopically in the human system, we established novel in vitro models which mimic normal human colon tissue (colon reproductions, CoRes) and primary colon carcinomas (artificial tumours, ArTs). These models are based on the isolated extracellular matrix (iECM) of the respective human tissues. Two isolation methods were established, the Digestion Method and the Lysis Method neither of which destroyed the characteristic architecture of the ECM found in the original tissues. BM components, i.e. laminin, fibronectin and collagen IV, were detectable in the iECM isolated with the Lysis Method but not those isolated with the Digestion Method. Scanning electron microscopic analysis of the normal colon iECM demonstrated that even if the BM was missing, the luminal surface consisted of densely packed ECM filaments which do not allow cell infiltration without degradation of the iECM. Furthermore, we demonstrated that iECM can be separately supplemented with different cell types, i.e. colorectal carcinoma cells, normal fibroblasts and immune cells at any desired concentration, combination and localisation. Therefore, these models could be used to determine the role of the BM and of the tumour cell/normal cell crosstalk in the infiltration process of human colorectal carcinoma cells.

Basement Membrane↗
PubMed1999

In vitro models to study mechanisms involved in cyclosporine A-mediated glomerular contraction.

The immunosuppressive drug, cyclosporin A (CsA), which is successfully used to prevent rejection in organ transplantation, induces renal side-effects as shown by a decrease in glomerular filtration rate and ultrafiltration coefficient regulated by the tone of mesangial cells.The aim of the present study was to investigate the effect of CsA on isolated glomeruli and mesangial cells, which constitute appropriate in vitro models for renal vasoreactivity studies. The roles of different intracellular and extracellular mediators such as calcium, endothelin-1 (ET-1), prostaglandins (TXA(2 )and PGI(2)) and reactive oxygen intermediates (ROIs) were analysed. CsA caused a concentration- and time-dependent decrease in the planar cross-sectional areas of isolated glomeruli and mesangial cells as determined by image analysis. Intracytosolic free calcium concentration determined by fluorimetric analysis was significantly increased after 30 min CsA (10 microM) incubation. In the contraction experiment, the calcium antagonist verapamil inhibited the CsA response. ET-1, TXB(2) and keto-PGF(1alpha) were determined directly, however no changes were found statistically significantly different from respective controls. In contrast to these results, the ET-1 specific antibody was able to reduce CsA-mediated cell contraction. In the presence of a prostacyclin agonist iloprost, CsA-induced contraction was also modified. The role of ROIs using a 2'7'-dichlorofluorescein diacetate (DCFdAc) fluorimetric method was directly determined by observing, with 10 microM CsA, a significant production of hydrogen peroxide (H(2)O(2)), which was able alone to induce mesangial cell contraction. Coincubation with the antioxidants led to a significant inhibition of mesangial cell contraction. These results suggest that CsA caused an imbalance in the normal level of all investigated vasoconstrictive and vasodilator mediators, which shifted towards the advantage of vasoconstrictive action.

Animals↗
PubMed1998

Dobutamine antagonizes epinephrine's biochemical and cardiotonic effects: results of an in vitro model using human lymphocytes and a clinical study in patients recovering from cardiac surgery.

BACKGROUND: Patients may receive more than one positive inotropic drug to improve myocardial function and cardiac output, with the assumption that the effects of two drugs are additive. The authors hypothesized that combinations of dobutamine and epinephrine would produce additive biochemical and hemodynamic effects. METHODS: The study was performed in two parts. Phase 1 used human lymphocytes in an in vitro model of cyclic adenosine monophosphate (cAMP) generation in response to dobutamine (10(-8) to 10(-4) M) or epinephrine (10(-9) M to 10(-5) M), and dobutamine and epinephrine together. Phase 2 was a clinical study in patients after aortocoronary artery bypass in which isobolographic analysis compared the cardiotonic effects of dobutamine (1.25, 2.5, or 5 microg x kg(-1) x min(-1)) or epinephrine (10, 20, or 40 ng x kg(-l) x min(-1)), alone or in combination. RESULTS: In phase 1, dobutamine increased cAMP production 41%, whereas epinephrine increased cAMP concentration approximately 200%. However, when epinephrine (10(-6) M) and dobutamine were combined, dobutamine reduced cAMP production at concentrations between 10(-6) to 10(-4) M (P = 0.001). In patients, 1.25 to 5 microg x kg(-1) x min(-1) dobutamine increased the cardiac index (CI) 15-28%. Epinephrine also increased the CI with each increase in dose. However, combining epinephrine with the two larger doses of dobutamine (2.5 and 5microg x kg(-1) x mi(-1)) did not increase the CI beyond that achieved with epinephrine and the lowest dose of dobutamine (1.25 microg x kg(-1) x min(-1)). In addition, the isobolographic analysis for equieffective concentrations of dobutamine and epinephrine suggests subadditive effects. CONCLUSIONS: Dobutamine inhibits epinephrine-induced production of cAMP in human lymphocytes and appears to be subadditive by clinical and isobolographic analyses of the cardiotonic effects. These findings suggest that combinations of dobutamine and epinephrine may be less than additive.

Adrenergic Agonists↗
PubMed1995

Canine bone marrow cell cultures infected with canine distemper virus: an in vitro model of Paget's disease.

We have previously shown that the canine paramyxovirus, canine distemper virus (CDV), is a possible aetiologic agent in Paget's disease of bone and in the canine bone disorder, metaphyseal osteopathy. More recently, we have examined the effects of CDV on the formation of multinucleated, tartrate resistant acid phosphatase positive, calcitonin receptor positive, osteoclast-like cells in cultures of canine bone marrow mononuclear cells, and shown that both in vitro and in vivo infection with CDV produced a dose dependent increase in the number and size of osteoclast-like cells. We have now extended these results to show that CDV infection induces interleukin-6 and c-Fos mRNA in these cells, similar to our recent findings in pagetic bone cells. These results further support the hypothesis that CDV might be involved in the aetiopathogenesis of Paget's disease and metaphyseal osteopathy and suggest that canine marrow culture systems will prove useful as an in vitro model to examine the disease processes in more detail.

Animals↗
PubMed2002

Mixing during intravertebral arterial infusions in an in vitro model.

Regional delivery of drugs can offer a pharmacokinetic advantage in the treatment of localized tumors. One method of regional delivery is by intra-arterial infusion into the basilar/vertebral artery network that provides local access to infratentorial tumors, which are frequent locations of childhood brain cancers. Proper delivery of drug by infused solutions requires adequate mixing of the infusate at the site of infusion within the artery lumen. Our mixing studies with an in vitro model of the vertebral artery network indicate that streaming of drug solution is likely to occur at low, steady infusion rates of 2 ml/min. Streaming leads to maldistribution of drug to distal perfused brain regions and may result in toxic levels in some regions while concurrently yielding subtherapeutic levels in adjacent regions. According to our model findings, distribution to both brain hemispheres is not likely following infusion into a single vertebral artery even if the infusate is well-mixed at the infusion site. This outcome results from the unique fluid flow properties of two converging channels, which are represented by the left and right vertebral branches converging into the basilar. Fluid in the model remains stratified on the side of the basilar artery served by the infused vertebral artery. Careful thought and planning of the methods of intravertebral drug infusions for treating posterior fossa tumors are required to assure proper distribution of the drug to the desired tissue regions. Improper delivery may be responsible for some noted toxicities or for failure of the treatments.

Antineoplastic Agents↗
PubMed2005

The potential for dental plaque to protect against erosion using an in vivo-in vitro model--a pilot study.

BACKGROUND: Tooth erosion is a problem for professional wine tasters (exogenous erosion from frequent exposure to wine acids) and for people with gastro oesophageal reflux disease (GORD) and bulimia who experience frequent reflux of gastric contents into the mouth (endogenous erosion from mainly HCl). The objective in this study was to determine whether plaque/pellicle could provide teeth with any protection from two common erosive acids, using an in vivo-in vitro technique. METHODS: Tiles of human tooth enamel and root surfaces were prepared from six extracted, unerupted third molar teeth and sterilized. Mandibular stents were prepared for six volunteer subjects and the tiles bonded to the buccal flanges of these stents. They were worn initially for three days to permit a layer of pellicle and plaque to form over the tile surfaces, and for a further 10 days of experimentation. Following cleaning of the plaque/ pellicle layer from the tiles on the right side flange, all the tiles were submerged in either 0.06M HCl or white wine for an accumulated time of 600 and 1500 minutes, respectively. Depths of erosion were determined using light microscopy of sections of the enamel and root tiles. SEM of the lesion surfaces was carried out to investigate the nature of erosive damage and of plaque/pellicle remnants. RESULTS: Retained plaque was found to significantly inhibit dental erosion on enamel, from contact with both HCl and wine, compared with that resulting following its removal. However, it was found to provide no significant protection on root surfaces. SEM analysis of the tile surfaces revealed marked etching of enamel on the cleaned surfaces, and considerable alteration to the appearance of remaining plaque and pellicle on most surfaces. CONCLUSION: Within the limitations of numbers of specimens, dental plaque/pellicle provided a significant level of protection to tooth enamel against dental erosion from simulated gastric acids and from white wine, using an in vivo-in vitro model. It was unable to provide any significant protection to root surfaces from these erosive agents. Possible reasons for this difference are explored.

Calcium Phosphates↗
PubMedDate not supplied

Effects of stem design and pre-cooling prostheses on the heat generated by bone cement in an in vitro model.

The necrotizing effects of the heat, particularly at more than 50 degrees C, produced by the exothermic polymerization process associated with the acrylic implant cement polymethylmethacrylate (PMMA) are well documented. The temperature changes that occur are dependent on the thickness of the PMMA. The current study investigates the hypothesis that the heat produced by the bone cement may be reduced by the choice of stem design and by pre-cooling the hip prosthesis. The thermal alterations at the bone-cement interface were measured in an in vitro model. The results indicated that a temperature decrease of approximately 7 degrees C could be achieved by pre-cooling the prosthesis, and by changing the shape of the prosthesis stem from flat and wide to round.

Bone Cements↗
PubMed2005

An in vitro model of chlorhexidine-induced tooth staining.

BACKGROUND: Tooth staining is a common feature of chlorhexidine treatment for periodontal disease and there is a large variation between patients as to the degree of their tooth staining. Although the mechanism of tooth staining is uncertain, diet, smoking and oral hygiene appear probable factors. OBJECTIVES: This study investigated the role of saliva in chlorhexidine-induced tooth staining and used tea as the staining agent in an in vitro model with hydroxyapatite mimicking teeth. METHODS: Saliva has been used to create an acquired pellicle and in solution to mimic its effects in vivo. Using different combinations of tea, chlorhexidine and parotid saliva, substances binding to hydroxyapatite were analysed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Using this system, tea, chlorhexidine and salivary proteins were clearly identifiable following staining by Coomassie Brilliant Blue. RESULTS: The results indicated that tea interacted with many salivary proteins, in particular proline-rich proteins and histatins. Chlorhexidine did not appear to complex with or precipitate salivary proteins nor prevent the formation of an acquired pellicle on the hydroxyapatite. In isolation, tea and chlorhexidine bound in small amounts to hydroxyapatite, but when added in combination, binding of both to hydroxyapatite was greatly increased. The acquired pellicle reduced chlorhexidine and tea binding, but conversely increased the binding of either tea or chlorhexidine alone to hydroxyapatite. CONCLUSION: In conclusion, salivary proteins play an important role in the staining process and the combination of tea and chlorhexidine appears to be a very potent staining factor.

Anti-Infective Agents, Local↗