bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Application of in Situ Models for Evaluation of New Fluoride-Containing Systems
Authors: Faller R.V. 
Published: January 2009

Many in situ models have assessed the anticaries potential of fluoride-containing systems (Stookey et al., 1985; Mellberg et al., 1986, 1992a,b; Corpron et al., 1986; Featherstone and Zero, 1992; Ogaard and Rolla, 1992; Stephen et al., 1992). Several models have reportedly been validated according to guidelines proposed by Proskin et al. (1992). The proposed guidelines cover only dentifrices containing sodium fluoride (NaF) or sodium monofluorophosphate (SMFP) as active ingredients. These compounds are the most widely used sources of fluoride in dentifrices, and dose-response clinical standards are available for both. Other fluoride compounds, such as amine fluoride (AmF) and stannous fluoride (SnF2), have also been proven effective in reducing caries (Muehler et al., 1957, 1958; Marthaler, 1968; Lu et al., 1980; Cahen et al., 1982). Profile standards for these fluorides were not included in the proposed guidelines, primarily due to the lack of clinical data necessary to establish a dose response for these ingredients. Criteria for demonstrating the efficacy of these ingredients, along with methods to assess new fluoride compounds, need to be established. In situ models are used to evaluate the anticaries potential of new compounds added to mouthrinses, gums, slow-release devices, etc. (Creanor et al., 1992; Manning and Edgar, 1992; Lamb et al., 1993; Toumba and Curzon, 1993; Wang et al., 1993). Ingredients are often added to dentifrices previously proven effective against caries in order to provide additional benefits of gum health, tartar control, cleaning, etc. Proposals are made regarding the in situ testing of new dentifrices containing clinically proven fluoride compounds other than NaF and SMFP, as well as alternative delivery systems, in order to assist in their evaluation.
Models for Evaluating New Fluoride-Containing Systems: Reaction Paper
Authors: Duckworth R.M. 
Published: January 2009

The type and number of control formulations to be used in model studies to evaluate new fluoride systems require careful consideration. While many controls may be justified on the grounds of scientific interest, some models can handle only small numbers of treatments without the statistical power of studies being compromised. In those cases, the results of more than one study may need to be combined. Current models for evaluating fluoride products have most often been developed with systems containing ionic fluoride in mind. To test new types of delivery vehicles or formulations which contain new fluoride agents, model protocols may need to be revised in order to account properly for differences in modes of action-for example, in rates of reaction with enamel or site specificity of active ingredient delivery in the mouth.
Surface Changes of Fluoride-Releasing Composites: a Comparison of in Vivo and in Vitro Results
Authors: Dijkman G.E.H.M. , De Vries J. , Jongebloed W.L. , Arends J. 
Published: January 2009

Fluoride-releasing composites lose fluoride very slowly over time. An interesting question is the possible change in mechanical properties related to the F release. If this happens, it might be expected that the mechanical properties of the outer surface of a fluoridating composite are affected first. The purpose of this study was to investigate in vivo and in vitro the changes in surface microhardness and surface structure of three fluoride-releasing composites and a non-F-containing control after 28 days. In the in vitro experiment, the composites were stored in tap water at 37°C. The results show that all composites stored in water were significantly softened after 28 days. In vivo, however, a very different picture emerged: The surface microhardness of the fluoride-releasing composites did not change significantly. In vitro, the data indicate that the amount of softening of the fluoridating composites is related to the amount of fluoride released. No relation was found between the amount of F released in one month in vitro and the microhardness changes in vivo. SEM micrographs of fluoridating composites do not reflect the microhardness changes mentioned.
Review of Fluoride Release and Secondary Caries Reduction by Fluoridating Composites
Authors: Arends J. , Dijkman G.E.H.M. , Dijkman A.G. 
Published: January 2009

Secondary caries is one of the main reasons to replace restorations. Due to the pressure to eliminate or reduce the number of amalgam restorations in many countries, fluoride-releasing composites have gained in importance. This review limits itself to information relevant to secondary caries near fluoride-releasing anterior or posterior composites. Although many parameters are very important in composite functioning, a weak spot near a filling is always the interface and the locally present interfacial gap between the composite and the hard tissues, where secondary caries takes place due to plaque action. Relevant parameters such as the amount of fluoride released in vitro in μg.cm-2, the rate of fluoride release, and the period of fluoride release are compared for several composites. In vitro F release has been measured for some fluoridating composites for more than five years. Unfortunately, F release in vivo or in situ cannot be measured adequately. The fluoride released by the composites considered is partly taken up by the surrounding tissues, partly released to the saliva, and partly efficacious in possible marginal gaps and defects. A major part of this paper pertains to in vitro, in situ, and in vivo secondary caries reduction experiments. In vitro caries reductions in the order of 40% from F-releasing composites vs. controls have been found. In in situ model investigations under plaque and saliva conditions, secondary caries reduction percentages of between 40 and 50% have been experimentally measured in gaps in enamel near F composites.
Prenatal Craniofacial Development: New Insights On Normal and Abnormal Mechanisms
Authors: Johnston M.C. , Bronsky P.T. 
Published: January 2009

Technical advances are radically altering our concepts of normal prenatal craniofacial development. These include concepts of germ layer formation, the establishment of the initial head plan in the neural plate, and the manner in which head segmentation is controlled by regulatory (homeobox) gene activity in neuromeres and their derived neural crest cells. There is also a much better appreciation of ways in which new cell associations are established. For example, the associations are achieved by neural crest cells primarily through cell migration and subsequent cell interactions that regulate induction, growth, programmed cell death, etc. These interactions are mediated primarily by two groups of regulatory molecules: "growth factors" ( e.g., FGF and TGFa) and the so-called steroid/thyroid/retinoic acid superfamily. Considerable advances have been made with respect to our understanding of the mechanisms involved in primary and secondary palate formation, such as growth, morphogenetic movements, and the fusion/merging phenomenon. Much progress has been made on the mechanisms involved in the final differentiation of skeletal tissues. Molecular genetics and animal models for human malformations are providing many insights into abnormal development. A mouse model for the fetal alcohol syndrome (FAS), a mild form of holoprosencephaly, demonstrates a mid-line anterior neural plate deficiency which leads to olfactory placodes being positioned too close to the mid-line, and other secondary changes. Work on animal models for the retinoic acid syndrome (RAS) shows that there is major involvement of neural crest cells. There is also major crest cell involvement in similar syndromes, apparently including hemifacial microsomia. Later administration of retinoic acid prematurely and excessively kills ganglionic placodal cells and leads to a malformation complex virtually identical to the Treacher Collins syndrome. Most clefts of the lip and/or palate appear to have a multifactorial etiology. Genetic variations in TGFas, RARas, NADH dehydrogenase, an enzyme involved in oxidative metabolism, and cytochrome P-450, a detoxifying enzyme, have been implicated as contributing genetic factors. Cigarette smoking, with the attendant hypoxia, is a probable contributing environmental factor. It seems likely that few clefts involve single major genes. In most cases, the pathogenesis appears to involve inadequate contact and/or fusion of the facial prominences or palatal shelves. Specific mutations in genes for different FGF receptor molecules have been identified for achondroplasia and Crouzon's syndrome, and in a regulatory gene (Msx2) for one type of craniosynostosis. Poorly co-ordinated control of form and size of structures, or groups of structures (e.g., teeth and jaws), by regulatory genes should do much to explain the very frequent "mismatches" found in malocclusions and other dentofacial "deformities". Future directions for research, including possibilities for prevention, are discussed.
Molecular Mechanisms of Dental Enamel Formation
Authors: Simmer J.P. , Fincham A.G. 
Published: January 2009

Tooth enamel is a unique mineralized tissue in that it is acellular, is more highly mineralized, and is comprised of individual crystallites that are larger and more oriented than other mineralized tissues. Dental enamel forms by matrix- mediated biomineralization. Enamel crystallites precipitate from a supersaturated solution within a well-delineated biological compartment. Mature enamel crystallites are comprised of non-stoichiometric carbonated calcium hydroxyapatite. The earliest crystallites appear suddenly at the dentino-enamel junction (DEJ) as rapidly growing thin ribbons. The shape and growth patterns of these crystallites can be interpreted as evidence for a precursor phase of octacalcium phosphate (OCP). An OCP crystal displays on its (100) face a surface that may act as a template for hydroxyapatite (OHAp) precipitation. Octacalcium phosphate is less stable than hydroxyapatite and can hydrolyze to OHAp. During this process, one unit cell of octacalcium phosphate is converted into two unit cells of hydroxyapatite. During the precipitation of the mineral phase, the degree of saturation of the enamel fluid is regulated. Proteins in the enamel matrix may buffer calcium and hydrogen ion concentrations as a strategy to preclude the precipitation of competing calcium phosphate solid phases. Tuftelin is an acidic enamel protein that concentrates at the DEJ and may participate in the nucleation of enamel crystals. Other enamel proteins may regulate crystal habit by binding to specific faces of the mineral and inhibiting growth. Structural analyses of recombinant amelogenin are consistent with a functional role in establishing and maintaining the spacing between enamel crystallites.
Dynamics of the Pulpo-Dentin Complex
Authors: Pashley D.H. 
Published: January 2009

Dentin has a relatively high water content due to its tubular structure. Once dentin is exposed, this intratubular water is free to move in response to thermal, osmotic, evaporative, or tactile stimuli. Fluid shifts across dentin are thought to cause sufficient shear forces on odontoblasts, nerve endings, nearby fibroblasts, and blood vessels to cause significant mechanical irritation, disruption, or damage, depending on the magnitude of the fluid shift. Even in the absence of fluid shifts, the water-filled tubules provide diffusion channels for noxious (i.e., bacterial products) substances which diffuse inward toward the pulp, where they can activate the immune system, provide chemotactic stimuli, cytokine production, and produce pain and pulpal inflammation. Viewed from this perspective, dentin is a poor barrier to external irritants. However, pulpal tissues react to these challenges by increasing the activity of nerves, blood vessels, the immune system, and interstitial fluid turnover, to make the exposed dentin less permeable either physiologically, via increased outward fluid flow, or microscopically, by lining tubules with proteins, mineral deposits, or tertiary dentin, thereby enhancing the barrier properties of dentin, and providing additional protection to pulpal tissues. These reactions involve dentin and pulp, both in the initiation of the processes and in their resolution. These responses of the dental pulp to irritation of dentin demonstrate the dynamic nature of the pulpo-dentin complex.
Is All Bone the Same? Distinctive Distributions and Properties of Non-Collagenous Matrix Proteins in Lamellar Vs. Woven Bone Imply the Existence of Different Underlying Osteogenic Mechanisms
Authors: Gorski J.P. 
Published: January 2009

The purpose of this review is to summarize recent functional and structural findings regarding non-collagenous matrix proteins in bone and teeth, to compare gene locations for bone and tooth matrix proteins with loci for hereditary skeletal diseases, and to present several provocative hypotheses which integrate this new information into a physiological context. Hypothesis 1 proposes that the molecular composition of rapidly deposited and mineralized woven bone, as well as the responsiveness of cells synthesizing woven bone to stimuli, is different from that for more slowly synthesized lamellar bone, implying the existence of distinctive osteogenic mechanisms. This review of recent research strongly supports this proposal. Briefly, the protein composition of woven bone matrix is enriched in acidic phosphoproteins BAG-75 and BSP, which are not expressed in lamellar bone, which is itself enriched in osteocalcin. De novo deposition and mineralization of woven bone occurs faster than in lamellar bone by means of a matrix-vesicle-assisted mechanism. Deposition of woven bone occurs at sites experiencing biomechanical strains higher than those experienced by lamellar bone. In addition, woven bone in metaphyseal regions is more susceptible to osteoclastic resorption after space flight, ovariectomy, and loss of weightbearing than is lamellar bone. Finally, osteoprogenitor cells responsive to parathyroid hormone reside in the metaphyseal region of long bones. Taken together, these findings suggest that Hypothesis I represents a useful paradigm for future studies. Specific functions mediated by most individual bone and tooth matrix proteins remain uncertain A review of current literature suggests that the functionality of skeletal matrix proteins is expressed through specific binding sites composed of particular species-conserved structural motifs (Hypothesis 2). Examples include the previously recognized Asp-Ser-Ser motif of dentin phosphophoryns and the gamma-carboxyglutamic acid motif of matrix GLA protein and osteocalcin. A new polyacidic amino acid motif composed of consecutive Asp and Glu residues (n > 7) was defined in extracellular matrix components osteopontin, bone sialoprotein, and bone acidic glycoprotein-75 on the basis of strong functional analogies with similar polyacidic stretches in divalent metal storage proteins of the endoplasmic reticulum and sarcoplasmic reticulum. These structural motifs represent prime targets for future structure-function studies in vivo and in vitro.
The Vascular and Biochemical Effects of Cilostazol in Diabetic Patients With Peripheral Arterial Disease
Authors: O'Donnell Mark E. , Badger Stephen A. , Sharif Muhammad A. , Makar Ragai R. , Young Ian S. , Lee Bernard , Soong C.V. 
Published: January 2009

Objectives: Cilostazol improves walking in patients with peripheral arterial disease (PAD). We hypothesized that cilostazol reduces diabetic complications in PAD patients. Methods: Diabetic PAD patients were prospectively recruited to a randomized double-blinded, placebo-controlled trial, using cilostazol 100mg twice a day. Clinical assessment included ankle-brachial index, arterial compliance, peripheral transcutaneous oxygenation, treadmill walking distance and validated quality of life (QoL) questionnaires. Biochemical analyses included glucose and lipid profiles. All tests were at baseline, 6, and 24 weeks. Results: 26 diabetic PAD patients (20 men) were recruited. Cilostazol improved absolute walking distance at 6 and 24 weeks (86.4% vs. 14.1%, P = .049; 143% vs. 23.2%, P = .086). Arterial compliance and lipid profiles improved as did some QoL indices for cilostazol at 6 and 24 weeks. Blood indices were similar at baseline and at follow-up points for both treatment groups. Conclusions: Cilostazol is a well-tolerated and efficacious treatment, which improves claudication distances in diabetic PAD patients with further benefits in arterial compliance, lipid profiles, and QoL.
Role of K+ATPChannels, Endothelin A Receptors, and Effect of Angiotensin II on Blood Flow in Oral Tissues
Authors: Berggreen E. , Heyeraas K.J. 
Published: January 2009

K+ATPchannels are involved in CGRP-mediated vasodilation and in the vasoconstriction induced by endothelin or angiotensin II. In this study, we examined the effects of a K+ATPchannel antagonist and an ET(A) receptor antagonist on resting blood flow in the pulp and gingiva, and observed their role in the vasodilation induced by tooth stimulation. We also investigated whether receptors for angiotensin II exist in the pulp and gingiva. Blood flow was measured with laser-Doppler flowmetry. Under control conditions, the K+ATPchannel antagonist and angiotensin II caused a significant drop in blood flow in both target tissues. Blocking of ET(A) receptor did not change basal blood flow. The vasodilation observed after tooth stimulation remained unchanged following blockade of K+ATPchannels and ET(A) receptors. Analysis of the data shows that open K+ATPchannels exist during resting conditions in the pulp and gingiva, but that CGRP seems to induce vasodilation mainly via mechanisms other than K+ATPchannels. ET(A) and AT1receptors are found in the pulp and gingiva, but ET(A) receptors are not involved in modulation of a basal vascular tone in these tissues or in the vasodilation observed after tooth stimulation.Open K+ATPchannels exist during resting conditions in both the dental pulp and gingiva, but calcitonin gene-related peptide seems to induce vasodilation via mechanisms other than the K+ATPchannels.
Methods for Enhancing the Efficiency of Dental/Oral Health Clinical Trials: Current Status, Future Possibilities
Authors: Barnett M.L. , Pihlstrom B.L. 
Published: January 2009

BACKGROUND In recent years, there has been an increasing demand for clinical trials to study oral, dental, and craniofacial diseases and conditions. This has resulted from such factors as the increasing pace of discoveries requiring translational research to develop them for clinical use, FDA requirements for product approval, a need for additional data to support evidence-based dental practice, and the expansion of the NIDCR’s clinical research programs. The complexity, size, and duration of clinical trials often make them quite costly to conduct, and may impede the development of novel diagnostic, preventive, and therapeutic methods that could have a significant impact on clinical practice and inform public health policy. Recent advances in such areas as genomics and proteomics, coupled with the development of new technologies, have expanded our knowledge of the etiology and pathogenesis of disease and, from this, have provided new insights into the design and conduct of clinical trials. The workshop, “Methods for Enhancing the Efficiency of Dental/Oral Health Clinical Trials: Current Status, Future Possibilities”, held on May 6–7, 2004, considered a variety of ways in which these insights are being, or have the potential to be, applied to clinical trials so as to enhance their efficiency and, hence, their cost-effectiveness, without diminishing the quality of information produced. The focus of this workshop was to assess the state of the science and identify research needs for the use of biomarkers, surrogate endpoints, and new technologies in oral disease clinical trials. Examples of ways in which clinical trials of other diseases have benefited from the use of new methods and technologies and FDA considerations were also discussed.
Balancing integrity vs. risk of falling – nurses’ experiences of caring for elderly people with dementia in nursing homes
Authors: Johansson Inger , Bachrach-Lindström Margareta , Struksnes Solveig , Hedelin Birgitta 
Published: January 2009

Abstract Dementia is recognized as being a major risk for falls that cause suffering and increase dependency for the individual. The purpose of this study was to explore registered nurses’ and nurse assistants’ experiences of caring for elderly people with dementia who are at risk of falling, and factors that contribute or reduce falls in this group. A phenomenographic design was chosen. Ten nurses and 18 nurse assistants with experience of fall events were strategically selected for a recorded interview. The informants were chosen from 10 nursing homes in Sweden and Norway. They were asked to describe a fall situation they had been involved in when caring for elderly people with dementia. The findings shed light on an ethical dilemma in the main category ‘Balancing integrity and autonomy versus risk of falling’ which was comprehensively related to two descriptive categories. The first one was ‘Adjusting to the older person’s condition’ with the concepts of forgetfulness, anxiety and confusion, ability to express oneself and understand, bodily build and function. The second category was ‘Adjusting the care environment’, comprising these conceptions: the physical environment, the psychosocial environment, organization and human resources. Based on the staff’s perceived difficulties in preventing falls in elderly people with dementia, there is a need for additional support or professional supervision in their work to enhance possibilities for successful fall prevention.
Dose-dense induction with sequential high-dose cytarabine and mitoxantone (S-HAM) and pegfilgrastim results in a high efficacy and a short duration of critical neutropenia in de novo acute myeloid leukemia: a pilot study of the AMLCG
Authors: Braess Jan , Spiekermann Karsten , Staib Peter , Grüneisen Andreas , Wörmann Bernhard , Ludwig Wolf-Dieter , Serve Hubert , Reichle Albrecht , Peceny Rudolf , Oruzio Daniel , Schmid Christoph , Schiel Xaver , Hentrich Marcus , Sauerland Christina , Unterhalt Michael , Fiegl Michael , Kern Wolfgang , Buske Christian , Bohlander Stefan , Heinecke Achim , Baurmann Herrad , Beelen Dietrich W. , Berdel Wolfgang E. , Büchner Thomas , Hiddemann Wolfgang 
Published: January 2009

AbstractDose density during early induction has been demonstrated to be one of the prime determinants for treatment efficacy in acute myeloid leukemia (AML). The German AML Cooperative Group has therefore piloted a dose-dense induction regimen sequential high-dose AraC and mitoxantrone followed by pegfilgrastim (S-HAM) in which 2 induction cycles are applied over 11 to 12 days instead of 25 to 29 days as used in conventional double induction, thereby increasing dose density 2-fold. Of 172 de novo AML patients (excluding acute promyelocytic leukemia), 61% reached a complete remission, 22% a complete remission with incomplete peripheral recovery, 7% had persistent leukemia, 10% died (early death) resulting in an overall response rate of 83%. Kaplan-Meier estimated survival at 2 years was 61% for the whole group (patients with unfavorable karyotypes, 38%; patients with favorable karyotypes, 69%; patients with intermediate karyotypes, 75%) after S-HAM treatment. Importantly, the compression of the 2 induction cycles into the first 11 to 12 days of treatment was beneficial for normal hematopoiesis as demonstrated by a significantly shortened duration of critical neutropenia of 31 days compared with 46 days after conventionally timed double induction. (European Leukemia Trial Registry LN_AMLINT_2004_230.)