People with dementia at times exhibit threatening and physically aggressive behavior toward care staff in residential aged care facilities (RACFs). Current clinical guidelines recommend judicious use of antipsychotic (AP) medications when there is an immediate risk of harm to care staff in RACFs and non-pharmacological interventions have failed to avert the threats. This article examines an account of how this recommendation can be ethically defensible: caregivers in RACFs may have a prima facie ethical justification, in certain cases, to use APs as an act of self-defense. The author examines whether such uses of APs meet the three commonly invoked conditions of ethically permissible acts of self-defense-namely, the conditions of liability, proportionality, and necessity-and argues that such conditions obtain only in a restricted range of cases. The liability constraint can be satisfied if residents are the only ones who are causally responsible for the threats they pose. Further, the condition of proportionality obtains if there is sufficient objective ground to demonstrate that the harm of using the medications does not outweigh the good to be secured. Lastly, the necessity condition obtains when the medications are used at their lowest effective dosage and caregivers in RACFs can reasonably assume that, for the purpose of averting threats posed by residents, the use of APs is the only available course of action. Not meeting any of these fairly stringent conditions renders uses of APs as acts of self-defense in RACFs morally impermissible actions.
......................................................................................................... ii ACKNOWLEDGMENTS ...................................................................................... iv LIST OF TABLES ............................................................................................... vii LIST OF FIGURES .............................................................................................. ix LIST OF ABBREVIATIONS ................................................................................. x INTRODUCTION ................................................................................................. 1 LITERATURE REVIEW ....................................................................................... 6 Acellular Dermal Matrix Allografts (ADMA) ............................................... 6 ADMA to Increase the Width of Keratinized Gingiva ................................. 7 ADMA versus CTG in the Treatment of Recessions ................................. 8 ADMA versus CAF in the Treatment of Recessions ............................... 10 ADMA versus ADMA in the Treatment of Recessions ............................ 11 Role of Orientation of the Basement Membrane of ADMA...................... 12 Long-term Stability of Root Coverage with ADMA .................................. 12 Histology of ADMA-Treated Sites ........................................................... 14 SPECIFIC AIMS OF THE STUDY ..................................................................... 16 MATERIAL AND METHODS ............................................................................. 17 Study Design and Population .................................................................. 17 Study Device ........................................................................................... 23 Surgical Procedure ................................................................................. 26 Post-Surgical Care .................................................................................. 29 Statistical Analysis .................................................................................. 32 RESULTS ......................................................................................................... 34 DISCUSSION .................................................................................................... 49 SUMMARY AND CONCLUSIONS .................................................................... 58
Statement of problem Virtually every prosthodontic rehabilitation involves making diagnostic casts for analysis and prosthesis fabrication Frequently, these casts are produced using irreversible hydrocolloid (IH) impression materials in stock metal or plastic trays However, it is unclear whether one technique produces a more accurate castPurpose The purpose of this randomized clinical trial was to compare the linear accuracy of diagnostic casts produced using IH with 1 of 3 different tray types (1) perforated metal trays, (2) stock plastic trays, and (3) directed-flow stock plastic trays All groups were compared to casts produced with custom trays and vinyl polysiloxane (VPS) impression materials, which were considered the controlMaterial and methods Seven subjects participated in this trial IH impressions were made in a random order using 1 of 3 tray types stock plastic, perforated metal, or plastic directed flow These were compared to VPS impressions using custom trays (control group) Each impression technique was repeated 3 times per subject, for a total of 84 observations Impressions were disinfected and poured in a type IV stone Linear accuracy of casts was measured using computer software analysis of scanned images of the casts at x30 magnification Three linear measurements were made on each cast second molar to second molar, right second molar to left first premolar, and left second molar to right first premolar Measurements were compared among techniques using mixed model analysis of variance to account for correlation among the multiple measurements made on each subject Dunnett's adjustment for multiple comparisons with control was used (alpha = 05)Results For molar-to molar and right second molar to the left first premolar measurements, there were no significant differences in linear dimensions between casts made from different trays However; linear measurements from the left second molar to the right first premolar demonstrated significant differences for casts made with stock metal, directed-flow, and stock plastic trays compared to custom trays In this group, casts produced by stock metal, directed-flow, and stock plastic trays differed from controls by 102, 68, and 71 um, respectively Generally, casts made with plastic trays (stock plastic and directed flow) had values closer to those of custom trays than did casts made with metal traysConclusions Impressions made with irreversible hydrocolloid produced casts that were significantly different in linear dimension than casts produced by custom trays and VPS impressions These differences were not uniform, but varied by location on the cast (J Prosthet Dent 2010,104 364-371)
OBJECTIVE:To compare the mineralisation density (MD), morphology and histology of alveolar bone and cementum amongst VDR +/+, VDR -/-, and VDR -/- groups supplemented with a diet TD 96348, containing 20% lactose, 2.0% calcium and 1.25% phosphorous. METHODS:Four groups of mice (6 mice/group) were identified by genotyping: VDR +/+ mice (VDR wild type), VDR -/- mice (VDR deficient), VDR -/- offsprings derived from VDR -/- parents receiving a supplemental diet (early rescued), and VDR -/- mice fed with a supplemental diet beginning at age one month (late rescued). All mice were sacrificed at age 70.5 days. Micro-CT was used to compare MD and morphology of alveolar bone and cementum. H-E and Toluidine blue staining was used to examine the ultrastructure of the alveolar bone and cementum at matched locations. RESULTS:In VDR -/- group, alveolar bone and cementum failed to mineralise normally. Early rescue increased MD of alveolar bone in VDR -/- mice with excessive alveolar bone formation, but which not observed in late rescue group. MD and morphology of cementum-dentine complex in both early and late rescue groups were comparable with VDR +/+ group when feeding with high-calcium rescue diet. CONCLUSIONS:VDR affects alveolar bone mineralisation and formation systemically and locally. However, cementum apposition and mineralisation is mainly regulated by calcium concentrations in serum.
BACKGROUND:Vitamin D plays an important role in bone mineralization. Enamel and dentin are two mineralized tissues of different origins that are part of the tooth structure, but the mechanism by which vitamin D regulates the mineralization of these tissues remains unclear. We examined the mineral deposition pattern of enamel and dentin in continuously erupting incisors in a vitamin D receptor (VDR) deficient mouse model to determine the effect of vitamin D receptor pathway on enamel and dentin mineralization.METHODS:VDR wild-type mice (VDR+/+) and VDR-deficient (VDR--/--) littermates were sacrificed at 70.5 days of age, and their mandibles were dissected. Immunostaining of biglycan and decorin was used to evaluate the dentin maturation. Micro-computerized tomography (micro-CT) was used to compare the mineral density (MD) of enamel and dentin of the two groups at different regions along the axis of the mandibular incisors. Scanning electronic microscopy (SEM) was employed to examine the ultrastructure of enamel and dentin at the levels corresponding to those examined in the micro-CT studies. Furthermore, an accelerated eruption procedure was performed to exclude the effect of delayed eruption on enamel and dentin mineralization.RESULTS:Different mineral deposition patterns of enamel and dentin were observed at different levels of the incisors in the VDR+/+ and VDR--/-- groups. Early enamel maturation and mineralization, and dentin hypomineralization were observed in the VDR--/-- group.CONCLUSION:Vitamin D affects enamel and dentin mineralization through different mechanisms. It may affect the mineralization of dentin systemically while enamel mineralization may be regulated locally.
Vitamin D plays an important role in the bone mineralization process. Enamel and dentin are two mineralized tissues of different origins that combine to form teeth, but the mechanism by which vitamin D regulates these tissues remains unclear. We hypothesized that vitamin D affects enamel and dentin mineralization through different mechanisms.Objective: To examine enamel and dentin mineralization in a vitamin D receptor (VDR) deficient mouse model by micro-computerized tomography (micro-CT) and scanning electronic microscopy (SEM).Methods: VDR wild type mice (VDR+/+) and VDR deficient (VDR-/-) littermates were sacrificed at 70.5 days old, and their mandibles were dissected. Micro-CT was used to compare mineral density (MD) of enamel and dentin of the two groups at different levels along the axis of mandibular incisors. SEM was employed to examine the ultrastructure of incisors at the levels corresponding to the levels used for the micro-CT studies. Furthermore, an accelerated eruption procedure was performed to exclude the effect of delayed eruption on enamel and dentin mineralization.Results: Different distribution patterns of enamel and dentin MD were observed between VDR+/+ and VDR-/- groups. Early enamel maturation, mineralization, and hypomineralization. in dentin were observed in the VDR deficient mice.Conclusion: Vitamin D may affect the mineralization of dentin systemically, and enamel mineralization may be regulated locally. Published by Elsevier Ltd.
Objective: To determine the effects of vitamin D receptor (VDR) deficiency on mouse dentin and enamel mineralisation, and how normalisation of serum calcium level affects dentin and enamel phenotypes in VDR knockout mice.Materials and methods: Groups of VDR wild-type (VDR+/+), VDR deficient (VDR-/-) and VDR-/- rescued mice were sacrificed at 70.5 days of life. The rescued group was established by a high-calcium diet feeding the VDR-/- mice from postnatal 19 days. Micro-CT was used to compare enamel and dentin mineralisation density (MD) at different levels of mandibular incisors among the groups. The scanning electron microscope (SEM) was used to examine the ultrastructure of the enamel and dentin in the corresponding levels and of surface enamel after acidic treatment.Results: Micro-CT showed that in VDR-/- rescued group, dentin phenotype was reversed and dentin MD was reversed to normal; however, enamel mineralisation was not reversible, and remained as hypermineralisation in molar region and apical region of the incisors. SEM also revealed enamel hypermineralisation in the VDR-/- rescued group. This early enamel hypermineralisation was more susceptible to acidic erosion.Conclusion: Vitamin D affects dentin mineralisation systemically, and it regulates enamel mineralisation locally. Published by Elsevier Ltd.
Background and Objective: Erbium lasers are potential tools to remove caries and dental hard tissue but bond strengths of composites to those preparations are reported to be lower than conventional methods. The purpose of this study was to evaluate the effect of mechanical excavation and/or chemical alteration on bond strength of composites to laser irradiated enamel and dentin.Materials and Methods: Seventy-two premolars were ground to obtain flat enamel (E, n, = 36) or dentin (D, n = 36) surfaces in both buccal and lingual cusps, divided into: LaserExcavation (LEx), LaserNo-excavation (LNex), and Bur (B) groups. The laser groups were irradiated for 10 seconds by Er,Cr:YSGG laser [4.5 W, 60% air, 80% water (enamel) 3W, 60% air, 70% water (dentin)]. Irradiated surfaces in the excavation groups (Ex) were then mechanically smoothed with a dental excavator, prepared Surfaces werethen etched (37% H(3)PO(4)) for 20 or 40 seconds (enamel) and 15 or 30 seconds (dentin), washed (20 seconds), adhesive was applied(Single Bond Plus), and light cured (20 seconds). A composite cylinder (Filtek Supreme Plus) formed, placed and light cured (40 seconds). The specimens were stored (37 degrees C,48 hours,), shear bond tested (1 mm/minute), and statistically analyzed (P < 0.05).Results: Mixed-model ANOVA showed significant differences between enamel (P = 0.0091) and between dentin groups (P=0.0035). Tukey/Kramer showed mean shear bond strength (SBS +/- SE) of EB40 (27.01 +/- 2.38 MPa) was significantly higher than ELNoExc20 (14.39 +/- 2.5 MPa) and ELExc40 (14.90 +/- 2.28MPa). Also DB30 (17.57 +/- 1.67MPa) and DLExc30 (18.6 +/- 1.74MPa) were significantly higher than DLNoExc15 (9.56 +/- 1.86 MPa).Conclusion: Increasing the etching time up to 40 seconds or excavation of' the laser prepared surface (but not the combination) may increase the bond strength to the level of conventional methods in enamel but excavation has a greater influence in dentin. Also the combination of both methods [excavation+longer etching time (30 seconds)] exhibit significantly better results in dentin. Mode offailure study showed mechanical excavation in both enamel and dentin can significantly reduce the cohesive failure in tooth structure. Lasers Surg. Med. 41:454-462,2009. (C) 2009Wiley-Liss, Inc.
Our laboratory has shown that a human autosomal recessive (AR) form of radicular dentin dysplasia (RDD) is caused by an alteration in the transcription factor NFI-C. Gene array analysis of AR RDD versus normal periodontal ligament cells has revealed that Sox11 is dramatically down regulated associated with the disease. SOX11 is a member of the SRY-related high-mobility-group box (Sox) family of transcription factors. Although Sox11 expression has been previously reported, characterized associated with tooth or root formation has not been performed. Objectives: 1) To characterize the temporal spatial expression pattern of Sox11 during tooth formation; and 2) to determine if Sox11 is potentially regulated by NFI-C. Methods: Mouse maxillas & mandibles (Embryonic day 16 through post-natal day 28) were fixed, embedded, demineralized if necessary, sectioned and mounted on silane-treated slides. Sox11 expression was determined by by immunohistochemistry using a rabbit anti-Sox11 polyclonal antibody. Levels of Sox11 transcripts in established dental cell lines are determined by quantitative real-time polymerase chain reaction analysis (QRT-PCR). Studies using a bioinformatics approach will determine the presence of potential NFIC binding sites contained within the Sox11 promoter that are conserved across various species. Results: In the early stages of tooth development (E-16) Sox11 is strongly expressed in both inner and outer enamel epithelium, as well as the dental papilla. Increased staining is seen with the cytodifferentiation of the ameloblasts and odontoblasts
Background: The purpose of this study was to evaluate if the healing of full-thickness skin wounds was accelerated by platelet-rich plasma (PRP).Methods: Four 2.5 x 2.5-cm full-thickness skin wounds were created on the backs of 15 New Zealand white rabbits. One wound on each animal received 0.3, 0.6, or 0.9 ml PRP, and the fourth wound served as a control. Seven and eight animals were sacrificed after 1 or 2 weeks, respectively, to determine histomorphometrically the epithelialization rate, contraction rate, healing rate, tissue fill, and volume fractions of fibroblasts, neutrophils, macrophages, and blood vessels.Results: Only the 0.6- and 0.9-ml groups had significantly lower contraction rates than the controls after 2 weeks (P <0.05). Although no statistically significant differences were found in other parameters between the PRP-treated wounds and the controls, the PRP treatment led to increases in average epithelialization rates and volume fraction of blood vessels at both time periods. The PRP also seemed to have the most positive effect on healing rate, tissue fill, and volume fraction of fibroblasts during week 1 compared to week 2.Conclusions: The PRP treatment enhanced healing in full-thickness wounds by reducing the contraction rate with a trend toward acceleration of the epithelial migration and the angiogenic response. Further studies with larger sample sizes should be conducted to improve statistical sensitivity. Longer time intervals and modifications of PRP volume should also be explored to evaluate the long-term efficacy of PRP on wound healing.
Mutation of vitamin D receptors (vdr) results in resistance to the vitamin's normal effects which may compromise dentin formation. The objective of this study was to investigate the effect of vdr deficiency on post-natal dentin maturation in mice. The dentin in mandibular incisors of 70.5-day-old vdr wild-type and vdr knockout mice was compared at different levels along the long axis. Expression of biglycan and decorin was detected by immunolocalisation. Scanning electron microscopy was used to observe the ultrastructure of the dentin, and micro-computerised tomography was used to determine the degree of dentin mineralisation density. In the vdr knockout mice, the pulp chamber was larger and the dentin wall was thinner compared with the wild-type mice. In addition, the pre-dentin layer was thickened with an irregular front line and diffuse expression of biglycan and decorin. Fewer tubules, lower mineralisation density and pore-like defects were observed in the dentin at the eruptive region and level with the first molar. In conclusion, vdr deficiency compromises dentin maturation.
Background: Alveolar bone loss is often a sequelae of edentulism. However, several reconstruction procedures with bone grafts and barrier membranes are used to restore the lost bony architecture. The value of titanium mesh barriers has been shown to be reliable both in vertical and horizontal ridge augmentation procedures. However, there is a paucity of literature supporting the role of pore size of barrier membranes in preventing soft tissue ingrowth during ridge augmentation procedures. There are multiple reports describing a layer of soft tissue with varying thickness beneath the mesh and adhering to the newly regenerated bone. The objective of this study was 1) to identity the presence of an optimal pore size that facilitates qualitative bone regeneration, 2) to identify the critical pore size that excludes soft tissue ingrowth into regenerative sites, 3) to determine if cortical perforations have any effect on bone regeneration, and 4) to reiterate that bone graft containment is an important parameter for successful regeneration. Methods: The study involved 4 adult hound dogs that were randomly divided into 3 groups. Groups 1 and 2 consisted of one animal each, sacrificed at one month and two months respectively. Group 3 consisted of two animals, sacrificed at the end of four months after the surgical procedure. All the animals received corticocancellous tibial bone grafting to the bilateral mandibular body/ramus areas. The left mandible received
Surfaces of biocompatible alloys used as implants play a significant role in their osseointegration. Surface sol-gel processing (SSP), a variant of the bulk sol-gel technique, is a relatively new process to prepare bioreactive nanostructured titanium oxide for thin film coatings. The surface topography, roughness, and composition of sol-gel processed Ti6Al4V titanium alloy coatings was investigated by atomic force microscopy (AFM) and X-ray electron spectroscopy (XPS). This was correlated with corrosion properties, adhesive strength, and bioreactivity in simulated body fluids (SBF). Electroimpedance spectroscopy (EIS) and polarization studies indicated similar advantageous corrosion properties between sol-gel coated and uncoated Ti6Al4V, which was attributed to the stable TiO2 composition, topography, and adhesive strength of the sol-gel coating. In addition, inductive coupled plasma (ICP) and scanning electron microscopy with energy dispersive spectrometry (SEM-EDS) analysis of substrates immersed in SBF revealed higher deposition of calcium and phosphate and low release rates of alloying elements from the sol-gel modified alloys. The equivalent corrosion behavior and the definite increase in nucleation of calcium apatite indicate the potential of the sol-gel coating for enhanced bioimplant applications.
To analyze the growth-related changes in extracellular matrix components in temporomandibular joint (TMJ) discs, the expression and localization of the core protein of a large chondroitin sulphate proteoglycan, versican, in rat TMJ discs during postnatal development (2-32 weeks) were examined using Western blot analysis, real-time quantitative PCR and immunohistochemistry. Western blot analysis showed that rat TMJ discs predominantly expressed one isoform (V1) and the core protein sharply increased after birth, reached a peak at 8 weeks, and then gradually decreased up to 32 weeks. Real-time quantitative PCR with TaqMan probes indicated that mRNA expression of versican was highest at 2 weeks and gradually decreased with growth. An immunohistochemical study showed that staining for versican was weak and evenly distributed in TMJ discs at 2 weeks. Regional differences in staining for versican became prominent after 8 weeks; staining was intense in the anterior and posterior peripheral attachments, and weak in the central part of the discs. These results demonstrate that growth-related changes and regional differences exist in the expression of versican in the TMJ discs of growing rats, and these probably reflect the changes in the biomechanical environment caused by the development of orofacial functions.
This study evaluated the cytotoxicity of the root canal sealing materials Resilon and Epiphany versus guttapercha, Grossman's sealer, Thermaseal, and Sealapex. Using human gingival fibroblasts the fibroblasts cultures were incubated for either 1 or 24 h to test the cytotoxicity after freshly mixing or after 24 h of setting. Fibroblasts were then stained with trypan blue, to determine number of dead cells. Data were analyzed using ANOVA and t tests. Resilon was similar to guttapercha and the control. Epiphany was less cytotoxic than Grossman's sealer at both the 1 and 24 h time periods. Epiphany was more cytotoxic than Sealapex at the 1-h time period but less cytotoxic at the 24 h time period. These results indicated that Resilon had a lower cytotoxicity and that Epiphany was more cytotoxic than conventional materials.
The biological events occurring at the bone–implant interface are influenced by the topography, chemistry and wettability of the implant surface. The surface properties of titanium alloy prepared by either surface sol–gel processing (SSP), or by passivation with nitric acid, were investigated systematically using X-ray photoelectron spectroscopy, scanning electron microscopy, atomic force microscopy and contact angle metrology. The bioreactivity of the substrates was assessed by evaluating MC3T3-E1 osteoblastic cell adhesion, as well as by in vitro formation of mineralized matrix. Surface analysis of sol–gel-derived oxide on Ti6Al4V substrates showed a predominantly titanium dioxide (TiO2) composition with abundant hydroxyl groups. The surface was highly wettable, rougher and more porous compared to that of the passivated substrate. Significantly more cells adhered to the sol–gel-coated surface, as compared with passivated surfaces, at 1 and 24h following cell seeding, and a markedly greater number of mineralized nodules were observed on sol–gel coatings. Collectively our results show that the surface properties of titanium alloy can be modified by SSP to enhance the bioreactivity of this biomaterial.
Epithelial cells lining the oral cavity are exposed to HIV-1 through breast-feeding and oral-genital contact. Genital secretions and breast milk of HIV-1-infected subjects contain both cell-free and cell-associated virus. To determine if oral epithelial cells can be infected with HIV-1 we exposed gingival keratinocytes and adenoid epithelial cells to cell-free virus and HIV-1-infected peripheral blood mononuclear cells and monocytes. Using primary isolates we determined that gingival keratinocytes are susceptible to HIV-1 infection via cell-free CD4-independent infection only. R5 but not X4 viral strains were capable of infecting the keratinocytes. Further, infected cells were able to release infectious virus. In addition, primary epithelial cells isolated from adenoids were also susceptible to infection; both cell-free and cell-associated virus infected these cells. These data have potential implications in the transmission of HIV-1 in the oral cavity.
The present study investigated the localization of versican in odontogenic tumors by immunohistochemistry, using paraffin-embedded sections obtained from 27 patients with odontogenic tumors (17 ameloblastomas, 1 adenomatoid odontogenic tumor, 4 odontogenic keratocysts, 1 calcifying odontogenic cyst, 2 ameloblastic fibromas, and 2 malignant ameloblastomas). Deparaffinized sections were immersed in a buffered 1 : 1000 solution of an antibody, 5D5 (raised against a large chondroitin sulfate proteoglycan from bovine sclera), which mainly recognizes versican. All samples showed a positive reaction for versican in connective tissues, whereas positive staining of epithelial nests was observed in only some samples. The positive staining in epithelial nests was in areas showing stellate reticulum-like, cuboidal, columnar cells at the periphery, and tear-drop structures. These results indicated that versican might be involved in, at least in part, the morphogenesis of neoplastic epithelium and mesenchymal tissues in odontogenic tumors.
In this study, we report the immunohistochemical localization of versican in healthy porcine gingival epithelia. The monoclonal antibody (mAb), 5D5, specifically recognizes core proteins of large chondroitin sulphate proteoglycans such as versican, neurocan and brevican, but not the core protein of aggrecan. Because neurocan and brevican appear to be specific to nervous tissue, the large chondroitin sulphate proteoglycans examined in this study is most likely versican. In the keratinized layer of the attached gingival epithelium, the basal and spinous cell surfaces showed intense staining for mAb 5D5. In the parakeratinized layer of the sulcus epithelium, the localization was restricted to the basal and lower spinous layers. In the junctional epithelium, intense staining was observed in one or two cell layers near the enamel surface. Immunoelectron microscopy revealed high-density depositions of 5D5 immunoreactivity on epithelial cell surfaces. At the enamel surface, 5D5 immunoreactivity was localized to the dental cuticle of the junctional epithelium but was not present in the internal basal lamina. These results suggest that versican, a large chondroitin sulphate proteoglycan, is involved in epithelial differentiation and downgrowth.