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Sökning: L773:0022 0345 OR L773:1544 0591

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1.
  • Abtahi, Jahan, et al. (författare)
  • Effect of Local vs. Systemic Bisphosphonate Delivery on Dental Implant Fixation in a Model of Osteonecrosis of the Jaw
  • 2013
  • Ingår i: Journal of Dental Research. - : Sage Publications. - 0022-0345 .- 1544-0591. ; 92:3, s. 279-283
  • Tidskriftsartikel (refereegranskat)abstract
    • Locally applied bisphosphonates may improve the fixation of metal implants in bone. However, systemic bisphosphonate treatment is associated with a risk of osteonecrosis of the jaw (ONJ). We hypothesized that local delivery of bisphosphonate from the implant surface improves the fixation of dental implants without complications in a setting where systemic treatment induces ONJ. Forty rats were randomly allocated to 4 groups of 10. All groups received a titanium implant inserted in an extraction socket. Group I received the implants only. Group II received dexamethasone (0.5 mg/kg). Group III received dexamethasone as above plus alendronate (200 µg/kg). Group IV received zoledronate-coated implants and dexamethasone as above. The animals were sacrificed 2 weeks after tooth extraction. All 10 animals with systemic alendronate treatment developed large ONJ-like changes, while all with local treatment were completely healed. Implant removal torque was higher for the bisphosphonate-coated implants compared with the other groups (p < 0.03 for each comparison). Micro-computed tomography of the maxilla showed more bone loss in the systemic alendronate group compared with groups receiving local treatment (p = 0.001). Local bisphosphonate treatment appears to improve implant fixation in a setting where systemic treatment caused ONJ.
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2.
  • af Geijersstam, E, et al. (författare)
  • Mercury uptake and kinetics after ingestion of dental amalgam
  • 2001
  • Ingår i: Journal of dental research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 80:9, s. 1793-1796
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of the present study was to investigate the G-I uptake of mercury (Hg) after intake of a single dose of amalgam-Hg, followed by pharmacokinetic analysis of the data. Eleven volunteers without amalgam fillings ingested 1.00 g amalgam powder. Hg in plasma vs. time was analyzed with a two-compartment model by means of mixed-effects modeling. A fraction of the absorption rate of Hg to the central compartment was inversely proportional to the plasma ferritin levels. The population mean half-life of the terminal phase of Hg in plasma was 37 days, with a considerable standard deviation in the population. The absorbed fraction of the administered dose was estimated to be about 0.04%. It is concluded that the G-I uptake of Hg is of quantitative importance during dental treatment.
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3.
  • Akhi, R, et al. (författare)
  • Salivary IgA to MAA-LDL and Oral Pathogens Are Linked to Coronary Disease
  • 2019
  • Ingår i: Journal of dental research. - : SAGE Publications. - 1544-0591 .- 0022-0345. ; 98:3, s. 296-303
  • Tidskriftsartikel (refereegranskat)abstract
    • A large body of literature has established the link between periodontal disease and cardiovascular disease. Oxidized low-density lipoproteins (OxLDLs) have a crucial role in atherosclerosis progression through initiation of immunological response. Monoclonal IgM antibodies to malondialdehyde-modified low-density lipoprotein (MDA-LDL) and to malondialdehyde acetaldehyde–modified low-density lipoprotein (MAA-LDL) have been shown to cross-react with the key virulence factors of periodontal pathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. We have previously shown that salivary IgA antibodies to MAA-LDL cross-react with P. gingivalis in healthy humans. In this study, we aim to assess whether oral mucosal immune response represented by salivary IgA to MAA-LDL and oral pathogens is associated with coronary artery disease (CAD). Also, the molecular mimicry through antibody cross-reaction between salivary IgA to MAA-LDL and oral pathogens was evaluated. The study subjects consisted of 451 patients who underwent a coronary angiography with no CAD ( n = 133), stable CAD ( n = 169), and acute coronary syndrome (ACS, n = 149). Elevated salivary IgA antibody levels to MAA-LDL, Rgp44 (gingipain A hemagglutinin domain of P. gingivalis), and Aa-HSP60 (heat shock protein 60 of A. actinomycetemcomitans) were discovered in stable-CAD and ACS patients when compared to no-CAD patients. In a multinomial regression model adjusted for known cardiovascular risk factors, stable CAD and ACS were associated with IgA to MAA-LDL ( P = 0.016, P = 0.043), Rgp44 ( P = 0.012, P = 0.004), Aa-HSP60 ( P = 0.032, P = 0.030), Tannerella forsythia ( P = 0.002, P = 0.004), Porphyromonas endodontalis ( P = 0.016, P = 0.020), Prevotella intermedia ( P = 0.038, P = 0.005), and with total IgA antibody concentration ( P = 0.002, P = 0.016). Salivary IgA to MAA-LDL showed cross-reactivity with the oral pathogens tested in the study patients. The study highlights an association between salivary IgA to MAA-LDL and atherosclerosis. However, whether salivary IgA to MAA-LDL and the related oral humoral responses play a causal role in the development in the CAD should be elucidated in the future.
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4.
  • Almståhl, Annica, 1973, et al. (författare)
  • Oral microflora in subjects with reduced salivary secretion
  • 1999
  • Ingår i: Journal of Dental Research. - 0022-0345 .- 1544-0591. ; 78:8, s. 1410-1416
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract. It is generally assumed that a decreased salivary secretion rate will promote plaque accumulation and increase the risk for caries, gingival inflammation, and mucosal infections. In this study, the effect of hyposalivation on the oral microflora was examined. The following microorganisms were analyzed in rinsing samples from 14 subjects with hyposalivation: the total number of anaerobically growing micro-organisms, alpha-hemolytic streptococci, mutans streptococci, lactobacilli, Fusobacterium nucleatum, Prevotella intermedia/Prevotella nigrescens, Staphylococcus aureus, Candida albicans, and enterics. The study group, age 53 ± 7 years, had no history of radiation therapy and showed no signs of inflammation in their salivary glands on biopsy. All were dentate with a mean of 24 ± 3 teeth. Their salivary secretion rates were 0.03 ± 0.02 mL/min (unstimulated) and 0.84 ± 0.65 mL/min (stimulated). The control group was matched to the hyposalivation group according to age, sex, and number of teeth. There was a significantly increased number of lactobacilli, and a tendency, not statistically significant and with large variations within the groups, toward a higher proportion of mutans streptococci and a lower proportion of alpha-hemolytic streptococci in the hyposalivation group. The presence of micro-organisms associated with gingival inflammation and mucosal infections was comparable with that in the healthy controls. The results indicated that a low salivary secretion rate mainly promotes a flora associated with the development of caries.
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5.
  • Andersson, Jennie, 1978, et al. (författare)
  • HEMA enhances IgG1 production by human B-cells in vitro.
  • 2010
  • Ingår i: Journal of Dental Research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 89:12, s. 1461-1464
  • Tidskriftsartikel (refereegranskat)abstract
    • We have previously shown that the resin monomer 2-hydroxyethylmethacrylate (HEMA) affects mouse B-lymphocyte activity, leading to increased IgG1 antibody production in vivo. In the present study, we tested, in vitro, the hypothesis that HEMA also affects human B-lymphocyte activity. The in vitro production of IgG1, IgM, and IgA in supernatants from purified human CD19+ B-lymphocyte cultures, containing different concentrations of HEMA, was assayed with ELISA. Proliferation was measured by [methyl-3H] thymidine incorporation. Of the different HEMA concentrations used, the lower concentrations caused a significant increase in IgG1 production, but not in IgM or IgA production, in vitro. The lower HEMA concentrations did not significantly change B-cell proliferation. At the highest concentration, HEMA significantly suppressed IgG1 and IgM production, as well as B-cell proliferation, in vitro. In conclusion, HEMA can, at certain concentrations, selectively enhance human B-lymphocyte IgG1 production. Abbreviations: 2-hydroxyethylmethacrylate (HEMA), Dulbecco’s Modified Eagle’s Medium supplemented with heat-inactivated fetal bovine serum, gentamycin, penicillin, and streptomycin (D-MEM++++), Enzyme-linked Immuno-sorbent Assay (ELISA), phosphate-buffered saline (PBS), ovalbumin (OVA), pokeweed mitogen (PWM), counts per minute (CPM).
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8.
  • Bai, Y., et al. (författare)
  • A Brief History of the Discovery of Amelogenin Nanoribbons In Vitro and In Vivo
  • 2021
  • Ingår i: Journal of Dental Research. - : SAGE Publications. - 0022-0345 .- 1544-0591.
  • Tidskriftsartikel (refereegranskat)abstract
    • Without evidence for an organic framework, biological and biochemical processes observed during amelogenesis provided limited information on how extracellular matrix proteins control the development of the complex fibrous architecture of human enamel. Over a decade ago, amelogenin nanoribbons were first observed from recombinant proteins during in vitro mineralization experiments in our laboratory. In enamel from mice lacking the enzyme kallikrein 4 (KLK4), we later uncovered ribbon-like protein structures that matched the morphology, width, and thickness of the nanoribbons assembled by recombinant proteins. Interestingly, similar structures had already been described since the 1960s, when enamel sections from various mammals were demineralized and stained for transmission electron microscopy analysis. However, at that time, researchers were not aware of the ability of amelogenin to form nanoribbons and instead associated the filamentous nanostructures with possible imprints of mineral ribbons in the gel-like matrix of developing enamel. Further evidence for the significance of amelogenin nanoribbons for enamel development was stipulated when recent mineralization experiments succeeded in templating and orienting the growth of apatite ribbons along the protein nanoribbon framework. This article provides a brief historical review of the discovery of amelogenin nanoribbons in our laboratory in the context of reports by others on similar structures in the developing enamel matrix.
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9.
  • Ballo, Ahmed, 1978, et al. (författare)
  • Prepolymerized vs. in situ-polymerized fiber-reinforced composite implants--a pilot study.
  • 2011
  • Ingår i: Journal of dental research. - : SAGE Publications. - 1544-0591 .- 0022-0345. ; 90:2, s. 263-7
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to investigate bone response to bioactive fiber-reinforced composite (FRC) implants under two polymerization conditions. Glass-fiber-dimethacrylate composite was tested as prepolymerized cylinder-shaped FRC implants and as cylindrical FRC implants polymerized in situ with blue light transmitted and scattered by the glass fibers. Ten FRC implants (6 prepolymerized and 4 in situ-polymerized implants) were placed in the right tibias of 3 pigs by means of a press-fit technique. After 12 weeks, light microscopy revealed only mild foreign-body reaction, with no accumulation of inflammatory cells on both the prepolymerized and the in situ-polymerized implants. The prepolymerized implants appeared to be fully integrated, whereas the in situ-polymerized implants were almost completely surrounded by a fibrous capsule. The present study suggests that in situ polymerization of FRC implants results in fibrous capsule formation and prevents integration with bone.
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10.
  • Bastos, JL, et al. (författare)
  • Racial Inequalities in Oral Health
  • 2018
  • Ingår i: Journal of dental research. - : SAGE Publications. - 1544-0591 .- 0022-0345. ; 97:8, s. 878-886
  • Tidskriftsartikel (refereegranskat)abstract
    • Together with other social categories, race has been at the core of much scholarly work in the area of humanities and social sciences, as well as a host of applied disciplines. In dentistry, debates have ranged from the use of race as a criterion for the recommendation of specific dental procedures to a means of assessing inequalities in a variety of outcomes. What is missing in these previous discussions, though, is a broader understanding of race that transcends relations with genetic makeup and other individual-level characteristics. In this review, we provide readers with a critique of the existing knowledge on race and oral health by answering the following 3 guiding questions: (1) What concepts and ideas are connected with race in the field of dentistry? (2) What can be learned and what is absent from the existing literature on the topic? (3) How can we enhance research and policy on racial inequalities in oral health? Taken together, the reviewed studies rely either on biological distinctions between racial categories or on other individual characteristics that may underlie racial disparities in oral health. Amidst a range of individual-level factors, racial inequalities have often been attributed to lower socioeconomic status and “health-damaging” cultural traits, for instance, patterns of and reasons for dental visits, dietary habits, and oral hygiene behaviors. While this literature has been useful in documenting large and persistent racial gaps in oral health, wider sociohistorical processes, such as systemic racism, as well as their relationships with economic exploitation, social stigmatization, and political marginalization, have yet to be operationalized among studies on the topic. A nascent body of research has recently begun to address some of these factors, but limited attention to structural theories of racism means that many more studies are needed to effectively mitigate racial health differentials.
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