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Sökning: WFRF:(Bratthall G.)

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1.
  • Bratthall, G., et al. (författare)
  • Comparison of ready-to-use EMDOGAIN®-gel and EMDOGAIN® in patients with chronic adult periodontitis. A multicenter clinical study
  • 2001
  • Ingår i: Journal of Clinical Periodontology. - : John Wiley & Sons. - 0303-6979 .- 1600-051X. ; 28:10, s. 923-929
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: The aim of this multicenter trial was to compare the clinical and radiographical outcome of a ready-to-use Emdogain®-gel (test) with the marketed Emdogain® (control). Methods: Subjects with bilateral infrabony defects ≥4 mm deep and ≥2 mm wide according to radiographs were selected. 88 subjects with probing pocket depth (PPD) ≥6 mm ≥1 month after supervised oral hygiene and scaling participated. At baseline plaque index, bleeding on probing, PPD and probing attachment level were recorded and reproducible radiographs for computer-based bone level measurements were taken. In each subject, 1 tooth was randomly treated with the test and 1 tooth with the control gel. Examinations were repeated 8 and 16 months post-operatively. Results: After 16 months, the mean test PPD was 4.1 mm and the mean control PPD 4.2 mm. The mean gain of attachment was 2.7 mm for test and 2.9 mm for the control sites, and the radiographic measurements demonstrated a mean gain of 1 mm for both test and control sites. Conclusion: This series of cases demonstrated a statistically significant reduction of pocket depths and gain of attachment and bone after 8 and 16 months with no difference between the 2 preparations.
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  • Hänsel Petersson, G, et al. (författare)
  • Comparing caries risk factors and caries risk profiles in children and elderly.
  • 2004
  • Ingår i: Swedish dental journal. ; 28:3, s. 119-128
  • Tidskriftsartikel (refereegranskat)abstract
    • The aims of this study were to compare the caries risk profiles of children and elderly, the actual annual caries increment and the impact of some selected caries related factors. Another aim was to find out if there were gender differences among the participants. The risk profiles were created by a computerised risk assessment program, the Cariogram, which evaluates data and presents the weighted and summarized result as one figure, illustrating the ‘percent chance of avoiding caries’ in the future. Methods: The Cariogram was earlier evaluated in two longitudinal studies for its capacity to assess caries risk. One study comprised about 400 children, 10-11 years of age and the other study included about 150 elderly (age 55, 65 and 75). At baseline, information on past caries experience, diet, oral hygiene and use of fluoride was obtained. Saliva analyses included mutans streptococci and lactobacilli, buffering capacity and secretion rate. The caries risk was assessed and the participants were divided into five groups according to the calculated Cariogram risk profiles. After two and five years, respectively, caries was re-evaluated and the incidence was compared with the predictions. Results: The Cariogram risk predictions were statistically in agreement with the actual caries increment. Fifty percent of the children, but only two percent of the elderly appeared in the lowest caries risk group. Of the elderly, 26.4% belonged to the highest caries risk group versus 3.1% of the children. The median value ‘chance of avoiding caries’ was 44% for the elderly and 80% for the children. The main Cariogram sectors contributing to the observed higher caries risk among elderly was the bacterial components in combination with higher susceptibility. Individual factors contributing significantly to the higher risk profiles for the adults compared to the children were higher plaque scores, higher counts of mutans streptococci and lower buffering capacity. Conclusion: comparing the risk profiles of the children and the elderly showed that the elderly were at a higher risk developing caries lesions. Overall one may say that the risk for caries, as assessed by the Cariogram, was twice as high for the elderly.
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  • Jansson, Henrik, et al. (författare)
  • Analysis of the interleukin-1 and interleukin-6 polymorphisms in patients with chronic periodontitis. A pilot study
  • 2006
  • Ingår i: Swedish Dental Journal. - 0347-9994. ; 30:1, s. 17-23
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to analyse whether the interleukin-1 (IL-1) and IL-6 gene polymorphisms were associated with the susceptibility of chronic periodontitis. Genomic DNA was obtained from 20 patients with chronic periodontitis and 31 periodontally healthy subjects. All subjects were of North European heritage. The test subjects were kept in a maintenance program after periodontal treatment but yet showing signs of recurrent disease. Genotyping of the IL-1 alpha[+4845C>T], IL-1 beta [-3954C>T] and IL-6 [-174G>C] polymorphisms was carried out using an allelic discrimination Assay-by-Design method on ABI PRISM 7900 Sequence Detection System. All genotypes were analyzed using the GeneMapper 2.0 software. A similar distribution of Single Nucleotide Polymorphism (SNP) was seen in both groups. Analysis by logistic regression including gender, IL-1 alpha [+4845C>T], IL-1 beta [-3954C>T], IL-6 [-174G>C] genotypes, the composite IL-1 genotype, the combination of the composite IL-1 genotype and the IL-6 -174G>C genotype and adjusting for smoking did not result in any statistically significant difference. SNPs in IL-1 alpha[+4845C>T], IL-1 beta [-3954C>T] and IL-6 [-174G>C] do not seem to increase the susceptibility to chronic periodontitis in this group of subjects.
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  • Jansson, Henrik, et al. (författare)
  • Type 2 diabetes and risk for periodontal disease: a role for dental health awareness
  • 2006
  • Ingår i: Journal of Clinical Periodontology. - 1600-051X .- 0303-6979. ; 33:6, s. 408-414
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Several studies have found correlations between diabetes and an increased prevalence of periodontitis. Objective: To analyse, in a group of subjects with type 2 diabetes (T2D), (i) the association between medical characteristics and severe periodontal disease and (ii) dental care habits and knowledge of oral health. Methods: One hundred and ninety-one subjects with T2D were examined. Based on assessment of marginal bone height in panoramic radiographs, two periodontal subgroups were identified: one periodontally diseased (PD+) and one periodontally healthy (PD-) group. All subjects completed a questionnaire about their medical and oral health. Results: Twenty per cent of the subjects were classified as PD+. This was verified by clinical parameters. PD+ individuals had higher haemoglobin A1c (HbA1c) levels (p=0.033) and higher prevalences of cardiovascular complications (p=0.012). They were also less likely to be of Scandinavian origin (p=0.028) and more likely to smoke (p < 0.001) than the PD- group. The PD+ group rated their oral health as poor (p < 0.0001) and believed that T2D had an influence on their oral status (p < 0.0001). Conclusion: The best predictor for severe periodontal disease in subjects with T2D is smoking followed by HbA1c levels. T2D subjects should be informed about the increased risk for periodontal disease when suffering from T2D.
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7.
  • Jönsson, Daniel, et al. (författare)
  • Differential effects of estrogen on DNA synthesis in human periodontal ligament and breast cancer cells.
  • 2005
  • Ingår i: Journal of Periodontal Research. - : Wiley. - 1600-0765 .- 0022-3484. ; 40:5, s. 401-406
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: It is important to clarify the biological function of the female sex hormones estrogen and progesterone in periodontal ligament cells, as these hormones may affect periodontal health. We have previously shown that human periodontal ligament cells express estrogen receptor beta (ERbeta) but not ERalpha, whereas human breast cancer cells (MCF7) express both ERalpha and ERbeta. Data on progesterone receptor (PgR) expression in human periodontal ligament cells have not been reported. OBJECTIVES: Determine PgR expression in human periodontal ligament and MCF7 cells and to investigate how estrogen affects DNA and collagen synthesis in these two cell types showing different pattern of expression for ERalpha and beta. METHODS: Periodontal ligament cells were obtained from the periodontal ligament of premolars extracted for orthodontic reasons and MCF7 cells from the American Type Culture Collection (ATCC). PgR expression was determined by immunocytochemistry. DNA and collagen synthesis was determined by [(3)H]thymidine and L-[(3)H]proline incorporation, respectively. RESULTS: PgR immunoreactivity was observed in nuclei of MCF7 but not periodontal ligament cells. Treatment with estrogen (17beta-estradiol, E(2)) at physiological concentrations for 24 h stimulated DNA synthesis by more than two times in MCF7 cells, whereas there was no effect on periodontal ligament cell DNA synthesis. The ER blocker ICI 182780 fully reversed the stimulatory effect of E(2). Not only short-term (24 h) but also long-term (5 days) treatment with E(2) lacked effect on DNA synthesis in periodontal ligament cells. Neither periodontal ligament cell viability nor collagen synthesis was affected by E(2) treatment. Identical results were observed in periodontal ligament cells from male and female subjects. CONCLUSIONS: Human MCF7 but not periodontal ligament cells express PgR, suggesting that progesterone via PgR affects MCF7 but not periodontal ligament cells. Further, estrogen stimulates breast cancer MCF7 cell proliferation, whereas it has no effect on proliferation of periodontal ligament cells, probably reflecting cell type specific ER expression pattern in these two cell types.
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8.
  • Jönsson, Daniel, et al. (författare)
  • Functional effects of female sex hormones in the periodontium
  • 2006
  • Ingår i: Swedish Dental Journal. - 0347-9994. ; 30, s. 185-185
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: Several studies have addressed the association between changes in the female sex hormones estrogen and progesterone levels and changes in parameters of periodontitis. In order to understand how these hormones affect periodontal health it is of major importance to obtain information on their physiological importance. We have previously shown that periodontal ligament cells (PDL cells) express estrogen receptor beta (ER beta) but not ER alfa immunoreactivity. The PDL cells express no immunoreactivity for progesterone receptors, suggesting that this cell type is not affected by progesterone. Treatment with a physiological concentration (100 nM) of estrogen increases DNA synthesis in human breast cancer cells but has no effect on PDL cell DNA and collagen synthesis. The purpose of this project is to investigate how and by which mechanisms estrogen influences structure and function of the periodontal ligament by affecting PDL cell functional properties. Methods: Human PDL cells were obtained from teeth extracted for orthodontic reasons. The cells were cultured from periodontal tissue explants and used in passages 3-5. Subcellular distribution of ER beta was determined by immunogold electron microscopy and confocal imagining using the mitochondrial selective probe MitoTracker and ER beta immunostaining. Expression of mitochondrial protein cytochrome c oxidase subunit I was investigated using Western blotting. The amounts of IL-6 and c-reactive protein (CRP) were determined by ELISA. Results: Confocal imaging revealed that ER beta immunoreactivity was distributed not only in the nucleus but also in the mitochondria. These results were confirmed using immunogold electron microscopy. Incubation with estrogen down-regulated the mitochondrial enzyme cytochrome c oxidase subunit I expression by about 30%, showing functional significance of mitochondrial ER. Preliminary data show that lipopolysaccharide (LPS) induces IL-6 but not CRP expression in PDL cells. The LPS induced IL-6 production is not affected by estrogen. Conclusion: Our data show that estrogen, preferably via ER beta, affects PDL cell functional properties, suggesting that estrogen and other ER specific ligands may modulate the periodontal tissue structure and function in health and disease.
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  • Jönsson, Daniel, et al. (författare)
  • Immunocytochemical demonstration of estrogen receptor beta in human periodontal ligament cells.
  • 2004
  • Ingår i: Archives of Oral Biology. - 1879-1506 .- 0003-9969. ; 49:1, s. 85-88
  • Tidskriftsartikel (refereegranskat)abstract
    • Two transcription associated estrogen receptor (ER) subtypes have been identified and named ERα and ERβ. In the present study we investigate the expression of these ER subtypes in cultured human periodontal ligament (PDL) cells by immunocytochemistry. ERβ immunoreactivity was observed in the nuclei of about 40% of the PDL cells, while no ERα immunoreactivity was detected. In human breast cancer MCF-7 cells, serving as positive controls, both ERα and ERβ immunoreactivities were demonstrated. No immunoreactivity was observed after omission of the primary antibodies. This study suggests that estrogen acts on gene transcription preferentially via ERβ in human PDL cells.
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12.
  • Jönsson, Daniel, et al. (författare)
  • LPS induces GROalpha chemokine production via NF-kappaB in oral fibroblasts.
  • 2009
  • Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 58:11, s. 791-796
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective and design Chemotaxis of neutrophils from blood to the inflammation process plays an important role in development of periodontal inflammation. The novel chemokine GRO alpha, also named CXCL1, is a strong chemoattractant for neutrophils. Data on production and regulation of GRO alpha by oral fibroblasts have not previously been presented. Materials and methods GRO alpha mRNA and protein levels were determined in human periodontal ligament cells and mouse gingival fibroblasts by quantitative real-time PCR and ELISA. Results We disclose that both human periodontal ligament cells and mouse gingival fibroblasts produce GRO alpha in response to LPS stimulation. Stimulation with LPS for 24 h increased both mRNA for GRO alpha and GRO alpha protein. The steroid hormone estrogen had no effect on LPS-induced GRO alpha mRNA expression. Treatment with the glucocorticoid dexamethasone attenuated LPS-induced GRO alpha production, and the NF-kappa B blocker MG 132 fully prevented LPS-induced GRO alpha. Conclusions Oral fibroblasts respond to LPS stimulation by increasing GRO alpha production via the transcription factor NF-kappa B, suggesting that this mechanism may be involved in development of periodontal inflammation.
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13.
  • Nebel, Daniel, et al. (författare)
  • Differential regulation of chemokine expression by estrogen in human periodontal ligament cells
  • 2010
  • Ingår i: Journal of Periodontal Research. - : John Wiley & Sons. - 0022-3484 .- 1600-0765. ; 45:6, s. 796-802
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Objective: Estrogen modulates inflammatory responses, but the mechanisms involved have not yet been identified. Periodontal ligament (PDL) cells produce chemokines (a group of chemoattractant molecules that recruit leukocytes) and it has been suggested that estrogen modulates periodontal inflammation by regulating the expression of chemokines by PDL cells. Therefore, the objectives of this study were to investigate the regulation of chemokine ligand 2 [CCL2/monocyte chemoattractant protein 1 (MCP-1)], chemokine ligand 3 [CCL3/macrophage inflammatory protein-1α (MIP-1α)] and chemokine ligand 5 (CCL5/RANTES) by estrogen in human PDL cells.Material and Methods: PDL cells were obtained from the PDL of premolars, extracted for orthodontic reasons, from two boys and two girls (16 and 17 years of age). PDL cell CCL2, CCL3 and CCL5 mRNA transcripts were determined by quantitative real-time PCR. The concentrations of CCL2, CCL3 and CCL5 proteins were determined by ELISAs.Results: Treatment with 0.5 μg/mL of lipopolysaccharide (LPS, from Escherichia coli) + 100 nm 17β-estradiol (E2) for 24 h reduced the expression of CCL3 mRNA by about 40% compared to PDL cells treated with LPS alone. Attenuation of CCL3 mRNA was not associated with a decrease in CCL3 protein within 48 h, suggesting a slow turnover of the CCL3 protein. Interindividual differences in the effects of E2 on CCL5 mRNA expression were observed. E2 (100 nm) increased the expression of CCL5 by 40-60% in PDL cells derived from two subjects but reduced the expression of CCL5 by about 30% in cells from another subject. CCL2 mRNA and CCL2 protein were highly expressed, but not regulated by E2. Similar data were observed in cells obtained from both boys and girls.Conclusion: Regulation, by estrogen, of chemokine expression in PDL cells shows a complex pattern involving the down-regulation as well as the up-regulation of chemokines, suggesting that estrogen exerts both anti-inflammatory and proinflammatory effects through these mechanisms.
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14.
  • Nebel, Daniel, et al. (författare)
  • Estrogen regulates DNA synthesis in human gingival epithelial cells displaying strong estrogen receptor β immunoreactivity
  • 2011
  • Ingår i: Journal of Periodontal Research. - : John Wiley & Sons. - 0022-3484 .- 1600-0765. ; 46:5, s. 622-628
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Objective: Estrogen acts via estrogen receptor (ER) α and β. The expression pattern of ERs and their importance in gingival tissues are not fully understood. In this study, we investigate gingival ER expression and effects of estrogen on gingival epithelial cell proliferation.Material and Methods: Gingival biopsies were obtained from both healthy and diseased sites in three male and three female subjects. Expression of ERα and β was determined by immunohistochemistry. Effects of 17β-estradiol (E 2) on cell proliferation, monitored by measuring DNA synthesis, were studied in cultured human gingival epithelial HGEPp.05 cells.Results: Estrogen receptorβ, but not ERα, immunoreactivity was demonstrated in nuclei of epithelial cells in all layers of the gingival epithelium, but also in cells of the lamina propria. No differences were observed between male and female subjects. The same pattern, i.e. high ERβ expression but no ERα expression, was observed in both healthy and diseased sites within each individual. No differences in the intensity of the ERβ immunoreactive signal and the number of ERβ-positive nuclei were observed between healthy and diseased gingiva. Treatment with a physiological concentration of E 2 (10nm) had no effect on DNA synthesis in ERβ- and ERα-expressing HGEPp.05 cells. In contrast, E 2 at high concentrations (500nm and 10μm) reduced DNA synthesis by 60-70%.Conclusion: Human gingival epithelial cells display strong ERβ but low ERα immunoreactivity both in vivo and in culture. Estrogen attenuates gingival epithelial cell DNA synthesis at high but not low concentrations, suggesting a concentration-dependent mechanism.
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