1.
Mårtensson, Carina, et al.
(författare)
Factors behind change in knowledge after a mass media campaign targeting periodontitis
2006
Ingår i: International Journal of Dental Hygiene. - 1601-5029 .- 1601-5037. ; 4:1, s. 8-14
Tidskriftsartikel (refereegranskat) abstract
The aim of this study was to investigate changes in knowledge before and after a mass media campaign, in relation to social attributes, care system attributes and oral health aspects. The study was based on a questionnaire in a cohort design, sent out to 900 randomly sampled people aged 50–75 in Sweden. The response rate to the questionnaire before and after the campaign was 70% and 65% respectively. Sixty-four percent answered both questionnaires. Two questions addressed knowledge, while 10 questions aimed to measure social attributes, care system attributes and oral health aspects. Data were analysed for bivariate relations as to change in knowledge and social attributes, care system attributes and oral health aspects. Data were also analysed in multiple regression analysis with knowledge before, knowledge after and knowledge differences as dependent variables. The results showed that there were a number of independent variables with influence on the dependent variables. Of the social attributes, secondary education gave almost 10% (P < 0.001) better knowledge both before and after the campaign. Among care system attributes, high care utilization was related to knowledge both before and after the campaign. The most important factors for knowledge about periodontitis were education, care utilization and perceived importance of oral health. In conclusion, this study demonstrates that mass media might increase knowledge about periodontitis as a health promotion strategy.
2.
Niemann-Jönsson, Audrey, et al.
(författare)
Medial Expression of TNF-α and TNF Receptors Precedes the Development of Atherosclerotic Lesions in Apolipoprotein E/LDL Receptor Double Knockout Mice
2007
Ingår i: International Journal of Biomedical Science. - 1550-9702 .- 1555-2810. ; 3:2, s. 117-123
Tidskriftsartikel (refereegranskat) abstract
TNF-α is present in atherosclerotic lesions, activates endothelial adhesion molecule expression, stimulates the release of proinflammatory cytokines and matrix metalloproteinases and promotes smooth muscle cell proliferation and migration. Taken together these observations suggest that TNF-α may be functionally involved in early atherosclerosis development. To further evaluate this hypothesis we compared vascular TNF-α and TNF receptor expression in atherosclerosis-susceptible apoE-/-/LDL receptor-/- mice and control C57BL/6 mice. The aortas of 8 week old apoE-/-/LDLreceptor-/- mice displayed immunoreactivity for TNF-α as well as TNF p55 and p75 receptors (2.1 ± 1.6%, 5.6 ± 1.5% and 3.6 ± 1.3% of total media area, respectively), but did not have any detectable lesions. A marginal increase in TNF-α and TNF receptor immunoreactivity was observed at 12 weeks and atherosclerotic plaques were detected in 1 out of 5 animals. At 16 weeks TNF-α expression in the media was increased more than four-fold as compared with 8 week old mice, and atherosclerosis was widespread. TNF-α immunoreactivity was also observed in all plaques. In addition, at the same age a tendency towards increased TNF-α mRNA levels was detected in the double knockout mice compared to age-matched controls. A further increase in TNF-α and TNF receptor immunoreactivity as well as plaque size was observed at 20 weeks. With only a few exceptions, no TNF-α or TNF receptor immunoreactivity was detected in C57BL/6 control mice. These findings demonstrate that medial TNF-α and TNF receptor expression precedes lesion formation in apoE-/-/LDL receptor-/- mice.
3.
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.
4.
Jönsson, Daniel, et al.
(författare)
LPS-induced MCP-1 and IL-6 production is not reversed by oestrogen in human periodontal ligament cells.
2008
Ingår i: Archives of Oral Biology. - : Elsevier BV. - 1879-1506 .- 0003-9969. ; Jun 11, s. 896-902
Tidskriftsartikel (refereegranskat) abstract
OBJECTIVE: Periodontal ligament (PDL) cells express oestrogen receptors but the functional importance of oestrogen in PDL cells exposed to bacterial endotoxins is not known. Here we investigate if the inflammation promoter lipopolysaccharide (LPS) affects PDL cell production of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), C-reactive protein (CRP) and/or normal functional PDL cell characteristics such as collagen synthesis and cell proliferation and if oestrogen modulates the effects of LPS. METHODS: PDL cells were obtained from periodontal ligament of premolars. PDL cells were treated with Escherichia coli LPS in the absence or presence of oestrogen (17beta-oestradiol, E(2)). Cellular concentration of IL-6, MCP-1 and CRP was determined by enzyme-linked immunosorbent assay (ELISA). Collagen synthesis was determined by l-[(3)H]proline incorporation. Cell proliferation was assessed by DNA synthesis measurement using [(3)H]thymidine incorporation. RESULTS: Stimulation with LPS (500ng/ml to 10mug/ml) increased IL-6 production in a concentration-dependent manner. Lower concentration (100ng/ml) of LPS had no effect. LPS-induced stimulation of IL-6 was not reversed by a physiologically high concentration (100nM) of E(2). LPS increased also MCP-1 production which was unaffected by E(2). Treatment with E(2) alone had no effect on either IL-6 or MCP-1. Stimulation with LPS had no effect on CRP. LPS did not affect collagen synthesis and cell proliferation, reflecting normal physiological properties of PDL cells. CONCLUSIONS: LPS stimulates PDL cell IL-6 and MCP-1 production but has no effect on the normal physiological properties of PDL cells. LPS-induced IL-6 and MCP-1 is not reversed by oestrogen suggesting that oestrogen exerts no anti-inflammatory effect via this mechanism.
5.
Svensson, Daniel, et al.
(författare)
The host defense peptide LL-37 is detected in human parotid and submandibular/sublingual saliva and expressed in glandular neutrophils
2018
Ingår i: European Journal of Oral Sciences. - : Blackwell Munksgaard. - 0909-8836 .- 1600-0722. ; 126:2, s. 93-100
Tidskriftsartikel (refereegranskat) abstract
The human host defense peptide, LL-37, is an important player in the first line of defense against invading microorganisms. LL-37 and its precursor, hCAP18, have been detected in unstimulated whole saliva but no reports showing hCAP18/LL-37 in isolated, parotid, and/or submandibular/sublingual saliva have been presented. Here, we measured the levels of hCAP18/LL-37 in human parotid and submandibular/sublingual saliva and investigated the expression of hCAP18/LL-37 in parotid and submandibular gland tissue. Parotid and submandibular/sublingual saliva was collected from healthy volunteers, and the levels of hCAP18/LL-37 in saliva were analyzed by dot blot, ELISA, and western blotting. Cellular expression of hCAP18/LL-37 in human parotid and submandibular glands was investigated by immunohistochemistry. Immunoreactivity for hCAP18/LL-37 was detected in both parotid and submandibular/sublingual saliva of all individuals. The concentration of hCAP18/LL-37 was similar in parotid and submandibular/sublingual saliva, and was determined by densitometric scanning of each dot and normalization to the total protein concentration of each sample, and by ELISA. Double immunohistochemistry revealed that intravascular neutrophils of both parotid and submandibular glands express hCAP18/LL-37. For the first time, we demonstrate hCAP18/LL-37 in isolated human parotid and submandibular/sublingual saliva and expression of hCAP18/LL-37 in glandular intravascular neutrophils, indicating that neutrophils of the major salivary glands contribute to the LL-37 content of whole saliva.
6.
Jönsson, Daniel, et al.
(författare)
Gingival tissue transcriptomes in experimental gingivitis.
2011
Ingår i: Journal of clinical periodontology. - : John Wiley & Sons. - 1600-051X .- 0303-6979. ; 38:7, s. 599-611
Tidskriftsartikel (refereegranskat) abstract
We investigated the sequential gene expression in the gingiva during the induction and resolution of experimental gingivitis.
7.
Wickström, Claes, et al.
(författare)
Proteolytic degradation of human salivary MUC5B by dental biofilms.
2009
Ingår i: Microbiology. - : Microbiology Society. - 1465-2080 .- 1350-0872.
Tidskriftsartikel (refereegranskat) abstract
The degradation of complex substrates, like salivary mucins, requires an arsenal of glycosidases and proteases to sequentially degrade the oligosaccharides and polypeptide backbone. MUC5B is a complex oligomeric glycoprotein, heterogeneous in molecular mass (14-40 x 106 Da), with a diverse repertoire of oligosaccharides, differing in composition and charge. The aim of this study was to investigate whether proteolytic degradation of the mucin polypeptide backbone could be identified and if cooperation of dental biofilm bacteria was required. Cooperative bacterial-mediated proteolysis of MUC5B was determined by comparing individual and mixed consortia of strains isolated from supragingival plaque and freshly harvested supragingival plaque. Proteolytic activity was analyzed using fluorescent labelled substrate and by visualizing mucin degradation by SDS-PAGE. Dental plaque degraded the polypeptide backbone of the salivary MUC5B mucin. The mucin also was degraded by a specific consortium of isolated species from supragingival plaque, although individual species and other consortia did not. Select bacteria in supragingival dental plaque, therefore, cooperate as a consortium to proteolyze human salivary MUC5B and hydrolyze glycosides.
8.
Ahlkvist, Linda, et al.
(författare)
Synergism by individual macronutrients explains the marked early GLP-1 and islet hormone responses to mixed meal challenge in mice
2012
Ingår i: Regulatory Peptides. - : Elsevier. - 0167-0115 .- 1873-1686. ; 178:1-3, s. 29-35
Tidskriftsartikel (refereegranskat) abstract
Apart from glucose, proteins and lipids also stimulate incretin and islet hormone secretion. However, the glucoregulatory effect of macronutrients in combination is poorly understood. We therefore developed an oral mixed meal model in mice to 1) explore the glucagon-like peptide-1 (GLP-1) and islet hormone responses to mixed meal versus isocaloric glucose, and 2) characterize the relative contribution of individual macronutrients to these responses. Anesthetized C57BL/6J female mice were orally gavaged with 1) a mixed meal (0.285 kcal; glucose, whey protein and peanut oil; 60/20/20% kcal) versus an isocaloric glucose load (0.285 kcal), and 2) a mixed meal (0.285 kcal) versus glucose, whey protein or peanut oil administered individually in their mixed meal caloric quantity, i.e., 0.171, 0.055 and 0.055 kcal, respectively. Plasma was analyzed for glucose, insulin and intact GLP-1 before and during oral challenges. Plasma glucose was lower after mixed meal versus after isocaloric glucose ingestion. In spite of this, the peak insulin response (P=0.02), the peak intact GLP-1 levels (P=0.006) and the estimated β-cell function (P=0.005) were higher. Furthermore, the peak insulin (P=0.004) and intact GLP-1 (P=0.006) levels were higher after mixed meal ingestion than the sum of responses to individual macronutrients. Compared to glucose alone, we conclude that there is a marked early insulin response to mixed meal ingestion, which emanates from a synergistic, rather than an additive, effect of the individual macronutrients in the mixed meal and is in part likely caused by increased levels of GLP-1.
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