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Träfflista för sökning "WFRF:(Bratthall Gunilla) srt2:(2011)"

Search: WFRF:(Bratthall Gunilla) > (2011)

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1.
  • Jönsson, Daniel, et al. (author)
  • The human periodontal ligament cell : a fibroblast-like cell acting as an immune cell
  • 2011
  • In: Journal of Periodontal Research. - : John Wiley & Sons. - 0022-3484 .- 1600-0765. ; 46:2, s. 153-157
  • Research review (peer-reviewed)abstract
    • BACKGROUND: Periodontal ligament cells are fibroblast-like cells characterized by collagen production but also possessing some osteoblastic features. In the light of numerous studies presented during recent times, which show that human periodontal ligament cells also produce cytokines and chemokines in response to inflammation promoters, it is reasonable to suggest that periodontal ligament cells play a role as promoters of periodontal inflammation through these mechanisms. MATERIAL AND METHODS: The periodontal ligament, which harbours the periodontal ligament cells, is a part of the attachment apparatus comprised of periodontal ligament cells, extracellular matrix and fibres, attaching the root cement to the alveolar bone. Periodontal ligament cells are in close proximity to bacteria within the plaque and the pocket, and thus these cells are readily accessible to bacterial endotoxins and other promoters of inflammation. RESULTS: Cytokines and chemokines, released by periodontal ligament cells upon stimulation with inflammation promoters, reach the blood vessels easily thanks to rich vascularization of the periodontium stimulating recruitment of white blood cells to the site of inflammation. In addition to classical inflammatory cells, such as leucocytes, macrophages and mast cells, the periodontal ligament cells also contribute to periodontal inflammation via their production and release of cytokines and chemokines. CONCLUSION: Therefore, pharmacological treatment of periodontitis should aim to reduce the release of proinflammatory agents not only from classical inflammatory cells but also from periodontal ligament cells.
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2.
  • Wallin Bengtsson, Viveca, et al. (author)
  • Alpha-1 antitrypsin deficiency and periodontitis, a pilot study
  • 2011
  • In: Swedish Dental Journal. - : Swedish Dental Association. - 0347-9994. ; 35:1, s. 33-40
  • Journal article (peer-reviewed)abstract
    • Målet med studien var att undersöka om parodontala parametrar och elastas i gingivalvätska (GCF) skilde sig hos individer med alfa-1-antrypsin-brist (AAT-brist) jämfört med individer med normal AAT-halt. I studien ingick 30 individer, varav 20 med allvarlig AAT-brist, fenotyp PiZZ. Tio individer med AAT- brist led av kronisk obstruktiv lungsjukdom (KOL) (grupp 1) och 10 var symptomfria (grupp 2). Tio individer med normal AAT-halt, fenotyp PiMM (grupp 3), utgjorde kontrollgrupp och rekryterades från en allmäntandvårdsklinik. Undersökningen bestod av insamling av GCF, gingivalindex (GI), plackindex (PlI), fickdjupsmätning (PPD) och röntgen. GCF samlades in med hjälp av pappers-strips (Periopaper®). AAT i plasma mättes med nefelometri och AAT i GCF mättes med ELISA. Elastasaktivitet och proteinmängd i GCF bestämdes med spektrofotometri. Medelvärden för GI, PlI, PPD och röntgenmätningar visade inga statistiskt signifikanta skillnader mellan grupperna. AAT i plasma och GCF visade mycket låga värden i grupp 1 och 2 utan några signifikanta skillnader mellan grupperna men en signifikant skillnad i jämförelse med grupp 3. Elastas i gingivalvätska visade inga skillnader mellan de tre grupperna. Sammanfattningsvis visade varken parodontala värden eller elastas i GCF några skillnader hos individer med AAT- brist, fenotyp PiZZ, jämfört med individer med normal AAT-halt, fenotyp PiMM, i detta material.
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3.
  • Wallin-Bengtsson, Viveca, et al. (author)
  • Alpha-1-antitrypsin deficiency and periodontitis, a pilot study
  • 2011
  • In: Swedish Dental Journal. - 0347-9994. ; 35:1, s. 33-40
  • Journal article (peer-reviewed)abstract
    • The aim of this study was to investigate if periodontal parameters and elastase in gingival crevicular fluid (GCF) are different in alpha-1-antitrypsin deficient (AATD) subjects compared to subjects with normal AAT level. Thirty subjects were included, 20 of whom with severe AATD, phenotype PiZZ. Ten AATD subjects suffered from chronic obstructive pulmonary disease (COPD, group 1) and 10 were asymptomatic (group 2). Ten control subjects, phenotype PiMM, (group 3) were recruited from a public dental clinic. The examination comprised of sampling of GCF, Gingival Index (GI), Plaque Index (PII), probing pocket depth (PPD) and radiography. GCF was collected with paper strips (Periopaper (R)). Plasma AAT concentration was measured by nephelometry and AAT in GCF with ELISA. Elastase activity and protein in GCF were determined by spectrophotometry. The mean values for GI, PII, PPD and the radiological measurements did not show any statistically significant differences between the groups. AAT in plasma and GCF demonstrated very low values in groups 1 and 2 with no significant difference between these groups but a statistical difference in comparison with group 3. Elastase in GCF did not show any difference between the three groups. In conclusion, neither the periodontal parameters nor the elastase in GCF were different in AATD subjects, phenotype PiZZ, when compared to subjects with normal AAT level, phenotype PiMM, in this material.
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