Interaction Between Immune Cells and Bacteria Associated With Periodontitis
NCT ID: NCT03225950
Last Updated: 2020-03-24
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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COMPLETED
90 participants
OBSERVATIONAL
2017-02-01
2020-03-23
Brief Summary
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Detailed Description
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The onset of periodontitis is caused by an immunologic imbalance between host immune cells and residing microorganisms in subgingival pockets. The host immune cells are capable of enhancing both a protective and a destructive inflammatory response towards the microorganisms through the release of inflammatory mediators e.i. proinflammatory and antiinflammatory cytokines.
The role of antibodies in periodontitis is also unclear. Some studies show an excessive antibody level against bacteria associated with periodontitis e.g. Porphyromonas gingivalis (P.g.).
In general, this study contributes to a profound understanding of the host immune cells role in the onset and pathogenesis of periodontitis by comparing healthy versus diseased donors immunologic responses toward pathogene and apathogene microorganisms and their genetic background.
Conditions
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Study Design
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CASE_CONTROL
CROSS_SECTIONAL
Study Groups
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Chronic periodontitis donors
* Donors are medically healthy.
* Slow to moderate attachment loss and bone destruction.
* Good correlation between etiological factors and serverity of attachment loss.
In vitro stimulation of blood with periodontitis-associated- and control bacteria
Peripheral mononuclear blood cells are stimulated with periodontitis-associated- and control bacteria to measure the amount of positive cytokine-producing cells.
Anti-CCP- and anti-P.g.-antibodies titers
Anitbody titers will be measured in saliva and serum samples.
Analysis of selected single nucleotide polymorphisms (SNPs)
DNA obtained from saliva samples will be used to determine the genotype of the participants for selected SNPs.
periodontitis-associated bacteria presence
Determination of the presence of periodontitis-associated bacteria e.i. Porphyromonas gingivalis in saliva and blood samples.
Aggressive periodontitis donors
* Donors are medically healthy.
* Rapid attachment loss and bone destruction.
* Familial aggregation.
* No correlation between etiological factors and serverity of attachment loss.
In vitro stimulation of blood with periodontitis-associated- and control bacteria
Peripheral mononuclear blood cells are stimulated with periodontitis-associated- and control bacteria to measure the amount of positive cytokine-producing cells.
Anti-CCP- and anti-P.g.-antibodies titers
Anitbody titers will be measured in saliva and serum samples.
Analysis of selected single nucleotide polymorphisms (SNPs)
DNA obtained from saliva samples will be used to determine the genotype of the participants for selected SNPs.
periodontitis-associated bacteria presence
Determination of the presence of periodontitis-associated bacteria e.i. Porphyromonas gingivalis in saliva and blood samples.
Control donors
* Donors are medically healthy.
* No sign of inflammatory conditions.
In vitro stimulation of blood with periodontitis-associated- and control bacteria
Peripheral mononuclear blood cells are stimulated with periodontitis-associated- and control bacteria to measure the amount of positive cytokine-producing cells.
Anti-CCP- and anti-P.g.-antibodies titers
Anitbody titers will be measured in saliva and serum samples.
Analysis of selected single nucleotide polymorphisms (SNPs)
DNA obtained from saliva samples will be used to determine the genotype of the participants for selected SNPs.
periodontitis-associated bacteria presence
Determination of the presence of periodontitis-associated bacteria e.i. Porphyromonas gingivalis in saliva and blood samples.
Interventions
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In vitro stimulation of blood with periodontitis-associated- and control bacteria
Peripheral mononuclear blood cells are stimulated with periodontitis-associated- and control bacteria to measure the amount of positive cytokine-producing cells.
Anti-CCP- and anti-P.g.-antibodies titers
Anitbody titers will be measured in saliva and serum samples.
Analysis of selected single nucleotide polymorphisms (SNPs)
DNA obtained from saliva samples will be used to determine the genotype of the participants for selected SNPs.
periodontitis-associated bacteria presence
Determination of the presence of periodontitis-associated bacteria e.i. Porphyromonas gingivalis in saliva and blood samples.
Eligibility Criteria
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Inclusion Criteria
* Interproximal attachment loss at minimum 3 teeth besides molars and incisors.
* Clinical attachment loss at minimum 10 sites identified by bleeding and pus upon probing.
* Visible radiographic bone loss.
* Medically healthy donors.
* 19-40 years of age.
* Interproximal attachment loss at minimum 3 teeth besides molars and incisors.
* Clinical attachment loss at minimum 10 sites identified by bleeding and pus upon probing.
* Visible radiographic bone loss.
* Medically healthy donors.
* No sign of inflammatory conditions or other general systemic diseases.
* Medically healthy donors.
Exclusion Criteria
* Antibiotic treatment within 6 months.
* Suffer from periodontal manifestations caused by systemic diseases e.i. genetic diseases, haematologic anomalies or syndromes.
19 Years
60 Years
ALL
Yes
Sponsors
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Copenhagen University Hospital, Denmark
OTHER
University of Copenhagen
OTHER
Responsible Party
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Anne Katrine Danielsen
Research Assistant
Principal Investigators
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Palle Holmstrup, DDS, PhD, Dr Odont
Role: STUDY_DIRECTOR
University of Copenhagen
Claus Henrik Nielsen, PhD, MSc, MD
Role: STUDY_DIRECTOR
Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Locations
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Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital.
Copenhagen, , Denmark
Section for Periodontology, Microbiology and Community Dentistry, Department of Odontology, Faculty of Health and Medical Sciences, University of Copenhagen
Copenhagen, , Denmark
Countries
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References
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Bartold PM, Van Dyke TE. Periodontitis: a host-mediated disruption of microbial homeostasis. Unlearning learned concepts. Periodontol 2000. 2013 Jun;62(1):203-17. doi: 10.1111/j.1600-0757.2012.00450.x.
Neely AL, Holford TR, Loe H, Anerud A, Boysen H. The natural history of periodontal disease in man. Risk factors for progression of attachment loss in individuals receiving no oral health care. J Periodontol. 2001 Aug;72(8):1006-15. doi: 10.1902/jop.2001.72.8.1006.
Eke PI, Dye BA, Wei L, Slade GD, Thornton-Evans GO, Borgnakke WS, Taylor GW, Page RC, Beck JD, Genco RJ. Update on Prevalence of Periodontitis in Adults in the United States: NHANES 2009 to 2012. J Periodontol. 2015 May;86(5):611-22. doi: 10.1902/jop.2015.140520. Epub 2015 Feb 17.
Armitage GC. Development of a classification system for periodontal diseases and conditions. Northwest Dent. 2000 Nov-Dec;79(6):31-5.
Haffajee AD, Socransky SS, Patel MR, Song X. Microbial complexes in supragingival plaque. Oral Microbiol Immunol. 2008 Jun;23(3):196-205. doi: 10.1111/j.1399-302X.2007.00411.x.
Damgaard C, Holmstrup P, Van Dyke TE, Nielsen CH. The complement system and its role in the pathogenesis of periodontitis: current concepts. J Periodontal Res. 2015 Jun;50(3):283-93. doi: 10.1111/jre.12209. Epub 2014 Jul 5.
Liu YC, Lerner UH, Teng YT. Cytokine responses against periodontal infection: protective and destructive roles. Periodontol 2000. 2010 Feb;52(1):163-206. doi: 10.1111/j.1600-0757.2009.00321.x. No abstract available.
Kinane DF, Preshaw PM, Loos BG; Working Group 2 of Seventh European Workshop on Periodontology. Host-response: understanding the cellular and molecular mechanisms of host-microbial interactions--consensus of the Seventh European Workshop on Periodontology. J Clin Periodontol. 2011 Mar;38 Suppl 11:44-8. doi: 10.1111/j.1600-051X.2010.01682.x.
Pussinen PJ, Jousilahti P, Alfthan G, Palosuo T, Asikainen S, Salomaa V. Antibodies to periodontal pathogens are associated with coronary heart disease. Arterioscler Thromb Vasc Biol. 2003 Jul 1;23(7):1250-4. doi: 10.1161/01.ATV.0000072969.71452.87. Epub 2003 Apr 24.
Pussinen PJ, Nyyssonen K, Alfthan G, Salonen R, Laukkanen JA, Salonen JT. Serum antibody levels to Actinobacillus actinomycetemcomitans predict the risk for coronary heart disease. Arterioscler Thromb Vasc Biol. 2005 Apr;25(4):833-8. doi: 10.1161/01.ATV.0000157982.69663.59. Epub 2005 Feb 3.
Berglundh T, Donati M. Aspects of adaptive host response in periodontitis. J Clin Periodontol. 2005;32 Suppl 6:87-107. doi: 10.1111/j.1600-051X.2005.00820.x.
Fillatreau S. Cytokine-producing B cells as regulators of pathogenic and protective immune responses. Ann Rheum Dis. 2013 Apr;72 Suppl 2:ii80-4. doi: 10.1136/annrheumdis-2012-202253. Epub 2012 Dec 19.
Belstrom D, Paster BJ, Fiehn NE, Bardow A, Holmstrup P. Salivary bacterial fingerprints of established oral disease revealed by the Human Oral Microbe Identification using Next Generation Sequencing (HOMINGS) technique. J Oral Microbiol. 2016 Jan 14;8:30170. doi: 10.3402/jom.v8.30170. eCollection 2016.
Belstrom D, Holmstrup P, Bardow A, Kokaras A, Fiehn NE, Paster BJ. Comparative analysis of bacterial profiles in unstimulated and stimulated saliva samples. J Oral Microbiol. 2016 Mar 16;8:30112. doi: 10.3402/jom.v8.30112. eCollection 2016.
Danielsen AK, Damgaard C, Massarenti L, Ostrup P, Riis Hansen P, Holmstrup P, Nielsen CH. B-cell cytokine responses to Porphyromonas gingivalis in patients with periodontitis and healthy controls. J Periodontol. 2023 Aug;94(8):997-1007. doi: 10.1002/JPER.22-0438. Epub 2023 Mar 5.
Other Identifiers
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H-16024734
Identifier Type: -
Identifier Source: org_study_id
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