Trial record 1 of 5 for:    periodontal dendritic cells
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Effects of Periodontal Pathogens, Porphyromonas Gingivalis and Tannerella Forsythensis, on Cytokine Production From Human Monocyte-Derived Dendritic Cells

The recruitment status of this study is unknown because the information has not been verified recently.
Verified May 2003 by National Taiwan University Hospital.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00162838
First received: September 12, 2005
Last updated: November 22, 2005
Last verified: May 2003
  Purpose

Periodontitis develops due to subgingival infection with specific microbial pathogen from dental plaque. The bacteria can activate immunoinflammatory mechanisms within the local periodontal tissues that lead to destruction of collagen and alveolar bone. Human gingiva contains Langerhans and connective tissue dendritic cells. Signals from periodontal pathogen can induce dendritic cells to maturation,rapidly increasing surface expression of MHC class II, costimulatory molecules, and secrete proinflammatory cytokines to regulate adaptive T cell immune response. Studies on cytokines have led to controversy about different T cell subsets associated with the progression of periodontitis. Seymour proposed that susceptibility to periodontal disease progression involve a predominantly Th2 response while Ebersole speculated that Th2 cells providing protective function. It is possible that a given pathogen may produce different maturation signals by activating DCs induce a given type of immune response. In this study, we observed the profiles and amounts of cytokine production of DCs stimulated with P. gingivalis and T. forsythensis compared with E. coli, to see whether the periodontal pathogens may induce different response of dendritic cells in the innate immunity.


Condition
Periodontal Disease

Study Type: Observational
Study Design: Observational Model: Defined Population
Time Perspective: Cross-Sectional
Official Title: Effects of Periodontal Pathogens, Porphyromonas Gingivalis and Tannerella Forsythensis, on Cytokine Production From Human Monocyte-Derived Dendritic Cells.

Further study details as provided by National Taiwan University Hospital:

Estimated Enrollment: 20
Study Start Date: October 2003
Detailed Description:

Periodontitis develops due to subgingival infection with specific microbial pathogen from dental plaque. The bacteria can activate immunoinflammatory mechanisms within the local periodontal tissues that lead to destruction of collagen and alveolar bone. Bacterial antigens can release from the supra and subgingival dental plaque on the tooth surface as well as from bacteria attached to mucosal surfaces. The sulcular epithelium served as a physical barrier to the insult of the bacteria, the presence of Langerhans cells is also responsible for communication with the immune system. Dendritic cells (DCs), the most effective antigen-presenting cells, contact and process the antigens. Signals from pathogen induce dendritic cells to maturation. Mature DCs rapidly increase surface expression and stability of MHC class I and class II-peptide complexes, upregulate the surface expression of adhesion and co-stimulatory molecules (CD40, CD54, CD80, and CD86) and secrete proinflammatory cytokines such as IL-1, IL-6, IL-12…….. then they migrate to lymphoid organs, where they regulate T cell immune response. Human gingiva contains Langerhans and connective tissue dendritic cells. Immature dendritic cells appeared to be limited to the epithelium, whereas mature dendritic cells were restricted to the connective tissue. Studies on cytokines have led to controversy about the the different T cell subsets associated with the progression of periodontitis. Seymour proposed that susceptibility to periodontal disease progression involve a predominantly Th2 response while Ebersole speculated that Th2 cells providing protective function. Progression of periodontitis is also associated with the presence of gram-negative anaerobic microorganism such as Porphyromonas gingivalis, Bacteroides forsythus. Different bacteria and their LPS can elicit strikingly different response. It is possible that a given pathogen may produce different maturation signals by selectively activating a particular DC subset to induce a given type of immune response. In this study, we observed the profiles and amounts of cytokine production of DCs stimulated with P. gingivalis and T. forsythensis compared with E. coli, to see whether the periodontal pathogens may induce different response of dendritic cells in the innate immunity.

  Eligibility

Ages Eligible for Study:   20 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

  • Healthy

Exclusion Criteria:

-

  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00162838

Locations
Taiwan
National Taiwan University Hospital Recruiting
Taipei, Taiwan
Contact: Man ying Wong    +886-2-23123456 ext 7700    veronica@ha.mc.ntu.edu.tw   
Principal Investigator: Man ying Wong         
Sponsors and Collaborators
National Taiwan University Hospital
Investigators
Principal Investigator: Man-ying Wong, DDS, MS Department of Periodontics, National Taiwan University Hospital
  More Information

No publications provided

ClinicalTrials.gov Identifier: NCT00162838     History of Changes
Other Study ID Numbers: 9261700824, NTUH-93S039
Study First Received: September 12, 2005
Last Updated: November 22, 2005
Health Authority: Taiwan: Department of Health

Additional relevant MeSH terms:
Periodontal Diseases
Mouth Diseases
Stomatognathic Diseases

ClinicalTrials.gov processed this record on July 31, 2014