Document Detail


Periodontal ligament fibroblasts sustain destructive immune modulators of chronic periodontitis.
MedLine Citation:
PMID:  20450375     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: In healthy periodontal tissue, innate immune responses effectively confine and suppress a bacterial insult. However, a disruption of the host-bacterial equilibrium may produce an overexpression of cytokines and lead to permanent, host-mediated tissue damage. Although such periodontal destruction primarily results from activated immune mechanisms, the site-specific damage suggests that local tissues participate in these pathologic changes. Periodontal ligament fibroblasts (PDLFs) are prominent in the periodontium and are critical in homeostasis and regeneration because they have the ability to produce multiple cytokines in response to a bacterial insult. These cells could play a role in the local pathogenesis of periodontal disease.
METHODS: We studied alkaline phosphatase (ALP) activity, interleukin (IL)-6 production, and morphologic characteristics of cultured PDLFs that were isolated from periodontally healthy sites (H-PDLFs) and diseased sites (D-PDLFs) in humans. Quantitative analyses of 84 genes that are related to inflammation were performed using real-time polymerase chain reaction arrays.
RESULTS: A mineralizing medium induced a significant increase of ALP in H-PDLFs, but no significant enzymatic changes were detected in D-PDLFs after such treatment. The protein and gene expression of IL6 showed a significant upregulation in D-PDLFs, which also demonstrated a significant upregulation of 54% of genes in the inflammatory gene arrays.
CONCLUSIONS: To our knowledge, these results represent the first biologic evidence that D-PDLFs retain uniquely inflammatory phenotypes that could maintain localized destructive signals in periodontitis. The overexpression of proinflammatory cytokines by PDLFs could amplify local inflammation by the continuous triggering of immune responses. In addition, the location of these cells could be critical in the progression of the inflammatory front into the deeper tissues.
Authors:
Ahmed R El-Awady; Regina L W Messer; Ahmed Y Gamal; Mohamed M Sharawy; Karl H Wenger; Carol A Lapp
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of periodontology     Volume:  81     ISSN:  1943-3670     ISO Abbreviation:  J. Periodontol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-03     Completed Date:  2010-12-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8000345     Medline TA:  J Periodontol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1324-35     Citation Subset:  D; IM    
Affiliation:
Department of Periodontology, School of Dentistry, Al-Azhar University, Cairo, Egypt.
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MeSH Terms
Descriptor/Qualifier:
Alkaline Phosphatase / genetics,  metabolism
Case-Control Studies
Cells, Cultured
Chemokines / biosynthesis,  genetics
Chronic Periodontitis / immunology*
Fibroblasts / immunology
Gene Expression
Gene Expression Profiling
Humans
Immunologic Factors / genetics,  metabolism*
Inflammation Mediators / metabolism*
Interleukin-6 / analysis,  biosynthesis*,  genetics
Periodontal Ligament / cytology,  immunology*
Up-Regulation
Chemical
Reg. No./Substance:
0/Chemokines; 0/Immunologic Factors; 0/Inflammation Mediators; 0/Interleukin-6; EC 3.1.3.1/Alkaline Phosphatase

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