Gene expression in periodontal tissues following treatment

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Abstract

Background

In periodontitis, treatment aimed at controlling the periodontal biofilm infection results in a resolution of the clinical and histological signs of inflammation. Although the cell types found in periodontal tissues following treatment have been well described, information on gene expression is limited to few candidate genes. Therefore, the aim of the study was to determine the expression profiles of immune and inflammatory genes in periodontal tissues from sites with severe chronic periodontitis following periodontal therapy in order to identify genes involved in tissue homeostasis.

Gingival biopsies from 12 patients with severe chronic periodontitis were taken six to eight weeks following non-surgical periodontal therapy, and from 11 healthy controls. As internal standard, RNA of an immortalized human keratinocyte line (HaCaT) was used. Total RNA was subjected to gene expression profiling using a commercially available microarray system focusing on inflammation-related genes. Post-hoc confirmation of selected genes was done by Realtime-PCR.

Results

Out of the 136 genes analyzed, the 5% most strongly expressed genes compared to healthy controls were Interleukin-12A (IL-12A), Versican (CSPG-2), Matrixmetalloproteinase-1 (MMP-1), Down syndrome critical region protein-1 (DSCR-1), Macrophage inflammatory protein-2β (Cxcl-3), Inhibitor of apoptosis protein-1 (BIRC-1), Cluster of differentiation antigen 38 (CD38), Regulator of G-protein signalling-1 (RGS-1), and Finkel-Biskis-Jinkins murine osteosarcoma virus oncogene (C-FOS); the 5% least strongly expressed genes were Receptor-interacting Serine/Threonine Kinase-2 (RIP-2), Complement component 3 (C3), Prostaglandin-endoperoxide synthase-2 (COX-2), Interleukin-8 (IL-8), Endothelin-1 (EDN-1), Plasminogen activator inhibitor type-2 (PAI-2), Matrix-metalloproteinase-14 (MMP-14), and Interferon regulating factor-7 (IRF-7).

Conclusion

Gene expression profiles found in periodontal tissues following therapy indicate activation of pathways that regulate tissue damage and repair.

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Most cited references 41

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Versican: a versatile extracellular matrix proteoglycan in cell biology.

Thomas N. Wight (2002)

Versican is a large extracellular matrix proteoglycan that is present in a variety of tissues. Successful cloning of the gene in man, mouse, cow and chicken has revealed the existence of at least four splice variants of versican, which differ in the size of the core protein and the number of glycosaminoglycan chains. The highly interactive nature of versican provides a basis for its importance as a structural molecule, creating loose and hydrated matrices during key events in development and disease; and by interacting either directly with cells or indirectly with molecules that associate with cells to, in part, regulate cell adhesion and survival, cell proliferation, cell migration and extracellular matrix assembly. Several studies within the past two years have confirmed a significant role for versican in regulating cell phenotype.

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Periodontitis.

Thomas Flemmig (1999)

The purpose of this review was to assess the scientific and clinical bases for the proposed classification of periodontitis. The clinical and histopathological signs and the etiology of periodontitis were described. Cross-sectional studies were analyzed to determine when onset of periodontitis most frequently occurs in adults. In addition, the progression rates of periodontitis have been assessed from longitudinal studies. No clinical, histopathological, or microbiological features could be identified that would characterize different disease entities of chronic periodontitis. The prevalence, extent, and severity of periodontitis were found to increase continually with higher age and there was no age when onset of disease would most likely occur. The rate of periodontitis progression varies largely between patients and there is no natural threshold for distinguishing various rates of disease progression. The incidence of periodontitis unresponsive to treatment depends on pretreatment progression rate, extent and severity of disease, tooth type, smoking, high levels of putative periodontal pathogens, a deficient immune response, and the type of therapy provided. There is no scientific basis for the classification "adult periodontitis" and "refractory adult periodontitis." Extensive clinical examinations are required for the diagnosis of "rapidly progressive adult periodontitis." It appears unrealistic that these examinations can be performed routinely in clinical practice. Therefore, the classification proposed by the Organizing Committee to define adult, rapidly progressive, and refractory periodontitis as specific disease entities was replaced with a simplified classification of periodontitis based on the scientific data available.

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Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection.

J. B. Singh, Caroline X. Gao, R Gorczynski … (2000)

Periodontitis, a prime cause of tooth loss in humans, is implicated in the increased risk of systemic diseases such as heart failure, stroke, and bacterial pneumonia. The mechanisms by which periodontitis and antibacterial immunity lead to alveolar bone and tooth loss are poorly understood. To study the human immune response to specific periodontal infections, we transplanted human peripheral blood lymphocytes (HuPBLs) from periodontitis patients into NOD/SCID mice. Oral challenge of HuPBL-NOD/SCID mice with Actinobacillus actinomycetemcomitans, a well-known Gram-negative anaerobic microorganism that causes human periodontitis, activates human CD4(+) T cells in the periodontium and triggers local alveolar bone destruction. Human CD4(+) T cells, but not CD8(+) T cells or B cells, are identified as essential mediators of alveolar bone destruction. Stimulation of CD4(+) T cells by A. actinomycetemcomitans induces production of osteoprotegerin ligand (OPG-L), a key modulator of osteoclastogenesis and osteoclast activation. In vivo inhibition of OPG-L function with the decoy receptor OPG diminishes alveolar bone destruction and reduces the number of periodontal osteoclasts after microbial challenge. These data imply that the molecular explanation for alveolar bone destruction observed in periodontal infections is mediated by microorganism-triggered induction of OPG-L expression on CD4(+) T cells and the consequent activation of osteoclasts. Inhibition of OPG-L may thus have therapeutic value to prevent alveolar bone and/or tooth loss in human periodontitis.

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Author and article information

Journal

Journal ID (nlm-ta): BMC Med Genomics

Title: BMC Medical Genomics

Publisher: BioMed Central

ISSN (Electronic): 1755-8794

Publication date Collection: 2008

Publication date (Electronic): 7 July 2008

Volume: 1

Page: 30

Affiliations

[1 ]Department of Periodontics, University of Washington, Seattle, USA

[2 ]University of Veterinary Medicine, University of Hannover, Hannover, Germany

[3 ]Department of Periodontology, Westfalian-Wilhelms-University, Muenster, Germany

[4 ]Institute of Medical Proteomics, Ruhr-University, Bochum, Germany

Article

Publisher ID: 1755-8794-1-30

DOI: 10.1186/1755-8794-1-30

PMC ID: 2491649

PubMed ID: 18606014

SO-VID: 3f546813-a9d7-4be5-8b5d-32cb6b4d8f83

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene expression in periodontal tissues following treatment

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Most cited references 41

Versican: a versatile extracellular matrix proteoglycan in cell biology.

Periodontitis.

Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection.

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