Influence of lipopolysaccharide and interleukin-6 on RANKL and OPG expression and release in human periodontal ligament cells

Recent research into periodontal disease pathology focuses on the role of receptor activator of nuclear factor‐κB ligand (RANKL) and osteoprotegerin (OPG) in periodontal bone destruction processes. RANKL regulates the differentiation of osteoclast by binding to its specific receptor RANK, while OPG...

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Published inAPMIS : acta pathologica, microbiologica et immunologica Scandinavica Vol. 117; no. 10; pp. 746 - 754
Main Authors KRAJEWSKI, ANNA C., BIESSEI, JANINE, KUNZE, MELANIE, MAERSCH, Stephan, PERABO, LUCA, NOACK, MICHAEL J.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.10.2009
Blackwell
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Summary:Recent research into periodontal disease pathology focuses on the role of receptor activator of nuclear factor‐κB ligand (RANKL) and osteoprotegerin (OPG) in periodontal bone destruction processes. RANKL regulates the differentiation of osteoclast by binding to its specific receptor RANK, while OPG inhibits the differentiation of osteoclasts by binding RANKL and therefore preventing RANKL to bind RANK. The aim of the present study was to investigate the influence of Porphyromonas gingivalis lipopolysaccharide (LPS) and interleukin‐6 (IL‐6) on RANKL and OPG expression and release in periodontal ligament (PDL) cells. Human PDL cells were stimulated for 48 h with purified P. gingivalis LPS and IL‐6. OPG and sRANKL release were assessed by using enzyme‐linked immunosorbent assay technique. OPG and RANKL expression was quantitatively measured by using the real‐time PCR technique. Whereas P. gingivalis LPS induced sRANKL release, expression was only slightly increased, IL‐6 did not show an effect on RANKL expression or release. In conclusion the data demonstrate that stimulation of PDL cells with P. gingivalis LPS leads to an increased release of sRANKL, rather than increased RANKL expression. Through this action, P. gingivalis LPS may exert its biological effect on osteoclast formation and bone resorption.
Bibliography:ark:/67375/WNG-8KRZ630L-7
ArticleID:APM2532
istex:530B41547DBEFE8B5ED3614BB8B8A346F0CEF98B
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:0903-4641
1600-0463
DOI:10.1111/j.1600-0463.2009.02532.x