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Enamel Matrix Derivative Exhibits Anti‐Inflammatory Properties in Monocytes
Author(s) -
Sato Sunao,
Kitagawa Masae,
Sakamoto Kiyako,
Iizuka Shinji,
Kudo Yasusei,
Ogawa Ikuko,
Miyauchi Mutsumi,
Chu Emily Y.,
Foster Brian L.,
Somerman Martha J.,
Takata Takashi
Publication year - 2008
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2008.070311
Subject(s) - enamel matrix derivative , derivative (finance) , matrix (chemical analysis) , materials science , composite material , biology , microbiology and biotechnology , regeneration (biology) , financial economics , economics
Background: Enamel matrix derivative (EMD) is used clinically to promote periodontal tissue regeneration with variable efficacy. EMD application results in significantly higher frequencies of sites without clinical signs of inflammation; additionally, patients receiving EMD therapy report significantly less post‐treatment discomfort. However, there are few reports that focus on defining the biologic mechanisms for the observed anti‐inflammatory effects of EMD. The aim of this study was to evaluate the influence of EMD on inflammatory‐associated markers using an in vitro monocyte assay. Methods: Rat monocytes were exposed to lipopolysaccharide (LPS; 100 ng/ml from Escherichia coli or Actinobacillus actinomycetemcomitans ) along with EMD (0, 50, 100, or 200 μg/ml). Levels of tumor necrosis factor‐alpha (TNF‐α) and prostaglandin E 2 (PGE 2 ) in conditioned media were analyzed by enzyme‐linked immunosorbent assay. In addition, the effects of exogenous PGE 2 on TNF‐α production from LPS‐stimulated monocytes were determined. Results: LPS‐stimulated monocytes exposed to EMD exhibited a decrease in TNF‐α production (0.10‐ to 0.52‐fold) and an increase in PGE 2 production (1.31‐ to 2.71‐fold) compared to controls not treated with EMD. Exogenously applied PGE 2 decreased TNF‐α production by LPS‐stimulated monocytes in a dose‐dependent manner, and EMD treatment enhanced this PGE 2 ‐mediated inhibition of TNF‐α production. Conclusion: In addition to EMD's published role in inducing proliferation, migration, adhesion, mineralization, and differentiation of periodontal ligament cells, our results indicated that EMD modulates two inflammation‐associated factors, TNF‐α and PGE 2 , in monocytes.

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