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Chitosan‐triclosan particles modulate inflammatory signaling in gingival fibroblasts
Author(s) -
Pavez L.,
Tobar N.,
Chacón C.,
Arancibia R.,
Martínez C.,
Tapia C.,
Pastor A.,
González M.,
Martínez J.,
Smith P. C.
Publication year - 2018
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12510
Subject(s) - triclosan , chitosan , microbiology and biotechnology , chemistry , dentistry , medicine , biology , biochemistry , pathology
Background and Objectives An important goal of periodontal therapy is the modulation of the inflammatory response. To this end, several pharmacological agents have been evaluated. Triclosan corresponds to an antibacterial and anti‐inflammatory agent currently used in periodontal therapy. Chitosan is a natural polymer that may act as a drug delivery agent and exerts antibacterial and anti‐inflammatory activities. Therefore, an association between both molecules might be useful to prevent inflammation and tissue destruction in periodontal tissues. Material and Methods In the present study, we have generated chitosan‐triclosan particles and evaluated their morphology, charge, biocompatibility and gene expression analysis in human gingival fibroblasts. Results The chitosan‐triclosan particles size and Z potential were 129 ± 47 nm and 51 ± 17 mV respectively. Human gingival fibroblast viability was not affected by chitosan‐triclosan. A total of 1533 genes were upregulated by interleukin ( IL) ‐1β. On the other hand, 943 were downregulated in fibroblasts stimulated with IL ‐1β plus chitosan‐triclosan particles. Fifty‐one genes were identified as molecular targets upregulated by IL ‐1 β and downregulated by the chitosan‐triclosan particles. The gene ontology analysis revealed that these genes were enriched in categories related to biological processes, molecular function and cellular components. Furthermore, using real‐time reverse transcription‐polymerase chain reaction beta‐actin , fibronectin , interleukin‐6 and IL‐1b genes were confirmed as targets upregulated by IL ‐1β and downregulated by chitosan‐triclosan particles. Conclusion Our results show that chitosan‐triclosan particles are able to modulate the inflammatory response in gingival fibroblasts. This effect might be useful in the prevention and/or treatment of inflammation in periodontal diseases.