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Article: Periodontal therapy: A novel non-drug-induced experimental model to study human inflammation

TitlePeriodontal therapy: A novel non-drug-induced experimental model to study human inflammation
Authors
KeywordsInterleukin-6
Interleukin-1 receptor antagonist
Inflammation
C-reactive protein
Periodontitis
Endotoxin-challenge
Issue Date2004
Citation
Journal of Periodontal Research, 2004, v. 39, n. 5, p. 294-299 How to Cite?
AbstractBackground: Chronic periodontitis causes a low-grade systemic inflammatory response; its standard treatment, however, induces an acute inflammatory response. The aim of this study was to describe the systemic inflammatory reactions to an intensive periodontal treatment regimen. Methods: Fourteen otherwise healthy subjects suffering from severe chronic periodontitis were enrolled in a 1 month pilot single-blind trial. Intensive periodontal treatment, consisting of full-mouth subgingival root debridement delivered within a 6-h period, was performed. Periodontal parameters were recorded before and 1 month after completion of treatment. Blood samples were taken at baseline and 1, 3, 5, 7 and 30 days after treatment. Interleukin-1 receptor antagonist (IL-1Ra), Interleukin-6 (IL-6) and C-reactive protein (CRP) serum concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Complete blood counts were also performed. Results: One day after treatment, mild neutrophilia and monocytosis (p < 0.05) and lymphopenia (p < 0.01) were accompanied by a sharp increase in inflammatory markers (IL-1Ra, IL-6, p < 0.01). A 10-fold increase in CRP (p < 0.001) was detected on day 1 and its kinetics followed a pattern of a classical acute phase response (significantly raised concentrations up to 1 week, p < 0.01). At 3-7 days after treatment, subjects presented also with a mild tendency towards a normocytic anaemic state (p < 0.01) and a degree of lympho-thrombocytosis (p < 0.05). The observed changes were similar to those expected following the well-characterized endotoxin-challenge model of inflammation. Conclusions: Intensive periodontal treatment produced an acute systemic inflammatory response of 1 week duration and might represent an alternative to classic endotoxin-challenge or drug-induced models to study acute inflammation in humans. © Blackwell Munksgaard 2004.
Persistent Identifierhttp://hdl.handle.net/10722/230817
ISSN
2015 Impact Factor: 2.474
2015 SCImago Journal Rankings: 0.932

 

DC FieldValueLanguage
dc.contributor.authorD'Aiuto, F.-
dc.contributor.authorNibali, L.-
dc.contributor.authorMohamed-Ali, V.-
dc.contributor.authorVallance, P.-
dc.contributor.authorTonetti, M. S.-
dc.date.accessioned2016-09-01T06:06:52Z-
dc.date.available2016-09-01T06:06:52Z-
dc.date.issued2004-
dc.identifier.citationJournal of Periodontal Research, 2004, v. 39, n. 5, p. 294-299-
dc.identifier.issn0022-3484-
dc.identifier.urihttp://hdl.handle.net/10722/230817-
dc.description.abstractBackground: Chronic periodontitis causes a low-grade systemic inflammatory response; its standard treatment, however, induces an acute inflammatory response. The aim of this study was to describe the systemic inflammatory reactions to an intensive periodontal treatment regimen. Methods: Fourteen otherwise healthy subjects suffering from severe chronic periodontitis were enrolled in a 1 month pilot single-blind trial. Intensive periodontal treatment, consisting of full-mouth subgingival root debridement delivered within a 6-h period, was performed. Periodontal parameters were recorded before and 1 month after completion of treatment. Blood samples were taken at baseline and 1, 3, 5, 7 and 30 days after treatment. Interleukin-1 receptor antagonist (IL-1Ra), Interleukin-6 (IL-6) and C-reactive protein (CRP) serum concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Complete blood counts were also performed. Results: One day after treatment, mild neutrophilia and monocytosis (p < 0.05) and lymphopenia (p < 0.01) were accompanied by a sharp increase in inflammatory markers (IL-1Ra, IL-6, p < 0.01). A 10-fold increase in CRP (p < 0.001) was detected on day 1 and its kinetics followed a pattern of a classical acute phase response (significantly raised concentrations up to 1 week, p < 0.01). At 3-7 days after treatment, subjects presented also with a mild tendency towards a normocytic anaemic state (p < 0.01) and a degree of lympho-thrombocytosis (p < 0.05). The observed changes were similar to those expected following the well-characterized endotoxin-challenge model of inflammation. Conclusions: Intensive periodontal treatment produced an acute systemic inflammatory response of 1 week duration and might represent an alternative to classic endotoxin-challenge or drug-induced models to study acute inflammation in humans. © Blackwell Munksgaard 2004.-
dc.languageeng-
dc.relation.ispartofJournal of Periodontal Research-
dc.subjectInterleukin-6-
dc.subjectInterleukin-1 receptor antagonist-
dc.subjectInflammation-
dc.subjectC-reactive protein-
dc.subjectPeriodontitis-
dc.subjectEndotoxin-challenge-
dc.titlePeriodontal therapy: A novel non-drug-induced experimental model to study human inflammation-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-0765.2004.00741.x-
dc.identifier.pmid15324349-
dc.identifier.scopuseid_2-s2.0-4644308729-
dc.identifier.volume39-
dc.identifier.issue5-
dc.identifier.spage294-
dc.identifier.epage299-

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