» Articles » PMID: 21730256

Local Inflammatory Markers and Systemic Endotoxin in Aggressive Periodontitis

Overview
Journal J Dent Res
Specialty Dentistry
Date 2011 Jul 7
PMID 21730256
Citations 41
Authors
Affiliations
Soon will be listed here.
Abstract

While much research has focused on local and systemic factors contributing to periodontal disease, little is known regarding mechanisms linking these factors. We have previously reported a systemic hyper-inflammatory response to bacterial endotoxin in localized aggressive periodontitis (LAP). The objectives of this study were to delineate cyto/chemokines in gingival crevicular fluid (GCF) and evaluate systemic levels of endotoxin associated with LAP. Clinical parameters, GCF, and peripheral blood were collected from: 34 LAP, 10 healthy siblings, and nine healthy unrelated control individuals. Cyto/chemokines were quantified in GCF, systemic endotoxin levels were quantified in plasma, and correlation analysis was performed among all parameters. Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNFα, INFγ, IL1β, IL2, IL6, IL10, Il12p40, GMCSF, and MIP1α, p < 0.001), while MCP1, IL4, and IL8 were elevated in healthy sites (p < 0.01). Four- to five-fold-higher endotoxin levels were detected in LAP plasma compared with that from healthy participants (p < 0.0001), which correlated with all clinical parameters and most cyto/chemokines analyzed. In conclusion, higher systemic levels of endotoxin were found in LAP, which correlates with an exacerbated local inflammatory response and clinical signs of disease. (Clinicaltrials.gov number, NCT01330719).

Citing Articles

Gingival Crevicular Fluid Biomarkers During Periodontitis Progression and After Periodontal Treatment.

Teles F, Martin L, Patel M, Hu W, Bittinger K, Kallan M J Clin Periodontol. 2024; 52(1):40-55.

PMID: 39278722 PMC: 11671168. DOI: 10.1111/jcpe.14061.


Grade C Molar-Incisor Pattern Periodontitis in Young Adults: What Have We Learned So Far?.

Miguel M, Shaddox L Pathogens. 2024; 13(7).

PMID: 39057807 PMC: 11279578. DOI: 10.3390/pathogens13070580.


Cytokine levels in the gingival crevicular fluid and their association with periodontal status of down syndrome patients: a cross-sectional study.

Mouchrek M, Franco M, da Silva L, Martins K, Conceicao S, de Azevedo Dos Santos A Clin Oral Investig. 2024; 28(7):391.

PMID: 38907162 DOI: 10.1007/s00784-024-05789-x.


Modulation of allograft immune responses by Porphyromonas gingivalis lipopolysaccharide administration in a rat model of kidney transplantation.

Sato Y, Noguchi H, Kubo S, Kaku K, Okabe Y, Onishi H Sci Rep. 2024; 14(1):13969.

PMID: 38886503 PMC: 11183068. DOI: 10.1038/s41598-024-64771-5.


The Novel Insight of Gut Microbiota from Mouse Model to Clinical Patients and the Role of NF-κB Pathway in Polycystic Ovary Syndrome.

Kong F, Huang P, Chen J, Ma Y Reprod Sci. 2024; 31(11):3323-3333.

PMID: 38653859 DOI: 10.1007/s43032-024-01562-3.


References
1.
Pussinen P, Paju S, Mantyla P, Sorsa T . Serum microbial- and host-derived markers of periodontal diseases: a review. Curr Med Chem. 2007; 14(22):2402-12. DOI: 10.2174/092986707781745604. View

2.
Shapira L, Warbington M, Van Dyke T . TNF alpha and IL-1 beta in serum of LJP patients with normal and defective neutrophil chemotaxis. J Periodontal Res. 1994; 29(5):371-3. DOI: 10.1111/j.1600-0765.1994.tb01236.x. View

3.
Kim M, Day C, Morrison N . MCP-1 is induced by receptor activator of nuclear factor-{kappa}B ligand, promotes human osteoclast fusion, and rescues granulocyte macrophage colony-stimulating factor suppression of osteoclast formation. J Biol Chem. 2005; 280(16):16163-9. DOI: 10.1074/jbc.M412713200. View

4.
Van Dyke T, Offenbacher S, Kalmar J, Arnold R . Neutrophil defects and host-parasite interactions in the pathogenesis of localized juvenile periodontitis. Adv Dent Res. 1988; 2(2):354-8. DOI: 10.1177/08959374880020022601. View

5.
Pussinen P, Vilkuna-Rautiainen T, Alfthan G, Palosuo T, Jauhiainen M, Sundvall J . Severe periodontitis enhances macrophage activation via increased serum lipopolysaccharide. Arterioscler Thromb Vasc Biol. 2004; 24(11):2174-80. DOI: 10.1161/01.ATV.0000145979.82184.9f. View