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Journal ArticleDOI

Gingival crevicular fluid levels of monocyte chemoattractant protein-1 in patients with aggressive periodontitis.

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TLDR
Investigation of gingival crevicular fluid levels of monocyte chemoattractant protein (MCP)-1 in aggressive periodontitis reveals that MCP-1 can be used to understand the disease pathogenesis of LAgP and GAgP.
Abstract
OBJECTIVES The purpose of this study was to investigate the gingival crevicular fluid (GCF) levels of monocyte chemoattractant protein (MCP)-1 in aggressive periodontitis (AgP) and whether GCF MCP-1 levels differ among localized (L) AgP and generalized (G) AgP. MATERIAL AND METHODS A total of 160 subjects including 80 AgP and 80 age- and gender-matched periodontally healthy (H) controls were recruited in this cross-sectional study (NCT02927704). GCF samples were collected from 160 patients including 50 LAgP, 30 GAgP, and 80 H. Volume of GCF was measured by Periotron 8000® , and enzyme-linked immunosorbent assay was used to assess MCP-1 levels. RESULTS Compared to H controls, all clinical parameters and total amounts (pg 30 s-1 ) of MCP-1 were significantly higher in subjects with LAgP and GAgP (P   0.05), total amounts of MCP-1 were higher in GAgP than LAgP (P < 0.05). CONCLUSION It can be concluded that the total amount of MCP-1 level in GCF may be a potential determinant in AgP subjects. Increased MCP-1 levels in line with the degree of periodontal destruction in GAgP patients reveal that MCP-1 can be used to understand the disease pathogenesis of LAgP and GAgP.

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Journal ArticleDOI

Classification and diagnosis of aggressive periodontitis

TL;DR: It is predicted that progress can be made in identifying a robust group of genetic, host, and microbial risk-markers associated with periodontal disease that can improve diagnostic capability in disease associated with juveniles, adolescents, and post-adolescent individuals.
Journal ArticleDOI

Urea and creatinine levels in saliva of patients with and without periodontitis

TL;DR: It is found that periodontitis increases the concentration of salivary urea, but this is not likely to be a result of contamination with blood, and Salivary creatinine seems to beA more robust non-invasive marker of renal functions than salivARY urea.
Journal ArticleDOI

Globular C1q receptor (p33) binds and stabilizes pro-inflammatory MCP-1: a novel mechanism for regulation of MCP-1 production and function.

TL;DR: It is proposed that endogenous gC1qR/p33 physically interacts with MCP-1 causing stabilization of the M CP-1 protein and stimulation of its activity in human periodontal ligament cells, suggesting a novel gC 1qR /p33-mediated pro-inflammatory mechanism of action.
Journal ArticleDOI

Dysregulation of genes and microRNAs in localized aggressive periodontitis.

TL;DR: The profile of genes and miRNAs overexpressed here are directly or indirectly related to immune response and inflammation and supports previous findings that suggests LAP patients have a `hyper-responsive` phenotype upon activation of TLR-pathway by periodontal pathogens.
Journal ArticleDOI

The host defense peptide LL‐37 is internalized by human periodontal ligament cells and prevents LPS‐induced MCP‐1 production

TL;DR: LL-37 abolishes LPS-induced MCP-1 production in human PDL cells through an intracellular, NF-κB-independent mechanism which probably involves direct interaction between LL-37 and DNA.
References
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Journal ArticleDOI

Periodontal Disease in Pregnancy II. Correlation Between Oral Hygiene and Periodontal Condition

TL;DR: In this paper, the correlation between oral hygiene and periodontal condition was investigated in the context of pregnant women with Periodontal Disease in Pregnancy II (PDI II).
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Development of a Classification System for Periodontal Diseases and Conditions

TL;DR: How the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics is summarized.
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The role of inflammatory mediators in the pathogenesis of periodontal disease.

TL;DR: The role of bacteria in the initiation of periodontitis is well-documented and the end result, destruction of the alveolar bone and periodontal connective tissue, is readily observed; but the events occurring between these two points in time remain obscure and are the focus of this paper.
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Inflammatory and immune pathways in the pathogenesis of periodontal disease.

TL;DR: Current knowledge of the host response in periodontitis is delineated to delineate the role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered.
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