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

Günpınar, Sadiye; Alptekin, Nilgün Özlem; Dündar, Niyazi

doi:10.1111/odi.12658

Cited by 18 publications

(21 citation statements)

References 58 publications

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“…Twelve current studies related to local host responses in AgP were examined (Table 3). 30,[41][42][43][44][45][46][47][48][49][50][51] Of these, 9 studies 41,42,44-46,49-52 looked at multiple crevice sites within a patient population. Of these, 5 manuscripts 46,[48][49][50]52 reported multiple mediators at the local site.…”

Section: Relevant Findingsmentioning

confidence: 99%

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Classification and diagnosis of aggressive periodontitis

Fine

Patil

Loos

2018

J Clinic Periodontology

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Conflicting data resulted for several reasons; 1) the classification was too broad, 2) the disease (AgP) was not studied from its inception, at differing time points (temporal), and at different locations (topographic). New technologic advances coupled with a more delimiting definition of disease will allow for genetic, host and microbial factor analyses in an unbiased manner. As such we predict 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.

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Section: Relevant Findingsmentioning

confidence: 99%

“…Undoubtedly these cytokines could drive immune responsiveness at that site. Other more restrictive studies 44,45,51 examined individual pre-selected factors, i.e., lactic acid dehydrogenase and matrixmetalloproteinases (MMPs), and thus had a built-in bias ( Table 3).…”

Section: Relevant Findingsmentioning

confidence: 99%

Classification and diagnosis of aggressive periodontitis

Fine

Patil

Loos

2018

J Clinic Periodontology

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“…Changes in bacterial metabolism might not be the only explanation of the altered concentrations of salivary urea. Higher GCF volumes were found in patients with periodontitis compared with healthy individuals . Thus, another potential factor that could influence the concentration of salivary urea is production of a larger volume of GCF.…”

Section: Discussionmentioning

confidence: 97%

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

Kovalčíková

Pančíková

Konečná

et al. 2019

European J Oral Sciences

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Despite the fact that saliva contains measurable concentrations of urea and creatinine, it is not widely used in clinical nephrology. One of the reasons is the high inter‐ and intra‐individual variability in the salivary markers of kidney function. We hypothesized that gingival bleeding in patients with periodontitis could contribute to this variability by increasing the concentration of salivary urea or creatinine. Samples were collected from 25 patients with periodontitis and 29 healthy controls. In addition, saliva samples from five healthy volunteers were artificially contaminated with blood. The concentration of urea, but not that of creatinine, was more than twice as high in patients with periodontitis than in controls. Artificial contamination of saliva with blood did not affect the salivary concentration of creatinine. Salivary urea increased only with very high levels of contamination (≥2.5% blood in saliva), but that did not occur in patients. In conclusion, periodontitis increases the concentration of salivary urea, but this is not likely to be a result of contamination with blood. Future studies should investigate the composition of the oral microbiome, specifically regarding how it affects the concentration of salivary urea. Salivary creatinine seems to be a more robust non‐invasive marker of renal functions than salivary urea.

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“…Stimulation of human PDL cells with LPS enhances their production of MCP‐1, suggesting that PDL cells via this mechanism may contribute to the recruitment of monocytes in periodontitis . MCP‐1 is regarded to play a key role in progression of periodontitis, and thus, it is of high clinical relevance to study the regulation of MCP‐1 production by PDL cells …”

Section: Introductionmentioning

confidence: 99%

“…18 MCP-1 is regarded to play a key role in progression of periodontitis, and thus, it is of high clinical relevance to study the regulation of MCP-1 production by PDL cells. [19][20][21][22] In the present study, we investigate the hypothesis that LL-37 interacts with toll-like receptor (TLR) signaling and the production of MCP-1 in human PDL cells. LL-37 has been shown to trigger rapid and efficient sensing of bacterial DNA by human B lymphocytes and plasmacytoid dendritic cells, suggesting that LL-37 may interact with DNA and thereby regulate gene activity.…”

Section: Introductionmentioning

confidence: 99%

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

Aidoukovitch

Anders

Dahl

et al. 2019

J of Periodontal Research

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Objective The human host defense peptide LL‐37 both shows antimicrobial effects and modulates host cell properties. Here, we assess the effects of synthesized LL‐37 on lipopolysaccharide (LPS)‐induced inflammation in human periodontal ligament (PDL) cells and investigates underlying mechanisms. Background LL‐37 has been detected in the periodontal tissues, but its functional importance for PDL cell innate immune responses is not known. Methods Human PDL cells were obtained from premolars extracted on orthodontic indications. Cellular pro‐inflammatory monocyte chemoattractant protein‐1 (MCP‐1) mRNA expression was determined using quantitative real‐time RT‐PCR. MCP‐1 protein production was assessed by western blot and ELISA. Internalization of LL‐37 by PDL cells was visualized by immunocytochemistry. Nuclear factor kappa‐light‐chain‐enhancer of activated B‐cell (NF‐κB) activity was assessed by western blot of phosphorylated p65, phosphorylated p105, and IκBα proteins. Binding of LL‐37 to PDL cell DNA was determined by isolation and purification of DNA and dot blot for LL‐37 immunoreactivity. Results Treatment with LL‐37 (1 µmol/L) for 24 hours prevented LPS‐induced stimulation of MCP‐1 expression analyzed both on transcript and on protein levels. Stimulation with LL‐37 (1 µmol/L) for 24 hours had no effect on toll‐like receptor (TLR)2 and TLR4 transcript expression, suggesting that LL‐37 acts downstream of the TLRs. Preincubation with LL‐37 for 60 minutes followed by stimulation with LPS for 24 hours in the absence of LL‐37 completely prevented LPS‐evoked MCP‐1 transcript expression, implying that LL‐37 acts intracellularly and not via binding and neutralization of LPS. In PDL cells stimulated with LL‐37 for 60 minutes, the peptide was internalized as demonstrated by immunocytochemistry, suggesting an intracellular mechanism of action. LL‐37 immunoreactivity was observed both in the cytosol and in the nucleus. Downregulation of LPS‐induced MCP‐1 by LL‐37 was not mediated by reduction in NF‐κB activity as shown by unaltered expression of phosphorylated p65, phosphorylated p105, and IκBα NF‐κB proteins in the presence of LL‐37. Immunoreactivity for LL‐37 was observed in PDL cell DNA treated with but not without 0.1 and 1 µmol/L LL‐37 for 60 minutes in vitro. Conclusion 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.

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

Abstract: 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.

Cited by 18 publications

References 58 publications

Classification and diagnosis of aggressive periodontitis

Classification and diagnosis of aggressive periodontitis

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

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

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