Gingival Crevicular Fluid Levels of Monocyte Chemoattractant Protein‐1 and Tumor Necrosis Factor‐Alpha in Patients With Chronic and Aggressive Periodontitis

Kurtiş, Bülent; Tüter, Gülay; Serdar, Muhittin; Akdemir, Pelin; Uygur, C; Fıratlı, Erhan; Bal, Belgin

doi:10.1902/jop.2005.76.11.1849

Cited by 129 publications

(136 citation statements)

References 31 publications

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“…This later hypothesis is supported by studies showing that periodontal subjects with specific polymorphisms in the IL-1 gene produce 2.5 more IL-1β in shallow pockets than subjects having periodontitis but without these polymorphisms [25]. IL-6, TNF-α, IL-17, IL-8 and MCP-1 have also been found to be increased in GCF of patients with PD [47,59].…”

Section: Local Host Response In Periodontitismentioning

confidence: 85%

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Kamer¹,

Dasanayake²,

Craig³

et al. 2008

JAD

152

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Abstract. Alzheimer's disease (AD) affects approximately 4.5 million people in the U.S. and this number will increase as the population ages and the life-span increases. Therefore, of paramount importance is identifying mechanisms and factors that affect the risk of developing AD. The etiology and pathogenic mechanisms for AD have not been defined, although inflammation within the brain is thought to play a role. Consistent with this hypothesis, studies suggest that peripheral infections contribute to the inflammatory state of the central nervous system. Periodontitis is a prevalent, persistent peripheral infection associated with gram negative, anaerobic bacteria that are capable of exhibiting localized and systemic infections in the host. This review offers a hypothetical link between periodontitis and AD and will present possible mechanistic links between periodontitis related inflammation and AD. It will review the pathogenesis of periodontitis and the mechanisms by which periodontal infections may affect the onset and progression of AD. Since periodontitis is a treatable condition, it may be a readily modifiable risk factor for AD.

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Section: Local Host Response In Periodontitismentioning

confidence: 85%

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Kamer¹,

Dasanayake²,

Craig³

et al. 2008

JAD

152

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“…There is considerable evidence that diabetes enhances the innate immune response in the periodontium. IL-1beta, TNF-alpha and the chemokine MCP-1 are elevated in the gingival crevicular fluid or serum of diabetic patients and are correlated with increased periodontal tissue destruction (69)(70)(71)(72). Monocytes from patients with type 1 diabetes produce significantly greater amounts of TNF-alpha, IL-1beta and PGE2 in response to LPS compared to matched normoglycemic individuals (72,73).…”

Section: Periodontal Diseasementioning

confidence: 99%

Diabetic complications and dysregulated innate immunity

Graves

Kayal²

2008

Front Biosci

223

188

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Diabetes mellitus is a metabolic disorder that leads to the development of a number of complications. The etiology of each diabetic complication is undoubtedly multifactorial. We will focus on one potential component that may be common in many diabetic complications, dysregulation of innate immunity associated with an increased inflammatory response. High glucose levels lead to shunting through the polyol pathway, an increase in diacylglycerol which activates protein kinase C, an increase in the release of electrons that react with oxygen molecules to form superoxides, and the non-enzymatic glycosylation of proteins that result in greater formation of advanced glycation end products. Each of these can lead to aberrant cell signalling that affects innate immunity for example, by activating the MAP kinase pathway or inducing activation of transcription factors such as NF-kappaB. This may be a common feature of several complications including periodontal disease, atherosclerosis, nephropathy, impaired healing and retinopathy. These complications are frequently associated with increased expression of inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 and enhanced generation of reactive oxygen species. Cause and effect relationship between dysregulation of key components of innate immunity and diabetic complications in many instances have been demonstrated with the use of cytokine blockers and antioxidants.

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“…Therefore, it is believed that the intensity of periodontal inflammation could be assessed objectively by analyzing GCF components, because many inflammatory and immune mediators implicated in periodontal destruction have been detected in GCF. Several researchers have reported that the expression of inflammatory cytokines such as IL-1, IL-6, IL-8 and TNF-α in GCF from chronic periodontitis patients was significantly elevated when compared with healthy patients [22] [23] [24] [25]. Furthermore, there are some reports investigating the effect of nonsurgical periodontal therapy involving SRP on GCF from patients with chronic periodontitis [26] [27].…”

Section: Discussionmentioning

confidence: 99%

Decreased Ratios of Interleukin-1<i>β</i> and Intercellular Adhesion Molecule 1 in Gingival Crevicular Fluid after Scaling and Root Planing Associated with Periodontal Pocket Healing

Hieda¹,

Usui²,

Nakamura³

et al. 2017

OJST

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Objectives: Several researchers have investigated inflammatory cytokines in gingival crevicular fluid (GCF) from chronic periodontitis with clinical parameters after periodontal treatment. The aim of the present study was to identify the inflammatory cytokines present in GCF associated with periodontal pocket healing after scaling and root planing (SRP). Methods: Twenty patients were enrolled, and clinical examinations including probing pocket depth (PPD) and bleeding on probing (BOP) were performed at the first visit, and before and after SRP. The periodontal epithelial surface area (PESA) and periodontal inflamed surface area (PISA) were also calculated. GCF samples were collected before and after SRP to measure the levels of 40 inflammatory cytokines using antibody array. Correlations between changes in cytokine levels and clinical improvements were assessed by single and multiple regression analyses. Results: PPD, PESA and PISA significantly decreased after SRP, while there were no significant differences in the levels of cytokines before (PreSRP) and one week after SRP (PostSRP). Clinical improvements (ΔPPD, ΔPESA and ΔPISA) were calculated using the formula PreSRP-PostSRP, while changes in the levels of inflammatory cytokines were calculated using three formulas: PreSRP-PostSRP, PostSRP/PreSRP and Log(PostSRP/PreSRP). Log (PostSRP/PreSRP) for interleukin-1β (IL-1β) significantly correlated with ΔPESA (R = −0.512). PostSRP/PreSRP and Log(PostSRP/PreSRP) for intercellular adhesion molecule 1 (ICAM-1) significantly correlated with ΔPISA (R = −0.669, −0.573). Two good fit models were generated by multiple linear regression. Log(PostSRP/PreSRP) for IL-1β significantly affected ΔPESA (R 2 = 0.566). PostSRP/PreSRP for ICAM-1 significantly affected ΔPISA (R 2 = 0.615). were not associated with clinical improvements. However, the present study indicates that lower PostSRP/PreSRP ratios for IL-1β and ICAM-1 in GCF lead to a greater decrease in PESA and PISA, respectively. Periodontal pocket healing might be affected by a decreased ratio of inflammatory cytokines such as IL-1β and ICAM-1 at an early stage after SRP.

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Gingival Crevicular Fluid Levels of Monocyte Chemoattractant Protein‐1 and Tumor Necrosis Factor‐Alpha in Patients With Chronic and Aggressive Periodontitis

Cited by 129 publications

References 31 publications

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Diabetic complications and dysregulated innate immunity

Decreased Ratios of Interleukin-1<i>β</i> and Intercellular Adhesion Molecule 1 in Gingival Crevicular Fluid after Scaling and Root Planing Associated with Periodontal Pocket Healing

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Gingival Crevicular Fluid Levels of Monocyte Chemoattractant Protein‐1 and Tumor Necrosis Factor‐Alpha in Patients With Chronic and Aggressive Periodontitis

Cited by 129 publications

References 31 publications

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Diabetic complications and dysregulated innate immunity

Decreased Ratios of Interleukin-1&lt;i&gt;β&lt;/i&gt; and Intercellular Adhesion Molecule 1 in Gingival Crevicular Fluid after Scaling and Root Planing Associated with Periodontal Pocket Healing

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Decreased Ratios of Interleukin-1<i>β</i> and Intercellular Adhesion Molecule 1 in Gingival Crevicular Fluid after Scaling and Root Planing Associated with Periodontal Pocket Healing