Clinical benefits of oral irrigation for periodontitis are related to reduction of pro‐inflammatory cytokine levels and plaque

Cutler, Christopher W.; Stanford, Thomas W.; Abraham, Celeste M; Cederberg, Robert A.; Boardman, Thomas J.; Ross, Candy B.

doi:10.1034/j.1600-051x.2000.027002134.x

Cited by 100 publications

(92 citation statements)

References 18 publications

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“…Initial studies (not shown) established the dilution of test samples that yielded sufficient volume and sensitivity for detection of the four cytokines within the linear range of their respective standard curves (32). Dilutions ranged from 1/2.5 to 1/5 v/v.…”

Section: Analysis Of Gcf Cytokines By Elisamentioning

confidence: 99%

“…Sections were stained with H&E to confirm the clinical diagnosis by histological means (not shown). The experimental design for the induction of active (n ϭ 12) or "quiescent" (n ϭ 20) gingival inflammation (Table I) in subjects with preexisting mild CP (minimum of three probing pocket depths of Ն 5 mm, clinical attachment levels of Ն 5 mm, bleeding on probing, and horizontal bone loss at the same sites), as well as the technique for sampling gingival crevicular fluid (GCF), have been described previously (32). All four periopaper strips from each tooth were placed in one glass screw-capped vial and stored at Ϫ80°C.…”

Section: Collection and Handling Of Clinical Specimens Disease Categmentioning

confidence: 99%

“…The clinical criteria for these disease categories have been described previously (5,31,32). Gingival tissue was properly oriented in OCT medium by inserting a tooth landmark (3-mm strip of filter paper) alongside the tissue specimen, was flash frozen, and then was stored at Ϫ80°C.…”

Section: Collection and Handling Of Clinical Specimens Disease Categmentioning

confidence: 99%

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Mature Dendritic Cells Infiltrate the T Cell-Rich Region of Oral Mucosa in Chronic Periodontitis: In Situ, In Vivo, and In Vitro Studies

Jotwani

Palucka

Al-Quotub

et al. 2001

The Journal of Immunology

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183

239

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Previous studies have analyzed the lymphoid and myeloid foci within the gingival mucosa in health and chronic periodontitis (CP); however, the principal APCs responsible for the formation and organizational structure of these foci in CP have not been defined. We show that in human CP tissues, CD1a+ immature Langerhans cells predominantly infiltrate the gingival epithelium, whereas CD83+ mature dendritic cells (DCs) specifically infiltrate the CD4+ lymphoid-rich lamina propria. In vivo evidence shows that exacerbation of CP results in increased levels of proinflammatory cytokines that mediate DC activation/maturation, but also of counterregulatory cytokines that may prevent a Th-polarized response. Consistently, in vitro-generated monocyte-derived DCs pulsed with Porphyromonas gingivalis strain 381 or its LPS undergo maturation, up-regulate accessory molecules, and release proinflammatory (IL-1β, PGE2) and Th (IL-10, IL-12) cytokines. Interestingly, the IL-10:IL-12 ratio elicited from P. gingivalis-pulsed DCs was 3-fold higher than that from Escherichia coli-pulsed DCs. This may account for the significantly (p < 0.05) lower proliferation of autologous CD4+ T cells and reduced release of IFN-γ elicited by P. gingivalis-pulsed DCs. Taken together, these findings suggest a previously unreported mechanism for the pathophysiology of CP, involving the activation and in situ maturation of DCs by the oral pathogen P. gingivalis, leading to release of counterregulatory cytokines and the formation of T cell-DC foci.

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Section: Analysis Of Gcf Cytokines By Elisamentioning

confidence: 99%

Section: Collection and Handling Of Clinical Specimens Disease Categmentioning

confidence: 99%

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Mature Dendritic Cells Infiltrate the T Cell-Rich Region of Oral Mucosa in Chronic Periodontitis: In Situ, In Vivo, and In Vitro Studies

Jotwani

Palucka

Al-Quotub

et al. 2001

The Journal of Immunology

Self Cite

183

239

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“…Actions focused exclusively on the tooth surface, associated plaque and invading bacterium can indeed reduce pro-inflammatory cytokine levels in crevicular fluid [15]. However, non-compliance -poor sustained oral hygiene regimen and missed returns for regular professional maintenance care -heavily influence undesirable therapeutic outcomes.…”

Section: Targeting Plaque -Current Tools Of Soft Tissue Managementmentioning

confidence: 99%

Molecular basis for soft tissue management of gingivitis, periodontitis and peri-implant mucositis using an FDA cleared inflammation-targeting hydrogel – high potency polymerized cross-linked sucralfate - A case series illustrated profile of a drug device (Orafate) and the clinical rationale for use

McCullough¹

2017

Dent Oral Craniofac Res

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Background: Current practice of soft tissue management (STM) targets the biofilm and its invasion into gingival soft tissue and periodontal space. Prior to FDA clearance of high potency polymerized cross-linked sucralfate (Orafate) there were not therapeutic options that targeted inflammation of the gingival and periodontal soft tissue structures. High potency polymerized cross-linked sucralfate (HPPCLS) for soft tissue management of oral inflammation represents an advance toward balanced medical management of oral inflammatory disease and wounds of oral surgery.

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“…The excess formation of prostaglandin E 2 (PGE 2 ) has been described in a number of conditions characterized by increased susceptibility to infection, rheumatoid arthritis and inflammation, including periodontal diseases (8,17,25,29). PGE 2 mediates its biological functions via binding to four types of membrane-bound, G protein-coupled receptors, termed E prostanoid (EP)1 to EP4 (6, 22).…”

Section: Introductionmentioning

confidence: 99%

C2-ceramide inhibits the prostaglandin E2-induced accumulation of cAMP in human gingival fibroblasts

et al. 2010

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Ceramide is generated by the hydrolysis of membrane sphingomyelin by sphingomyelinase and is implicated in multiple signaling pathways, including those regulating differentiation, inflammation and immune responses. Excess formation of prostaglandin E 2 (PGE 2 ) is thought to increase susceptibility to infection, rheumatoid arthritis and inflammation, including periodontal diseases. We investigated the inhibitory effect of C 2 -ceramide, a short-chain ceramide analog, on the PGE 2 -stimulated accumulation of cAMP in human gingival fibroblasts. In human gingival fibroblasts pre-treated with C 2 -ceramide for 18 h, the PGE 2 -stimulated accumulation of cAMP was reduced, but an inactive C 2 -ceramide analog had no such effect. The accumulation of cAMP induced by EP2 and EP4 receptor agonists (ONO-AE1-259 and ONO-AE1-329, respectively) was inhibited in cells treated with C 2 -ceramide. However, treatment with C 2 -ceramide had no effect on the expression of mRNAs encoding the EP2 and EP4 receptors. Accumulation of cAMP could be induced by cAMP-elevating agents (forskolin, isobutylmethylxanthine and mastparan) but was not reduced by treatment with C 2 -ceramide. These observations suggest that C 2 -ceramide attenuates PGE 2 receptor function and consequently inhibits the accumulation of cAMP in human gingival fibroblasts.Prostaglandins are lipid mediators that are involved in many physiological and pathophysiological processes. The excess formation of prostaglandin E 2 (PGE 2 ) has been described in a number of conditions characterized by increased susceptibility to infection, rheumatoid arthritis and inflammation, including periodontal diseases (8,17,25,29). PGE 2 mediates its biological functions via binding to four types of membrane-bound, G protein-coupled receptors, termed E prostanoid (EP)1 to EP4 (6, 22). EP receptors stimulated by ligand binding activate different signal transduction pathways. Activation of the EP1 receptor raises intracellular Ca 2+ levels. Activation of EP2 and EP4 receptors increases intracellular cAMP levels by activating adenylate cyclase via G s proteins. Activation of the EP3 receptor reduces or increases cAMP levels by activating inhibitory G (G i ) or stimulatory G (G s ) proteins depending on the particular splice variant expressed by the cell (15). In human gingival fibroblasts, PGE 2 inhibited the DNA synthesis and proliferation (1, 37), and downregulated intercellular adhesion molecule-1 expression by cAMP-dependent signaling pathways (24). Therefore, cAMP is thought to be the main intracellular second messenger for response to PGE 2 , and is the crucial modulator of the functional activity of inflammation. Ceramide, an intracellular second messenger in the sphingomyelin transmembrane signaling pathway, can be generated by the cleavage of sphingomyelin by sphingomyelinase or by de novo biosynthesis by ceramide synthase (14). Increases in intracellular ceramide have been reported in many

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Clinical benefits of oral irrigation for periodontitis are related to reduction of pro‐inflammatory cytokine levels and plaque

Abstract: Oral irrigation with water for 14 days had an improved therapeutic benefit for AP over that of routine oral hygiene alone and this improvement was accompanied by a down-modulation of the pro-inflammatory cytokine profile in GCF.

Cited by 100 publications

References 18 publications

Mature Dendritic Cells Infiltrate the T Cell-Rich Region of Oral Mucosa in Chronic Periodontitis: In Situ, In Vivo, and In Vitro Studies

Mature Dendritic Cells Infiltrate the T Cell-Rich Region of Oral Mucosa in Chronic Periodontitis: In Situ, In Vivo, and In Vitro Studies

C2-ceramide inhibits the prostaglandin E2-induced accumulation of cAMP in human gingival fibroblasts

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