Are Cytokines Linked to Collagen Breakdown During Periodontal Disease Progression?

Ejeil, Anne-Laure; Gaultier, Fréderick; Igondjo-Tchen, Sylvie; Senni, Karim; Pellat, B.; Godeau, Gaston; Gogly, Bruno

doi:10.1902/jop.2003.74.2.196

Cited by 87 publications

(83 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As inflammatory cell infiltration and subsequent collagen degradation are hallmarks of periodontitis [7][8][9][10], and because IR spectral analyses can determine such tissue events, in addition to multiple other tissue changes at the molecular and sub-molecular level, then this IR microspectroscopic methodology can now be applied to hypothesis-driven research that aims to identify diseaserelated pathological changes in periodontal tissues. Figure 7 Cluster mapping of periodontal tissue.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

A Three-Dimensional Multivariate Image Processing Technique for the Analysis of FTIR Spectroscopic Images of Multiple Tissue Sections

2016

Spectroscopy

View full text Add to dashboard Cite

Background: Chronic periodontitis is an inflammatory disease of the supporting structures of the teeth. Infrared microspectroscopy has the potential to simultaneously monitor multiple disease markers, including cellular infiltration and collagen catabolism, and hence differentiate diseased and healthy tissues. Therefore, our aim was to establish an infrared microspectroscopy methodology with which to analyze and interpret molecular maps defining pathogenic processes in periodontal tissues.

show abstract

Section: Resultsmentioning

confidence: 99%

“…Inflammation-driven collagen degradation is a hallmark of periodontitis [7,8], with strong dissolution of collagen types I and III observed [9,10]. Particular absorptions are assigned to various functional groups in an attempt to extract biochemical information.…”

Section: Introductionmentioning

confidence: 99%

A Three-Dimensional Multivariate Image Processing Technique for the Analysis of FTIR Spectroscopic Images of Multiple Tissue Sections

2016

Spectroscopy

View full text Add to dashboard Cite

show abstract

“…A variety of immune-associated cell populations are responsible for the pathogenesis of periodontal diseases. Within periodontal lesions, activated monocytes, macrophages, and fibroblasts all produce cytokines, such as TNF-␣, IL-1␤, prostaglandin E 2 , and IL-6, and have all been found to be significantly elevated in diseased periodontal sites compared with healthy or inactive sites (Stashenko et al, 1991;Lee et al, 1995;Ejeil et al, 2003). These cytokines orchestrate the cascade of destructive events that occur in the periodontal tissues and trigger the production of an array of inflammatory enzymes and mediators, including matrix metalloproteinases, prostaglandins, and osteoclasts, thus resulting in irreversible hard and soft tissue damage (Assuma et al, 1998;Graves, 1999).…”

Section: Discussionmentioning

confidence: 99%

A p38α Selective Mitogen-Activated Protein Kinase Inhibitor Prevents Periodontal Bone Loss

Kirkwood¹,

Li²,

Rogers³

et al. 2006

J Pharmacol Exp Ther

View full text Add to dashboard Cite

In the oral microbial environment, Gram-negative bacterial derived lipopolysaccharide (LPS) can initiate inflammatory bone loss as seen in periodontal diseases. p38 Mitogen-activated protein kinase (MAPK) signaling is critical to inflammatory cytokine and LPS-induced cytokine expression, which may contribute toward periodontal bone loss. The purpose of this proof-of-principle study was to evaluate the ability of an orally active p38␣ MAPK inhibitor (SD-282) to reduce periopathogenic LPS-induced alveolar bone loss in an experimental rat model. Five groups of Sprague-Dawley rats received one of the following treatments: LPS injected to the palatal gingiva adjacent to the maxillary molars three times per week for 8 weeks, LPS plus two doses of SD-282 (15 or 45 mg/kg) twice daily by oral gavage, or control groups given drug vehicle (1% polyethylene glycol) or SD-282 (45 mg/kg) only. Baseline and 8-week alveolar bone loss was assessed by microcomputed tomography (CT) and histological examination. LPS induced severe bone loss over this time period, whereas control groups were unchanged from baseline measurements. Both doses of SD-282 showed significant protection from LPSinduced bone loss. Bone area and volumetric analysis of maxillas by CT indicated significant loss of bone volume with LPS treatment, which was blocked with the p38 inhibitor. Histological examination indicated significantly fewer tartate-resistant acid phosphatase-positive osteoclasts and a significant decrease in interleukin (IL)-6, IL-1␤, and tumor necrosis factor ␣ expression in p38 inhibitor-treated groups compared with LPS groups by immunostaining. Results from this in vivo study suggest that orally active p38 MAPK inhibitors can reduce LPS-induced inflammatory cytokine production and osteoclast formation and protect against LPS-stimulated alveolar bone loss.

show abstract

“…Periodontal disease and rheumatoid arthritis have remarkably similar inflammatory mediator profiles (22). Within periodontal lesions, activated monocytes, macrophages, and fibroblasts produce cytokines, such as TNF-␣, IL-1␤, and IL-6, which have been found to be significantly elevated in diseased periodontal sites compared with healthy or inactive sites (11). These cytokines orchestrate the cascade of destructive events that occur in the periodontal tissues and trigger the production of an array of inflammatory enzymes and mediators, resulting in irreversible hard and soft tissue damage (15).…”

Section: Fig 5 Veillonella Lps Activates P38 Mapk (A) Effects Of Tmentioning

confidence: 99%

Receptor Recognition of and Immune Intracellular Pathways for Veillonella parvula Lipopolysaccharide

Matera

Muto

Vinci

et al. 2009

Clin Vaccine Immunol

View full text Add to dashboard Cite

Veillonella parvula is an anaerobic gram-negative coccus that is part of the normal flora of the animal and human mouth and gastrointestinal and genitourinary tracts. Oral V. parvula is involved in the development of early periodontal disease as well as different types of serious infections. Present data on molecular mechanisms responsible for innate immune response against Veillonella are very scanty. The aim of this study was to investigate the Toll-like receptor (TLR) pathways responsible for V. parvula lipopolysaccharide (LPS) and to identify the intracellular pathways induced by this recognition. V. parvula LPS stimulated tumor necrosis factor alpha (TNF-␣) and interleukin-6 (IL-6) release in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner. Pretreatment of cells with a TLR4 antagonist significantly reduced TNF-␣ and IL-6 production in PBMC stimulated with either Veillonella or Escherichia coli LPS. However, V. parvula LPS was 10-to 100-fold less active than E. coli LPS for cytokine induction. TNF-␣, IL-1␤, IL-6, and IL-10 were released in wild-type and TLR2 ؊/؊ , but not TLR4 ؊/؊ , mouse macrophage cultures. V. parvula LPS was able to activate the human PBMC p38 mitogen-activated protein kinase (MAPK). A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-␣, IL-1␤, IL-6, and IL-10. In conclusion, V. parvula LPS is able to induce cytokine production in both human and murine in vitro models, although it is less effective than Enterobacteriaceae LPS. V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features.Veillonella organisms are small, nonfermentative, strictly anaerobic, gram-negative cocci which form part of the normal flora of the oral, genitourinary, respiratory, and intestinal tracts of humans and animals (10). The genus Veillonella was first isolated by Veillon and Zuber in 1898 and currently consists of eight species (28).Veillonella species have been reported as causes of serious infections, including meningitis (6), osteomyelitis and discitis (7, 28), prosthetic joint infection (26), and acute and chronic pleuropulmonary infection (33).Risk factors for Veillonella infection include periodontal disease, immunodeficiency, intravenous drug use, and premature birth (28). V. parvula is an important pathogen implicated in periodontitis and other dental infections (3, 18), and it is one of the most common anaerobic pathogens in chronic maxillary sinusitis and deep neck infections (9, 37). V. parvula has also been reported as a pathogen for osteomyelitis (34) and abscessed orchiepididymitis with sepsis (4). Endovascular infections reportedly may range from bacteremia to severe endocarditis and fatal cases of sepsis (8,14,25).Lipopolysaccharides (LPS) are major pathogenic factors of gram-negative bacteria. LPS from aerobic and facultative bacteria have been extensively studied (5). On the contrary, very little is known regarding the biological activity of LPS from anaerobic microorganisms such as Veillonella (1...

show abstract

Are Cytokines Linked to Collagen Breakdown During Periodontal Disease Progression?

Abstract: The present study showed that EGF was not changed in inflamed gingival tissue and that IL-1beta and IL-4 were particularly and intensively correlated with collagen loss. These 2 cytokines could be markers of clinical severity during active periodontitis.

Cited by 87 publications

References 25 publications

A Three-Dimensional Multivariate Image Processing Technique for the Analysis of FTIR Spectroscopic Images of Multiple Tissue Sections

A Three-Dimensional Multivariate Image Processing Technique for the Analysis of FTIR Spectroscopic Images of Multiple Tissue Sections

A p38α Selective Mitogen-Activated Protein Kinase Inhibitor Prevents Periodontal Bone Loss

Receptor Recognition of and Immune Intracellular Pathways for Veillonella parvula Lipopolysaccharide

Contact Info

Product

Resources

About