Cytokine pattern determines the progression of experimental periodontal disease induced by <i>Actinobacillus actinomycetemcomitans</i> through the modulation of MMPs, RANKL, and their physiological inhibitors

Garlet, Gustavo; Cardoso, Cristina Ribeiro de Barros; Silva, T. A.; Ferreira, Beatriz Rossetti; Ávila-Campos, Mário Júlio; Cunha, Fernando; Silva, J. S.

doi:10.1111/j.1399-302x.2005.00245.x

Cited by 204 publications

(285 citation statements)

References 53 publications

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“…Furthermore, the increased ePD severity correlates with the significant increase in the levels of RANKL and MMP-13, and with the increase of RANKL/OPG and MMP-13/TIMPs ratios, characteristically associated with periodontal destruction. 13,19,45 Looking for the reason of the altered adaptive response because of RA/ PD interaction, we found that the submandibular LNs (the major draining LNs of oral cavity), which are significantly enlarged by the ePD induction, presented an even higher enlargement because of the pristane injection (data not shown), being an indicative of systemic immune reactivity to the PIA. Furthermore, the pattern of the transcription factors responsible for T-cell polarization expressed in submandibular LN was modulated by the PIA, the levels of Tbet and RORg being significantly increased in AIRmax mice submitted to both PIA and ePD protocols.…”

Section: Experimental Periodontitis and Arthritis Interaction Ap Trommentioning

confidence: 92%

“…10,13 Furthermore, in both diseases, these cytokines present a catabolic function over the periodontal tissues, mediated by the production of matrix metalloproteinases (MMPs) and the osteoclastogenic factor RANKL. 10,[13][14][15][16][17][18][19][20] On the other hand, Th2-and anti-inflammatory cytokines such as IL-4 and IL-10 exert the reverse effect, mediating the direct downregulation of inflammatory cytokines and their signaling pathways, and also upregulating the expression of TIMPs and OPG, the endogenous inhibitors of MMPs and RANKL, respectively. 10,13,19,21,22 However, a major unanswered question is how a joint lesion could influence the host response at periodontal environment to affect PD outcome.…”

Section: Introductionmentioning

confidence: 99%

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Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

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Periodontitis (PD) and rheumatoid arthritis (RA) have been found to be clinically associated and to share the chronic nature of the inflammatory reaction associated with bone resorption activity. However, the mechanisms underlying such association are unknown. Therefore, we examined the basis of Actinobacillus actinomycetemcomitans-and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) interaction in mice. Higher severity PD in the genetically inflammation prone acute inflammatory reactivity maximum (AIRmax) mice strain was associated with higher levels of TNF-a, IL-1b, IL-17, matrix metalloproteinase (MMP)-13, and RANKL, whereas PD/PIA co-induction resulted in even higher levels of IL-1b, IFN-g, IL-17, RANKL, and MMP-13 levels. Conversely, PD/PIA co-induction in AIRmin strain did not alter the course of both pathologies. PIA/PD co-induction resulted in altered expression of T-cell subsets transcription factors expression, with T-bet and RORg levels being upregulated, whereas GATA-3 levels were unaltered. Interestingly, PIA induction resulted in alveolar bone loss, such response being highly dependent on the presence of commensal oral bacteria. No differences were found in PIA severity parameters by PD co-induction. Our results show that the interaction between experimental PD and arthritis in mice involves a shared hyper-inflammatory genotype and functional interferences in innate and adaptive immune responses.

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Section: Experimental Periodontitis and Arthritis Interaction Ap Trommentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

View full text Add to dashboard Cite

show abstract

“…Mice with A. actinomycetemcomitans-induced periodontitis demonstrated upregulation of Th1 cytokines (IFN-γ and IL-12) in the early stage and that of Th2 cytokines (IL-4 and IL-10) in the late stage, indicating the involvement of each T cell subset in different disease stages [9]. Destructive effects of Th1 and Th2 cytokines were suggested in an experiment that showed that IFN-γ-and IL-6-deficient mice were resistant to P. gingivalis-induced alveolar bone loss [7].…”

Section: Cd4mentioning

confidence: 99%

The Role of Distinct T Cell Subsets in Periodontitis—Studies from Humans and Rodent Models

Okui

Aoki-Nonaka

Nakajima

et al. 2014

Curr Oral Health Rep

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“…Also, genetic factors have an important role on the balance between protective and destructive chemical mediators [17,18]. Genetic components may determine the roles of the immune system, host response, and cytokines in periodontal disease [19].…”

Section: Periodontitismentioning

confidence: 99%

Oral and Periodontal Diseases in Consanguineous Marriages

Çalışır¹

2017

Insights Into Various Aspects of Oral Health

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Periodontitis is deined as an inlammatory disease of supporting tissues of teeth characterized by progressive destruction of the periodontal ligament and alveolar bone. Periodontal manifestations of these genetic disorders or syndromes, such as familial and cyclic neutropenias, granulomatous disease, agranulocytosis, Langerhans' cell disease, glycogen storage disease, hypophosphatasia, leucocyte adhesion deiciency, and Papillon-Lefèvre, Chédiak-Higashi, Cohen, Ehlers-Danlos, Marfan, Down, Haim-Munk, and Kindlers syndromes, imitate some types of periodontal diseases. Most of these syndromes have autosomal-recessive characterization and can be seen commonly in consanguineous marriages. Therefore, consanguineous marriages have generally been accepted as having important detrimental efects on ofspring. There is a lot of genetic research about consanguineous marriage and its detrimental efects on ofspring. Although consanguineous marriages are common in the world, the relationship with oral and periodontal diseases has not been thoroughly investigated. We do not have enough of an understanding of the efects of consanguineous marriage on oral and periodontal diseases. In this chapter, previous studies in the literature related to this subject will be investigated and evaluated, and then this research will be related to oral and periodontal diseases. Therefore, this chapter will guide further research. The aim of this chapter is to show the relation between consanguineous marriages and oral-periodontal diseases.

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Cytokine pattern determines the progression of experimental periodontal disease induced by Actinobacillus actinomycetemcomitans through the modulation of MMPs, RANKL, and their physiological inhibitors

Cited by 204 publications

References 53 publications

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

The Role of Distinct T Cell Subsets in Periodontitis—Studies from Humans and Rodent Models

Oral and Periodontal Diseases in Consanguineous Marriages

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