Relationships between clinical parameters, interleukin 1B and histopathologic findings of gingival tissue in periodontitis patients

Liu, Cheng-Meei; Hou, Linlin; Wong, Man-Ying; Rossomando, Edward F.

doi:10.1006/cyto.1996.0023

Cited by 41 publications

(37 citation statements)

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“…Elevation of circulating serum cytokines as seen in this study shows that abdominal obesity and moderate to severe periodontal inflammation are associated and is in accordance with study by Fujihashi et al [27]. Moreover, a significant positive correlation between serum interleukin-1␤ and measures of abdominal obesity and periodontal inflammation seen here confirm their association with systemic inflammation.…”

Section: Discussionsupporting

confidence: 93%

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Serum interleukin-1β in subjects with abdominal obesity and periodontitis

Satpathy

Ravindra²,

Thakur

et al. 2015

Obesity Research & Clinical Practice

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Section: Discussionsupporting

confidence: 93%

“…The findings of this study supplement earlier information on cytokine synthesis in response to periodontopathogenic bacteria and their products [27]. Evidence suggested that both keratinocytes and gingival fibroblasts produce interleukin-1␤ in response to stimulation by bacterial products [28].…”

Section: Discussionsupporting

confidence: 83%

Serum interleukin-1β in subjects with abdominal obesity and periodontitis

Satpathy

Ravindra²,

Thakur

et al. 2015

Obesity Research & Clinical Practice

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“…IL-1b or IL-1b receptor antagonists are thus potential therapeutics for the treatment of inflammatory diseases through the targeting of the NLRP3 activation pathway (Hoffman et al, 2004;Dinarello, 2005). IL-1b is a key mediator for gingival inflammation and is a strong enhancer of PGE 2 and TNF-a, leading to the degradation of the extracellular matrix of the periodontal tissues and alveolar bone, which are the characteristics of periodontitis (Liu et al, 1996). Because IL-1b is tightly controlled by the separate regulation at transcriptional and posttranslation levels, the simultaneous induction of proIL-1b and its maturation by Td92 could lead to uncontrollable inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…The proinflammatory and bone-resorptive characteristics of IL-1b are associated with the immunopathology of periodontitis, leading to periodontal tissue destruction (Liu et al, 1996). IL-1b is increased in the gingival crevicular fluid of periodontitis patients and correlates to the presence of major periodontopathogens, such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, the so-called red complex (Teles et al, 2010), and to disease severity (Ferreira et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Integrin α5β1 Activates the NLRP3 Inflammasome by Direct Interaction with a Bacterial Surface Protein

Jun

Lee

et al. 2012

Immunity

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Integrins are cell-surface heterodimeric glycoproteins composed of alpha and beta subunits that mediate cell-cell, cell-extracellular matrix, and cell-pathogen interactions. In this study, we report a specific role of integrin α5β1 in NLRP3 inflammasome activation in macrophages stimulated by Td92, a surface protein of the periodontopathogen, Treponema denticola. The direct interaction of Td92 with the cell membrane integrin α5β1 resulted in ATP release and K(+) efflux, which are the main events in NLRP3 activation. This interaction was arginine-glycine-aspartate (RGD)-independent, and Td92 internalization was not required for the activity. An integrin α5β1 antibody and oxATP, an ATP receptor antagonist, inhibited NLRP3 expression, caspase-1 activation, interleukin-1β (IL-1β) secretion, and proIL-1β synthesis, all of which were regulated by NF-κB activation. Therefore, our data has identified the integrin α5β1 as a principal cell membrane receptor for both NLRP3 inflammasome activation and IL-1β transcription by a bacterial protein, which could exaggerate inflammation, a characteristic of periodontitis.

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“…11 There is a strong correlation between IL-1β level and both gingival index and probing depth. [13][14][15] IL-1β was found in high levels in gingival tissue and gingival crevicular fluid of patients with periodontal disease [13][14][15][16] and decreased remarkably after periodontal therapy. 14,17 Therefore, due to the fact that endotoxin is the most potent stimulator of IL-1β production, the removal of endotoxin embedded in diseased cementum is believed to be a critical procedure during various periodontal treatments.…”

mentioning

confidence: 99%