aggressive periodontitis/hypoxia

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Effect of non-surgical periodontal treatment on gingival crevicular fluid hypoxia inducible factor-1 alpha, vascular endothelial growth factor and tumour necrosis factor- alpha levels in generalized aggressive periodontitis patients.

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Hypoxia-inducible angiogenic pathway involving hypoxia inducible factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and tumour necrosis factor- alpha (TNF-α) may regulate several biological processes related to inflammation. The present study aimed to assess the effect

A disintegrin-like And metalloproteinase with thrombospondin-1 (ADAMTS-1) levels in gingival crevicular fluid correlate with vascular endothelial growth factor-A, hypoxia-inducible factor-1α, and clinical parameters in patients with advanced periodontitis.

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ADAMTS (A disintegrin-like and metalloproteinase with thrombospondin) are a family of proteinases that are structurally similar to the family of matrix metalloproteinases with critical roles in damage and repair of the extracellular matrix. Their functions are closely related to

Ceruloplasmin induces polymorphonuclear leukocyte priming in localized aggressive periodontitis.

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BACKGROUND Polymorphonuclear leukocytes (PMNs) from subjects with localized aggressive periodontitis (LAgP) present multiple functional abnormalities associated with a phenotypically primed PMN phenotype. Local inflammation is characterized by hypoxia, which leads to increased production of

Evaluation of serum ceruloplasmin in aggressive and chronic periodontitis patients.

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BACKGROUND Pro-inflammatory markers are seen to increase in inflammatory diseases like periodontitis. Detecting an increase in these markers is one of the diagnostic modality. One such marker, which can be detected, is the ceruloplasmin. Ceruloplasmin induces hypoxia and generates oxygen radicals at

Gingival crevicular fluid and salivary HIF-1α, VEGF, and TNF-α levels in periodontal health and disease.

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Hypoxia-inducible factor-1 alpha (HIF-1α) is expressed as an adaptive response to hypoxia, mediates angiogenesis through the expression of vascular endothelial growth factor (VEGF) and can be induced by tumor necrosis factor-alpha (TNF-α). This study aimed to investigate the gingival

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