Stimulation of osteoclastic bone resorption by hydrogen peroxide

Bax, Bridget E.; Alam, A. S. M. Towhidul; Banerji, Bashab; Bax, Christopher M.R.; Bevis, Peter J. R.; Stevens, CR; Moonga, Baljit S.; Blake, David R.; Zaidi, Mone

doi:10.1016/s0006-291x(05)80311-0

Cited by 190 publications

(111 citation statements)

References 18 publications

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“…RANKL also stimulates ROS generation, which has been suggested to be crucial for the activation of the RANK-signaling cascades leading to osteoclast differentiation (12). This is supported by the observations that addition of exogenous hydrogen peroxide stimulates osteoclastic bone resorption and cell motility (26). Alternatively, antioxidants can block the RANKL-dependent signaling (27,28).…”

Section: Discussionmentioning

confidence: 88%

NADPH oxidase-derived reactive oxygen species are essential for differentiation of a mouse macrophage cell line (RAW264.7) into osteoclasts

et al. 2009

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Section: Discussionmentioning

confidence: 88%

NADPH oxidase-derived reactive oxygen species are essential for differentiation of a mouse macrophage cell line (RAW264.7) into osteoclasts

et al. 2009

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“…O 2 -is released into the phagosomal space and also into the extracellular environment [30]. It has been suggested that reactive oxygens such as O 2 -and H 2 O 2 play a role in the activation of osteoclasts, in addition to their bactericidal function [32]. It has also been demonstrated that reactive oxygen molecules are capable of activating latent PMN collagenase in gingival crevices [33,34] and damaging connective tissues as part of the pathology of periodontal disease.…”

Section: Discussionmentioning

confidence: 99%

Surface protease of Treponema denticola hydrolyzes C3 and influences function of polymorphonuclear leukocytes

Yamazaki

Miyamoto

Yamada

et al. 2006

Microbes and Infection

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Treponema denticola is a dominant microorganism in human periodontal lesions. One of the major virulence factors of this microorganism is its chymotrypsinlike surface protease, dentilisin. The purpose of this study was to evaluate the effect of dentilisin on human polymorphonuclear leukocytes (PMNs). We used chemiluminescence to assess production of O 2 -by PMNs against T. denticola ATCC 35405 and dentilisin deficient mutant K1. T. denticola ATCC 35405 induced production of O 2 -, whereas dentilisin deficient K1 did not. We found that chymostatin, a protease inhibitor, strongly reduced the ability of T. denticola ATCC 35405 to induce production of, O 2 -, whereas K1 was relatively unaffected. We also usedImmunoblot and ELISA to evaluate the activation of complement by this microorganism in relation to PMNs. T. denticola ATCC 35405 hydrolyzed the α-chain of C3, producing iC3b.Furthermore, strain ATCC 35405 induced a larger release of MMP-9 from PMNs than strain K1. Dentilisin, activated PMNs via complement pathways, and may play a role in establishing periodontal lesions.

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“…One such cell is the osteoclast, which has been shown to be activated by ROS (17,18). Several signals essential for osteoclasts are sensitive to activation by ROS, including NF-κB, c-Jun amino-terminal kinase (JNK), PI3K, and p38 MAP kinase (see refs.…”

Section: Introductionmentioning

confidence: 99%