Sonic extracts from a bacterium related to periapical disease activate gelatinase A and inactivate tissue inhibitor of metalloproteinases TIMP‐1 and TIMP‐2

Sato, Yuzo; Kishi, Jun-Ichi; Suzuki, Kensuke; Nakamura, Hiroshi; Hayakawa, Taro

doi:10.1111/j.1365-2591.2009.01640.x

Cited by 14 publications

(19 citation statements)

References 36 publications

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“…Plaque rupture, leading to leakage of the prothrombotic plaque core in the circulation and thrombus formation, can be due to the bacteria-dependent release of matrix metalloproteinases with concomitant suppression of the matrix metalloproteinase antagonist, tissue inhibitor of metalloproteinases [84,85]. …”

Section: Proatherogenic Sequelae Of Bacterial Presence In Vascular Cellsmentioning

confidence: 99%

Bacterial Invasion of Vascular Cell Types: Vascular Infectology and Atherogenesis

Kozarov

2011

Future Cardiol.

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To portray the chronic inflammation in atherosclerosis, leukocytic cell types involved in the immune response to invading pathogens are often the focus. However, atherogenesis is a complex pathological deterioration of the arterial walls, where vascular cell types are participants with regards to deterioration and disease. Since other recent reviews have detailed the role of both the innate and adaptive immune response in atherosclerosis, herein we will summarize the latest developments regarding the association of bacteria with vascular cell types: infections as a risk factor for atherosclerosis; bacterial invasion of vascular cell types; the atherogenic sequelae of bacterial presence such as endothelial activation and blood clotting; and the identification of the species that are able to colonize this niche. The evidence of a polybacterial infectious component of the atheromatous lesions opens the doors for exploration of the new field of vascular infectology and for the study of atherosclerosis microbiome.

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Section: Proatherogenic Sequelae Of Bacterial Presence In Vascular Cellsmentioning

confidence: 99%

Bacterial Invasion of Vascular Cell Types: Vascular Infectology and Atherogenesis

Kozarov

2011

Future Cardiol.

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“…MMPs play an important role during periapical pathology development (11– 13), and it has been suggested that the modality of root canal treatment could interfere with MMPs expression (14). Moreover, elevated MMP levels have also been reported to correlate with non-healing (15, 16).…”

Section: Introductionmentioning

confidence: 99%

Genetic Susceptibility to Periapical Disease: Conditional Contribution of MMP2 and MMP3 Genes to the Development of Periapical Lesions and Healing Response

Menezes-Silva

Khaliq

Deeley

et al. 2012

Journal of Endodontics

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“…Without prior demineralization, it is unlikely that bacterial enzymes can affect dentinal collagen protected by minerals: even in periodontal diseases, host‐derived MMPs instead of bacterial proteases are considered key players in the extracellular matrix degradation and bacterial proteases have been shown not to be directly involved in root dentin destruction. However, they might be able to activate host proteolytic enzymes , which in turn may under certain conditions degrade the organic matrix of dentin. In 2009, using a gelatin zymography assay, Itoh and co‐workers showed that whole‐cell extracts from Prevotella nigrescens , an anaerobe Gram‐negative species regularly found in the microflora of infected root canals , could noticeably activate pro‐MMP‐2 and pro‐MMP‐9, both gelatinases that are found in coronal and root dentin , and could play an important role in the degradation of dentin collagen fibrils .…”

Section: Dentin Management: Microbial and Biofilm Factors Altering Thmentioning

confidence: 99%

Chemical, microbial, and host‐related factors: effects on the integrity of dentin and the dentin–biomaterial interface

Carrilho¹,

Piveta²,

Tjäderhane³

2015

Endodontic Topics

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Dentin is the largest substrate available whenever restorative procedures are implemented on the exposed crown or root of teeth. In endodontics, restorative/obturating procedures are practically restricted to dentin. It is well recognized that the incidence of fracture in endodontically treated teeth is intrinsically related to the amount of remaining dentin. Ideally, it is expected that a gap‐free, solid interface can be formed between the restorative/obturating materials and root dentin, providing an impervious seal and, simultaneously, fracture resistance to root‐filled teeth. Over the past years, a number of new obturating biomaterials have been launched in the market, bringing to endodontists the expectation of achieving consistent sealing/reinforcing of the root canal system. However, the successful sealing of root dentin remains one of the greatest challenges in restorative dentistry. This article will focus on reviewing some factors that affect the formation and integrity of dentin–biomaterial interfaces from the perspective of the dentin substrate. Because other articles in preceding issues of Endodontic Topics have already covered dentin structure and composition, the objective here is not to review these aspects. Specific attention is given, however, to depicting how chemical treatments affect existing root filling/restorative mechanisms and how some microbial and host‐related aspects can compromise the interaction of dentin with new biomaterials.

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Sonic extracts from a bacterium related to periapical disease activate gelatinase A and inactivate tissue inhibitor of metalloproteinases TIMP‐1 and TIMP‐2

Abstract: These findings suggest that P. gingivalis SBE may cause connective tissue to be destroyed, contributing to the process of periapical disease, by activating pro-MMP-2 as well as by inactivating TIMP-1 and TIMP-2.

Cited by 14 publications

References 36 publications

Bacterial Invasion of Vascular Cell Types: Vascular Infectology and Atherogenesis

Bacterial Invasion of Vascular Cell Types: Vascular Infectology and Atherogenesis

Genetic Susceptibility to Periapical Disease: Conditional Contribution of MMP2 and MMP3 Genes to the Development of Periapical Lesions and Healing Response

Chemical, microbial, and host‐related factors: effects on the integrity of dentin and the dentin–biomaterial interface

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