Evidence of bacterial etiology: a historical perspective

Socransky, S. S.; Haffajee, A. D.

doi:10.1111/j.1600-0757.1994.tb00016.x

Cited by 308 publications

(258 citation statements)

References 185 publications

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“…18,19 Once bacteria gain access to these sites, their byproducts incite periods of exacerbation and remission of inflammation, leading to increased production of proinflammatory cytokines and matrix metalloproteinases, often by augmenting mechanisms linked to evasion of host defenses. 20,21 A consequence of this heavy burden of cytokines and tissue-destructive mediators is the development of hyperpermeability and loss of epithelial integrity, which creates an opportunity for invading bacteria, and their byproducts, to gain access to the systemic circulation.…”

Section: Discussionmentioning

confidence: 99%

Oral Infection With a Periodontal Pathogen Accelerates Early Atherosclerosis in Apolipoprotein E–Null Mice

Lalla

Lamster

Hofmann

et al. 2003

ATVB

359

334

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Objective-Because recent epidemiologic evidence suggests that periodontal infections may increase the risk of atherosclerosis and related events in humans, we assessed the impact of oral inoculation with the periodontal pathogen Porphyromonas gingivalis on atherogenesis in hypercholesterolemic apolipoprotein E-null mice. Methods and Results-In the absence of alterations in distinct risk factors, P gingivalis infection exacerbated the early stages of atherogenesis in this model. Infected animals displayed evidence of local periodontal infection, as the severity of alveolar bone loss, the hallmark of periodontitis, was increased.

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Section: Discussionmentioning

confidence: 99%

Oral Infection With a Periodontal Pathogen Accelerates Early Atherosclerosis in Apolipoprotein E–Null Mice

Lalla

Lamster

Hofmann

et al. 2003

ATVB

359

334

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“…During the development and progression of periodontitis, there is a well‐documented shift from a symbiotic microbiota to a dysbiotic community, from predominantly facultative Gram‐positive species to Gram‐negative anaerobes (Socransky & Haffajee, 1994). As these periodontal pathogens aggregate subgingivally, they inhibit the growth of other commensal species in the biofilm and work synergistically in pathogenesis (Thurnheer et al, 2014).…”

mentioning

confidence: 99%

Multiplex real‐time PCR detection and relative quantification of periodontal pathogens

Coffey

Choudhry

Shlossman

et al. 2016

Clinical & Exp Dental Res

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Periodontitis is a chronic inflammatory disease, which is strongly associated with certain pathogenic bacteria. The aim of this study was to develop a real‐time multiplex polymerase chain reaction (PCR) assay to detect and quantify bacterial species associated with periodontitis. We targeted detection and relative quantification of the following five bacterial species relevant to periodontal diseases: Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. The conserved regions of the genome of these species were targeted with oligos and TaqMan probes in real‐time PCR assays. The species‐specific TaqMan oligos and TaqMan probes showed no cross‐amplification, and there was no loss of amplification yield in multiplex real‐time PCR assays. All five bacterial targets were amplified analogous to the template concentrations used in these assays. This multiplex real‐time PCR strategy could potentially be used to detect the bacterial species in periodontal pockets of patients with periodontal diseases. This assay may also serve as a quick tool for profiling and quantifying bacteria relevant to periodontal diseases and likely be a valuable tool for clinical translational research.

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“…Periodontopathogens also produce a variety of virulence factors such as proteases (13), lipopolysaccharide (LPS) (14), and fimbria (3,15), as well as SCFAs. Even if monocytes/macrophages have varying butyric acidsusceptibility to other immune cells, it is still unclear whether apoptosis is induced in monocytes/macrophages as well as lymphocytes by pathogens.…”

Section: Introductionmentioning

confidence: 99%

Butyric acid induces apoptosis in both human monocytes and lymphocytes equivalently

Abe

2012

J Oral Sci

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Evidence of bacterial etiology: a historical perspective

Cited by 308 publications

References 185 publications

Oral Infection With a Periodontal Pathogen Accelerates Early Atherosclerosis in Apolipoprotein E–Null Mice

Oral Infection With a Periodontal Pathogen Accelerates Early Atherosclerosis in Apolipoprotein E–Null Mice

Multiplex real‐time PCR detection and relative quantification of periodontal pathogens

Butyric acid induces apoptosis in both human monocytes and lymphocytes equivalently

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