2016
DOI: 10.1080/21505594.2016.1235128
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Virulence factors associated withAggregatibacter actinomycetemcomitansand their role in promoting periodontal diseases

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Cited by 12 publications
(8 citation statements)
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“…Aqueous-acetone PSRE was efficient in decreasing growth of antibiotic-resistant S. aureus strains [39]. The present study for the first time demonstrated the growth-suppressing efficiency of PSRE and PACN on Aggregatibacter actinomycetemcomitans , one of the most important gram-negative anaerobic periodontal pathogens [40]. Similarly as in the previously demonstrated case of P. gingivalis [19], PACN demonstrated significantly higher toxicity on A. actinomycetemcomitans , compared to the effect of PSRE.…”
Section: Discussionsupporting
confidence: 76%
“…Aqueous-acetone PSRE was efficient in decreasing growth of antibiotic-resistant S. aureus strains [39]. The present study for the first time demonstrated the growth-suppressing efficiency of PSRE and PACN on Aggregatibacter actinomycetemcomitans , one of the most important gram-negative anaerobic periodontal pathogens [40]. Similarly as in the previously demonstrated case of P. gingivalis [19], PACN demonstrated significantly higher toxicity on A. actinomycetemcomitans , compared to the effect of PSRE.…”
Section: Discussionsupporting
confidence: 76%
“…The capnophilic A. actinomycetemcomitans is most sensitive to amoxicillin but resistant to metronidazole, while the other Gram-negative but strictly anaerobe bacteria (e.g., P. gingivalis ) are most highly sensitive to metronidazole [ 19 , 20 , 21 ]. Contrastingly, there is not always a high susceptibility of bacteria in the subgingival biofilm to amoxicillin [ 22 ].…”
Section: Introductionmentioning
confidence: 99%
“…Along with this, inhibition of local nonspecific protective factors is observed. Pro-inflammatory mediators, including cytokines, chemokines and metalloproteinases are known to increase dramatically in periodontal tissues and GCF in periodontitis [ 45 , 46 ]. Cytokines are produced by resident cells, such as epithelial cells and fibroblasts, and by phagocytes (neutrophils and macrophages) in the acute and early chronic phases of inflammation, and by immune cells (lymphocytes) in established and advanced lesions [ 47 ].…”
Section: Discussionmentioning
confidence: 99%