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2014
DOI: 10.15406/jhvrv.2014.01.00007
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Chronic Periodontitis and Herpes Viruses

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Cited by 2 publications
(2 citation statements)
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“…Plaque accumulation is considered the primary initiating agent in the etiology of gingivitis and chronic periodontitis� Attachment and bone loss are associated with an increase in the proportion of Gram-negative organisms in the subgingival biofilm, with specific increase in organisms such as P. gingivalis, Tannerella forsythia, and Treponema denticola -otherwise known as the "red complex�" [9] A�a has been considered the primary pathogen for AgP, especially in its localized form� Six serotypes of A�a (a, b, c, d, e, and f) are described� Filifactor alocis is Gram-positive anaerobic rod which is elevated in AgP patients� Treponema lecithinolyticum and Treponema socranskii are elevated in GAP along with P�g� sulfate-reducing bacteria and desulfomicrobium orale Yamabe suggested Archaea a methanogenic organism, especially methanobrevibacter oralis as putative periodontal pathogen for AgP� [10] Virus Plaque-induced gingivitis has increased inflammatory content and virus exists in latent state, which gets activated in conditions such as immunosuppression, infection, stress level, and hormonal effect leads to induction of periodontopathogenic property further causing periodontal destruction� [11] Herpes virus-infected sites show more break down and the presence of virus enhances the bacterial adherence which results in increased bacterial load which further increase and alter the inflammatory mediators� [12] Herpes was less associated with aggressive when compared to chronic� [13]…”
Section: Bacteriamentioning
confidence: 99%
“…Plaque accumulation is considered the primary initiating agent in the etiology of gingivitis and chronic periodontitis� Attachment and bone loss are associated with an increase in the proportion of Gram-negative organisms in the subgingival biofilm, with specific increase in organisms such as P. gingivalis, Tannerella forsythia, and Treponema denticola -otherwise known as the "red complex�" [9] A�a has been considered the primary pathogen for AgP, especially in its localized form� Six serotypes of A�a (a, b, c, d, e, and f) are described� Filifactor alocis is Gram-positive anaerobic rod which is elevated in AgP patients� Treponema lecithinolyticum and Treponema socranskii are elevated in GAP along with P�g� sulfate-reducing bacteria and desulfomicrobium orale Yamabe suggested Archaea a methanogenic organism, especially methanobrevibacter oralis as putative periodontal pathogen for AgP� [10] Virus Plaque-induced gingivitis has increased inflammatory content and virus exists in latent state, which gets activated in conditions such as immunosuppression, infection, stress level, and hormonal effect leads to induction of periodontopathogenic property further causing periodontal destruction� [11] Herpes virus-infected sites show more break down and the presence of virus enhances the bacterial adherence which results in increased bacterial load which further increase and alter the inflammatory mediators� [12] Herpes was less associated with aggressive when compared to chronic� [13]…”
Section: Bacteriamentioning
confidence: 99%
“…Loss of alveolar bone and attachment loss are the peculiar features of periodontal inflammation [ 2 ]. There is a larger inflammatory content and a latent virus in plaque-induced gingivitis, both of which become active in response to factors such as immunosuppression, infection, stress, and hormonal impact, ultimately inducing the periodontopathogenic characteristic and resulting in periodontal damage [ 3 ]. Sites infected with the herpes virus are more likely to break down, and the presence of the virus improves bacterial adhesion, leading to an increase in bacterial load that, in turn, increases and modifies inflammatory mediators [ 4 ].…”
Section: Introductionmentioning
confidence: 99%