Abstract
The microbial profile of aggressive periodontitis patients is considered to be complex with variations among populations in different geographical areas. The aim of this study was to assess the presences of 4 putative periodontopathic bacteria (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola) and 2 periodontal herpes viruses (Epstein–Barr virus type 1 [EBV‐1] and human cytomegalovirus [HMCV]) in subgingival plaque of Sudanese subjects with aggressive periodontitis and healthy controls. The study group consisted of 34 subjects, 17 aggressive periodontitis patients and 17 periodontally healthy controls (14–19 years of age). Pooled subgingival plaque samples were collected and analyzed for detection of bacteria and viruses using loop‐mediated isothermal amplification. Prevalence of subgingival A. actinomycetemcomitans, HCMV, and P. gingivalis were significantly higher among aggressive periodontitis patients than periodontally healthy controls. Coinfection with A. actinomycetemcomitans, HCMV, and/or EBV‐1 was restricted to the cases. Increased risk of aggressive periodontitis was the highest when A. actinomycetemcomitans was detected together with EBV‐1 (OD 49.0, 95% CI [2.5, 948.7], p = .01) and HCMV (OD 39.1, 95% CI [2.0, 754.6], p = .02). In Sudanese patients, A. actinomycetemcomitans and HCMV were the most associated test pathogens with aggressive periodontitis.
Highlights
There is ample evidence that the etiopathogenesis of aggressive periodontitis is multifactorial, involving genetic predisposition (de Carvalho, Tinoco, Govil, Marazita, & Vieira, 2009) and complex interactions between specific oral microbiota and the host tissues (Socransky & Haffajee, 2005)
A. actinomycetemcomitans, P. gingivalis, T. forsythia, and T. denticola were detected in 70–82% and 5–82% of the subgingival plague of cases and controls, respectively
The odds ratio of having aggressive periodontitis was substantially higher when A. actinomycetemcomitans was detected together with Epstein–Barr virus type 1 (EBV‐1) or human cytomegalovirus (HCMV)
Summary
There is ample evidence that the etiopathogenesis of aggressive periodontitis is multifactorial, involving genetic predisposition (de Carvalho, Tinoco, Govil, Marazita, & Vieira, 2009) and complex interactions between specific oral microbiota and the host tissues (Socransky & Haffajee, 2005). In the case of aggressive periodontitis, the oral biofilms constitute complex and dynamic bacterial mixed‐species communities, and this hampers the task of accurately identifying the causative periodontopathic microorganisms (Haffajee & Socransky, 2006). Gram‐negative anaerobic bacteria residing in the dental pocket have extensively been incriminated as the primary etiological factors for initiation and progression of aggressive periodontitis (Armitage, 2010).
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