The epidemiology of childhood cytomegalovirus infections in a large city of southern Italy

Leogrande, G

doi:10.1007/bf02592292

Cited by 5 publications

(3 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Young individuals experience frequent herpesvirus infection. Primary HCMV infection, which is thought to commence at about 4 yr of age, affects 89.1% of 4±7-yr-old children (43). Primary EBV infection also occurs early in life, frequently at or shortly after 4 yr of age (44).…”

Section: Discussionmentioning

confidence: 99%

Herpesviruses in localized juvenile periodontitis

Ting

Contreras

Slots

2000

J of Periodontal Research

121

172

View full text Add to dashboard Cite

Herpesvirus genomic sequences can be detected in gingival crevicular fluid of adult periodontitis lesions. Herpesviruses are immunosuppressive and may facilitate establishment of subgingival pathogens. Electron microscopic studies have identified nuclear and cytoplasmic virus-like inclusions in gingival inflammatory cells from localized juvenile periodontitis (LJP). The present study aimed to determine if herpesviruses occur in LJP lesions and if human cytomegalovirus (HCMV) activation is associated with elevated levels of subgingival Actinobacillus actinomycetemcomitans, the putative bacterial pathogen of LJP. Eleven systemically healthy patients exhibiting LJP (10-23 yr) were studied. In each patient, subgingival samples were pooled from 3 periodontitis lesions around first molar and incisor teeth (5-11 mm periodontal pocket depth) and from 3 gingivitis/healthy sites around canines (2-3 mm periodontal pocket depth). Polymerase chain reaction (PCR) was used to detect herpesvirus DNA and HCMV cDNA of major capsid protein transcripts, indicative of viral activation. Selective culture and 16S rRNA PCR were used to identify A. actinomycetemcomitans. Of 11 deep periodontal samples, 8 showed HCMV, 7 showed Epstein-Barr virus type 1 (EBV-1), 1 showed EBV type 2, 6 showed herpes simplex virus (HSV) and 8 showed viral co-infection. Of 11 shallow periodontal samples, 2 showed HCMV, 2 showed EBV-1, 1 showed HSV and 2 showed viral co-infection. The difference in occurrence of HCMV and viral co-infection between deep and shallow periodontal sites was statistically significant (p =0.031). HCMV activation was detected in deep pockets of all 5 virally positive patients with early LJP (aged 10-14 years) but only in 1 of 3 virally positive LJP patients older than 14 years, and not in any shallow pocket tested. HCMV activation appeared related to absence of radiographic crestal alveolar lamina dura, a possible indication of periodontal disease progression. A. actinomycetemcomitans tended to be more prevalent in samples showing active than latent HCMV infection. The present findings are consistent with the notion that periodontal herpesvirus infection and possibly HCMV activation constitute important features of the etiopathogenesis of LJP.

show abstract

Section: Discussionmentioning

confidence: 99%

Herpesviruses in localized juvenile periodontitis

Ting

Contreras

Slots

2000

J of Periodontal Research

121

172

View full text Add to dashboard Cite

show abstract

“…20 Primary cytomegalovirus infection may occur at about the same 4 years of age and affect about 90% of 4-7-year-old children. 30 Primary Epstein-Barr infection also occurs early in life, frequently at or shortly after 4 years of age. 31 An active cytomegalovirus infection can change the morphology of developing murine 32 and human 33 teeth, and viruses infecting odontogenic cells of developing hamster teeth can disrupt normal cell differentiation.…”

Section: Prop Osed Infec Tious -Dise a Se Model For J U Venile Period...mentioning

confidence: 99%

“…To account for the site‐specificity of localized juvenile periodontitis, it is hypothesized that a periodontal cytomegalovirus infection at the time of root formation of permanent first molars and incisors at 3–5 years of age results in defective root cementum 20 . Primary cytomegalovirus infection may occur at about the same 4 years of age and affect about 90% of 4–7‐year‐old children 30 . Primary Epstein–Barr infection also occurs early in life, frequently at or shortly after 4 years of age 31 .…”

Section: Proposed Infectious‐disease Model For Juvenile Periodontitismentioning

confidence: 99%

Herpesvirus‐Bacteria pathogenic interaction in juvenile (aggressive) periodontitis. A novel etiologic concept of the disease

Slots

Rams

2023

Periodontology 2000

View full text Add to dashboard Cite

Localized juvenile (aggressive) periodontitis starts at puberty in otherwise healthy individuals and involves the proximal surfaces of permanent incisors and first molars. The disease destroys a sizeable amount of periodontal bone within a few months despite minimal dental plaque and gingival tissue inflammation. Cytomegalovirus and Epstein–Barr virus, as well as the two main periodontopathic bacteria Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, are linked to juvenile periodontitis. Juvenile periodontitis‐affected teeth show cementum hypoplasia. We hypothesize that an active herpesvirus infection, at the time of root formation, hampers cementum formation and, at puberty, herpesvirus reactivation triggers an upgrowth of bacterial pathogens which produce rapid periodontal destruction on teeth with a defective periodontium. A pathogenic interaction between active herpesviruses and bacterial pathogens can potentially explain the etiology and incisor‐first molar destructive pattern of juvenile periodontitis. Effective treatment of juvenile periodontitis may target the herpesvirus‐bacteria co‐infection.

show abstract