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Human Cytomegalovirus and Epstein-Barr Virus in Etiopathogenesis of Apical Periodontitis: A Systematic Review

期刊

JOURNAL OF ENDODONTICS
卷 40, 期 1, 页码 6-15

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.joen.2013.10.001

关键词

Apical periodontitis; Epstein-Barr virus; human cytomegalovirus; review

资金

  1. Ministry of Education, Science and Technological Development of the Republic of Serbia [175075]

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Introduction: During the last decade, a hypothesis has been established that human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) may be implicated in the pathogenesis of apical periodontitis. The aim of this review was to analyze the available evidence that indicates that HCMV and EBV can actually contribute to the pathogenesis of periapical lesions and to answer the following focused question: is there a relationship between HCMV and EBV DNA and/or RNA detection and the clinical features of human periapical lesions? Methods: The literature search covered MEDLINE, Science Citation Index Expanded (SCIexpanded), Scopus, and The Cochrane Library database. Quantitative statistical analysis was performed on the pooled data of HCMV and EBV messenger RNA transcripts in tissues of symptomatic and asymptomatic pedapical lesions. Results: The electronic database search yielded 48 hits from PubMed, 197 hits from Scopus, 40 hits from Web of Science, and 1 from the Cochrane Library. Seventeen cross-sectional studies have been included in the final review. The pooled results from quantitative systematic method analysis showed no statistically significant relationship between the presence of HCMV and EBV messenger RNA transcripts (P = .083 and P = .306, respectively) and the clinical features of apical periodontitis. Conclusions: The findings of HCMV and EBV transcripts in apical periodontitis were controversial among the included studies. Herpesviruses were common in symptomatic and large-size periapical lesions, but such results failed to reach statistical significance. Further studies, including those based on an experimental animal model, should provide more data on herpesviruses as a factor in the pathogenesis of periapical inflammation.

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