Relationship between human cytomegalovirus transcription and symptomatic apical periodontitis in Iran.

BACKGROUND/AIMS: Apical periodontitis of endodontic origin may develop as a result of cooperative interactions among herpesviruses, specific pathogenic bacteria and tissue-destructive inflammatory mediators. This study sought to identify the presence of Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) transcripts in symptomatic and asymptomatic periapical lesions of individuals living in Iran. MATERIAL AND METHODS: Fifty endodontic patients (28 with symptomatic periapical lesions and 22 with asymptomatic periapical lesions) were included in the study. In each study subject, a microbiological periapical sample was collected using a curette in conjunction with periapical surgery. A reverse transcription-polymerase chain reaction assay was used to identify transcripts of EBV and HCMV. RESULTS: Human cytomegalovirus transcript was detected in 15 of the 28 (53.6%) symptomatic and in six of the 22 (27.3%) asymptomatic periapical study lesions (significant difference between symptomatic and asymptomatic lesions; P = 0.03, chi-square test). Epstein-Barr virus transcript was identified in one symptomatic and in two asymptomatic periapical lesions. CONCLUSION: This study establishes that HCMV transcription is common in apical periodontitis and is most frequent in symptomatic lesions. The high frequency of active herpesvirus infections in severe apical periodontitis changes the pathogenic paradigm of the disease and may also have preventive and therapeutic implications.

Natural killer cells and alterations in collagen density: signs of periradicular herpesvirus infection?

This study evaluated the presence and density of natural killer (NK) cells as well as collagen density in chronic apical periodontitis lesions and tried to find any correlations with concomitant herpesvirus infection or histopathological status of the lesion. Surgical specimens of chronic apical periodontitis lesions were surveyed for the presence and density of NK cells by immunohistochemical analysis. Collagen density in these lesions was quantified by means of histochemistry. All specimens were positive for the presence of CD57-positive cells. Topographically, CD57-positive cells were found singly or forming clusters in the granulomatous tissue, as well as subjacent and within the cystic epithelium. No significant differences in the density of CD57-positive cells were found between nonepithelialized and epithelialized lesions or between herpesvirus-positive and herpesvirus-negative lesions. Significant differences were found in volumetric density of collagen when comparing nonepithelialized and epithelialized lesions, with the latter demonstrating higher values. When no distinction of lesion type was made, there was no significant difference in collagen density between herpesvirus-positive and herpesvirus-negative lesions. When comparing the collagen density in herpesvirus-positive and herpesvirus-negative specimens from the same lesion type, a significant difference was found in nonepithelialized lesions, with herpesvirus-positive lesions showing lower values. The presence of CD57-positive cells in all chronic apical periodontitis specimens may indicate that activated NK cells play a role in the pathogenesis of this disease, possibly by participating in innate immunity events involved in the control of virus infection. Collagen density may vary in function of the type of lesion and presence of herpesvirus infection.

Cytomegalovirus and Epstein-Barr virus DNA transcription in endodontic symptomatic lesions.

OBJECTIVES: Productive Herpesviridae infections are implicated in the etio-pathogenesis of aggressive periodontitis. However, virtually nothing is known about a possible role of herpesviruses in pulpal and periapical pathosis. This study employed a cDNA analysis to determine transcription of human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV) in 14 recalcitrant periapical lesions and in 2 periapical healthy control sites. METHODS: Periapical samples were collected in conjunction with periapical surgery and kept frozen until virologic examination. RNA was isolated from periapical tissue by using a guanidinium isothiocyanate-acid phenol procedure (TRIZOL LS Reagent, GIBCO BRL, Rockville, MD). cDNAs were amplified by means of oligonucleotides targeting highly conserved regions of the test viruses and the RT-PCR-100 amplification kit (Sigma-Aldrich, St Louis, MO). Standardization of PCR primer sensitivity and validation was carried out according to established methods. Amplification products were identified by agarose gel electrophoresis. RESULTS: HCMV transcript was detected in 12 of 13 symptomatic and in 1 asymptomatic periapical lesion. EBV transcript was demonstrated in 8 of the 13 symptomatic lesions but not in the asymptomatic periapical lesion. HCMV and EBV dual transcription occurred at higher frequency in periapical lesions showing radiographic bone destruction of 5 mm x 7 mm or larger than in smaller size lesions (P = 0.03; Chi-squared test). No HCMV or EBV transcription was identified in the 2 healthy control sites. HSV transcript was not detected in any study site. CONCLUSION: The present data suggest that HCMV or EBV infections participate in the pathogenesis of periapical symptomatic lesions. Herpesviruses may produce periapical pathosis as a direct result of viral infection and replication, or as a consequence of virally induced impairment of the host defense and subsequent increased virulence of resident bacterial pathogens.