[The prevalance of herpesviruses in human apical periodontitis samples]. / Herpeszvírusok elofordulása humán periodontitis apicalis mintákban.

Apical periodontitis is primarily initiated by the endodonto-patogen bacteria spreading from the inflamed or necrotic pulp tissues to the periapical area. Nevertheless, findings within the past years have established a pathogenic role of human herpesviruses such as Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) in periapical inflammations. The authors analysed the prevalence, activity and disease association of EBV, HCMV and human herpesvirus 6 (HHV-6) in 40 apical periodontitis samples and 40 healthy pulp controls. Based on the viral DNA results, EBV (29/40) was the most frequent herpesvirus in apical periodontitis, followed by HHV-6 (8/40) and HCMV (4/40). According to the mRNA results approximately two-third of the EBV DNA-positive lesions had active EBV infections. However, the HHV-6 and the HCMV infections seemed to be of latent state. Our findings suggest that EBV and HHV-GB infections primarily occurred in large sized and symptomatic periapical lesions. The co-occurrence of large lesion size and active EBV infection was strongly associated (OR = 8.80) with the symptomatic manifestation of apical periodontitis.

Detection of presence or absence of herpes simplex virus, Epstein Barr virus and human cytomegalovirus in infected pulp using a polymerase chain reaction.

The development of methods to amplify nucleic acids has provided a way of identifying and quantifying infectious pathogens in infected pulp and periapical region. Recent studies have detected human herpes virus in periapical pathosis and periodontitis. The aim of this study is to detect the presence or absence of herpes simplex virus, human cytomegalovirus and Epstein Barr virus in an infected pulp. Ten pulp tissue samples from teeth with irreversible pulpitis and eight control samples were subjected to polymerase chain reaction(Perkin - Elmer Gene Amplification System) for detection of human herpesvirus. The results of this study did not reveal any human herpes virus in both the control and infected pulp tissue samples. According to this study, human herpes virus may not have an entry through the infected pulp to reach the periapical region and may not be a causative organism in the pulp.

Herpes zoster associated with tooth resorption and periapical lesions.

A 72-year-old woman presented with multiple periapical lesions and resorption of teeth in a single quadrant 17 years after an attack of herpes zoster (shingles) of the maxillary division of the trigeminal nerve. It is possible that cases of tooth resorption that were previously classified as idiopathic may have a viral aetiology and we suggest that these patients should be asked about a previous attack of shingles.

Multiple Apical Radiolucencies and External Cervical Resorption Associated with Varicella Zoster Virus: A Case Report.

Varicella zoster virus (VZV) is responsible for the primary infection chickenpox. After the initial infection, it remains latent but can reactivate, resulting in shingles (herpes zoster). Previous reports have implicated VZV in the pathogenesis of apical periodontitis, but the involvement of the virus has not been investigated fully. The present case describes a patient who suffered from a severe episode of shingles and subsequently developed periapical radiolucencies of all the teeth in the affected nerve distribution. Molecular and culture techniques showed the presence of VZV DNA in the root canal system in the absence of bacteria. This confirms that VZV can cause localized pulp necrosis and apical periodontitis. The lesions healed after endodontic treatment, implying chemomechanical debridement using sodium hypochlorite irrigation and a calcium hydroxide interim dressing may be effective against the virus.

Herpesviral-bacterial coinfection in periapical pathosis.

Two members of the herpesvirus family, human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV), seem to be important putative pathogens of human periodontitis and symptomatic periapical lesions, causing pathosis either by inducing immunosuppression with a subsequent risk of aggressive bacterial infections or by infecting of periodontal cells directly. This study aimed to relate periapical occurrence of HCMV, EBV, and herpes simplex virus active infections to clinical characteristics of periapical lesions and periapical bacterial flora. Microbial samples were collected from 34 periapical lesions in conjunction with periapical surgery. Part of the periapical specimen was frozen for virologic examination, and another part was transferred to anaerobic transport medium for bacteriologic examination. RNA was isolated by means of a guanidinium isothiocyanate-acid phenol procedure, and cDNA was produced using herpesvirus-specific primers and reverse-transcription polymerase chain reaction amplification. Bacteriologic examination was performed according to established anaerobic culture methods. Of the 34 periapical lesions studied, 20 showed both HCMV and EBV, seven showed only HCMV, one showed only EBV, and six showed neither HCMV nor EBV. Herpes simplex virus was detected in two lesions. Higher occurrence of herpesvirus was detected in large versus small periapical lesions (p < 0.001) and in symptomatic versus asymptomatic periapical lesions (p < 0.001). A total of 18 microbial groups and an average of 2.1 to 3.0 bacterial groups were isolated from various categories of periapical lesions. The important finding of this study was that most teeth with necrotic pulp and periapical lesions harbored herpesviruses in periapical granulomatous tissue. Herpesvirus species in cooperation with endodontopathic bacteria may play major roles in the etiopathogenesis of aggressive types of periapical pathosis in humans.

Is herpes simplex virus associated with pulp/periapical inflammation?

OBJECTIVES: This study focuses on the detection of herpes simplex virus (HSV) DNA in dental pulp and inflamed periapical tissue. STUDY DESIGN: Dental pulp tissue (vital and necrotic) and periapical tissue samples were collected under strictly sterile conditions and examined for the presence of HSV DNA. Saliva samples were also examined for the presence of the viral DNA. The polymerase chain reaction assay was used to detect viral DNA. Blood samples were collected, and the enzyme-linked immunosorbent assay (ELISA) for immunoglobulin G (IgG) and immunoglobulin M (IgM) antibodies against HSV was carried out. RESULTS: According to the ELISA test, 19 of the 23 blood samples were IgG-positive and IgM-negative to HSV, whereas 4 were IgG-negative and IgM-negative. HSV DNA was not detected in the tissue and the saliva samples tested. CONCLUSION: HSV is not present and therefore is probably not involved in the pathology of tooth neural tissue.