The Expression Of Human Cytomegalovirus And Estein-barr Virus In Periapical Lesions Of Deciduous Teeth

Previous researches showed that a positive relationship exists between periapical human cytomegalovirus and Esptein-Barr virus infections and symptomatic and large-size periapical lesions in adult patients. Slots et al. hypothesized that human cytomegalovirus and Epstein-Barr virus infections may cause periapical pathosis by inducing cytokine and chemokine release from inflammatory or connective tissue cells, or by impairing local host defenses, resulting in heightened virulence of resident bacterial pathogens. However, there is few investigation on the relationship between periapical periodontitis in deciduous tooth and infections by human cytomegalovirus and Esptein-Barr virus.The periapical pathosis of deciduous teeth is inflammation disease of the cementum, periodontal ligament and alveolar bone in the periapical or root furcation region. Since periapical pathosis of deciduous teeth is extremely easy to cause corresponding maxillofacial cellulitis for its loose tissue and rich blood circulation, it is especially important to give proper medication, which also needs to understand the concrete pathogenesis of periapical pathosis comprehensively. In the past, people thought that endodontic disease and periapical pathosis are mainly caused by the bacterial infection, but the research in recent years has already realized that HCMV, EBV and other herpesvirus may partly be responsible for large periapical lesions. Herpesvirus may cause disease as a direct result of viral infection and replication, or as a result of virally induced impairment of the host defense. Herpesvirus-mediated endodontic disease may take place via several mechanisms, operating alone or in combination, and may involve both cellular and humoral host responses. Herpesvirus family members are all found in periapical lesions in adults. The research also indicates HCMV, EBV and other herpesvirus have been implicated in the pathogenesis of aggressive periodontitis and in acute inflammation of gingiva and oral mucosa. Similarly to severe periodontitis, some scholars hypothesize that some aggressive types of periapical pathosis develop as a result of a series of interactions between bacteria, herpesvirues and host immune reactions. Initially, pulpal infection by oral bacteria causes herpesvirus-infected inflammatory celles to enter the root canal and the periapical region.Subsequent herpesvirus reactivation may then aggravate the inflammatory response and further diminish the resistance of periapical tissue, leading to overgrowth of pathogenic bacteria and release of pro-inflammatory cytokines and chemokines from macrophages and orther host cells to stimulate the bone resorption. And other research also confirmed the existence of HCMV in odontogenic cysts. But many researches also think that herpesvirus are present, but not required for development of periapical lesions. This study intends to investigate the expressive difference of HCMV, EBV in periapical lesion and normal dental pulp of deciduous teeth, to discuss herpesvirus'role in the pathogenesis of periapical lesion of deciduous teeth.Objective:1. To examine the gene fragment of HCMV, EBV in chronic periapical lesion through PCR assay.2. To discuss the role plaid by human cytomegalovirus and Esptein-Barr virus in the progresses of periapical infection of deciduous teeth and the possible antiviral treatment for the disease.Methods:1. To collect tissue in seriously infective periapical granulation of deciduous teeth and normal dental pulp respectively.2. To detect the expression of HCMV, EBV mRNA by PCR method.Results:1. In serious chronic periapical granulation of deciduous teeth,the detection rate of HCMV is 64.3%, and the detection rate of EBV is 57.1%.2. In normal dental pulp of deciduous teeth, the detection rate of HCMV is 7.1%, and the detection rate of EBV is 14.3%.3. In the two groups, the distinction of the detection rates of HCMV is significant (p=0.004<0.05); And that of EBV is also significant (p=0.046<0.05)Conclusion:1. A positive relationship exists between HCMV and EBV infections and large-size periapical lesions in deciduoud teeth.2. HCMV and EBV infections may cause periapical pathosis in deciduous teeth by causing direct cytopathic effects and by impairing local host defenses, or by eliciting proflammatory cytokine and chemokine release from inflammatory cells and by inducing host immune responses.3. The periapical pathosis of deciduous teeth caused by pulp infection is the multiple factor infection mainly because of bacterial infection and partly viral infection and host immune responses.