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ePaper created 2015-11-17, 15:11:47 | version 1.38.0
38 Volume 1 | Issue 1/2015 Journal of Oral Science & Rehabilitation Discussion Periimplantitis is one of the most controversial problems affecting the outcome of implant treatment. Different hypotheses have been proposed about its etiology and definition— even if the term “periimplantitis” appears to have been improperly used to describe any periimplantboneloss,irrespectiveofthecomplex- ityofthenumerousfactorsthatmaycontributeto lossofmarginalbonearoundimplants.11 Various authors have putforwardthe hypothe- sis that periimplantitis could be associated with EBV or HCMV. These viruses have been suggested to alter the local host immune re- sponse in combination with periodontopathic bacteria,withthe potentialto leadto periodon- tal and periimplant tissue destruction.7 Infact,itiswellknownthatthegreatmajor- ity of the human population (more than 90%) are infected with EBV. This particular virus es- tablishes specific communication with the host, changing the expression of its own genes in different cell types, depending on its differ- entialstatus.Duringprimaryinfection,EBVini- tiallyinfectsoralepithelialcellsinthelyticform and subsequently infects B cells, where the virus assumes one of three different types of latency lifelong. Occasionally, the latent infec- tion reactivates and changes into lytic infec- tion.The differentiation ofmemoryB cellswith the EBVgenome into plasma cells afterantigen stimulation activates the lytic EBV infection. Thereactivationmostcommonlyoccursinton- sillar plasma cells, as well as in tonsillar B cells. This is one of the reasons that the saliva from immunocompromised but also immunocom- petent persons often contains infectious EBV, with or without any signs of infection. EBV can change the immune response of the host with a specific influence on the immunopatho- geneses of infection. The cytokines secreted during EBV infection can influence local im- munopathology. The results of the present study rejected the hypothesis that periimplantitis could be associ- atedwith EBV; in fact, no statisticallysignificant differences were found regarding the presence of EBV in healthy or periimplantitis-affected sites(28.6%ofthehealthypatientsand37.2%of the periimplantitis-affected patients presented atleastonesitewithEBV). This is in contrast to previous studies, in which a significantly higher presence of EBV was found in subgingival samples from peri- implantitislesionsthanfromhealthyperiimplant sites. In fact, both Jankovic et al. and Verdugo et al.foundasignificantlyhigherpresenceofEBVin theperiimplantitis-affectedsites.7,8 The absence of significant differences be- tween the groups could lead to the rejection of thehypothesisofthepathogenickeymechanism of viruses in the incidence of periimplantitis. However, this could be because the present study had a retrospective design. This limitation could jeopardize the detection of EBV, which is thought to activate immunological response only in the early stage of disease.12 This could be indirectly confirmed by the fact that most parts ofthe sites in the periimplantitis group were un- der the limit of quantification. At the same time, interactions between EBV and herpesviruses could be supposed to have an effect on the host response.7 E ps tein – Ba rr v irus a n d pe r i i mplanti ti s Fig. 3 Distribution of EBV in internal sites in both groups. Fig. 4 Distribution of EBV in external sites in both groups. Fig. 4Fig. 3