In the pathogenesis of severe periodontitis, there is increasing evidence regarding the involvement of herpes
viral, bacterial and host immune factors but there is no clarity on the relative importance of each of these factors.
Herpes viruses are re-activated by immunosuppressive factors and, maybe for this reason, they are also major
risk factors for periodontitis. When the periodontitis is in a progressive phase, it seems that the inflamed
periodontium is a major site for accumulation and re-activation of Epstein-Barr virus and cytomegalovirus.
Matrix metalloproteinases and osteoclasts are activated by cytokines. Cytokines in turn are released by herpes
viruses. Herpes viruses may thus act as pathogens in the progression of periodontitis. Antibacterial immune
mechanisms are weakened because of an active herpesvirus infection resulting in a rise in the number of bacteria
which are considered to be periodontopathogens. A suppressed herpesvesvirus infection may be re-activated by
some of the periodontopathogenic bacteria. This synergy between the bacteria and herpesviruses may play a
significant part in the commencement and advancement of periodontitis. Herpesvirus-induced periodontitis
suggests that the immunity against herpesviruses forms a crucial feature in attaining a stable periodontium.
There is a need for further investigation on the part played by herpesviruses in periodontitis which will result in
enhanced diagnosis, better therapy and disease prevention. Vaccines specific to human cytomegalovirus
(HCMV) and Epstein Barr virus (EBV) that shape treatment strategies against herpesvirus, may be effectively
utilized in the inhibition and therapy for diseases of periodontal origin, specifically the periodontitis.
herpes viruses, periodontitis, pathogenesis, bacteria
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