Introduction:The objectives of this study were to compare the qualitative and quantitative profiles of herpes simplex virus type I (HSV-1) in implant surfaces between participants with periimplantitis (PI) and Healthy peri-implant tissues and to quantitatively assess the relation between HSV-1 and periopathogens inside the microbiological profile associated with PI.
Materials and methods:A total of 40 patients with PI and 40 with healthy peri-implant tissues (HI) were recruited. Plaque samples from peri-implant sulcus and internal implant connections were analyzed using quantitative real-time polymerase chain reaction to detect and quantify HSV-1 and periodontopathogens. Frequencies of detection and levels of microorganisms were compared between PI and HI; the frequencies and levels of periodontopathogens were compared between HSV-1+ and HSV-1− PI to assess qualitative relations between HSV-1 and bacteria. Correlation between HSV-1 and periodontopathogens levels was assessed in PI and HI.Results: A total of 77 dental implants affected by PI, and 113 HIs were included. The HSV-1 prevalence was slightly higher in PI compared with controls (33.3 vs 23.8%; p > 0.05); HSV-1 was detected in external samples more frequently compared with internal samples. The HSV-1-positive patients revealed higher median loads of Prevotella intermedia (Pi) and Campylobacter rectus (Cr) compared with HSV-1-negative patients. In the PI group, a significant positive correlation was evidenced between HSV-1 and Tannerella forsythia, Parvimonas micra (Pm), Fusobacterium nucleatum, and Cr levels, while in the HI, positive correlation between HSV-1 and Aggregatibacter actinomycetemcomitans, Pi, and Pm was established.
Conclusion:The HSV-1 prevalence cannot be used to identify PI. The HSV-1 was found in similar levels of PI and HI patients after an average of 6 years of loaded implants. The HSV-1 prevalence cannot be used to identify implants with or without the presence of PI.
HerpesClinical significance: Although HSV-1 is detected in PI site, HSV-1 may represent an unspecific indicator for the host response to the bacterial challenge observed in PI.