Comparative biology of chronic and aggressive periodontitis vs. peri-implantitis

This review was undertaken to address the similarities and dissimilarities between the two disease entities of periodontitis and peri-implantitis. The overall analysis of the literature on the etiology and pathogenesis of periodontitis and peri-implantitis provided an impression that these two diseases have more similarities than differences. First, the initiation of the two diseases is dependent on the presence of a biofilm containing pathogens. While the microbiota associated with periodontitis is rich in gram-negative bacteria, a similar composition has been identified in peri-implant diseases. However, increasing evidence suggests that S. aureus may be an important pathogen in the initiation of some cases of peri-implantitis. Further research into the role of this gram-positive facultative coccus, and other putative pathogens, in the development of peri-implantitis is indicated. While the initial host response to the bacterial challenge in peri-implant mucositis appears to be identical to that encountered in gingivitis, persistent biofilm accumulation may elicit a more pronounced inflammatory response in peri-implant mucosal tissues than in the dentogingival unit. This may be a result of structural differences (such as vascularity and fibroblast-to-collagen ratios). When periodontitis and peri-implantitis were produced experimentally by applying plaque-retaining ligatures, the progression of mucositis to peri-implantitis followed a very similar sequence of events as the development of gingivitis to periodontitis. However, some of the peri-implantitis lesions appeared to have periods of rapid progression, in which the infective lesion reached the alveolar bone marrow. It is therefore reasonable to assume that peri-implantitis in humans may also display periods of accelerated destruction that are more pronounced than that observed in cases of chronic periodontitis. From a clinical point of view the identified and confirmed risk factors for periodontitis may be considered as identical to those for peri-implantitis. In addition, patients susceptible to periodontitis appear to be more susceptible to peri-implantitis than patients without a history of periodontitis. As both periodontitis and peri-implantitis are opportunistic infections, their therapy must be antiinfective in nature. The same clinical principles apply to debridement of the lesions and the maintenance of an infection-free oral cavity. However, in daily practice, such principles may occasionally be difficult to apply in peri-implantitis treatment. Owing to implant surface characteristics and limited access to the microbial habitats, surgical access may be required more frequently, and at an earlier stage, in periimplantitis treatment than in periodontal therapy. In conclusion, it is evident that periodontitis and peri-implantitis are not fundamentally different from the perspectives of etiology, pathogenesis, risk assessment, diagnosis and therapy. Nevertheless, some difference in the host response to these two infections may explain the occasional rapid progression of peri-implantitis lesions. Consequently, a diagnosed peri-implantitis should be treated without delay.