A Novel Rat Model of Polymicrobial Peri-Implantitis: A Preliminary Study

• Autores: Theofilos Koutouzis, Christie Eastman, Sasanka Chukkapalli, Hannu Larjava, Lakshmyya Kesavalu
• Localización: Journal of periodontology, ISSN 0022-3492, Vol. 88, Nº. 2, 2017, págs. 32-41
• Idioma: inglés
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• Resumen

  • Background: Peri-implantitis is a complex polymicrobial biofilm-induced inflammatory osteolytic gingival infection that results in orofacial implant failures. To the best knowledge of the authors, there are no preclinical in vivo studies in implant dentistry that have investigated the inflammatory response to known microbial biofilms observed in humans. The aim of this study is to develop a novel peri-implant rat model using an established model of polymicrobial periodontitis.

    Methods: Wistar rats were used for the study of experimental peri-implantitis. One month after extraction of maxillary first molars, a titanium mini-implant was inserted. Two months after implant healing, implants were uncovered, and abutment fixing was done using cyanoacrylate to prevent abutment loosening. Rats were separated into two groups (group A: polymicrobial-infected and group B: sham-infected). One week after healing of abutments, rats were infected with Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia for 12 weeks. Bacterial colonization, bone resorption, and implant inflammation were evaluated by polymerase chain reaction (PCR), microcomputed tomography, and histology, respectively.

    Results: Three rats with four implants in the infection group and two rats with three implants in the sham-infection group were analyzed. PCR analysis revealed presence of bacterial genomic DNA, and infection elicited significant immunoglobulin (Ig)G and IgM antibody responses, indicating bacterial colonization/infection around implants. Infection induced an enhanced mean distance from implant platform to the first bone-to-implant contact, extensive peri-implantitis with advanced bone resorption, and extensive inflammation with granulation tissue and polymorphonuclear leukocytes.

    Conclusions: To the best knowledge of the authors, this is the first study to develop a novel rat model of polymicrobial peri-implantitis. With modifications to improve implant retention it could offer significant advantages for studies of initiation and progression of peri-implantitis.

    Over the last few decades, dental implants have been a common treatment alternative for missing teeth replacement, improving the quality of life of millions of patients and preventing disuse atrophy of the alveolar bone.1 However, biologic complications, such as peri-implant diseases, commonly occur.2 Peri-implant disease is a collective phrase for inflammatory reactions that are infectious in nature in the tissues around an implant.3 Peri-implant mucositis is a common term to describe the existence of inflammation in the mucosa at an implant with no signs of loss of supporting bone in addition to inflammation in the mucosa.2-4 While peri-implant mucositis represents the host response of the peri-implant tissues against a bacterial challenge, gingivitis is a sum of responses of the host to a bacterial challenge in the gingiva. Peri-implantitis may also differ from periodontitis, both in the extent of lesions and composition of cells in the lesion, as well as the rate of progression.5-7 Using a ligature-induced defect model the association between bacterial biofilm formation and the pathogenesis of peri-implant diseases was demonstrated in animal studies.8 In this experimental model, mucositis and peri-implantitis lesions were induced by terminating the plaque control regimen8 and the placement and exchange of ligatures around the implant neck in a submucosal position.9 At peri-implantitis sites, this active breakdown period is usually terminated by ligature removal, which was associated with spontaneous disease progression in a majority of sites (i.e., progression period).10 It is critical to note that the ligature-induced breakdown is an experimentally induced invasive procedure to achieve a certain degree of breakdown so the final result can mimic a natural peri-implantitis lesion. Thus, it fails to serve as an ideal model to study progression as the investigator controls the ligature-induced breakdown process artificially. Further, the type of ligature, coronal-apical position of the ligature, and how often the ligature is replaced during the plaque formation interval determines the amount and rate of breakdown. Therefore, the ligature-induced tissue destruction model fails to recapitulate in vivo peri-implant pathogenesis.11 Rodent models serve as important tools for exploring molecular mechanisms behind the pathogenesis of infection-induced inflammatory diseases.12 In relation to the process of periodontal disease, rodent models have revealed that periodontal pathogens play a primordial role in initiating gingival inflammation and alveolar bone resorption, and humoral immune response to bacteria significantly influences periodontal tissue destruction.13,14 Later studies have demonstrated that Porphyromonas gingivalis (Pg), Treponema denticola (Td), and Tanneralla forsythia (Tf) can colonize the rat and mouse gingival cavity, leading to gingival inflammation with induction of an enhanced immunoglobulin (Ig)G immune response and significant alveolar bone loss, typical of polymicrobial periodontitis.15-19 At present there are only limited rodent models available for evaluating biofilm-mediated pathogenesis of peri-implant diseases.20 Thus, this study aimed to evaluate a rat model for polybacterial infection in the progression of peri-implantitis.