Periodontal disease has been substantial and growing in the last three decades. Estimate that in 2019 there were 1.1 billion prevalent cases of severe periodontitis worldwide. From 1990–2019, the age-standardized prevalence rate of severe periodontitis increased by 8.44 % (6.62–10.59 %), being highest among less developed countries and regions (GBD, Viewpoint Collaborators, 2019, 2020), characterized by an immunoinflammatory pathogenesis that affects the supporting tissues of the tooth (Chen et al., 2021, Jurdziński et al., 2020, Kassebaum et al., 2017) being dependent on and sustained by the oral microbial biofilm (Jurdziński et al., 2020, Lamont et al., 2018). Even though the presence of key pathogens, such as Porphyromonas gingivalis, reflects a dysbiotic state, it is now accepted that the host immune modulation may play an important role in this breakdown transmuting commensal homeostatic microbiota into a polymicrobial disease (Hajishengallis and Lamont, 2012, Tonetti et al., 2018) - activation of an systemic immunoinflammatory response is not only dependent on specific periodontal pathogens but an exacerbation of inflammatory condition that leads to underlying tissues destruction.

Despite a considerable number of investigations, the mechanisms involved in the pathogenicity of periodontal disease still need to be determined (Borges et al., 2020) as well as its correlation with systemic pathologies, which makes the study of the subject of paramount importance. For the study of periodontal disease, several methods are used such as the stimulation of periodontal disease by inducing pathogenic microorganisms through injections of inactivated bacteria or bacterial lipopolysaccharide (Klausen, 1991), through oral gavage (Fiehn et al., 1992), ligature (Rovin et al., 1966) and ligature soaked in bacteria (Kimura et al., 2000).

The great advantage of using experimental animal models are Ethical considerations in conducting studies in humans make it necessary to conduct them in animals and the benefit of allowing the longitudinal study of the disease from the initial onset to the progression of the lesion in the various tissues of the organs that make up the analysis (Graves et al., 2008, Graves et al., 2012). However, there are many uncertainties about which models are suitable for the induction of periodontitis, in part due to the issues of disease onset, progression, and the events that lead to the irreversible degradation of periodontal tissues, which allow them to maintain their chronic nature as in humans (Graves et al., 2008, Kinane and Hajishengallis, 2009; Oz Hs & Puleo DA 2011; Palioto et al., 2019).

Taking into account the need for more studies that help to understand the effectiveness of these models and analyze their local and systemic outcomes, this systematic review seeks to compare and help to better understand experimental models of periodontitis in mice.