Aim Materials and Methods Results Conclusions To investigate the bidirectional influence between periodontitis and psoriasis, using the respective experimental models of ligature‐ and imiquimod‐induced diseases on murine models.Thirty‐two C57/BL6J mice were randomly allocated to four experimental groups: control (P− Pso−), ligature‐induced periodontitis (P+ Pso−), imiquimod‐induced psoriasis (P− Pso+) and periodontitis and psoriasis (P+ Pso+). Samples (maxilla, dorsal skin and blood) were harvested immediately after death. Measures of periodontitis (distance between the cemento‐enamel junction and alveolar bone crest [CEJ–ABC] and the number of osteoclasts) and psoriasis (epidermal thickness and infiltrate cell [/0.03mm2]) severity as well as systemic inflammation (IL‐6, IL‐17A, TNF‐α) were collected.The P+ Pso+ group exhibited the most severe experimental periodontitis and psoriasis, with the highest values of CEJ–ABC, number of osteoclasts, epidermal thickness and infiltrate cells in the dorsal skin, as well as the highest blood cytokine concentration. The P+ Pso− group presented with higher cell infiltrate (/0.03mm2) compared to the control group (p <.05), while the P− Pso+ group showed substantially higher alveolar bone loss (CEJ–ABC) than the control group (p <.05).Experimental periodontitis may initiate and maintain psoriasiform skin inflammation and, vice versa, experimental psoriasis may contribute to the onset of periodontitis. In a combined model of the diseases, we propose a bidirectional association between periodontitis and psoriasis via systemic inflammation. [ABSTRACT FROM AUTHOR]