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AIM In this study, we aimed to explore the effects of microRNA-203 (miR-203) on P. gingivalis lipopolysaccharide (P.g. LPS)-stimulated periodontal ligament cells (PDLCs) and identify potential molecular targets for periodontitis treatment. METHODS PDLCs were stimulated by P.g. LPS, followed by quantification of miR-203 and AP-1 expression. Next, loss- and gain-of-function experiments were applied in P.g. LPS-induced PDLCs. The proliferation, apoptosis, and differentiation of PDLCs were determined and mineralized nodule numbers were counted. Functional assays were used to identify interactions among miR-203, activator protein 1 (AP-1), and intercellular adhesion molecule 1 (ICAM-1). In addition, expression of osteogenesis-related genes and release of proinflammatory factors were analyzed. RESULTS miR-203 was found to be downregulated while AP-1 was upregulated in PDLCs stimulated by P.g. LPS. The overexpression of miR-203 promoted P.g. LPS-stimulated PDLC proliferation and differentiation, inhibited apoptosis, and increased the number of mineralized nodules. miR-203 was verified to downregulate AP-1/ICAM-1 axis. miR-203 overexpression reduced the secretion of proinflammatory factors while increasing expression of osteogenesis-related genes in P.g. LPS-stimulated PDLCs, which was reversed by overexpressing AP-1 and ICAM-1. CONCLUSION These experimental data demonstrated the potential inhibitory effects of overexpressed miR-203 on periodontitis development by promoting PDLC differentiation and suppressing inflammatory responses through AP-1/ICAM-1 axis.