Objective：This study aimed to investigate the role of interleukin 17A（IL-17A） in the regulation of bone destruction in experimental periodontitis model. Methods：Male IL-17A knockout C57BL/6 mice and C57BL/6 wild type mice induced with ligation and Porphyromonasgingivalis infection were used to establish experimental periodontitis model in this study. Wild type mice and IL-17A knockout mice were divided into the normal group and the periodontitis group，respectively. The experimental periodontitis model mice were sacrificed 4 weeks after ligation to collect maxillary bones. Micro-computed tomography（Micro-CT），HE staining，TRAP staining，immunohistochemistry and histopathological analysis were performed to reveal the role of IL-17A on bone destruction and inflammation. Results：In the experimental periodontitis mice model induced with Porphyromonasgingivalis infection and ligation，IL-17A knockout mice showed less alveolar bone resorption in the three-dimensional reconstruction of Micro-CT than wild-type mice did. The mesial and distal linear distance from the alveolar bone crest（ABC） to the cementoenamel junction（CEJ） of maxillary second molars in the IL-17A knockout mice was（0.51 ± 0.11）mm and （0.45 ± 0.04）mm respectively，significantly less than those in wild-type mice（P < 0.05），which was（0.61 ± 0.09）mm and（0.65 ± 0.08）mm respectively. In addition，compared to wild-type mice，the mean bone volume fraction in IL-17A knockout mice was 41.88 ± 1.82，significantly higher than that in wild-type mice（36.55 ± 2.08，P < 0.05），and the bone mineral density in IL-17A knockout mice was 84.39 ± 2.11，significantly higher than that in wild-type mice（76.90 ± 2.55，P < 0.05）. On the other hand，IL-17A knockout mice exhibited significantly less alveolar bone resorption in periodontal tissue in HE staining than wild-type mice；TRAP-positive cells and the expression of receptor activator of nuclear factor κB ligand（RANKL） in periodontal tissue were reduced as well. Conclusion：IL-17A may promote the development of periodontitis and alveolar bone resorption.