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Interleukin (IL)‑17A exhibits pleiotropic biological activities and serves a role in the progression of periodontitis. However, data describing the association between IL‑17 and osteogenesis are not conclusive. It was previously demonstrated that RAC‑β serine/threonine protein kinase (AKT2)‑specific knockdown in MC3T3‑E1 cells weakened osteogenic effects. The role of AKT2 in the regulation of IL‑17A for osteoblast differentiation and calcification remains unclear. The MTT method was adopted in the present study to assess cell proliferation; cell cycle distribution was analyzed by flow cytometry. Following osteogenic induction treatment, the involvement of phosphatidylinositol 3‑kinase (PI3K) and phosphorylated‑PI3K was evaluated by western blotting. The effects of IL‑17A on osteogenesis‑associated markers, including Runt‑related transcription factor 2 (Runx‑2), alkaline phosphatase (ALP) and osteocalcin (OCN) were evaluated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis. An ALP activity assay and Alizarin Red S staining were used to assess the differentiation and calcification functions. AKT2 knockdown inhibited MC3T3‑E1 cell proliferation, inducing significantly increased G0/G1 cell counts, and reduced S and G2/M cell numbers. IL‑17A exerted no significant effects. The protein levels of p‑PI3K, gene expression levels of IL‑17A, Runx‑2, ALP and OCN, and relative ALP activity and calcification areas were increased in the induction group, and these effects were markedly promoted by treatment with IL‑17A. AKT2 knockdown in MC3T3‑E1 cells resulted in reduced IL‑17A‑induced differentiation and calcification, although it was not completely inhibited. The results of the present study suggested that AKT2 signaling was required for MC3T3‑E1 cell proliferation. IL‑17A promoted osteoblast differentiation and calcification in a partly AKT2‑dependent manner in MC3T3‑E1 cells in vitro, possibly reflecting compensation by other signaling pathways. The results of the present study may offer novel perspectives to guide the clinical strategy for the prevention and treatment of periodontitis. [ABSTRACT FROM AUTHOR]