One adverse effect of nifedipine, a long‐acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen‐free Fischer rats (male, 14 days old) were used . Gingival inflammation and dental plaque accumulation were induced by infection with Streptococccus mutans MT8148R. The nifedipine‐treated rats (experimental group) were fed a caries‐inducing diet contai ning nifedipine either with or without infection, while the nifedipine‐untreated rats (control group) were fed the same diet, similarly with or with out the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine‐treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans‐infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammatio n and/or dental plaque, although these factors can augment the effect of the drug. Our experimental system seems to be a useful model for studying the mechanism of this side effect.