To investigate the mechanisms underlying impaired hippocampal function resulting from masticatory dysfunction, we examined the effects of the molarless condition on cell proliferation and the effect of the administration of metyrapone, which suppresses the stress-induced rise in plasma corticosterone levels, on cell proliferation in the hippocampal dentate gyrus (DG) of aged senescence-accelerated prone (SAMP8) mice. In addition, we examined whether chewing under restraint stress prevents the stress-induced suppression of cell proliferation. In aged mice, the molarless condition suppressed cell proliferation in the hippocampal DG. Vehicle-injected molarless mice had significantly higher plasma corticosterone levels than vehicle-injected control and metyrapone-injected molarless mice, in association with decreased cell proliferation in the hippocampal DG. Pretreatment with metyrapone inhibited the increase in plasma corticosterone levels induced by the bite-raised condition, and also attenuated the reduction in cell proliferation. Immobilization stress suppressed cell proliferation in the hippocampal DG, but chewing under restraint stress blocked the stress-induced suppression of cell proliferation in the DG. These results suggest that the morphologic deficits induced by the molarless condition in aged SAMP8 mice are a result of increased plasma corticosterone levels, and that chewing under restraint stress prevents the stress-induced suppression of cell birth in the DG.