Masticatory function and cognitive function.

Recent studies have suggest that masticatory (chewing) function is useful for maintaining neurocognitive function in the elderly. For example, a reduced ability to masticate, such as that resulting from toothlessness or soft-diet feeding, causes learning and memory deficits in aged animals and pathologic changes in the hippocampus. In addition, occlusal disharmony impairs hippocampal memory processes via chronic stress, and induces similar hippocampal pathology. Chewing, however, rescues stress-induced suppression of long-term potentiation in the hippocampus and the stress-induced impairment of hippocampal-dependent learning. These findings strongly suggest a link between mastication and neurocognitive function.

Novel stress increases hypothalamic-pituitary-adrenal activity in mice with a raised bite.

BACKGROUND AND OBJECTIVE: In humans, occlusal disharmony may cause various physical complaints, including head and neck ache, stiffness in the shoulder and neck, and arthrosis of the temporomandibular joints. Occlusal disharmony induced by raising the bite in rodents, increases plasma corticosterone levels, which leads to morphologic changes in the hippocampus and altered hippocampus-related behavior. The paraventricular nucleus (PVN) of the hypothalamus regulates the hypothalamic-pituitary-adrenal system. Chronically stressed animals exposed to a novel stress exhibit higher adrenocorticotropic hormone levels than naive control animals. We hypothesized that there would be different response of the corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) to a novel acute stress with occlusal disharmony. DESIGN: In order to investigate how exposure of mice with occlusal disharmony to a novel acute stress (restraint stress) affects the PVN, we induced occlusal disharmony by raising the vertical dimension of the bite (bite-raised condition) and examined the expression of corticotrophin releasing hormone (CRH) mRNA and arginine vasopressin (AVP) mRNA in mouse PVN. RESULTS: CRH mRNA expression was increased in the PVN of the bite-raised group 90min after the bite-raising procedure, but the expression was recovered to the control level at 14days. AVP mRNA expression in the PVN was normal at 90min, and increased significantly 14days after the bite-raising procedure. Exposure to restraint stress in the bite-raised mice induced a significant increase in CRH mRNA expression in the PVN. CONCLUSIONS: The bite-raising procedure induced a rapid CRH mRNA response and a slower AVP mRNA response in the parvocellular PVN of the hypothalamus. Exposure to a novel stress following the bite-raising procedure further reinforced the CRH stress response. Thus, occlusal disharmony, such as that induced by raising the bite, may be a risk factor for hypersensitivity to a novel stress.

Occlusal disharmony leads to learning deficits associated with decreased cellular proliferation in the hippocampal dentate gyrus of SAMP8 mice.

Occlusal disharmony is associated with increased plasma corticosterone levels, learning deficits, and morphologic alterations in the hippocampus via chronic stress. Here, we investigated the occlusal disharmony-induced impairment of hippocampal function. We first examined the effects of raising the bite on newborn cell proliferation in the hippocampal dentate gyrus (DG) in senescence-accelerated prone mice. Raising the bite significantly decreased cell proliferation in the hippocampal DG in an age-dependent manner. Immediately after raising the bite, cell proliferation decreased abruptly in the aged mice, then gradually increased, but did not recover to control levels within 2wk. Further, learning-induced cell proliferation was impaired in aged bite-raised mice. These findings suggest that occlusal disharmony induced by raising the bite impaired cell proliferation in the hippocampal DG, leading to learning deficits.

Effect of bite-raised condition on the hippocampal cholinergic system of aged SAMP8 mice.

Occlusal disharmony induces chronic stress, which results in learning deficits in association with the morphologic changes in the hippocampus, e.g., neuronal degeneration and increased hypertrophied glial fibrillary acidic protein-positive cells. To investigate the mechanisms underlying impaired hippocampal function resulting from occlusal disharmony, we examined the effects of the bite-raised condition on the septohippocampal cholinergic system by assessing acetylcholine release in the hippocampus and choline acetyltransferase immunoreactivity in the medial septal nucleus in aged SAMP8 mice that underwent the bite raising procedure. Aged bite-raised mice showed decreased acetylcholine release in the hippocampus and a reduced number of choline acetyltransferase-immunopositive neurons in the medial septal nucleus compared to age-matched control mice. These findings suggest that the bite-raised condition in aged SAMP8 mice enhances the age-related decline in the septohippocampal cholinergic system, leading to impaired learning.