Relationship between the Early Toothless Condition and Hippocampal Functional Morphology

Previous studies suggested that mastication activity can affect learning and memory function. However, most were focused on mastication impaired models by providing long-term soft diet. The effects of chewing food with various hardness, especially during the growth period, remain unknown. Objective: To analyze the difference of hippocampus function and morphology, as characterized by pyramidal cell count and BDNF expression in different mastication activities. Materials and Methods: 28-day old, post-weaned, male-Wistar rats were randomly divided into three groups (n=7); the first (K0) was fed a standard diet using pellets as the control, the second (K1) was fed soft food and the third (K2) was fed hard food. After eight weeks, the rats were decapitated, their brains were removed and placed on histological plates made to count the pyramid cells and quantify BDNF expression in the hippocampus. Data collected were compared using one-way ANOVA. Results: Results confirmed the pyramid cell count (K0=169.14±27.25; K1=130.14±29.32; K2=128.14±39.02) and BDNF expression (K0=85.27±19.78; K1=49.57±20.90; K2=36.86±28.97) of the K0 group to be significantly higher than that of K1 and K2 groups (p<0.05); no significant difference in the pyramidal cell count and BNDF expression was found between K1 and K2 groups (p>0.05). Conclusion: A standard diet leads to the optimum effect on hippocampus morphology. Food consistency must be appropriately suited to each development stage, in this case, hippocampus development in post-weaned period.

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“… 27 , 28 Therefore, mastication activity is critical in maintaining hippocampus function for learning and memory. 29 , 30 …”

Section: Discussionmentioning

confidence: 99%

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

2019

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“…increase in the plasma corticosterone levels (Onozuka et al 2002;Furuzawa et al 2014;Iinuma et al 2014), we consider that tooth loss early in life may act as chronic stress in adult and aged SAMP8 mice. Previous studies demonstrated that exposure to various stressors, such as restraint, immobilization, forced swimming, psychological and social stressor led to sustained increase in the circulating corticosterone level.…”

Section: Discussionmentioning

confidence: 99%

Tooth Loss Early in Life Accelerates Age-Related Bone Deterioration in Mice

Kurahashi

Kondo

Iinuma

et al. 2015

Tohoku J. Exp. Med.

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Both osteoporosis and tooth loss are health concerns that affect many older people. Osteoporosis is a common skeletal disease of the elderly, characterized by low bone mass and microstructural deterioration of bone tissue. Chronic mild stress is a risk factor for osteoporosis. Many studies showed that tooth loss induced neurological alterations through activation of a stress hormone, corticosterone, in mice. In this study, we tested the hypothesis that tooth loss early in life may accelerate age-related bone deterioration using a mouse model. Male senescence-accelerated mouse strain P8 (SAMP8) mice were randomly divided into control and toothless groups. Removal of the upper molar teeth was performed at one month of age. Bone response was evaluated at 2, 5 and 9 months of age. Tooth loss early in life caused a significant increase in circulating corticosterone level with age. Osteoblast bone formation was suppressed and osteoclast bone resorption was activated in the toothless mice. Trabecular bone volume fraction of the vertebra and femur was decreased in the toothless mice with age. The bone quality was reduced in the toothless mice at 5 and 9 months of age, compared with the age-matched control mice. These findings indicate that tooth loss early in life impairs the dynamic homeostasis of the bone formation and bone resorption, leading to reduced bone strength with age. Long-term tooth loss may have a cumulative detrimental effect on bone health. It is important to take appropriate measures to treat tooth loss in older people for preventing and/or treating senile osteoporosis.

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“…Permanent tooth loss decreases the somatosensory stimuli from the oral cavity, inducing sustained increases in circulating GCs. Several studies demonstrated that loss of molar teeth for a long period of time in rodents induces chronic psychological stress [ 36 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 ]. We used dental tweezers to bilaterally remove the maxillary molars in senescence accelerated mouse prone 8 (SAMP8) mice at the age of one month [ 34 , 35 , 36 , 50 , 51 , 52 , 53 , 57 , 58 , 59 ].…”

Section: Masticatory Dysfunction Activates the Hypothalamic-pituitmentioning

confidence: 99%

“…The results demonstrated that circulating corticosterone levels increase with age. The circulating corticosterone levels were not significantly different between the young control and toothless mice, whereas circulating corticosterone levels were significantly higher in adult and old toothless mice than in the age-matched control mice [ 15 , 16 , 55 ]. As chronic stress causes a significant increase in the circulating corticosterone levels, we consider that tooth loss may act as chronic stressor in adult and aged SAMP8 mice [ 20 , 35 , 57 , 59 ].…”

Section: Masticatory Dysfunction Activates the Hypothalamic-pituitmentioning

confidence: 99%

Association between Mastication, the Hippocampus, and the HPA Axis: A Comprehensive Review

Chen

Zhou

Níwa³

et al. 2017

IJMS

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Mastication is mainly involved in food intake and nutrient digestion with the aid of teeth. Mastication is also important for preserving and promoting general health, including hippocampus-dependent cognition. Both animal and human studies indicate that mastication influences hippocampal functions through the end product of the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoid (GC). Epidemiologic studies suggest that masticatory dysfunction in aged individuals, such as that resulting from tooth loss and periodontitis, acting as a source of chronic stress, activates the HPA axis, leading to increases in circulating GCs and eventually inducing various physical and psychological diseases, such as cognitive impairment, cardiovascular disorders, and osteoporosis. Recent studies demonstrated that masticatory stimulation or chewing during stressful conditions suppresses the hyperactivity of the HPA axis via GCs and GC receptors within the hippocampus, and ameliorates chronic stress-induced hippocampus-dependent cognitive deficits. Here, we provide a comprehensive overview of current research regarding the association between mastication, the hippocampus, and HPA axis activity. We also discuss several potential molecular mechanisms involved in the interactions between mastication, hippocampal function, and HPA axis activity.

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Relationship between the Early Toothless Condition and Hippocampal Functional Morphology

Cited by 12 publications

References 48 publications

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

Tooth Loss Early in Life Accelerates Age-Related Bone Deterioration in Mice

Association between Mastication, the Hippocampus, and the HPA Axis: A Comprehensive Review

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