Molarless-induced changes of spines in hippocampal region of SAMP8 mice
Department of Oral Anatomy, Division of Oral Structure, Function and Development, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, Gifu 501-0296, Japan. Brain Research
(Impact Factor: 2.84).
10/2005; 1057(1-2):191-5. DOI: 10.1016/j.brainres.2005.07.038
We examined the effect of the molarless condition on the dendritic spines of hippocampal pyramidal cells in SAMP8 mice in comparison to its effect on learning ability in a maze test. The molarless condition caused a decrease in the number of the spines of CA1 pyramidal cells only in the aged mice showing a reduced learning ability. The results suggest the involvement of the molarless condition in an attenuation of input activities in the hippocampal synapses.
Available from: jstage.jst.go.jp
- "Both groups were subdivided into 3 age groups of 10 each, totaling 60 animals. Removal of the upper molar teeth was performed as described previously (Kubo et al. 2005). Briefly, at one month of age, mice were anesthetized with sodium pentobarbital and all upper (maxillary) molar teeth were extracted using dental tweezers. "
[Show abstract] [Hide abstract]
ABSTRACT: 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.
Available from: PubMed Central
- "In response to mastication, increased cerebral blood flows and higher oxygen levels were observed within the central nervous system, notably the hippocampus and the prefrontal cortex
[15-17]. Moreover, it is suggested that neuronal signals from teeth influence hippocampus functions
[18,19]. Within the central nervous system, the hippocampus and the prefrontal cortex are considered important for learning and memory; the prefrontal cortex is also viewed as being relevant for numeracy
[Show abstract] [Hide abstract]
The purpose of the present study was to examine the impact of oral health conditions on cognitive functioning on basis of data samples from several European countries.
Secondary analyses were conducted of data from wave 2 of the Survey of Health, Ageing, and Retirement in Europe (SHARE) which includes 14 European countries and is intended to be representative of each country’s middle and later adulthood population. Information on word recall, verbal fluency, and numeracy as well as information on chewing ability and denture wearing status was available for a total of 28,693 persons aged 50+. Multivariate regression analysis was used to detect influences of oral health parameters on cognitive functioning (p < 0.05).
Persons with good chewing ability or without dentures had significantly better word recall, verbal fluency, and numeracy skills than persons with chewing impairment or with dentures. The observed patterns of parameter estimates imply differential oral health impacts on numeracy compared to word recall and verbal fluency.
The present study provides novel large-scale epidemiological evidence supportive of an association between oral health and cognitive functioning. Future research should intend to verify the precise causal links between oral health conditions, various cognitive dimensions, and their neural correlates.
Available from: Cristiane S. F. Maia
- "It has been reported that masticatory dysfunction contributes to a decrease in the density of pyramidal neurons55 and dendritic spines60, and is associated with increased astrocytosis and hypertrophy in the hippocampal CA1 field in mice56,57. These morphological alterations were correlated with spatial memory impairment in a water maze test. "
[Show abstract] [Hide abstract]
ABSTRACT: Several studies have demonstrated that chewing helps to maintain cognitive functions in brain regions including the hippocampus, a central nervous system (CNS) region vital for memory and learning. Epidemiological studies suggest that masticatory deficiency is associated with development of dementia, which is related to spatial memory deficits especially in older animals. The purpose of this paper is to review recent work on the effects of masticatory impairment on cognitive functions both in experimental animals and humans. We show that several mechanisms may be involved in the cognitive deficits associated with masticatory deficiency. The epidemiological data suggest a positive correlation between masticatory deficit and Alzheimer's disease. It may be concluded that chewing has important implications for the mechanisms underlying certain cognitive abilities.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.