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Effect of Chewing on amyloid beta and beta secretase
Get PDFAlzheimer’s disease (AD) is a common form of dementia characterized by progressive neuronal dysfunction with cognitive impairment and memory loss.
Pathological findings in AD include senile plaques, which are deposits of mature amyloid beta (Aβ) fibers, and neurofibrillary tangles (NFT), which are aggregates of hyperphosphorylated tau. Aβ, in particular, is considered to be central to the pathogenesis of AD. Aβ is insoluble when deposited as mature fibers in brain tissue, but is soluble in the monomeric and oligomeric stages before maturation. These soluble oligomers are believed to be involved in the pathogenesis of AD, which eventually forms senile plaques. Aβ has various subtypes, such as Aβ40 and Aβ42, and Aβ42 is believed to play a major role in the development of AD. It is possible that Chewing influences the early signs of AD.
In this study, we investigated whether Chewing affects the production of Aβ, a key enzyme in the development of AD, and the concentrations of β−secretase and γ−secretase and their degrading enzyme, neprilysin (NEP), in the central tissues, and examined whether Chewing may contribute to the prevention of AD.
Experimental animals were 9−week−old male wild−type Wister/ST rats. After 3 months of rearing on each diet, the rats were euthanized with isoflurane, and cerebrospinal fluid and brain tissues were collected. The brain tissues were collected as a single mass, and divided into 5 parts : cerebellum, medulla oblongata, hypothalamus, mesencephalon−hippocampus−striatum complex, and cerebral cortex. The number of Aβ oligomers deposited in the cerebral cortex and the concentrations of Aβ42 and β−secretase in the cerebellum were significantly lower in the chewing group than in the non−chewing group.
These results suggest that Chewing may contribute to the prevention of AD by inhibiting the production of β−secretase, a synthetic enzyme, and at the same time inhibiting the production of Aβ42.departmental bulletin pape
In vitro and in vivo evaluation of bone regeneration using 3D bioprinted scaffolds containing osteoblasts and growth factors
Get PDFAutologous bone grafting is considered the gold standard for treating craniofacial bone defects due to its excellent osteoconductive and osteoinductive properties, as well as biocompatibility. However, limitations such as donor site morbidity and restricted graft availability have prompted the need for alternative bone substitutes. In particular, for orthodontic cases requiring postoperative tooth movement, conventional bone substitutes such as hydroxyapatite (HA) are inadequate, as their slow resorption impedes normal bone remodeling and may induce adverse effects such as root resorption and soft tissue ingrowth.
This study aimed to develop a novel bone scaffold capable of promoting normal bone remodeling through the incorporation of osteogenic cells and growth factors. We fabricated a scaffold using a bioink composed of sodium alginate (SA) and nanocellulose fibers (NCF), The bioink incorporated osteoblasts derived from rat calvaria along with bone morphogenetic protein−2 (BMP−2) . The constructs were printed using an extrusion−based 3D bioprinter and implanted into critical−sized calvarial defects in rats. Micro−computed tomography (micro−CT) and histological analyses were performed to evaluate bone regeneration and remodeling.
The scaffolds containing both osteoblasts and BMP−2 promoted robust new bone formation, characterized by thick, continuous trabecular structures connecting seamlessly with the surrounding native bone. The regenerated bone showed similar bone mineral density (BMD) and mechanical properties, including hardness and elastic modulus, compared to the host bone. Furthermore, the scaffold exhibited excellent cell viability, structural stability, and enhanced mineralization over time.
These findings suggest that a 3D bioprinted scaffold incorporating osteoblasts and BMP−2 effectively induces normal bone remodeling and could serve as a promising alternative to autologous bone grafts, particularly in clinical scenarios requiring subsequent orthodontic interventions.departmental bulletin pape
The effect of mastication on glucose metabolism via adiponectin in mice. An in Vivo study.
Get PDFAims :
Mastication is reported as a factor that controls glucose metabolism. The aim of this study is to investigate whether mastication affects glucose metabolism through adiponectin and/or leptin, which play key roles in maintaining glucose metabolic homeostasis.
Materials and Methods :
Male C57BL/6J mice (4 weeks old) were divided randomly into two groups : the non−masticatory group (n=10), which received liquid diet, and the masticatory group ( n = 10 ) , which received solid diet. After 12 weeks, the mice were fasted for 24 hours, followed by a glucose tolerance test in which 2 g/kg glucose was administered. Three days later, the mice were anesthetized with 4% isoflurane, and blood was collected via cardiac puncture. Serum levels of adiponectin and leptin were measured using ELISA. We calculated Incremental Area under the Curve (IAUC) trapezoid rule according to methods described by Wolever. Data from both groups were analyzed using the Mann−Whitney U test, with p < 0.05 considered statistically significant.
Results :
The serum concentration of adiponectin was 55.9 ± 16.6 ng/mL in the masticatory group and 32.1 ± 19.1 ng/mL in the non−masticatory group. The masticatory group exhibited a significantly higher adiponectin concentration compared to the non−masticatory group (p < 0.05). In contrast, serum leptin levels had no significant difference in both groups. In the glucose tolerance test, the blood glucose level at 120 minutes post−administration was significantly higher in the non−masticatory group compared to the masticatory group. IAUC in the non−masticatory group were significantly higher than in the masticatory group.
Conclusions :
This study suggests that mastication increases adiponectin secretion and maintains insulin sensitivity, thereby preventing impaired glucose tolerance.departmental bulletin pape
Effect of the psychological chronic stress on aging-related genes in oral mucosa in vivo and in vitro.
Get PDF北海道医療大学博士（歯学）令和6年度thesi
