Regional Inequalities in Oral Frailty and Social Capital.

INTRODUCTION: Oral frailty leads to poor nutritional status, which, in turn, leads to frailty. This cross-sectional study aimed to determine regional differences in the prevalence of oral frailty and to identify factors associated with oral frailty using 3-level multilevel models. METHODS: This study comprised 165,164 participants aged ≥65 y without long-term care requirements in the Japan Gerontological Evaluation Study. The dependent variable was oral frailty, which was calculated based on age, number of teeth, difficulty in eating tough foods, and choking. The individual-level independent variables included sociodemographics, present illness, social participation, frequency of meeting friends, and social capital. The local district-level independent variable was social capital (n = 1,008) derived from exploratory factor analyses. The municipality-level independent variable was population density (n = 62). Three-level multilevel Poisson regression analysis was performed to calculate the prevalence ratios (PRs). RESULTS: The prevalence of oral frailty in municipalities ranged from 39.9% to 77.6%. Regarding district-level factors, higher civic participation was significantly associated with a lower probability of oral frailty. At the municipality level, the PR of the rural-agricultural area was 1.17 (95% confidence interval, 1.11-1.23) (reference: metropolitan). CONCLUSION: These results highlight the usefulness of oral frailty prevention measures in encouraging social participation in rural areas. KNOWLEDGE TRANSFER STATEMENT: The results of the present study showed regional differences in oral frailty. In particular, rural-agricultural areas show higher prevalence rates of oral frailty than those in metropolitan cities. Promoting measures of social participation among older adults may help prevent oral frailty in rural areas.

Effects of electrical stimulation on periodontal tissue remodeling in rats.

BACKGROUND AND OBJECTIVE: Electric current is used to promote wound healing. However, it is unclear whether electrical stimulation contributes to gingival tissue remodeling. This study examined the effects of electrical stimulation on gingival tissue remodeling in a rat periodontitis model. MATERIAL AND METHODS: Male Wistar rats (n = 28, 8 wks of age) were divided into four groups of seven rats each. The control group did not receive any treatment for 6 wks. In the other groups, periodontitis was ligature-induced for 4 wks. After 4 wks, the rats with periodontitis were given daily electrical stimulation of 0, 50 or 100 µA for 2 wks. RESULTS: The periodontitis group stimulated with 0 µA showed a higher density of polymorphonuclear leukocytes and a lower density of collagen in gingival tissue compared with the control group (p < 0.05). The two remaining groups treated with 50 or 100 µA of electrical stimulation exhibited a lower density of polymorphonuclear leukocytes (p < 0.05) and a higher density of collagen than the group stimulated with 0 µA (p < 0.05). They also showed higher expression of fibroblast growth factor-2 than the group treated with 0 µA of electrical stimulation (p < 0.05). CONCLUSION: Electric stimulation may offer a novel approach to promote gingival tissue remodeling in periodontal lesions.

Contrast Injection from an Intermediate Catheter Placed in an Intradural Artery is Associated with Contrast-Induced Encephalopathy following Neurointervention.

BACKGROUND AND PURPOSE: Contrast-induced encephalopathy can result from neurotoxicity of contrast medium in the affected area. The development of intermediate catheters has allowed guidance of catheters to more distal arteries. This study focused on the association between contrast-induced encephalopathy and contrast injection from an intermediate catheter guided into a distal intradural artery during neurointervention for cerebral aneurysms. MATERIALS AND METHODS: We retrospectively reviewed 420 consecutive aneurysms in 396 patients who underwent neurointervention for extracranial aneurysms and unruptured intracranial aneurysms at our institution from February 2012 to January 2023. Patients were divided into a group with contrast-induced encephalopathy and a group without. To identify risk factors for contrast-induced encephalopathy, we compared clinical, anatomic, and procedural factors between groups by multivariate logistic regression analysis and stepwise selection. RESULTS: Among the 396 patients who underwent neurointervention for cerebral aneurysms, 14 (3.5%) developed contrast-induced encephalopathy. Compared with the group without contrast-induced encephalopathy, the group with contrast-induced encephalopathy showed significantly higher rates of patients on hemodialysis, previously treated aneurysms, intradural placement of a catheter for angiography, nonionic contrast medium, and flow-diversion procedures in univariate analyses. Stepwise multivariate logistic regression analysis revealed intradural placement of a catheter for angiography (OR = 40.4; 95% CI, 8.63-189) and previously treated aneurysms (OR = 8.20; 95% CI, 2.26-29.6) as independent predictors of contrast-induced encephalopathy. CONCLUSIONS: Contrast injection from an intradural artery and retreatment of recurrent aneurysms were major risk factors for contrast-induced encephalopathy. Attention should be paid to the location of the intermediate catheter for angiography to avoid developing contrast-induced encephalopathy.

Effects of topical application of inorganic polyphosphate on tissue remodeling in rat inflamed gingiva.

BACKGROUND AND OBJECTIVE: Inorganic polyphosphate [poly(P)] is a biopolymer found in almost all cells and tissues, and which promotes tissue remodeling. However, there is limited information on how poly(P) affects the connective tissue in inflamed gingiva. This study examined the effects of topical application of poly(P) on gingival connective tissue and its remodeling in a rat periodontitis model. MATERIAL AND METHODS: Male Wistar rats (n = 36, 8 wk of age) were used in this 6-wk study. The rats were divided into six groups of six rats each. The control group received no treatment. In the other groups, periodontitis was ligature-induced for 4 wk. After 4 wk, the rats with periodontitis were further divided into five groups, and were left untreated (periodontitis group) or subjected to topical application of oral rinses containing 0, 0.1, 1 or 5% poly(P) for 2 wk. RESULTS: The periodontitis and 0% poly(P) groups showed a higher density of polymorphonuclear leukocytes and a lower density of collagen in gingival tissue than the control group (p < 0.05). In contrast, groups treated with more than 1% poly(P) exhibited a lower density of polymorphonuclear leukocytes (p < 0.05) and a higher density of collagen than the periodontitis and 0% poly(P) groups (p < 0.05). A higher expression of fibroblast growth factor-2 was observed in the gingiva of rats treated with 1% poly(P) than in those treated with 0% poly(P) (p < 0.05). CONCLUSION: Topical application of poly(P) may induce connective tissue remodeling, contributing to improvement of inflamed gingiva in rats.

Load distribution and forearm muscle activity during cylinder grip at various grip strength values.

This study aimed to investigate load distribution and forearm muscle activity from strong to weak grip strength, using a cylindrical device (Grip Sensor). We invited 15 students and measured the pressure distribution and forearm muscle activity during grip tasks at 25%, 50%, 75%, and 100% maximum voluntary force (MVF). Pressure data from the Grip Sensor were assigned to seven anatomical regions; the sum of the data from the seven regions (Total force) and proportionate load distribution for each grip task were calculated. Electromyography recorded activity in the extensor carpi radialis longus (ECRL), flexor carpi radialis (FCR), extensor carpi ulnaris (ECU) and flexor carpi ulnaris (FCU) muscles. Forearm muscle activity increased significantly with grip strength (p < 0.05). The load proportion corresponding to the thumb did not significantly change with increasing strength. On the other hand, the fingertip ratio significantly decreased, and the palm ratio significantly increased with increasing strength (p < 0.05). The Grip Sensor showed a shift in the load distribution in the hand from fingertips to palm as grip strength increased. This result indicates that more detailed evaluations of hand function may be possible.

Gli1+-PDL Cells Contribute to Alveolar Bone Homeostasis and Regeneration.

The periodontal ligament (PDL) contains mesenchymal stem cells (MSCs) that can differentiate into osteoblasts, cementoblasts, and fibroblasts. Nevertheless, the distribution and characteristics of these cells remain uncertain. Gli1, an essential hedgehog signaling transcription factor, functions in undifferentiated cells during embryogenesis. Therefore, in the present study, the differentiation ability of Gli1+ cells was examined using Gli1-CreERT2/ROSA26-loxP-stop-loxP-tdTomato (iGli1/Tomato) mice. In 4-wk-old iGli1/Tomato mice, Gli1/Tomato+ cells were only slightly detected in the PDL, around endomucin-expressing blood vessels. These cells had proliferated over time, localizing in the PDL as well as on the bone and cementum surfaces at day 28. However, in 8-wk-old iGli1/Tomato mice, Gli1/Tomato+ cells were quiescent, as most cells were not immunoreactive for Ki-67. These cells in 8-wk-old mice exhibited high colony-forming unit fibroblast activity and were capable of osteogenic, chondrogenic, and adipogenic differentiation in vitro. In addition, after transplantation of teeth of iGli1/Tomato mice into the hypodermis of wild-type mice, Tomato fluorescence indicating the progeny of Gli1+ cells was detected in the osteoblasts and osteocytes of the regenerated bone. These results demonstrate that Gli1+ cells in the PDL were MSCs and could contribute to the alveolar bone regeneration.

Relationship between periodontal condition and arterial properties in an adult population in Japan.

UNLABELLED: Oral Diseases (2010) 16, 781-787 OBJECTIVE: This study addressed the relationship between periodontal condition and second derivative of the finger photoplethysmogram (SDPTG) in Japanese adults. SUBJECT AND METHODS: The Community Periodontal Index (CPI) and SDPTG were recorded in 415 subjects (mean age: 44.0 years). For assessing SDPTG, we mainly focused on the ratio of the absolute value of the height of the early negative 'b' wave and ratio of the late re-decreasing 'd' wave to the height of the initial positive 'a' wave, namely the b/a and d/a ratios. RESULTS: The CPI score was positively correlated with the b/a ratio (P < 0.001), and negatively correlated with the d/a ratio (P < 0.001). Logistic regression analysis showed that subjects with CPI scores ≥ 3 were more likely to have a higher level (male > -0.69, female > -0.64) of b/a ratio (Odds ratio = 1.7, P = 0.026) and lower level (male ≤ -0.29, female ≤ -0.32) of d/a ratio (Odds ratio = 2.2, P =0.001) than those with CPI scores 0-2, after adjusting for age, gender, smoking status, pulse rate and presence of hypertension. CONCLUSION: There was a statistical association between the CPI scores and SDPTG indices in Japanese adults.

Evidence for in vivo reaction of antibody and complement to surface antigens of human cancer cells.

The immune adherence test was used to determine whether antibody and complement in cancer patients are fixed in vivo to tumor cells. Human erythrocytes adhered in vitro to the surface of human cancer cells obtained from autopsy and biopsy. Adherence was enhanced by further addition of the C2 and C3 components of complement, and was diminished by preliminary treatment with antibody to C3 (that is, to beta1C-globulin). The results suggest that tumor associated membrane antigens form complexes in vivo with antibodies and complement.

Stimulatory effects of yeast and mammalian 14-3-3 proteins on the Raf protein kinase.

Intracellular signaling from receptor tyrosine kinases in mammalian cells results in activation of a signal cascade that includes the guanine nucleotide-binding protein Ras and the protein kinases Raf, MEK [mitogen-activated protein kinase (MAPK) or extracellular signal-regulated kinase (ERK) kinase], and MAPK. MAPK activation that is dependent on the coupling of Ras and Raf was reconstituted in yeast. Yeast genes were isolated that, when overexpressed, enhanced the function of Raf. One of them is identical to BMH1, which encodes a protein similar to members of the mammalian 14-3-3 family. Bacterially synthesized mammalian 14-3-3 protein stimulated the activity of Raf prepared from yeast cells expressing c-Raf-1. Thus, the 14-3-3 protein may participate in or be required for activation of Raf.

Identification of a member of the MAPKKK family as a potential mediator of TGF-beta signal transduction.

The mitogen-activated protein kinase (MAPK) pathway is a conserved eukaryotic signaling module that converts receptor signals into various outputs. MAPK is activated through phosphorylation by MAPK kinase (MAPKK), which is first activated by MAPKK kinase (MAPKKK). A genetic selection based on a MAPK pathway in yeast was used to identify a mouse protein kinase (TAK1) distinct from other members of the MAPKKK family. TAK1 was shown to participate in regulation of transcription by transforming growth factor-beta (TGF-beta). Furthermore, kinase activity of TAK1 was stimulated in response to TGF-beta and bone morphogenetic protein. These results suggest that TAK1 functions as a mediator in the signaling pathway of TGF-beta superfamily members.

TAB1: an activator of the TAK1 MAPKKK in TGF-beta signal transduction.

Transforming growth factor-beta (TGF-beta) regulates many aspects of cellular function. A member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family, TAK1, was previously identified as a mediator in the signaling pathway of TGF-beta superfamily members. The yeast two-hybrid system has now revealed two human proteins, termed TAB1 and TAB2 (for TAK1 binding protein), that interact with TAK1. TAB1 and TAK1 were co-immunoprecipitated from mammalian cells. Overproduction of TAB1 enhanced activity of the plasminogen activator inhibitor 1 gene promoter, which is regulated by TGF-beta, and increased the kinase activity of TAK1. TAB1 may function as an activator of the TAK1 MAPKKK in TGF-beta signal transduction.

Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways.

Mitogen-activated protein (MAP) kinase cascades are activated in response to various extracellular stimuli, including growth factors and environmental stresses. A MAP kinase kinase kinase (MAPKKK), termed ASK1, was identified that activated two different subgroups of MAP kinase kinases (MAPKK), SEK1 (or MKK4) and MKK3/MAPKK6 (or MKK6), which in turn activated stress-activated protein kinase (SAPK, also known as JNK; c-Jun amino-terminal kinase) and p38 subgroups of MAP kinases, respectively. Overexpression of ASK1 induced apoptotic cell death, and ASK1 was activated in cells treated with tumor necrosis factor-alpha (TNF-alpha). Moreover, TNF-alpha-induced apoptosis was inhibited by a catalytically inactive form of ASK1. ASK1 may be a key element in the mechanism of stress- and cytokine-induced apoptosis.

Periodontitis-induced lipid peroxidation in rat descending aorta is involved in the initiation of atherosclerosis.

BACKGROUND AND OBJECTIVE: Periodontitis is a risk factor for the development of atherosclerosis. Recent studies indicate that oxidative mechanisms, including lipid peroxidation, are involved not only in periodontitis but also in atherosclerosis. Lipid peroxidation may play an important role in the pathogenesis of atherosclerosis, particularly during its earliest stages. The purpose of this study was to investigate the relationship between lipid peroxidation induced by periodontitis and the initiation of atherosclerosis. MATERIAL AND METHODS: Sixteen rats were randomly divided into two groups of eight rats each. Periodontitis was ligature-induced for 4 wk in the experimental group, whereas the control group was left untreated. After the experimental period, the mandibular first molar regions were resected and then subjected to histological analysis and measurement of hexanoyl-lysine expression as an indicator of lipid peroxidation. Descending aorta was used for measuring the levels of hexanoyl-lysine, reactive oxygen species and lipid deposits, and for real-time polymerase chain reaction microarray analysis. The level of hexanoyl-lysine was also measured in serum. RESULTS: In the experimental group, the levels of hexanoyl-lysine in periodontal tissue and serum increased. Only aorta samples in the experimental group showed lipid accumulation, with increased expression of hexanoyl-lysine, reactive oxygen species and oxidative stress-related genes (including nitric oxide synthases 2 and 3), whereas the superoxide dismutase 1 gene level was down-regulated. CONCLUSION: In a ligature-induced periodontitis rat model, increased lipid peroxidation was found in serum and aorta as well as in periodontal tissue. Atherosclerosis-related gene expression and histological changes were also stimulated. Periodontitis-induced lipid peroxidation in the aorta may be involved in the early stage of atherosclerosis.

Delta 9-tetrahydrocannabinol-induced catalepsy-like immobilization is mediated by decreased 5-HT neurotransmission in the nucleus accumbens due to the action of glutamate-containing neurons.

Delta(9)-tetrahydrocannabinol (THC) has been reported to induce catalepsy-like immobilization, but the mechanism underlying this effect remains unclear. In the present study, in order to fully understand the neural circuits involved, we determined the brain sites involved in the immobilization effect in rats. THC dose-dependently induced catalepsy-like immobilization. THC-induced catalepsy-like immobilization is mechanistically different from that induced by haloperidol (HPD), because unlike HPD-induced catalepsy, animals with THC-induced catalepsy became normal again following sound and air-puff stimuli. THC-induced catalepsy was reversed by SR141716, a selective cannabinoid CB(1) receptor antagonist. Moreover, THC-induced catalepsy was abolished by lesions in the nucleus accumbens (NAc) and central amygdala (ACE) regions. On the other hand, HPD-induced catalepsy was suppressed by lesions in the caudate putamen (CP), substantia nigra (SN), globus pallidus (GP), ACE and lateral hypothalamus (LH) regions. Bilateral microinjection of THC into the NAc region induced catalepsy-like immobilization. This THC-induced catalepsy was inhibited by serotonergic drugs such as 5-hydroxy-L-tryptophan (5-HTP), a 5-HT precursor, and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), a 5-HT receptor agonist, as well as by anti-glutamatergic drugs such as MK-801 and amantadine, an N-methyl-d-aspartate (NMDA) receptor antagonist. THC significantly decreased 5-HT and glutamate release in the NAc, as shown by in vivo microdialysis. SR141716 reversed and MK-801 inhibited this decrease in 5-HT and glutamate release. These findings suggest that the THC-induced catalepsy is mechanistically different from HPD-induced catalepsy and that the catalepsy-like immobilization induced by THC is mediated by decreased 5-HT neurotransmission in the nucleus accumbens due to the action of glutamate-containing neurons.

Effects of ethanol consumption on periodontal inflammation in rats.

Studies suggest a correlation between ethanol consumption and periodontal disease. We hypothesized that elevated levels of blood reactive oxygen species following ethanol consumption may increase inflammation in periodontal tissue. Rats were divided into 4 groups (6-7 rats/group). Two groups were fed an ethanol-containing liquid diet, and 2 groups were fed a pair-fed control diet. In one of each dietary group, periodontitis was ligature-induced, while the other group was left unligated. Chronic ethanol feeding alone decreased the ratio of reduced/oxidized glutathione and increased 8-hydroxydeoxy-guanosine and tumor necrosis factor (TNF)-alpha levels in the gingiva. Blood hydroperoxides were also increased. In ligature-induced periodontitis lesions, ethanol feeding enhanced polymorpho-nuclear leukocyte infiltration and TNF-alpha expression. The results suggest that chronic alcohol consumption increased periodontal inflammation, oxidative damage, and TNF-alpha production and had an additive effect on polymorphonuclear leukocyte infiltration and gingival oxidative damage, increasing the severity of periodontal inflammation in the ligature model.

Select Calcium Compounds Reduce the Severity of Phytophthora Stem Rot of Soybean.

This study investigated the effects of several calcium compounds on Phytophthora stem rot of soybean (Glycine max) and fungal growth and zoospore release of a Phytophthora sojae isolate in vitro. All concentrations of five formulated calcium products [Ca(COOH)2-A, Ca(COOH)2-B, Ca(COOH)2-C, CaSO4-A, and CaCl2-A] and two chemical compounds [CaCl2 and Ca(NO3)2] applied prior to inoculation significantly suppressed disease incidence. Among all the products and chemicals, Ca(COOH)2-A was the most effective in suppressing the incidence of disease. In most cases, no significant relationship was observed between inhibition of growth rate in vitro and disease reduction in growth chamber tests. Therefore, disease suppression recorded in laboratory experiments using pathogen mycelium was likely due to the responses of plant tissues rather than the direct inhibition of pathogen fungal growth by the calcium compounds. The extent of disease reduction was related to increased calcium uptake by plants, suggesting that calcium was the effective element in reducing Phytophthora stem rot. Seedling tray experiments using zoospores indicated that the application of 10 mM Ca(COOH)2-A was more effective for reducing incidence of disease under growth chamber conditions, compared to other concentrations. The presence of 4 to 20 mM of all seven calcium solutions decreased the release of zoospores, although 0.4 mM of all compounds significantly increased zoospore release. Therefore, disease reduction in the growth-chamber experiments was due to the multiple effects of direct suppression on zoospore release and fungal growth in combination with the response of the host plant tissue to Ca(COOH)2-A.

Requirement of nectin, but not cadherin, for formation of claudin-based tight junctions in annexin II-knockdown MDCK cells.

Adherens junctions (AJs) and tight junctions (TJs) comprise a junctional complex which plays key roles not only in cell adhesion and polarization but also in regulation of cell movement and proliferation in epithelial cells. E-Cadherin and nectin are major cell-cell adhesion molecules (CAMs) at AJs, whereas claudin is a major CAM at TJs. We have shown that the cadherin-based cell-cell adhesion is not formed in MDCK cells in which annexin II, a Ca(2+)- and phospholipid-binding protein, is knocked down. Here, we found that TJs and the nectin-based cell-cell adhesions were formed in annexin II-knockdown cells. The formation of TJs in annexin II-knockdown MDCK cells required the nectin-based cell-cell adhesion and afadin, a nectin- and actin-filament-binding protein. In addition, it required the activation of Cdc42 and Rac small G proteins and subsequent reorganization of the IQGAP1-dependent actin cytoskeleton which were induced by the nectin-based cell-cell adhesion. These results indicate that the nectin-based cell-cell adhesion and afadin, but not the cadherin-based cell-cell adhesion, are necessary for the formation of TJs and that the signaling by nectin and the subsequent reorganization of the actin cytoskeleton are also necessary for the formation of TJs under certain conditions.