Effect of periodontitis induced by Fusobacterium nucleatum on the microbiota of the gut and surrounding organs.

Detection of the oral bacterium Fusobacterium nucleatum in colorectal cancer tissues suggests that periodontitis may alter gut microbiota. The purpose of this study was to analyze the influence and infection route of periodontal inflammation caused by F. nucleatum, and microbiota of the gut and surrounding organs (heart, liver, kidney). Wistar female rats were orally inoculated with F. nucleatum to establish an experimental periodontitis model that was confirmed by X-ray imaging and histopathological analysis. The mandibles, gut, liver, heart, and kidneys were collected from the experimental group at 2, 4, and 8 weeks, and from the uninfected control group at 0 weeks, for DNA extraction for PCR amplification and comprehensive microbiota analysis using the Illumina MiSeq platform. Imaging confirmed the onset of periodontitis at 2 weeks post-inoculation, and histopathology showed inflammatory cell infiltration from 2 to 8 weeks. PCR and comprehensive microbiota analysis showed the presence of F. nucleatum in the heart and liver at 2 weeks, and in the liver at 4 and 8 weeks. There were changes of microbiota of the gut, heart, liver, and kidneys at 4 weeks: namely, decreased Verrucomicrobia and Bacteroidetes, and increased Firmicutes. F. nucleatum induced the onset of periodontitis and infected the heart and liver in rats. As the periodontic lesion progressed, the microbiota of the gut, liver, heart, and kidneys were altered.

Regioselective Synthesis of 4-Aryl-1,3-dihydroxy-2-naphthoates through 1,2-Aryl-Migrative Ring Rearrangement Reaction and their Photoluminescence Properties.

4-Aryl-1,3-dihydroxy-2-naphthoates having the less accessible 1,2,3,4-tetrasubstituted naphthalene scaffold and that show photoluminescence emission from solid state as well as in solutions, were selectively synthesized from brominated lactol silyl ethers through the 1,2-aryl-migrative ring rearrangement reaction.

Imaging Tremor Quantification for Neurological Disease Diagnosis.

In this paper, we introduce a simple method based on image analysis and deep learning that can be used in the objective assessment and measurement of tremors. A tremor is a neurological disorder that causes involuntary and rhythmic movements in a human body part or parts. There are many types of tremors, depending on their amplitude and frequency type. Appropriate treatment is only possible when there is an accurate diagnosis. Thus, a need exists for a technique to analyze tremors. In this paper, we propose a hybrid approach using imaging technology and machine learning techniques for quantification and extraction of the parameters associated with tremors. These extracted parameters are used to classify the tremor for subsequent identification of the disease. In particular, we focus on essential tremor and cerebellar disorders by monitoring the finger-nose-finger test. First of all, test results obtained from both patients and healthy individuals are analyzed using image processing techniques. Next, data were grouped in order to determine classes of typical responses. A machine learning method using a support vector machine is used to perform an unsupervised clustering. Experimental results showed the highest internal evaluation for distribution into three clusters, which could be used to differentiate the responses of healthy subjects, patients with essential tremor and patients with cerebellar disorders.

Clinical Symptoms, Neurological Signs, and Electrophysiological Findings in Surviving Residents with Probable Arsenic Exposure in Toroku, Japan.

Chronic arsenic intoxication is known to cause multisystem impairment and is still a major threat to public health in many countries. In Toroku, a small village in Japan, arsenic mines operated from 1920 to 1962, and residents suffered serious sequelae of arsenic intoxication. We have performed annual medical examinations of these residents since 1974, allowing us to characterize participants' long-term health following their last exposure to arsenic. The participants could not be described as having "chronic arsenic intoxication," because their blood arsenic levels were not measured. In this study, we defined them as having "probable arsenic intoxication." Symptoms frequently involved the sensory nervous system, skin, and upper respiratory system (89.1-97.8%). In an analysis of neurological findings, sensory neuropathy was common, and more than half of the participants complained of hearing impairment. Longitudinal assessment with neurological examinations and nerve conduction studies revealed that sensory dysfunction gradually worsened, even after exposure cessation. However, we could not conclude that arsenic caused the long-term decline of sensory function due to a lack of comparisons with age-matched healthy controls. This is the first study to characterize the longitudinal sequelae after probable arsenic exposure. Our study will be helpful to assess the prognosis of patients worldwide who still suffer from chronic arsenic intoxication.

Hypometabolism of watershed areas of the brain in HTLV-1-associated myelopathy/tropical spastic paraparesis.

In previous studies of human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), areas of slow blood flow in the spinal cord were related to pathological changes. While the pathological changes in the brain are milder than those in the spinal cord, they are also more significant in sites with slow blood flow. In this study, we investigated brain glucose metabolism in slow blood flow areas using fluorine-18 fluorodeoxyglucose positron emission tomography ((18)F-FDG-PET). Clinical features and brain (18)F-FDG-PET parameters were analyzed in six patients with HAM/TSP. For comparison of PET data, eight healthy volunteers were enrolled as normal controls (NLs). Glucose metabolism in the watershed areas of the middle and posterior cerebral arteries, as compared with that in the occipital lobes as a control, was significantly lower in HAM/TSP patients than in NLs. This result confirmed the relationship between slow blood flow areas and hypometabolism in HAM/TSP, and is consistent with previous findings that pathological changes are accentuated in sites with slow blood flow.

PR Prolongation and Cardiac 123I-MIBG Uptake Reduction in Parkinson's Disease.

BACKGROUND: Cardiac 123I-metaiodobenzylguanidine scintigraphy (MIBG) previously demonstrated an uptake reduction in patients with Parkinson's disease (PD). However, epidemiologic research showed that electrocardiography (ECG) abnormalities occurred prior to motor signs in PD. Here we investigated whether the electrical conduction system of the heart was impaired in PD. METHODS: Clinical features, ECG and MIBG parameters were analyzed in 191 patients with PD, 42 with multiple system atrophy (MSA) and 124 normal controls (NL). RESULTS: The PR interval was significantly longer in patients with PD than in NL. The PR interval was significantly negatively correlated with early and delayed heart-to-mediastinum ratios in MIBG scintigraphy in PD and MSA patients. In 19 PD patients with PR prolongation, 17 patients also had abnormal MIBG findings, and the other 2 showed normal MIBG. CONCLUSIONS: The PR prolongation must show some sympathetic system abnormality because it is mainly controlled by the sympathetic nervous system. PR prolongation supports the objective biomarker value of MIBG for PD diagnosis.

Role of MAPKs in TGF-ß1-induced maturation and mineralization in human osteoblast-like cells.

OBJECTIVES: Our study aimed to clarify the role of mitogen-activated protein kinases (MAPKs) in transforming growth factor (TGF)-ß1-stimulated mineralization in the human osteoblast-like MG63 cells. METHODS: The viability of MG63 cells under TGF-ß1 stimulation was assessed by MTS assay. Western blotting determined TGF-ß1-mediated activation of extracellular signal-related protein kinase (ERK), p38, and c-Jun amino-terminal kinase (JNK). Mineralization-related gene expression was examined by quantitative real-time PCR, and mineral deposition levels were evaluated by alizarin red S staining. RESULTS: TGF-ß1 had no effect on MG63 cell proliferation. Activation of p38 was observed at 3 h post TGF-ß1 stimulation. Moreover, JNK phosphorylation was upregulated by TGF-ß1 from 1 to 6 h post stimulation, but had no activation on ERK phosphorylation throughout the experimental period. Treatment with JNK inhibitor diminished the alizarin red S-stained area in a dose-dependent manner. Mineral deposition was unaffected by MEK inhibitor, whereas p38 inhibitor increased the red-stained area. Gene expression levels of ALP and BSP were significantly decreased under treatment with JNK inhibitor and p38 inhibitor. The MEK inhibitor had no effect on the TGF-ß1-mediated upregulation of ALP and BSP. Although all three inhibitors suppressed expression of COL I, none were found to stimulate expression of OCN. CONCLUSIONS: Human osteoblast-like MG63 cells maturation and mineralization are induced through JNK activation of MAPK signaling in response to TGF-ß1.

Carbon Nanotubes Induce Mineralization of Human Cementoblasts.

INTRODUCTION: Carbon nanotubes (CNT) are 1 of the allotropes of carbon with unique properties. CNT shows good bone-tissue compatibility and has been reported to induce osteogenesis; therefore, it is regarded as an ideal material in a wide range of applications. However, the therapeutic effect of CNT-containing materials in the healing of apical periodontal tissue is unknown. The purpose of this study was to clarify the effect of CNT on the proliferation and mineralization of the human cementoblast cell line (HCEM). METHODS: The proliferation of HCEM cells with CNT stimulation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay performed from 24-72 hours. Calcium deposition levels were evaluated by alizarin red S staining on days 7 and 10, and mineralization-related gene expression was examined by quantitative real-time polymerase chain reaction on days 3, 7, and 10. Scanning electron microscopy was used to observe the culture with CNT on day 14. RESULTS: CNT showed no cytotoxicity to HCEM cell proliferation. Treatment was performed with mineralization medium, CNT-induced HCEM mineralization on day 7, and increased calcium deposition on days 7 and 14. Messenger RNA expression of alkaline phosphatase was significantly increased throughout the experimental period, and bone sialoprotein was significantly increased on day 3 by CNT, whereas no effect was found on mRNA expression of type I collagen. CNT was observed in attachment to the cell surface on day 14. CONCLUSIONS: CNT promotes the mineralization of HCEM cells, indicating the potential as a new bioactive component for apical periodontal tissue regeneration materials through the regulation of cementoblast mineralization.

Influence of IgA nephropathy on the progression of pulpitis and apical periodontitis in HIGA mice.

OBJECTIVES: Immunoglobulin (Ig)A nephropathy has been associated with oral infections such as periodontitis, but its pathogenesis is not fully understood; no treatments exist. This study analyzes the influence of IgA nephropathy, an autoimmune disease, on the pathogenesis of pulpitis and apical periodontitis. METHODS: Two groups of mice were used in pulp infection experiments: high serum IgA nephropathy model mice (HIGA) and control mice (BALB/c). Histologic analyses of the pulp and apical periodontal tissues were performed on days 3, 5, 7, 14, and 28 following oral bacterial infection. The dynamics of odontoblasts, apoptotic cells, and IgA expression were analyzed using anti-Nestin, TUNEL, and anti-IgA staining, respectively. RESULTS: Inflammatory cells infiltrated the exposed pulp at day three in both groups and by 14 days, these cells had infiltrated from the pulp to the apical periodontal tissue. The area of necrotic pulp tissue increased significantly in the control group at seven days. Odontoblasts decreased from day three onwards and disappeared by 28 days in both groups. The number of apoptotic cells in the pulp and apical periodontal tissues was significantly higher in the experimental group at day 28. The experimental group exhibited a significant increase in IgA production in the pulp after 14 days. Bone resorption in the apical periodontal tissue was significantly decreased in the experimental group at day 28. CONCLUSIONS: The results of this study suggest that IgA nephropathy may modulate the inflammatory response and sustain long-term biological defense responses in pulpitis and apical periodontitis in HIGA mice.

A rare case of concomitant Lambert-Eaton myasthenic syndrome and syndrome of inappropriate antidiuretic hormone secretion in a patient with small cell lung carcinoma.

Small cell lung carcinoma (SCLC) is a neuroendocrine carcinoma with a poor prognosis and is a common cause of paraneoplastic syndromes. Paraneoplastic syndromes are characterized by neurological and endocrinological problems in patients with malignancy and are often associated with difficulty in induction of chemotherapy. Here we report the case of a patient with SCLC concomitant with two paraneoplastic syndromes, syndrome of inappropriate antidiuretic hormone secretion (SIADH) and Lambert-Eaton myasthenic syndrome (LEMS), who was treated with a platinum-doublet chemotherapy regimen. A 66-year-old male patient presented with a 1-month history of progressive proximal muscle weakness, ataxia gait and 5 kg of body weight loss. The laboratory tests revealed hyponatremia due to SIADH and the existence of antibodies against P/Q-type voltage-gated calcium channels. The nerve conduction study showed a low amplitude of compound muscle action potential (0.38 mv), a 34% decrement on 3-Hz stimulation, and a 1939% increment after maximum voluntary contraction in 10 seconds (7.75 mv). The endobronchial ultrasound transbronchial needle aspiration biopsy revealed the pathological findings of SCLC. A 2-cycle chemotherapy regimen of irinotecan plus cisplatin resulted in temporary tumor shrinkage that lasted 2 months, but the improvement of proximal muscle weakness and hyponatremia were maintained over the tumor re-progression period after chemotherapy. Although paraneoplastic syndromes accelerate the decrease in performance status, chemotherapy for SCLC may improve symptoms related to paraneoplastic syndromes and could be considered in similar cases.

BMP-1-induced GBA1 nuclear accumulation provokes CCN2 mRNA expression via importin-ß-mediated nucleocytoplasmic pathway.

Bone morphogenetic protein (BMP)-1 is expressed by odontoblasts in the dentin-pulp complex. Although the functional effects of BMP-1 on the maturation of various preforms of proteins and enzymes involved in initiating mineralization have been widely observed, how BMP-1 affects cellular molecules remains unknown. We performed a comprehensive analysis of BMP-1-altered glycome profiles and subsequent assays to identify the target glycoproteins in human dental pulp cells (hDPCs) by a glycomic approach. In the presence of BMP-1, a lectin microarray analysis and lectin-probed blotting showed that α2,6-sialylation was significantly attenuated in insoluble fractions from hDPCs. Six proteins were identified by a mass spectrometry analysis of α2,6-sialylated glycoproteins purified using a lectin column. Among them, glucosylceramidase (GBA1) was found to accumulate in the nuclei of hDPCs in the presence of BMP-1. Moreover, BMP-1-induced cellular communication network factor (CCN) 2 expression, which is well known as the osteogenesis/chondrogenesis marker, was significantly suppressed in the cells transfected with GBA1 siRNA. Furthermore, importazole, a potent inhibitor of importin-ß-mediated nuclear import significantly suppressed BMP-1-induced GBA1 nuclear accumulation and BMP-1-induced CCN2 mRNA expression, respectively. Thus, BMP-1 facilitates the accumulation of GBA1 in the nucleus through the reduction of α2,6-sialic acid, which potentially contributes to the transcriptional regulation of the CCN2 gene via importin-ß-mediated nuclear import pathway in hDPCs. Our results offer new insights into the role of the BMP-1-GBA1-CCN2 axis in the development, tissue remodeling, and pathology of dental/craniofacial diseases.

Effects of Rheumatoid Arthritis on the Progression of Pulpitis and Apical Periodontitis in SKG Mice.

INTRODUCTION: Rheumatoid arthritis (RA) is an autoimmune disease that involves joint inflammation. Although periodontal disease reportedly contributes to RA onset, the associations of RA with pulpitis and apical periodontitis have not been described. The purpose of this study was to examine the effects of immune response disruption of RA for pulpitis and apical periodontitis with SKG mice. METHODS: SKG and BALB/c (control) mice were used to establish models of pulp infection. Histologic studies of pulp and apical periodontal tissue were performed at 3, 5, 7, 14, and 28 days; odontoblast dynamics were analyzed by antinestin staining, and apoptotic cells were examined by TdT-mediated digoxygenin (biotin)-dUTP nick end labeling staining. RESULTS: Inflammatory cell infiltration into the exposed pulp was observed at 3 days in the SKG and control group groups; the infiltration extended to the apical pulp area at 14 days after surgery. Inflammatory cell infiltration and bone resorption in the apical pulp area were observed from 14-28 days in the SKG and control groups; there were significant increases in inflammatory cell infiltration and bone resorption in the control group at 28 days. The numbers of apoptotic cells in pulp and apical periodontal tissue were higher in the SKG group than in the control group at 14 and 28 days. The number of odontoblasts decreased in the SKG and control groups until 14 days and then disappeared in the SKG and control groups at 28 days. CONCLUSIONS: This study suggested that immune response disruption in RA is involved in prolonging the inflammatory state of pulpitis and apical periodontitis.

Identification of Candidate Genes of Familial Multiple Idiopathic Cervical Root Resorption.

INTRODUCTION: Multiple idiopathic cervical root resorption (MICRR) is a disease with an unknown etiology that causes invasive cervical root resorption in multiple teeth. Although previous MICRR genomic studies have identified candidate gene variants, the etiology of the condition remains poorly understood. In the present study, we investigated the genetic causality of MICRR to explore candidate variants. METHODS: Saliva samples from a family containing 2 affected and two unaffected subjects with the dominant transmission of MICRR were subjected to whole-exome sequencing. RESULTS: As a result, we identified novel candidate variants of 10 genes. Each variant was confirmed by Sanger sequencing. Among them, the American College of Medical Genetics and Genomics and the Association for Molecular Pathology (ACMG/AMP) guidelines classified doublecortin domain containing 1 (c.1099 C > T) and ß-defensin 114 (c.189 T > G) as "pathogenic," and solute carrier family 45 member 2 (c.152_153del) as "likely pathogenic." CONCLUSIONS: These results provide new insight to help clarify the pathogenesis of MICRR, and the variants could be applied for further investigation to understand invasive cervical root resorption.

Effect of the Progression of Fusobacterium nucleatum-induced Apical Periodontitis on the Gut Microbiota.

INTRODUCTION: Fusobacterium nucleatum, which is involved in the development of periodontal disease and apical lesions, can be transmitted to the colon and metastasize to colorectal cancer, suggesting a link between oral and systemic diseases. We analyzed the effects of F. nucleatum on bacterial flora in the gut and surrounding organs in a rat model of apical periodontitis and analyzed the infection route to the gut and distant organs. METHODS: We induced apical periodontitis in rat molars by infecting the dental pulp with F. nucleatum and then took X-ray images and performed histopathologic analyses. Next, we removed the maxilla, gut, heart, liver, and kidney from the rats at 0, 2, 4, and 8 weeks postsurgery and then extracted DNA samples and performed polymerase chain reaction and microbiome analyses using the Illumina MiSeq (Illumina Co, Tokyo, Japan). RESULTS: The presence of inflammatory cell infiltration confirmed apical periodontitis from 2-8 weeks. Polymerase chain reaction and microbiome analyses revealed F. nucleatum in the rat gut from 2 weeks and in the kidney from 8 weeks. The rat gut, heart, liver, and kidney exhibited altered bacterial flora, including a marked decrease in Verrucomicrobia and an increase in Proteobacteria after 2 weeks and increases in Bacteroidetes and Firmicutes after 4 weeks. CONCLUSIONS: The onset of F. nucleatum-induced apical periodontitis changed the bacterial flora in the rat gut, heart, liver, and kidney, with a confirmed progressing infection in the large intestines.

Responses of BrdU label-retaining dental pulp cells to allogenic tooth transplantation into mouse maxilla.

Recently, we demonstrated that a pulse of BrdU given to prenatal animals reveals the existence of slow-cycling long-term label-retaining cells (LRCs), putative adult stem or progenitor cells, which reside in the dental pulp. This study aims to clarify responses of LRCs to allogenic tooth transplantation into mouse maxilla using prenatal BrdU-labeling, in situ hybridization for osteopontin and periostin, and immunohistochemistry for BrdU, nestin, and osteopontin. The upper-right first molars were allografted in the original socket between BrdU-labeled and non-labeled mice or between GFP transgenic and wild-type mice. Tooth transplantation caused degeneration of the odontoblast layer, resulting in the disappearance of nestin-positive reactions in the dental pulp. On postoperative days 5-7, tertiary dentin formation commenced next to the preexisting dentin where nestin-positive odontoblast-like cells were arranged in the successful cases. In BrdU-labeled transplanted teeth, dense LRCs were maintained in the center of the dental pulp beneath the odontoblast-like cells including LRCs, whereas LRCs disappeared in the area surrounding the bone-like tissue. In contrast, LRCs were not recognized in the pulp chamber of non-labeled transplants through the experimental period. Tooth transplantation using GFP mice demonstrated that the donor cells constituted the dental pulp of the transplant except for endothelial cells and some migrated cells, and the periodontal tissue was replaced by host-derived cells except for epithelial cell rests of Malassez. These results suggest that the maintenance of BrdU label-retaining dental pulp cells play a role in the regeneration of odontoblast-like cells in the process of pulpal healing following tooth transplantation.

Wnt5a plays a crucial role in determining tooth size during murine tooth development.

We have previously demonstrated that tooth size is determined by dental mesenchymal factors. Exogenous bone morphogenetic protein (BMP)4, Noggin, fibroblast growth factor (FGF)3 and FGF10 have no effect on tooth size, despite the expressions of Bmp2, Bmp4, Fgf3, Fgf10 and Lef1 in the dental mesenchyme. Among the wingless (Wnt) genes that are differentially expressed during tooth development, only Wnt5a is expressed in the dental mesenchyme. The aims of the present study were to clarify the expression pattern of Wnt5a in developing tooth germs and the role of Wnt5a in the regulation of tooth size by treatment with exogenous WNT5A with/without an apoptosis inhibitor on in vitro tooth germs combined with transplantation into kidney capsules. Wnt5a was intensely expressed in both the dental epithelium and mesenchyme during embryonic days 14-17, overlapping partly with the expressions of both Shh and Bmp4. Moreover, WNT5A retarded the development of tooth germs by markedly inducing cell death in the non-dental epithelium and mesenchyme but not widely in the dental region, where the epithelial-mesenchymal gene interactions among Wnt5a, Fgf10, Bmp4 and Shh might partly rescue the cells from death in the WNT5A-treated tooth germ. Together, these results indicate that WNT5A-induced cell death inhibited the overall development of the tooth germ, resulting in smaller teeth with blunter cusps after tooth-germ transplantation. Thus, it is suggested that Wnt5a is involved in regulating cell death in non-dental regions, while in the dental region it acts as a regulator of other genes that rescue tooth germs from cell death.

Biosynthesized selenium nanoparticles: characterization, antimicrobial, and antibiofilm activity against Enterococcus faecalis.

BACKGROUND: Control over microbial growth is a crucial factor in determining the success of endodontic therapy. Enterococcus faecalis is the most resistant biofilm-forming species leading to endodontic failure. Hence, the current researches are directed towards discovering materials with superior disinfection properties and lesser cytotoxicity. This study aimed to synthesize and characterize biogenically produced Selenium Nanoparticles, and to evaluate the antimicrobial and antibiofilm efficacy, against Enterococcus Faecalis, for the following test groups: Group I: Distilled water (control), Group II: SeNPs (1 mg/ml), Group III: Calcium hydroxide (1 mg/ml), Group IV: 2% Chlorhexidine gluconate (CHX), Group V: 5.25% Sodium hypochlorite (NaOCl). MATERIALS AND METHODS: Selenium nanoparticles were derived using fresh guava leaves (Psidium guajava) and were characterized. The antibacterial efficacy against E. faecalis was evaluated by agar well diffusion method. The antibiofilm efficacy of the test groups was observed by viable cell count, antibiofilm assay, and Anthrone and Bradford's tests. The morphology of the biofilms was analysed using the Scanning Electron Microscope and Fourier Transform Infrared spectroscopy. RESULTS: Antibacterial and antibiofilm efficacy of all tested solutions showed superior antibacterial and antibiofilm efficacy when compared to the control group. Overall, SeNPs (Group II) was the most effective against E. faecalis biofilm, followed by NaOCl (Group V), CHX (Group IV), and Ca(OH)2 (Group III). CONCLUSION: Biogenically produced SeNPs emerged as a novel antibacterial and antibiofilm agent against E. faecalis. This nano-formulation demonstrates the potential to be developed as a root canal disinfectant combating bacterial biofilm in endodontics after the results have been clinically extrapolated.

Detailed Analysis of Neurological Symptoms and Sensory Disturbances Due to Chronic Arsenic Exposure in Toroku, Japan.

As a result of population growth and the development of tube wells, humans' exposure to arsenic has increased over the past few decades. The natural course of organ damage secondary to arsenic exposure is not yet well understood. In Toroku, Japan, an arsenic mine was intermittently operated from 1920 to 1962, and residents were exposed to high concentrations of arsenic. In this paper, we analyzed 190 consecutive residents for whom detailed records of neurological symptoms and findings were obtained from 1974 to 2005. All participants were interviewed regarding the presence of general, skin, hearing, respiratory, and neurological symptoms. Neurological symptoms were classified into extremity numbness or pain, constipation, dyshidrosis, sensory loss, and muscle atrophy. Superficial and vibratory sensation was also evaluated. More than 80% of participants experienced extremity numbness, and numbness was the most common neurological symptom. Numbness was associated with superficial sensory disturbance, and was correlated with the subsequent development of other neurological symptoms, including autonomic and motor symptoms. No previous studies have investigated the natural course of chronic arsenic intoxication; thus, these data serve as a guide for detecting early symptoms due to arsenic exposure.

The effect of mineral trioxide aggregate on dental pulp healing in the infected pulp by direct pulp capping.

This study aimed to clarify the effect of mineral trioxide aggregate (MTA) on pulp healing in the infected pulp by direct pulp capping (DPC). Thirty-six male ICR mice were divided into infected and uninfected groups. The pulp tissue was exposed to the oral flora for 24 h after pulp exposure in the infected group, or not exposed in the uninfected group, followed by sealing with MTA, calcium hydroxide cement (CH), or no DPC. Pulpal healing process was analyzed by hematoxylin-eosin staining and immunohistochemistry for nestin and Ki67. The active cell proliferation occurred on 1 week in the both MTA and CH groups, followed by the differentiation of odontoblast-like cells on 2 weeks in the MTA group, whereas their differentiation were not facilitated in the CH group. MTA is suggested to be a useful material for DPC with the infected and uninfected pulp tissue.