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Aim: Recent evidence suggests that acute liver failure (ALF) in some patients may reflect a dysregulated immune response, and that corticosteroids improve survival of the native liver in ALF patients with high serum alanine aminotransferase levels, which are an indication of liver inflammation. However, it is unclear whether steroids are effective for pediatric acute liver failure (PALF). The aim of this retrospective case–control study is to examine whether steroid therapy for PALF accompanied by immune activation improves the survival of native liver and to identify factors that predict responses to steroid treatment. Methods: Of 38 patients with PALF treated at Kyoto University Hospital from February 2006 to August 2022, 19 receiving steroids who met the specific criteria for identifying the pathophysiology of immune activity in the liver (the "Steroid group"), and seven steroid‐free patients who also met the criteria ("Nonsteroid group") were enrolled. Patients in the "Steroid group" were categorized as "responders" or "nonresponders" according to treatment outcome. Clinical and histological data were analyzed. Results: Survival of the native liver in the Steroid group was significantly higher than that in the Nonsteroid group (68% vs. 0%, respectively; p = 0.0052). Nonresponders were significantly younger, with higher Model for End‐stage Liver Disease and pediatric end‐stage liver disease scores, higher prothrombin time – international normalized ratio, and higher serum ferritin levels than responders. Massive hepatic necrosis was more common in nonresponders. Conclusion: Steroid therapy is effective for PALF patients with liver inflammation; however, liver transplantation should be prioritized for young children with ALF accompanied by severe coagulopathy or massive hepatic necrosis. [ABSTRACT FROM AUTHOR]

Introduction Dementia is a devastating disorder in the aging population, progressively compromising cognitive performance. Alzheimer's disease (AD) is responsible for the development of 60% to 80% of all dementia cases [...], Carrying the [epsilon]4 allele of the APOE gene encoding apolipoprotein E (APOE4) markedly increases the risk for late-onset Alzheimer's disease (AD), in which APOE4 exacerbates the brain accumulation and subsequent deposition of amyloid-[beta] (A[beta]) peptides. While the LDL receptor-related protein 1 (LRP1) is a major apoE receptor in the brain, we found that its levels are associated with those of insoluble A[beta] depending on APOE genotype status in postmortem AD brains. Thus, to determine the functional interaction of apoE4 and LRP1 in brain A[beta] metabolism, we crossed neuronal LRP1-knockout mice with amyloid model APP/PS1 mice and APOE3-targeted replacement (APO3-TR) or APOE4-TR mice. Consistent with previous findings, mice expressing apoE4 had increased A[beta] deposition and insoluble amounts of A[beta]40 and A[beta]42 in the hippocampus of APP/PS1 mice compared with those expressing apoE3. Intriguingly, such effects were reversed in the absence of neuronal LRP1. Neuronal LRP1 deficiency also increased detergent-soluble apoE4 levels, which may contribute to the inhibition of A[beta] deposition. Together, our results suggest that apoE4 exacerbates A[beta] pathology through a mechanism that depends on neuronal LRP1. A better understanding of apoE isoform-specific interaction with their metabolic receptor LRP1 on A[beta] metabolism is crucial for defining APOE4- related risk for AD.

Objective: This study aims to investigate how experimental tooth loss affected learning, memory function, and brain pathophysiology in mice. Materials and Methods: The mice (C57BL/6 J, 2‐month‐old, male) were divided into tooth loss and control groups. The behavioral test battery was performed at 6 and 12 months after tooth extraction. The protein levels of the tight junctions in the brains of the mice were analyzed. Hippocampal astrocyte was measured using immunohistochemical staining. Results: The results of behavioral tests and biochemical analysis performed during the 6 months observation period did not show significant differences between the groups. However, the escape latency in the tooth loss group was significantly longer than that in the control group at the 12 months after tooth extraction. The level of claudin‐5 decreased in the tooth loss group. Additionally, hippocampal astrogliosis was found in the tooth loss group. Conclusions: Experimental tooth loss reduced the level of claudin‐5 and caused astrogliosis in the brains of mice, which was accompanied by deterioration of learning functions. This study may provide a new insight about the association between tooth loss and cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Background and Objective: Previous studies have reported that tooth loss is a risk factor of Alzheimer's disease (AD). However, the association between tooth loss and cognition and the impact of tooth loss on the molecular pathogenesis of AD remain elusive. In this study, we tested the effect of tooth loss on learning and memory and on the molecular pathogenesis of AD in an aged AD model mice.Materials and Methods: We divided 14-month-old amyloid precursor protein (APP) transgenic mice, an AD model mouse line, into upper molar extracted group (experimental) and molar intact group (control). At 18 months old, we analysed not only the changes of amyloid-beta (Aβ), pyramidal cells in the brain but also the learning and memory ability with step-through passive avoidance test.Results: The amount of Aβ and the number of pyramidal cells in the hippocampus were not significantly different between the experimental and control group. Similarly, the difference of learning and memory ability could not be distinguished between the groups.Conclusion: Neither molecular pathogenesis of AD nor associated learning and memory were aggravated by tooth loss in these mice. The limited results of this study which used the aged mice may help the dental profession to plan and explain treatments to patients with AD, which must be designed while taking into account the severity of the AD symptoms. [ABSTRACT FROM AUTHOR]

The aim of the study was to investigate the effect of parathyroid hormone (PTH) on primary stability of dental implants in a bone-reduced model. Ten female New Zealand white rabbits underwent ovariectomy and were administered glucocorticoid to induce osteoporosis. One group was administered PTH intermittently by subcutaneous injection for 4 weeks (PTH-group) and the other group was given injections of saline for 4 weeks (Osteoporosis; OP-group). After the administration period, implants were inserted into the distal femoral epiphyses of each animal. At implant placement, insertion torque (IT) and implant stability quotient (ISQ) were measured. Histological examination revealed newly formed trabecular bone around the implant socket in the PTH-group but not in the OP-group. The trabecular bone structures in the PTH-group appeared thicker than those in the OP-group. In the PTH-group, the mean IT value was significantly greater than that in the OP-group (29.8 ± 6.2 Ncm and 10.0 ± 2.1 Ncm, respectively; P < 0.05). The ISQ value in the PTH-group was significantly higher than that in the OP-group (74.7 ± 11.2 and 55.9 ± 13.5, respectively; P < 0.05). Intermittent PTH administration could be an effective treatment for achieving favorable primary stability of dental implants in patients with osteoporosis. (J Oral Sci 58, 241-246, 2016). [ABSTRACT FROM AUTHOR]

Background: We first reported that intraoral imaging with a color-imaging intraoral scanner could evaluate stained plaques and contribute to oral hygiene instructions. In this study, we aimed to evaluate the effects of red and blue staining on dental hygiene assessment with an intraoral scanner using plaque control record values and plaque-stained areas., Material and Methods: Fifteen patients (six males and nine females, aged 25-85 years) were included in this study. The patients' teeth were stained with a two-tone (blue and red) dental plaque staining solution, and images of their teeth were recorded with an intraoral scanner and a digital camera. The plaque control record was measured by direct viewing, as usual, and on a monitor using intraoral scanner image. In addition, the plaque deposition area was measured using images obtained using an intraoral scanner and images taken by a digital camera., Results: Most parts were stained red and blue dental plaque staining was also observed. Plaque control record values tended to be higher in the intraoral scanner evaluation than in the direct evaluation. The plaque-stained area was larger in intraoral scanner images than in camera images., Conclusions: It is possible to use a two-tone plaque-staining solution for oral health evaluation using an intraoral scanner. In the future, we need to investigate cases of blue-stained plaques. Key words: Intraoral scanner, oral hygiene, dental plaque, preventive dentistry., Competing Interests: The authors declare that they have no competing interests., (Copyright: © 2024 Medicina Oral S.L.)