Survival analysis of implants after surgical treatment of peri-implantitis based on bone loss severity and surgical technique: a retrospective study.

BACKGROUND: Few trials have compared the results of surgical treatment for peri-implantitis based on severity of peri-implantitis and surgical method. This study investigated the survival rate of implants based on type of surgical method used and initial severity of peri-implantitis. Classification of severity was determined based on bone loss rate relative to fixture length. METHODS: Medical records of patients who underwent peri-implantitis surgery from July 2003 to April 2021 were identified. Classification of peri-implantitis was divided into 3 groups (stage 1: bone loss < 25% (of fixture length), stage 2: 25% < bone loss < 50%, stage 3: bone loss > 50%) and performance of resective or regenerative surgery was investigated. Kaplan-Meier survival curves and Cox hazards proportional models were used to analyze the cumulative survival rate of implants. Median survival time, predicted mean survival time, hazard ratio (HR), and 95% confidence interval (CI) were calculated. RESULTS: Based on Kaplan-Meier analysis, 89 patients and 227 implants were included, and total median postoperative survival duration was 8.96 years. Cumulative survival rates for stage 1, 2, and 3 were 70.7%, 48.9%, and 21.3%, respectively. The mean survival time for implants in stage 1, 2, and 3 was 9.95 years, 7.96 years, and 5.67 years, respectively, with statistically significant difference (log-rank p-value < 0.001). HRs for stage 2 and stage 3 were 2.25 and 4.59, respectively, with stage 1 as reference. Significant difference was not found in survival time between resective and regenerative surgery groups in any peri-implantitis stage. CONCLUSIONS: The initial bone loss rate relative to the fixture length significantly correlated with the outcome after peri-implantitis surgery, demonstrating a notable difference in the long-term survival rate. Difference was not found between resective surgery and regenerative surgery in implant survival time. Bone loss rate could be utilized as a reliable diagnostic tool for evaluating prognosis after surgical treatment, regardless of surgical method used. TRIAL REGISTRATION: Retrospectively registered. (KCT0008225).

Natural Products as New Approaches for Treating Bladder Cancer: From Traditional Medicine to Novel Drug Discovery.

Bladder cancer (BC) is a heterogeneous disease that a tumor develops in the bladder lining and in some cases, the bladder muscle. Chemotherapy and immunotherapy are commonly used to treat bladder cancer. However, chemotherapy can cause burning and irritation in the bladder while BCG immunotherapy, which is the main type of intravesical immunotherapy for bladder cancer, can also cause burning in the bladder and flu-like symptoms. Thus, drugs originating from natural products have attracted much attention due to the reports that they have anti-cancer properties with low adverse effects. In this study, eighty-seven papers that dealt with natural products preventing or treating bladder cancer were reviewed. The studies were classified into the following mechanism: 71 papers on cell death, 5 papers on anti-metastasis, 3 papers on anti-angiogenesis, 1 paper on anti-resistance, and 7 papers on clinical trials. Most of the natural products that induced apoptosis up-regulated proteins such as caspase-3 and caspase-9. Regarding anti-metastasis, MMP-2 and MMP-9 are regulated frequently. Regarding anti-angiogenesis, HIF-1α and VEGF-A are down-regulated frequently. Nevertheless, the number of papers regarding anti-resistance and clinical trial are too few, so more studies are needed. In conclusion, this database will be useful for future in vivo studies of the anti-bladder cancer effect of natural products, in the process of selecting materials used for the experiment.

Stochastic chromatin packing of 3D mitotic chromosomes revealed by coherent X-rays.

DNA molecules are atomic-scale information storage molecules that promote reliable information transfer via fault-free repetitions of replications and transcriptions. Remarkable accuracy of compacting a few-meters-long DNA into a micrometer-scale object, and the reverse, makes the chromosome one of the most intriguing structures from both physical and biological viewpoints. However, its three-dimensional (3D) structure remains elusive with challenges in observing native structures of specimens at tens-of-nanometers resolution. Here, using cryogenic coherent X-ray diffraction imaging, we succeeded in obtaining nanoscale 3D structures of metaphase chromosomes that exhibited a random distribution of electron density without characteristics of high-order folding structures. Scaling analysis of the chromosomes, compared with a model structure having the same density profile as the experimental results, has discovered the fractal nature of density distributions. Quantitative 3D density maps, corroborated by molecular dynamics simulations, reveal that internal structures of chromosomes conform to diffusion-limited aggregation behavior, which indicates that 3D chromatin packing occurs via stochastic processes.

Hepatitis B virus X protein induces apoptosis by enhancing translocation of Bax to mitochondria.

Hepatitis B virus X protein (HBx) is essential for viral replication and plays an important role in viral pathogenesis. HBx transactivates many viral and cellular genes and participates in cellular signal transduction pathways, proliferation, and apoptosis. In the present study, we report that HBx induces apoptosis by enhancing the translocation of Bax to mitochondria, followed by inducing the loss of mitochondrial membrane potential and release of cytochrome C. In addition, Bcl-2, inhibitor of Bax, rescues the disruption of mitochondrial membrane potential and DNA fragmentation induced by serum starvation in HepG2-X cells expressing HBx. We also found that HBx binds directly to Bax and interferes with the interaction between Bax and 14-3-3epsilon to enhance the translocation of Bax to mitochondria. Taken together, our data suggest that HBx induces apoptosis by interacting with Bax and enhancing its translocation to mitochondria.