Progressive Destruction Research Articles

Comparative Evaluation of the Degree of Liver Fibrosis on Ultrasound-Based Fibroscan and Hyaluran Tests in Patients with Chronic Liver Disease

Abstract Background: Chronic liver disease (CLD) in the clinical context is a disease process affecting the liver, which involves a process of progressive destruction and regeneration of the liver parenchyma, leading to fibrosis and cirrhosis. Both FibroScan, which is an ultrasound study also known as transient elastography, and Hyaluran test (biochemical test) are rapid safe non-invasive examinations of the liver, which can be used to monitor the degree and progression of fibrotic changes in the liver. Objective: The purpose of this study was to compare the degree of liver fibrosis, as measured on ultrasound-based FibroScan and Hyaluran tests in CLD. Materials and Methods: This was a two-stage comparative study carried out on patients with clinically diagnosed CLD and non-CLD subjects at Jos University Teaching Hospital (JUTH) from January to June 2022. The first stage involved the use of ultrasound-based FibroScan to assess the degree of tissue stiffness in the liver of both CLD and non-CLD subjects. The unit of measurement of FibroScan is kilopascals (Kpa). In the second stage, blood samples were collected from CLD and non-CLD subjects for Hyaluran tests. The unit of measurement of Hyaluran tests is expressed in nanograms per milliliter (ng/mL). Results: This study comprises of 75 apparently normal subjects and 75 CLD patients. The mean FibroScan level was significantly higher (17.55 ± 7.5 kPa) in patients with CLD compared to apparently normal subjects (5.06 ± 3.1 kPa), t = 5.783; P < 0.001. The mean Hyaluran value in the patients with CLD was 30.01 ± 20.39 ng/mL, which was significantly higher than that in the normal subjects with the mean value of 20.39 ± 8.27 ng/mL, t = 3.784; P < 0.001. In evaluating the correlation between FibroScan and Hyaluran in assessing the degree of fibrosis using the Spearman correlation coefficient, it was observed that the degree of fibrosis at the earlier stage (minimal) signifies a positive but weak correlation (P = 0.151), but this was not statistically significant (P = 0.492). However, mild/moderate and severe fibrosis demonstrate moderate positive (P = 0.505 and 0.550) and statistically significant correlation with P value of 0.020 and 0.011, respectively. Conclusion: The study demonstrated a statistically significant difference in the mean FibroScan value in non-CLD and CLD cases. The results also indicated statistically significant difference in the mean Hyaluran value in non-CLD and the CLD cases. The study demonstrated a significant correlation between Hyaluran and FibroScan in assessing the degree of moderate and severe fibrosis in CLD.

Vitiligo-update on pathogenesis, diagnostics and therapy

Vitiligo is acommon skin disease leading to depigmentation that is associated with progressive destruction of melanocytes. The main subtype, nonsegmental vitiligo (NSV), is considered achronic autoimmune disease leading to activation of melanocyte-specific CD8+ lymphocytes and development of acutaneous immune memory. Vitiligo can result in significant impairment of quality of life and is associated with anumber of comorbidities. Despite the existence of national guidelines and international treatment recommendations, there is astrong need for improved health care for patients with vitiligo. The options in the treatment algorithm for vitiligo are similar and consisted until recently of only topical and systemic corticosteroids, topical calcineurin inhibitors, phototherapy, and surgical interventions. New insights into the pathobiological role of the interferon signature in vitiligo have most recently contributed to the approval of the first vitiligo-specific therapy with the topical Janus kinase1/2 inhibitor ruxolitinib for patients with NSV.

Smart biomaterial gels for periodontal therapy: A novel approach.

Periodontitis, a chronic inflammatory condition of the oral cavity, is characterized by the progressive destruction of the supporting structures of the teeth. The pathogenic effects of periodontopathogens extend beyond the local periodontal environment, contributing to systemic health complications, thereby underscoring the need for effective therapeutic strategies. Current standard treatments, which involve mechanical debridement coupled with systemic anti-inflammatory and antibiotic therapies, are often associated with limited efficacy, adverse effects, and the emergence of antibiotic resistance. Recent advancements in localized drug delivery systems present an innovative alternative, offering site-specific targeting with sustained therapeutic action. Smart drug delivery platforms, designed to respond to the unique microenvironment of periodontal pockets, undergo physicochemical transformations such as gelation or controlled drug release, enhancing treatment efficacy. This review comprehensively explores the etiological and prognostic factors of periodontitis, critical diagnostic biomarkers, and an in-depth analysis of stimuli-responsive biomacromolecule-based gels. These systems are evaluated for their structural properties, biological compatibility, and therapeutic potential while addressing their limitations and barriers to clinical translation. By integrating insights into the interplay between material properties and biological performance, this review highlights the future role of these advanced delivery systems in overcoming challenges in periodontal healthcare. Such approaches aim to bridge the gap between bench-side innovation and bedside application, offering the transformative potential to enhance therapeutic outcomes and improve patient quality of life in managing periodontal diseases.

Treatment advances in Vitiligo: An Updated Review

Introduction Vitiligo is a common disorder of depigmentation caused by the progressive destruction of melanocytes that affects the skin, hair, and mucous membranes, clinically presenting as depigmented macules and leukotrichia. This condition, affecting millions of people worldwide, has a significant psychosocial burden on patients’ quality of life, particularly in relation to skin colour. The etiopathogenesis of this disorder is obscure, but multiple factors contribute to the loss of melanocytes in the skin, like oxidative stress, inflammation, genetics, and autoimmunity. The treatment of vitiligo has been challenging over the past years, but recent developments in understanding the etiopathogenesis of the disease have paved the way for the development of more effective and promising therapeutic treatment options. Objective The aim of this review was to provide an overview of the underlying mechanisms and highlight the latest advances in the treatment of vitiligo. Methodology This review was performed according to PRISMA (Preferred Reporting Items for Systematic Reviews and Metanalyses) guidelines. A comprehensive search of the literature was carried out through the PubMed electronic database from inception to 31 December 2023 using the following search terms “vitiligo” AND “JAK inhibitors”, “vitiligo” AND “prostaglandin”, “vitiligo” AND “afamelanotide”, “vitiligo” AND “antioxidants”, “vitiligo” AND “vitamin D3”, “vitiligo AND “statins”, “vitiligo” AND “TNF-alpha”, “vitiligo” AND “interleukin”, “vitiligo” AND “light therapy”. Two independent reviewers screened titles, abstracts, and full texts to select papers dealing with vitiligo and its treatment. Conclusion The advent of treatment modalities like Janus kinase inhibitors, prostaglandin analogues, antioxidants, TNF-α inhibitors, targeted phototherapy, and excimer lasers has revolutionized the therapeutic possibilities, offering a ray of hope to the individuals suffering from this devastating condition.

Exploring the link between genetic disorders and early-onset periodontal disease

Periodontal disease is a complex, multifactorial condition characterized by chronic inflammation and progressive destruction of the tooth-supporting structures. Among its various forms, early-onset periodontitis is particularly aggressive and often associated with genetic predispositions. Genetic and epigenetic factors play pivotal roles in shaping host susceptibility to this disease by influencing immune responses, inflammatory regulation, and tissue homeostasis. Single-nucleotide polymorphisms (SNPs) in genes encoding cytokines, such as interleukin-1β and tumor necrosis factor-alpha, are linked to heightened inflammatory responses, amplifying tissue damage and accelerating disease progression. Additionally, polymorphisms in genes like TLR2 and TLR4 impair microbial recognition, promoting chronic inflammation and dysbiosis. Epigenetic modifications, including DNA methylation and histone acetylation, further modulate gene expression, contributing to the dynamic interplay between genetic predispositions and environmental factors like smoking or poor oral hygiene. Emerging research has also highlighted genetic markers such as human leukocyte antigen (HLA) alleles and matrix metalloproteinase (MMP) variants as predictors of disease severity and therapeutic outcomes. These insights have driven the development of targeted therapies, including inhibitors of pro-inflammatory mediators, MMP inhibitors, and potential miRNA-based interventions. High-throughput technologies, such as genome-wide association studies (GWAS), have expanded the understanding of genetic pathways involved in periodontal disease. These advances enable earlier disease detection and personalized treatment strategies, offering the potential to mitigate progression and reduce the burden of severe periodontitis. The integration of genetic and epigenetic research into clinical practice marks a significant step toward precision medicine, providing a framework for tailored prevention and therapeutic interventions aimed at improving patient outcomes. Future research must continue to explore these genetic mechanisms to uncover novel biomarkers and refine targeted treatment approaches for periodontal disease.

P1310 Role of gut pathobiont-derived membrane vesicles for biliary epithelium in PSC-IBD

Abstract Background Primary sclerosing cholangitis (PSC), a cholestatic liver disease highly associated with inflammatory bowel disease (IBD), is characterized by progressive inflammatory destruction of bile ducts. Bacterial membrane vesicles (bEVs) derived from gut pathobionts may play a significant role in the pathogenesis of PSC-IBD by disrupting the biliary barrier, promoting liver inflammation and contributing to liver fibrosis. A deeper understanding of how bEVs influence bile duct homeostasis is crucial for unraveling the mechanisms behind PSC-IBD and developing targeted therapeutic strategies. Methods Bile duct organoids were generated from WT mice and PSC-IBD patients. BEVs were isolated from commensals or PSC-associated gut pathobionts following MISEV guidelines. To assess the role of bEVs to ductal barrier dysfunction and inflammation, we employed an organoid based permeability assay, immunofluorescence staining, qPCR and bulk RNA sequencing. Furthermore, to investigate whether the presence and amount of bEVs in the systemic circulation were associated with PSC-IBD, we analyzed serum-derived EVs from either healthy control, as well as PSC and PSC-IBD patients using Nanoparticle Tracking Analysis (NTA), Transmission Electron Microscopy (TEM) and a TLR4-Receptor based reporter assay. Results Our results demonstrate that particularly bEVs isolated from gut pathobionts trigger signaling pathways associated with inflammation in both murine and human biliary epithelial cells. Furthermore, we observed a disease and strain specific fingerprint after bEV treatment, which was characterized by several significantly enriched terms related to PSC-related inflammation, including genes involved in T-helper 17 cell differentiation, and tumor necrosis factor (TNF) signaling. However, we did not observe a direct impact of bEVs on biliary barrier function. Consistent with this, we detected increased levels of bEVs in the systemic circulation of PSC-IBD patients, but not in those with PSC alone or in healthy controls, suggesting that these bacterial components may translocate across a compromised intestinal barrier into the bloodstream. Conclusion Overall, our study suggests that bEVs may contribute to biliary inflammation, but not barrier dysfunction and thereby may represent a novel player in the pathogenesis of PSC-IBD. Additionally, it underscores the critical role of bEVs in host-microbe communication, suggesting their potential as diagnostic biomarkers and highlighting, that therapeutic strategies targeting bEVs could offer promising avenues for managing PSC-IBD.

Targeting GABA signaling in type 1 diabetes and its complications- an update on the state of the art.

Type 1 diabetes (T1D) is an autoimmune disease that leads to the progressive destruction of insulin-producing β cells, resulting in lifelong insulin dependence and a range of severe complications. Beyond conventional glycemic control, innovative therapeutic strategies are needed to address the underlying disease mechanisms. Recent research has highlighted gamma-aminobutyric acid (GABA) as a promising therapeutic target for T1D due to its dual role in modulating both β cell survival and immune response within pancreatic islets. GABA signaling supports β cell regeneration, inhibits α cell hyperactivity, and promotes α-to-β cell transdifferentiation, contributing to improved islet function. Moreover, GABA's influence extends to mitigating T1D complications, including nephropathy, neuropathy, and retinopathy, as well as regulating central nervous system pathways involved in glucose metabolism. This review consolidates the latest advances in GABA-related T1D therapies, covering animal preclinical and human clinical studies and examining the therapeutic potential of GABA receptor modulation, combination therapies, and dietary interventions. Emphasis is placed on the translational potential of GABA-based approaches to enhance β cell viability and counteract autoimmune processes in T1D. Our findings underscore the therapeutic promise of GABA signaling modulation as a novel approach for T1D treatment and encourage further investigation into this pathway's role in comprehensive diabetes management.

Shorter telomere length in COPD cases secondary to biomass-burning smoke exposure

BackgroundChronic obstructive pulmonary disease (COPD) is characterized by progressive airflow obstruction and destruction of lung tissue, primarily attributed to tobacco smoking. However, other factors like biomass-burning smoke (BS) exposure are also implicated. COPD has been described as an accelerated aging disease, and telomere length is a biomarker of aging.MethodsThis study examined telomere length in 189 Mexican individuals, from which 93 developed COPD secondary to BS exposure (BE-COPD); the rest of the participants were exposed to BS but did not develop the disease. Lung function parameters were measured by spirometry, and relative telomere length (rTL) from peripheral blood DNA was determined using multiplex qPCR.ResultsResults showed rTL to inversely correlate with age (R2=-0.207, p = 0.006) and with the hours-a-day of BS exposure (R2=-0.297, p < 0.001). Within BE-COPD cases, rTL was associated with daily BS exposure, and BE-COPD individuals exhibited a reduced rTL compared to controls (1.39 ± 0.45 vs. 0.89 ± 0.50; p < 0.001). When compared by rTL length in BE-COPD cases, longer telomeres were associated with decreased COPD risk (β = 0.134, 95% CI = 0.053–0.339; p < 0.001). However, no significant relationship was found between rTL and clinical or lung function parameters in the BE-COPD group.ConclusionsThis is the first study to document that individuals with COPD secondary to biomass smoke exposure present shorter telomeres than BS-exposed subjects who did not develop the disease.

Anti-inflammatory effects of moxifloxacin and levofloxacin on cadmium-activated human astrocytes: Inhibition of proinflammatory cytokine release, TLR4/STAT3, and ERK/NF-κB signaling pathway.

Cadmium is a non-essential element and neurotoxin that causes neuroinflammation, which leads to neurodegenerative diseases and brain cancer. To date, there are no specific or effective therapeutic agents to control inflammation and alleviate cadmium-induced progressive destruction of brain cells. Fluoroquinolones (FQs), widely used antimicrobials with effective blood-brain barrier penetration, show promise in being repurposed as anti-inflammatory drugs. Therefore, we aimed to test the efficacy of repurposed FQs for the treatment of cadmium-induced inflammation using cultures of U-87 MG human astrocytes and primary human astrocytes. Both FQs abrogated cadmium-induced interleukin (IL)-6 and IL-8 release from human astrocytes in a concentration and time-dependent manner, although levofloxacin had a stronger inhibitory effect than moxifloxacin. The downregulation of inflammatory cytokine release occurred with a concomitant reduction in cadmium-induced elevations in p65 nuclear factor-κB (NF-κB) and extracellular signal-regulated kinases (ERKs) 1/2 phosphorylation. Additionally, levofloxacin treatment significantly alleviated cadmium-induced activation of phosphorylated NF-κB translocation and toll-like receptor (TLR)-4/signal transducer and activator of transcription (STAT) 3 signaling. Transcriptome analysis revealed that modulation of inflammation-related pathways was the most enriched after FQ treatment. Our data suggest that FQs, particularly levofloxacin, attenuate the inflammatory process mediated by cadmium in human astrocytes. These effects may be mediated, at least in part, by inhibition of immune pathways regulated by TLR4, STAT3, ERK MAPK, and NF-κB.

What is Rheumatoid factor-from screening to personalized management.

The rheumatoid factor (RF) is a representative autoantibody against the crystallizable fragment (Fc) of denatured immunoglobulin (Ig) G that are primarily detected in patients with rheumatoid arthritis (RA). Although five types of tumor necrosis factor (TNF) inhibitors can be used to treat RA, no guidelines are available for selecting the appropriate inhibitor for treatment. High serum RF levels are associated with high disease activity, progressive joint destruction, life prognosis associated with organ damage, decreased treatment responsiveness to TNF inhibitors and other drugs, and low treatment retention rates. Meanwhile, certolizumab pegol (CZP), a TNF inhibitor without the Fc region, remains at high concentrations in the blood. Unlike other antibody drugs with the Fc region, CZP maintains efficacy in patients with high serum RF levels. When serum IgM-RF levels are high, antibody drugs with the Fc region are more likely to bind to IgM-RF and be degraded. Thus, CZP without the Fc region may be more favorable for patients with high serum RF levels.

Microfluidic organ-on-chip systems for periodontal research: advances and future directions.

Advances in tissue engineering and microfluidic technologies have enabled the development of sophisticated in vitro models known as organ-on-a-chip (OoC) or microphysiological systems. These systems enable to potential to simulate the dynamic interactions between host tissues and their microenvironment including microbes, biomaterials, mechanical forces, pharmaceutical, and consumer-care products. These fluidic technologies are increasingly being utilized to investigate host-microbe and host-material interactions in oral health and disease. Of interest is their application in understanding periodontal disease, a chronic inflammatory condition marked by the progressive destruction of periodontal tissues, including gingiva, periodontal ligament, and alveolar bone. The pathogenesis of periodontal disease involves a complex interplay between microbial dysbiosis and host immune responses, which can lead to a loss of dental support structures and contribute to systemic conditions such as cardiovascular disease, diabetes, and inflammatory bowel disease. This provides a comprehensive overview of the latest developments in millifluidic and microfluidic systems designed to emulate periodontal host-microbe and host-material interactions. We discuss the critical engineering and biological considerations in designing these platforms, their applications in studying oral biofilms, periodontal tissue responses, and their potential to unravel disease mechanisms and therapeutic targets in periodontal disease.

The immunological landscape of primary biliary cholangitis: Mechanisms and therapeutic prospects.

Primary Biliary Cholangitis (PBC) is a chronic cholestatic liver disease characterized by the progressive destruction of intrahepatic bile ducts, leading to fibrosis, and potentially cirrhosis. PBC has been considered a prototypical autoimmune condition, given the presence of specific autoantibodies and the immune response against well-defined mitochondrial autoantigens. Further evidence supports the interaction of immunogenetic and environmental factors in the aetiology of PBC. An immunological attack on biliary epithelial cells (BECs) with secondary failure of biliary transporters, e.g. the anion exchange protein 2 (AE2), is traditionally considered the primum movens. A recent hypothesis proposes a primary failure of BECs with the downregulation of AE2 secondary to epigenetic mechanisms (miR-506 overexpression) which then triggers the immunological storm. This highlights the secretory defect as culprit and sustaining factor in the pathogenesis of PBC with UDCA helping to restore this protective mechanism by promoting bicarbonate secretion and reducing bile acid toxicity. In this review we aim to provide the most recent evidence on the immunopathogenesis of PBC. We will analyse the immune function of the biliary epithelium, assessing the immunomodulatory functions of the bile acids and the evidence of the immunological roles of the secretory pathways targeted by the current treatments.

The current progress and futural prospects of ultrasound-targeted microbubble destruction for liver diseases: a narrative review

The current progress and futural prospects of ultrasound-targeted microbubble destruction for liver diseases: a narrative review

Mitochondrial Dysfunction in Diabetic Periodontitis: Mechanisms and Therapeutic Potential.

Diabetic periodontitis is a common oral complication of diabetes characterized by progressive destruction of periodontal tissues. Recent evidence suggests that mitochondrial dysfunction plays a crucial role in the pathogenesis and progression of this condition. This review aims to systematically summarize the role and potential mechanisms of mitochondrial dysfunction in diabetic periodontitis. We first explore the relationship between diabetes and mitochondrial dysfunction, then analyze the specific manifestations of mitochondrial dysfunction in diabetic periodontitis, including morphological changes, energy metabolism disorders, increased oxidative stress, and enhanced apoptosis. We further delve into the connections between mitochondrial dysfunction and the pathogenic mechanisms of diabetic periodontitis, such as exacerbated inflammatory responses, decreased tissue repair capacity, and autophagy dysregulation. Finally, we discuss potential therapeutic targets based on mitochondrial function, including antioxidant strategies, mitochondria-targeted drugs, and autophagy regulators. We also propose future research directions, emphasizing the need for in-depth exploration of molecular mechanisms, development of new diagnostic markers and therapeutic strategies, and personalized treatment approaches. This review provides new insights into understanding the pathogenic mechanisms of diabetic periodontitis and offers a theoretical basis for developing targeted prevention and treatment strategies to improve oral health in diabetic patients.

Microstructural and Seismic Characteristics of Mantle Xenoliths From Damaping Area, and Their Geodynamic Implications of North China Craton Destruction

AbstractThe large‐volume lithospheric mantle xenoliths around the Damaping area provides valuable insights into the detailed destruction progression of the North China Craton (NCC). This paper presents a quantitative analysis of the microstructural and seismic properties of oriented mantle xenoliths (with distinct foliation and lineation). The selected peridotites all have coarse‐grained textures. The olivine crystallographic preferred orientations (CPOs) are predominantly axial‐[010] type (or AG‐type), with all xenoliths have girdled [100]OL and [001]OL characteristics. B‐type olivine CPO is newly discovered in the research area. Analysis of crystallographic vorticity axis (CVA) projections indicates that more than half of Damaping xenoliths have CVA maxima (sub)parallel to the lineation. These microstructure characteristics suggest that B‐type CPOs were formed before the onset of pure shear‐dominated transpression and pyroxene restriction, which significantly influenced the lithospheric mantle evolution. The upwelling asthenosphere beneath Eastern Block of the NCC not only delaminated its lithospheric mantle but also experienced rollback and flowed along the WNW‐SEE direction. This progression likely serves as the primary driving force of transpression. If foliation were vertical and lineation were horizontal, the valid S‐wave anisotropies range is 5%–12%. All selected samples are spinel facies, resulting in a maximum in situ depth of 90 km, and the calculated SKS splitting delay times (0.5–1.3 s) align with previous seismological observations. The SKS direction in the research area is predominantly oriented perpendicular (NNE‐SSW) to the flow direction of nearby asthenosphere. These characteristics are likely attributed to transpression. Therefore, the “fossil” anisotropy may have developed after the cessation of transpression.

&lt;b&gt;Activities limitation in patients with rheumatoid arthritis: A cross sectional study&lt;/b&gt;

Background: Rheumatoid arthritis (RA) is an auto immune disease leads to progressive destruction of synovial membrane of joints, causing pain, deformity and functional limitation, which results in severe disability in performing daily and professional activities. The burden of rheumatoid arthritis RA in general population varies high in females. The most common cause of rheumatoid arthritis in individual life is activities limitations. Rheumatoid arthritis is a disease that should be examined and assessed carefully in the general peoples as well as in patients , because if this disease is identified later can lead to a state of irreversible damage of the articular cartilage of the joints , which can lead further disability and increases activities limitation . Objective: to asses activities limitation in patients with rheumatoid arthritis Methodology: Total of 132 patients in the study. Data was collected at rheumatology OPD at arif diagnostic hospital and research center Hayatabad Peshawar. Data from patients were collected through health assessment questionnaire (HAQ) convenient sampling technique was used, data was analyzed using SPSS version 26. Result: total of 132 participated, ranging in age from 25-60 years, mean age was 47.6±10.3. Female patients were more than male patients. Out of 132 patients 2 67.4% have female patients and 32.6% were have male patients with rheumatoid arthritis Conclusion: most of the patients with rheumatoid arthritis were having activities limitations in their daily life. in term of severity most patients were have moderate pain . Keywords: activities limitation, rheumatoid arthritis, HAQ

Rhaponticin Alleviates Collagen-induced Arthritis by Inhibiting NLRP3/GSDMD-mediated Neutrophil Extracellular Traps.

Neutrophil extracellular traps (NETs) play an important role in the inflammatory response and progressive joint destruction in rheumatoid arthritis (RA). Rhaponticin (Rha) is a stilbene glycoside compound with antioxidant and anti-inflammatory effects. This study aimed to investigate the therapeutic potential of Rha in RA, with a specific focus on its effects on NETs and on the underlying mechanisms of Rha. NETs formation induced by phorbol 12-myristate 13-acetate (PMA) and a collagen-induced arthritis (CIA) mouse model were implemented to evaluate the pharmacological effects of Rha in vitro and in vivo. The potential mechanism of Rha in improving RA was screened and verified using the SuperPred and DisGeNET databases. Disulfiram (a GSDMD inhibitor) and S100a8cre GSDMDfl/fl mice were used to confirm whether GSDMD is key to the role of Rha.The findings demonstrate that Rha significantly inhibited reactive oxygen species and NETs production in PMA-activated neutrophils. In vivo, Rha treatment significantly relieved joint symptoms in CIA mice and NETs production. Mechanistically, Rha reduced NETs production via inhibition of NLRP3/GSDMD activation. Neutrophil-specific GSDMD depletion eliminated the effects of Rha on NETs production in vitro. Disulfiram eliminated the effects of Rha on the inhibition of NETs production and alleviated joint inflammation in mice in vivo and in vitro. Overall, our results indicated that Rha exerts a protective effect against CIA by inhibiting NETs production through the NLRP3/GSDMD pathway. The results of this study provide new strategies for treating RA.

Effectiveness of Total Hip Arthroplasty Combined With Hip Braces for Hip Charcot Arthropathy.

Charcot arthropathy is characterized by varying degrees of sensory loss and rapidly progressive joint destruction. Historically, limited studies indicated that Charcot arthropathy of the hip joint may be a contraindication for total hip arthroplasty (THA). Yet, some recent studies have shown that good clinical results and acceptable survival rate. Hence, this study aimed to investigate clinical outcomes, radiographic outcomes, complication rates and survivorship of primary THA in Charcot arthropathy. We retrospectively included 11 patients (11 hips) with Charcot arthropathy who underwent THA between 1998 and 2016. All involved patients were diagnosed as syphilis. All patients had classic radiographic findings of Charcot arthropathy. The hip braces were used in all patients for six weeks after surgery. Outcome measures included VAS, Oxford Hip Score, and UCLA score. Statistical analyses involved t-tests, chi-square tests, and Kaplan-Meier survival analysis. The average follow-up period was 81.73 months. The average VAS, Oxford Hip Score, and UCLA score were improved significantly. There was higher complication rate of 45.5% after THA. Reoperation was carried out in two patients due to dislocation and acetabular component loosening. The Kaplan-Meier survivorship with an end point of reoperation for any reason was 81.8%. THA is proved to be reasonable in improving hip joint function, which is suitable for patients with Charcot hip joint. Although the complication rate is high, we consider that THA combined with hip brace may be a valid treatment choice for Charcot arthropathy with detailed preoperative planning and proper precautions.

Analysis of structural safety of structures when accounting processes of progressive destruction

The reasons for the occurrence of failures are considered, the consequence of which can be considered the progressive collapse of structures and the consideration of structural safety in more expanded concepts than when assessing the first and second groups of limit states for low-rise buildings built from local materials.

Machine Learning Approaches for Integrating Clinical and Radiographic Data in the Early Detection of Osteonecrosis of the Jaw

Osteonecrosis of the jaw (ONJ) is a severe bone condition characterized by the progressive destruction of the jawbone, often associated with the long-term use of antiresorptive medications such as bisphosphonates. Early detection of ONJ remains a significant clinical challenge due to the subtle onset of symptoms and limitations in current diagnostic methods, which rely on clinical assessment and radiographic imaging. Conventional techniques, such as panoramic X-rays, computed tomography (CT), and magnetic resonance imaging (MRI), often fail to detect early-stage ONJ, delaying diagnosis until more advanced stages. Machine learning (ML) has emerged as a powerful tool for improving the early detection and diagnosis of ONJ by integrating clinical and radiographic data. ML algorithms, including supervised learning methods like random forests, support vector machines, and deep learning models such as convolutional neural networks, are particularly suited for analyzing complex datasets and identifying patterns that are undetectable by traditional methods. These models can enhance the sensitivity and specificity of ONJ detection, potentially leading to earlier interventions and improved patient outcomes. This paper reviews the current state of ML applications in ONJ detection, emphasizing the integration of clinical and radiographic data. It discusses various ML approaches, their potential to improve diagnostic accuracy, and the challenges involved in data integration. Also, this review highlights future directions of ML as a diagnostic tool that has the potential to revolutionize ONJ detection, offering a path toward earlier, more accurate diagnosis and better patient care.