Background: Acute bone loss after fracture is associated with various effects on the complete recovery process and a risk of secondary fractures among patients. Studies have reported similarities in pathophysiological mechanisms involved in acute bone loss after fractures and osteoporosis. However, given the silence nature of bone loss and bone metabolism complexities, the actual underlying pathophysiological mechanisms have yet to be fully elucidated.
Aim Of Review: To elaborate the latest findings in basic research with a focus on acute bone loss after fracture. To briefly highlight potential therapeutic targets and current representative drugs. To arouse researchers' attention and discussion on acute bone loss after fracture.
Key Scientific Concepts Of Review: Bone loss after fracture is associated with immobilization, mechanical unloading, blood supply damage, sympathetic nerve regulation, and crosstalk between musculoskeletals among other factors. Current treatment strategies rely on regulation of osteoblasts and osteoclasts, therefore, there is a need to elucidate on the underlying mechanisms of acute bone loss after fractures to inform the development of efficacious and safe drugs. In addition, attention should be paid towards ensuring long-term skeletal health.
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http://dx.doi.org/10.1016/j.jare.2022.08.019 | DOI Listing |
Curr Cardiol Rep
January 2025
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, 660 S Euclid Ave, Campus Box 8086, St. Louis, MO, 63110, USA.
Purpose Of Review: This review aims to explore the role of immune memory and trained immunity, focusing on how innate immune cells like monocytes, macrophages, and natural killer cells undergo long-term epigenetic and metabolic rewiring. Specifically, it examines the mechanisms by which trained immunity, often triggered by infection or vaccination, could impact cardiac processes and contribute to both protective and pathological responses within the cardiovascular system.
Recent Findings: Recent research demonstrates that vaccination and infection not only activate immune responses in circulating monocytes and tissue macrophages but also affect immune progenitor cells within the bone marrow environment, conferring lasting protection against heterologous infections.
Objectives: The goal of this systematic review was to critically appraise the existing evidence evaluating osteoporosis' effects on dental implant osseointegration and survival rate.
Data Source: A search was conducted in two databases, PubMed/MEDLINE and Scopus, until October 2024, using the keywords 'osteoporosis,' 'osteopenia,' 'osseointegration,' and 'dental implants'. The inclusion criteria were clinical studies that evaluated the implant placement, complications, and osseointegration results in patients with osteoporosis; literature reviews and clinical studies addressing the outcome were considered; and articles written in English and published since 2000.
J Cell Mol Med
January 2025
Department of Hematology, General Hospital, Tianjin Medical University, Tianjin, China.
Single-cell sequencing of lineage negative (Lin-) cells from patients with myelodysplastic syndromes (MDS) revealed a reduction in ferritin heavy chain 1 (FTH1) levels, yet the significance of this decrease in FTH1 in the pathophysiology of MDS remains unclear. In this study, we evaluated the role of FTH1 in patients with MDS. The mRNA expression of FTH1 in GlycoA nucleated erythrocytes from MDS patients was significantly lower than that in control group.
View Article and Find Full Text PDFJ Periodontal Res
January 2025
Section of Periodontology, Faculty of Odontology, University Complutense, Madrid, Spain.
Aim: This prospective cohort study aimed to evaluate the incidence and risk/protective factors of peri-implantitis over time.
Methods: A university-representative cohort was evaluated at baseline and after a mean follow-up time of 3.9 years.
Unlabelled: is one of the three most frequently mutated genes in age-related clonal hematopoiesis (CH), alongside and . CH can progress to myeloid malignancies including chronic monomyelocytic leukemia (CMML), and is also strongly associated with inflammatory cardiovascular disease and all-cause mortality in humans. DNMT3A and TET2 regulate DNA methylation and demethylation pathways respectively, and loss-of-function mutations in these genes reduce DNA methylation in heterochromatin, allowing de-repression of silenced elements in heterochromatin.
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