In recent years, the mechanisms and clinical significance of vascular calcification have been increasingly investigated. For over a century, however, pathologists have recognized that vascular calcification is a form of heterotopic ossification. In this review, we aim to describe the pathology and molecular processes of vascular ossification, to characterize its clinical significance and treatment options, and to elucidate areas that require further investigation. The molecular mechanisms of vascular ossification involve the activation of regulators including bone morphogenic proteins and chondrogenic transcription factors and the loss of mineralization inhibitors like fetuin-A and pyrophosphate. Although few studies have examined the gross pathology of vascular ossification, the presence of these molecular regulators and evidence of microfractures and cartilage have been demonstrated on heart valves and atherosclerotic plaques. These changes are often triggered by common inflammatory and metabolic disorders like diabetes, hyperlipidemia, and chronic kidney disease. The increasing prevalence of these diseases warrants further research into the clinical significance of vascular ossification and future treatment options.
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http://dx.doi.org/10.1016/j.bone.2017.07.006 | DOI Listing |
Calcif Tissue Int
January 2025
Department of Paediatric Endocrinology, Alder Hey Children's Hospital, Liverpool, UK.
Autosomal recessive hypophosphatemic rickets type 2 (ARHR2) is an uncommon hereditary form of rickets characterised by chronic renal phosphate loss and impaired bone mineralisation. This results from compound heterozygous or homozygous pathogenic variants in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), a key producer of extracellular inorganic pyrophosphate (PPi) and an inhibitor of fibroblast growth factor23 (FGF23). ENPP1 deficiency impacts FGF23 and increases its activity.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
ACS Biomater Sci Eng
January 2025
Research Center for Nano-Biomaterials, Analytical and Testing Center, Sichuan University, Chengdu 610064, PR China.
Oxidative stress induced by reactive oxygen species (ROS) can adversely affect tissue repair, whereas endowing biomaterials with antioxidant activity can improve the in vivo microenvironment, thereby promoting angiogenesis and osteogenesis. Accordingly, this study utilized epigallocatechin-3-gallate (EGCG), a material known for its reducing properties, oxidative self-polymerization capability, and strong binding characteristics, to modify a bioactive core-shell fibrous membrane (10RP-PG). Compared to the 10RP-PG fibrous membrane, the EGCG-modified fibrous membrane (E/10RP-PG) exhibited superior hydrophilicity, excellent cell adhesion, and compatibility.
View Article and Find Full Text PDFJ Korean Assoc Oral Maxillofac Surg
December 2024
Oral Oncology Clinic, Research Institute and Hospital, National Cancer Center, Goyang, Korea.
Adv Sci (Weinh)
December 2024
Department of Dental Materials & Dental Medical Devices Testing Center, Peking University School and Hospital of Stomatology, Beijing, 100081, P. R. China.
Regulation of the immune response is key to promoting bone regeneration by electroactive biomaterials. However, how electrical signals at the micro- and nanoscale regulate the immune response and subsequent angiogenesis during bone regeneration remains to be elucidated. Here, the distinctly different surface potential distributions on charged poly(vinylidene fluoridetrifluoroethylene) (P(VDF-TrFE)) matrix surfaces are established by altering the dimensions of ferroelectric nanofillers from 0D BaTiO nanoparticles (homogeneous surface potential distribution, HOPD) to 1D BaTiO nanofibers (heterogeneous surface potential distribution, HEPD).
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