Tissue Calcification in Normal and Pathological Environments

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 2400

Special Issue Editor


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Guest Editor
Department of Medicine, Medical School, University of Udine, Udine, Italy
Interests: ectopic calcification; aortic valve bioprostheses; valve interstitial cells; tissue remodeling; fibrillar collagen

Special Issue Information

Dear Colleagues,

It is well known that physiological calcification is a regulated process occurring during histogenesis or the remodeling of the so-called hard tissues bones, bone-forming cartilages, tooth enamel, dentin, and cementum. The pathological calcific processes are associated with aging and/or various diseases and are usually classified into the main types referred to as dystrophic, metastatic, iatrogenic, idiopathic, and calciphylaxis, words which are not dictated by univocal and/or exhaustive criteria so that supernumerary adjectives are often used, such as endocrine, metabolic, vascular, infectious, congenital, or neoplastic. Thus, the common term “calcification” is actually consistent with its culmination in tissue mineralization but indeed indicating a composite ensemble of distinct processes, of which physiological calcification at most remains a reference model for better elucidating the ectopic mineralization processes occurring in soft tissues in terms of underlying molecular mechanisms and inherent stimulatory, inhibitory, and propagatory factors.

Because of the conflicting results gained hitherto, a debate is still ongoing as to whether ectopic calcification depends on osteogenic differentiation, rather than protein-dysregulated secretory processes or cell-death-based degenerative pathways, thereby the detection of therapeutics exclusively targeted to the suppression of osteogenic-like factors or their genes might be not entirely effective in treating this multifaceted and likely multifactorial disorder.

Bearing in mind that surgery remains the only viable solution to date, future investigation on calcification will have to continue in all directions employing multidisciplinary approaches and aiming to develop appropriate therapeutic strategies counteracting dysregulated calcification, so preventing or delaying the progression of a disorder that is increasingly recognized as a major health problem leading to relevant morbidity and mortality in humans of any age.

Given the great number of open problems and the complexity of the different calcific events, any investigation adding information on biomineralization in both normal and pathological contexts will be welcomed in the setting of the present Special Issue project.

I look forward to receiving your valuable contributions.

Dr. Fulvia Ortolani
Guest Editor

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Keywords

  • calcification
  • ectopic mineralization
  • bone
  • heterotopic ossification
  • calcium phosphate
  • calcium carbonate
  • calcium oxalate
  • procalcific cell death

Published Papers (2 papers)

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Research

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13 pages, 4009 KiB  
Article
Micro-Osteoperforations Accelerate Tooth Movement without Exacerbating the Progression of Root Resorption in Rats
by Tadasu Sugimori, Masaru Yamaguchi, Jun Kikuta, Mami Shimizu and Shinichi Negishi
Biomolecules 2024, 14(3), 300; https://0-doi-org.brum.beds.ac.uk/10.3390/biom14030300 - 02 Mar 2024
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Abstract
A recent study reported that micro-osteoperforations (MOPs) accelerated tooth movement by activating alveolar bone remodeling. However, very little is known about the relationship between MOPs and external apical root resorption during orthodontic treatment. In this study, in order to investigate the mechanism through [...] Read more.
A recent study reported that micro-osteoperforations (MOPs) accelerated tooth movement by activating alveolar bone remodeling. However, very little is known about the relationship between MOPs and external apical root resorption during orthodontic treatment. In this study, in order to investigate the mechanism through which MOPs accelerate tooth movement without exacerbating the progression of root resorption, we measured the volume of the resorbed root, and performed the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL) method on exposed MOPs during experimental tooth movements in rats. Male Wistar rats (11 weeks old) were divided into three groups: 10 g orthodontic force (optimal force) applied to the maxillary first molar (optimal force: OF group), 50 g orthodontic force application (heavy force: HF group), and 10 g force application plus three small perforations of the cortical plate (OF + MOPs group). On days 1, 4, 7, 10, and 14 after force application, the tooth movement and root volume were investigated by micro-computed tomography. Furthermore, the number of apoptotic cells in the pressured sides of the periodontal ligament (PDL) and surrounding hard tissues were determined by TUNEL staining. The OF + MOPs group exhibited a 1.8-fold increase in tooth movement on days 7, 10, and 14 compared with the OF group. On days 14, the HF group had a higher volume of root loss than the OF and OF + MOPs groups. On the same day, the number of TUNEL-positive cells in the HF group increased at the root (cementum) site whereas that in the OF group increased at the alveolar bone site. Furthermore, the number of TUNEL-positive cells in the OF + MOPs group increased at the alveolar bone site compared with the OF group. These results suggest that MOPs accelerate orthodontic tooth movement without exacerbating the progression of root resorption. Full article
(This article belongs to the Special Issue Tissue Calcification in Normal and Pathological Environments)
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Review

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21 pages, 795 KiB  
Review
Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities
by Miguel A. Ortega, Diego De Leon-Oliva, Maria José Gimeno-Longas, Diego Liviu Boaru, Oscar Fraile-Martinez, Cielo García-Montero, Amador Velazquez de Castro, Silvestra Barrena-Blázquez, Laura López-González, Silvia Amor, Natalio García-Honduvilla, Julia Buján, Luis G. Guijarro, Elisa Castillo-Ruiz, Miguel Ángel Álvarez-Mon, Agustin Albillos, Melchor Álvarez-Mon, Raul Diaz and Miguel A. Saez
Biomolecules 2024, 14(3), 275; https://0-doi-org.brum.beds.ac.uk/10.3390/biom14030275 - 25 Feb 2024
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Abstract
Calcification is a process of accumulation of calcium in tissues and deposition of calcium salts by the crystallization of PO43− and ionized calcium (Ca2+). It is a crucial process in the development of bones and teeth. However, pathological calcification [...] Read more.
Calcification is a process of accumulation of calcium in tissues and deposition of calcium salts by the crystallization of PO43− and ionized calcium (Ca2+). It is a crucial process in the development of bones and teeth. However, pathological calcification can occur in almost any soft tissue of the organism. The better studied is vascular calcification, where calcium salts can accumulate in the intima or medial layer or in aortic valves, and it is associated with higher mortality and cardiovascular events, including myocardial infarction, stroke, aortic and peripheral artery disease (PAD), and diabetes or chronic kidney disease (CKD), among others. The process involves an intricate interplay of different cellular components, endothelial cells (ECs), vascular smooth muscle cells (VSMCs), fibroblasts, and pericytes, concurrent with the activation of several signaling pathways, calcium, Wnt, BMP/Smad, and Notch, and the regulation by different molecular mediators, growth factors (GFs), osteogenic factors and matrix vesicles (MVs). In the present review, we aim to explore the cellular players, molecular pathways, biomarkers, and clinical treatment strategies associated with vascular calcification to provide a current and comprehensive overview of the topic. Full article
(This article belongs to the Special Issue Tissue Calcification in Normal and Pathological Environments)
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