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Calcification in Human Pathology

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 43562

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Prof. Dr. Elena Bonanno

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Department of Anatomic Pathology, University of Rome Tor Vergata, Rome, Italy
Interests: breast cancer
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Dr. Virginia Tancredi

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Department of Systems Medicine and Centre of Space Biomedicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
Interests: synaptic plasticity; neurophysiology; aging; physical activity and wellness; cognitive perception; sport training; quality of life
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Dr. Manuel Scimeca

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Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133 Rome, Italy
Interests: environmental pollution; oncology; cardiovascular diseases; electron microscopy; histology
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Dr. Rita Bonfiglio

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Department of Experimental Medicine, University of Rome “Tor Vergata”, Via Montpellier 1, 00133 Rome, Italy
Interests: cisplatin; cancer; aporphine alkaloids
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Special Issue Information

Dear Colleagues,

Calcifications are mineral deposits accumulated in several human tissues that are often associated with the occurrence and development of diseases, such as cancer and/or inflammation. Recent studies have demonstrated that the formation of calcifications in human tissues, i.e., breast and prostate cancer, can be triggered by biological processes related to the epithelial to mesenchymal transition phenomenon. Therefore, the presence of microcalcifications could be considered an end-point sign of biological processes involved in human diseases. In fact, in some of them, such as breast cancer, the radiological detection of microcalcifications has a diagnostic value for predicting the presence of a breast lesion. In spite of the relevant role of microcalcifications in early detection of some human diseases, and their proposed activities in modulating cell behavior, little is known about their chemical composition or how this relates to pathology. Starting from these considerations, the aim of this Issue is to publish the latest discoveries and bring together researchers and clinicians working in the field of “Calcifications in Human Pathology”. Topics will include (but are not limited to):

Biological mechanisms related to the formation of calcifications;
Identification of cells involved in ectopic calcifications;
Prognostic value of calcifications;
Elemental composition of calcifications;
Molecular/pathologic/cellular image analysis of microcalcifications;
Diagnostic Imaging applications for the detection of microcalcifications;
Cardiovascular, breast, prostate and kidney calcifications;
Calcifications as a sign of tissue osteotropism.

Prof. Dr. Elena Bonanno
Prof. Dr. Virginia Tancredi
Dr. Manuel Scimeca
Dr. Rita Bonfiglio
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

ectopic calcifications
microcalcifications
cancer
osteoblast
hydroxyapatite
calcium oxalate
RANKL/OPG/RANK
inflammation
cardiovascular diseases

Related Special Issue

Calcification in Human Pathology 2.0 in International Journal of Molecular Sciences (2 articles)

Published Papers (11 papers)

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Research

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21 pages, 34601 KiB

Open AccessArticle

Pro-Calcific Environment Impairs Ischaemia-Driven Angiogenesis

by Jocelyne Mulangala, Emma J. Akers, Emma L. Solly, Panashe M. Bamhare, Laura A. Wilsdon, Nathan K. P. Wong, Joanne T. M. Tan, Christina A. Bursill, Stephen J. Nicholls and Belinda A. Di Bartolo

Int. J. Mol. Sci. 2022, 23(6), 3363; https://doi.org/10.3390/ijms23063363 - 20 Mar 2022

Viewed by 2387

Abstract

Peripheral arterial disease (PAD) is characterised by accelerated arterial calcification and impairment in angiogenesis. Studies implicate vascular calcification as a contributor to PAD, but the mechanisms remain unclear. We aimed to determine the effect of calcification on ischaemia-driven angiogenesis. Human coronary artery endothelial cells (ECs) were treated with calcification medium (CM: CaCl₂ 2.7 mM, Na₂PO₄ 2.0 mM) for 24 h and exposed to normoxia (5% CO₂) or hypoxia (1.2% O₂; 5% CO₂ balanced with N₂). In normoxia, CM significantly inhibited tubule formation and migration and upregulated calcification markers of ALP, BMP2, and Runx2. CM elevated levels of calcification-protective gene OPG, demonstrating a compensatory mechanism by ECs. CM failed to induce pro-angiogenic regulators VEGFA and HIF-1α in hypoxia and further suppressed the phosphorylation of endothelial nitric oxide synthase (eNOS) that is essential for vascular function. In vivo, osteoprotegerin-deficient mice (OPG^−/−), a calcification model, were subjected to hind-limb ischaemia (HLI) surgery. OPG^−/− mice displayed elevated serum alkaline phosphatase (ALP) activity compared to wild-type controls. OPG^−/− mice experienced striking reductions in blood-flow reperfusion in both 8-week-old and 6-month-old mice post-HLI. This coincided with significant impairment in tissue ischaemia and reduced limb function as assessed by clinical scoring (Tarlov). This study demonstrated for the first time that a pro-calcific environment is detrimental to ischaemia-driven angiogenesis. The degree of calcification in patients with PAD can often be a limiting factor with the use of standard therapies. These highly novel findings require further studies for full elucidation of the mechanisms involved and have implications for the development of therapies to suppress calcification in PAD. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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11 pages, 2828 KiB

Open AccessArticle

Vitamin D and Calcium Supplementation Accelerate Vascular Calcification in a Model of Pseudoxanthoma Elasticum

by Elise Bouderlique, Ellie Tang, Jeremy Zaworski, Amélie Coudert, Dominique Bazin, Ferenc Borondics, Jean-Philippe Haymann, Georges Leftheriotis, Ludovic Martin, Michel Daudon and Emmanuel Letavernier

Int. J. Mol. Sci. 2022, 23(4), 2302; https://doi.org/10.3390/ijms23042302 - 19 Feb 2022

Cited by 4 | Viewed by 3926

Abstract

Arterial calcification is a common feature of pseudoxanthoma elasticum (PXE), a disease characterized by ABCC6 mutations, inducing a deficiency in pyrophosphate, a key inhibitor of calcium phosphate crystallization in arteries. Methods: we analyzed whether long-term exposure of Abcc6^−/− mice (a murine model of PXE) to a mild vitamin D supplementation, with or without calcium, would impact the development of vascular calcification. Eight groups of mice (including Abcc6^−/− and wild-type) received vitamin D supplementation every 2 weeks, a calcium-enriched diet alone (calcium in drinking water), both vitamin D supplementation and calcium-enriched diet, or a standard diet (controls) for 6 months. Aorta and kidney artery calcification was assessed by 3D-micro-computed tomography, Optical PhotoThermal IR (OPTIR) spectroscopy, scanning electron microscopy coupled with energy-dispersive X-ray spectroscopy (SEM-EDS) and Yasue staining. Results: at 6 months, although vitamin D and/or calcium did not significantly increase serum calcium levels, vitamin D and calcium supplementation significantly worsened aorta and renal artery calcification in Abcc6^−/− mice. Conclusions: vitamin D and/or calcium supplementation accelerate vascular calcification in a murine model of PXE. These results sound a warning regarding the use of these supplementations in PXE patients and, to a larger extent, patients with low systemic pyrophosphate levels. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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23 pages, 5872 KiB

Open AccessArticle

BGP-15 Inhibits Hyperglycemia-Aggravated VSMC Calcification Induced by High Phosphate

by Annamária Nagy, Dávid Pethő, Rudolf Gesztelyi, Béla Juhász, György Balla, Zoltán Szilvássy, József Balla and Tamás Gáll

Int. J. Mol. Sci. 2021, 22(17), 9263; https://doi.org/10.3390/ijms22179263 - 26 Aug 2021

Cited by 4 | Viewed by 2752

Abstract

Vascular calcification associated with high plasma phosphate (Pi) level is a frequent complication of hyperglycemia, diabetes mellitus, and chronic kidney disease. BGP-15 is an emerging anti-diabetic drug candidate. This study was aimed to explore whether BGP-15 inhibits high Pi-induced calcification of human vascular smooth muscle cells (VSMCs) under normal glucose (NG) and high glucose (HG) conditions. Exposure of VSMCs to Pi resulted in accumulation of extracellular calcium, elevated cellular Pi uptake and intracellular pyruvate dehydrogenase kinase-4 (PDK-4) level, loss of smooth muscle cell markers (ACTA, TAGLN), and enhanced osteochondrogenic gene expression (KLF-5, Msx-2, Sp7, BMP-2). Increased Annexin A2 and decreased matrix Gla protein (MGP) content were found in extracellular vesicles (EVs). The HG condition markedly aggravated Pi-induced VSMC calcification. BGP-15 inhibited Pi uptake and PDK-4 expression that was accompanied by the decreased nuclear translocation of KLF-5, Msx-2, Sp7, retained VSMC markers (ACTA, TAGLN), and decreased BMP-2 in both NG and HG conditions. EVs exhibited increased MGP content and decreased Annexin A2. Importantly, BGP-15 prevented the deposition of calcium in the extracellular matrix. In conclusion, BGP-15 inhibits Pi-induced osteochondrogenic phenotypic switch and mineralization of VSMCs in vitro that make BGP-15 an ideal candidate to attenuate both diabetic and non-diabetic vascular calcification. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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12 pages, 689 KiB

Open AccessArticle

The Paradox Effect of Calcification in Carotid Atherosclerosis: Microcalcification Is Correlated with Plaque Instability

by Manuela Montanaro, Manuel Scimeca, Lucia Anemona, Francesca Servadei, Erica Giacobbi, Rita Bonfiglio, Elena Bonanno, Nicoletta Urbano, Arnaldo Ippoliti, Giuseppe Santeusanio, Orazio Schillaci and Alessandro Mauriello

Int. J. Mol. Sci. 2021, 22(1), 395; https://doi.org/10.3390/ijms22010395 - 1 Jan 2021

Cited by 27 | Viewed by 2861

Abstract

Background: this study aims to investigate the possible association among the histopathologic features of carotid plaque instability, the presence of micro- or macrocalcifications, the expression of in situ inflammatory biomarkers, and the occurrence of the major risk factors in this process in a large series of carotid plaques. Methods: a total of 687 carotid plaques from symptomatic and asymptomatic patients were collected. Histological evaluation was performed to classify the calcium deposits in micro or macrocalcifications according to their morphological features (location and size). Immunohistochemistry was performed to study the expression of the main inflammatory biomarkers. Results: results here reported demonstrated that calcifications are very frequent in carotid plaques, with a significant difference between the presence of micro- and macrocalcifications. Specifically, microcalcifications were significantly associated to high inflamed unstable plaques. Paradoxically, macrocalcifications seem to stabilize the plaque and are associated to a M2 macrophage polarization instead. Discussion: the characterization of mechanisms involved in the formation of carotid calcifications can lay the foundation for developing new strategies for the management of patients affected by carotid atherosclerosis. Data of this study could provide key elements for an exhaustive evaluation of carotid plaque calcifications allowing to establish the risk of associated clinical events. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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17 pages, 9956 KiB

Open AccessArticle

Ultrastructural Pathology of Atherosclerosis, Calcific Aortic Valve Disease, and Bioprosthetic Heart Valve Degeneration: Commonalities and Differences

by Alexander Kostyunin, Rinat Mukhamadiyarov, Tatiana Glushkova, Leo Bogdanov, Daria Shishkova, Nikolay Osyaev, Evgeniy Ovcharenko and Anton Kutikhin

Int. J. Mol. Sci. 2020, 21(20), 7434; https://doi.org/10.3390/ijms21207434 - 9 Oct 2020

Cited by 30 | Viewed by 3836

Abstract

Atherosclerosis, calcific aortic valve disease (CAVD), and bioprosthetic heart valve degeneration (alternatively termed structural valve deterioration, SVD) represent three diseases affecting distinct components of the circulatory system and their substitutes, yet sharing multiple risk factors and commonly leading to the extraskeletal calcification. Whereas the histopathology of the mentioned disorders is well-described, their ultrastructural pathology is largely obscure due to the lack of appropriate investigation techniques. Employing an original method for sample preparation and the electron microscopy visualisation of calcified cardiovascular tissues, here we revisited the ultrastructural features of lipid retention, macrophage infiltration, intraplaque/intraleaflet haemorrhage, and calcification which are common or unique for the indicated types of cardiovascular disease. Atherosclerotic plaques were notable for the massive accumulation of lipids in the extracellular matrix (ECM), abundant macrophage content, and pronounced neovascularisation associated with blood leakage and calcium deposition. In contrast, CAVD and SVD generally did not require vasculo- or angiogenesis to occur, instead relying on fatigue-induced ECM degradation and the concurrent migration of immune cells. Unlike native tissues, bioprosthetic heart valves contained numerous specialised macrophages and were not capable of the regeneration that underscores ECM integrity as a pivotal factor for SVD prevention. While atherosclerosis, CAVD, and SVD show similar pathogenesis patterns, these disorders demonstrate considerable ultrastructural differences. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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12 pages, 2483 KiB

Open AccessArticle

Circulating Long Non-Coding RNA GAS5 Is Overexpressed in Serum from Osteoporotic Patients and Is Associated with Increased Risk of Bone Fragility

by Virginia Veronica Visconti, Simona Fittipaldi, Simone Ciuffi, Francesca Marini, Giancarlo Isaia, Patrizia D’Amelio, Silvia Migliaccio, Claudio Marcocci, Salvatore Minisola, Ranuccio Nuti, Giuseppe Novelli, Maria Luisa Brandi, Annalisa Botta and Umberto Tarantino

Int. J. Mol. Sci. 2020, 21(18), 6930; https://doi.org/10.3390/ijms21186930 - 21 Sep 2020

Cited by 13 | Viewed by 2130

Abstract

Osteoporosis (OP) is a multifactorial disorder in which environmental factors along with genetic variants and epigenetic mechanisms have been implicated. Long non-coding RNAs (lncRNAs) have recently emerged as important regulators of bone metabolism and OP aetiology. In this study, we analyzed the expression level and the genetic association of lncRNA GAS5 in OP patients compared to controls. Quantitative RT-PCR analysis of GAS5 was performed on the serum of 56 OP patients and 28 healthy individuals. OP subjects were divided into three groups of analysis: 29 with fragility fractures of lumbar spine (OP_VF), 14 with fragility fractures of femoral neck (OP_FF) and 13 without fractures (OP_WF). Genotyping of the rs145204276 insertion/deletion polymorphism has also been performed by Restriction fragment length polymorphism (RFLP) and direct sequencing analyses. Expression of circulating GAS5 is significantly increased in OP patients compared to controls (p < 0.01), with a statistically higher significance in fractured OP individuals vs. healthy subjects (p < 0.001). No statistically significant change was found in female OP patients; conversely, GAS5 is upregulated in the subgroup of fractured OP women sera (p < 0.01) and in all OP males (p < 0.05). Furthermore, a direct correlation between GAS5 expression level and parathyroid hormone (PTH) concentration was found in OP patients (r = 0.2930; p = 0.0389). Genetic analysis of rs145204276 revealed that the deletion allele was correlated with a higher expression of GAS5 in OP patients (0.22 ± 0.02 vs. 0.15 ± 0.01, ** p < 0.01). Our results suggest circulating GAS5 as a putative biomarker for the diagnosis and prognosis of OP and OP-related fractures. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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Review

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14 pages, 1319 KiB

Open AccessReview

Molecular Aspects and Prognostic Significance of Microcalcifications in Human Pathology: A Narrative Review

by Rita Bonfiglio, Annarita Granaglia, Raffaella Giocondo, Manuel Scimeca and Elena Bonanno

Int. J. Mol. Sci. 2021, 22(1), 120; https://doi.org/10.3390/ijms22010120 - 24 Dec 2020

Cited by 9 | Viewed by 3103

Abstract

The presence of calcium deposits in human lesions is largely used as imaging biomarkers of human diseases such as breast cancer. Indeed, the presence of micro- or macrocalcifications is frequently associated with the development of both benign and malignant lesions. Nevertheless, the molecular mechanisms involved in the formation of these calcium deposits, as well as the prognostic significance of their presence in human tissues, have not been completely elucidated. Therefore, a better characterization of the biological process related to the formation of calcifications in different tissues and organs, as well as the understanding of the prognostic significance of the presence of these calcium deposits into human tissues could significantly improve the management of patients characterized by microcalcifications associated lesions. Starting from these considerations, this narrative review highlights the most recent histopathological and molecular data concerning the formation of calcifications in breast, thyroid, lung, and ovarian diseases. Evidence reported here could deeply change the current point of view concerning the role of ectopic calcifications in the progression of human diseases and also in the patients’ management. In fact, the presence of calcifications can suggest an unfavorable prognosis due to dysregulation of normal tissues homeostasis. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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34 pages, 2340 KiB

Open AccessReview

Breast Cancer and Microcalcifications: An Osteoimmunological Disorder?

by Alisson Clemenceau, Laetitia Michou, Caroline Diorio and Francine Durocher

Int. J. Mol. Sci. 2020, 21(22), 8613; https://doi.org/10.3390/ijms21228613 - 15 Nov 2020

Cited by 15 | Viewed by 4137

Abstract

The presence of microcalcifications in the breast microenvironment, combined with the growing evidences of the possible presence of osteoblast-like or osteoclast-like cells in the breast, suggest the existence of active processes of calcification in the breast tissue during a woman’s life. Furthermore, much evidence that osteoimmunological disorders, such as osteoarthritis, rheumatoid arthritis, or periodontitis influence the risk of developing breast cancer in women exists and vice versa. Antiresorptive drugs benefits on breast cancer incidence and progression have been reported in the past decades. More recently, biological agents targeting pro-inflammatory cytokines used against rheumatoid arthritis also demonstrated benefits against breast cancer cell lines proliferation, viability, and migratory abilities, both in vitro and in vivo in xenografted mice. Hence, it is tempting to hypothesize that breast carcinogenesis should be considered as a potential osteoimmunological disorder. In this review, we compare microenvironments and molecular characteristics in the most frequent osteoimmunological disorders with major events occurring in a woman’s breast during her lifetime. We also highlight what the use of bone anabolic drugs, antiresorptive, and biological agents targeting pro-inflammatory cytokines against breast cancer can teach us. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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28 pages, 1060 KiB

Open AccessReview

Current Evidence and Future Perspectives on Pharmacological Treatment of Calcific Aortic Valve Stenosis

by Maristella Donato, Nicola Ferri, Maria Giovanna Lupo, Elisabetta Faggin and Marcello Rattazzi

Int. J. Mol. Sci. 2020, 21(21), 8263; https://doi.org/10.3390/ijms21218263 - 4 Nov 2020

Cited by 26 | Viewed by 5163

Abstract

Calcific aortic valve stenosis (CAVS), the most common heart valve disease, is characterized by the slow progressive fibro-calcific remodeling of the valve leaflets, leading to progressive obstruction to the blood flow. CAVS is an increasing health care burden and the development of an effective medical treatment is a major medical need. To date, no effective pharmacological therapies have proven to halt or delay its progression to the severe symptomatic stage and aortic valve replacement represents the only available option to improve clinical outcomes and to increase survival. In the present report, the current knowledge and latest advances in the medical management of patients with CAVS are summarized, placing emphasis on lipid-lowering agents, vasoactive drugs, and anti-calcific treatments. In addition, novel potential therapeutic targets recently identified and currently under investigation are reported. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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20 pages, 2576 KiB

Open AccessReview

Molecular Aspects of Thyroid Calcification

by Luciana Bueno Ferreira, Etel Gimba, João Vinagre, Manuel Sobrinho-Simões and Paula Soares

Int. J. Mol. Sci. 2020, 21(20), 7718; https://doi.org/10.3390/ijms21207718 - 19 Oct 2020

Cited by 26 | Viewed by 7094

Abstract

In thyroid cancer, calcification is mainly present in classical papillary thyroid carcinoma (PTC) and in medullary thyroid carcinoma (MTC), despite being described in benign lesions and in other subtypes of thyroid carcinomas. Thyroid calcifications are classified according to their diameter and location. At ultrasonography, microcalcifications appear as hyperechoic spots ≤ 1 mm in diameter and can be named as stromal calcification, bone formation, or psammoma bodies (PBs), whereas calcifications > 1 mm are macrocalcifications. The mechanism of their formation is still poorly understood. Microcalcifications are generally accepted as a reliable indicator of malignancy as they mostly represent PBs. In order to progress in terms of the understanding of the mechanisms behind calcification occurring in thyroid tumors in general, and in PTC in particular, we decided to use histopathology as the basis of the possible cellular and molecular mechanisms of calcification formation in thyroid cancer. We explored the involvement of molecules such as runt-related transcription factor-2 (Runx-2), osteonectin/secreted protein acidic and rich in cysteine (SPARC), alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteopontin (OPN) in the formation of calcification. The present review offers a novel insight into the mechanisms underlying the development of calcification in thyroid cancer. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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19 pages, 3162 KiB

Open AccessReview

Sex-Specific Features of Calcific Aortic Valve Disease

by Volha I. Summerhill, Donato Moschetta, Alexander N. Orekhov, Paolo Poggio and Veronika A. Myasoedova

Int. J. Mol. Sci. 2020, 21(16), 5620; https://doi.org/10.3390/ijms21165620 - 6 Aug 2020

Cited by 49 | Viewed by 5097

Abstract

Calcific aortic valve disease (CAVD) is the most common valvular heart disease in developed countries predominantly affecting the elderly population therefore posing a large economic burden. It is a gradually progressive condition ranging from mild valve calcification and thickening, without the hemodynamic obstruction, to severe calcification impairing leaflet motion, known as aortic stenosis (AS). The progression of CAVD occurs over many years, and it is extremely variable among individuals. It is also associated with an increased risk of coronary events and mortality. The recent insights into the CAVD pathophysiology included an important role of sex. Accumulating evidence suggests that, in patients with CAVD, sex can determine important differences in the relationship between valvular calcification process, fibrosis, and aortic stenosis hemodynamic severity between men and women. Consequently, it has implications on the development of different valvular phenotypes, left ventricular hypertrophy, and cardiovascular outcomes in men and women. Along these lines, taking into account the sex-related differences in diagnosis, prognosis, and treatment outcomes is of profound importance. In this review, the sex-related differences in patients with CAVD, in terms of pathobiology, clinical phenotypes, and outcomes were discussed. Full article

(This article belongs to the Special Issue Calcification in Human Pathology)

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