Cellular and Molecular Mechanisms of Bone Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3169

Special Issue Editors


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Guest Editor
1. Faculty of Medicine and Biomedical Sciences, University of Algarve, Faro, Portugal
2. Centre of Marine Sciences, University of Algarve, Faro, Portugal
Interests: skeletal development; bone diseases; Gla proteins; fish models of human diseases; marine derived compounds for biotechnological applications
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Guest Editor
Centre of Marine Sciences (CCMAR), Universidade do Algarve, Faro, Portugal
Interests: extracellular vesicles; fish models of human diseases; cardiovascular diseases; regenerative medicine

Special Issue Information

Dear Colleagues,

Bone diseases (e.g., Osteoporosis, Osteogenesis imperfecta, and Paget’s diseases) are conditions in which bones are weaker and more prone to fractures. These disorders affect millions of people worldwide and current treatments have limited efficacy often accompanied by side effects. A better understanding of the cellular and molecular mechanisms associated with bone diseases is critical to prevent advances in disease progression and the identification of novel therapeutical strategies. This special issue will integrate the expertise of clinicians, basic scientists, and patient organizations and aims to contribute to the understanding of pathophysiological mechanisms associated with bone diseases and diseases associated with abnormal calcium accumulation (e.g., inflammation and ectopic calcification).

Prof. Dr. M. Leonor Cancela
Dr. João Miguel Almeida Santos
Guest Editors

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Keywords

  • bone diseases
  • calcium
  • osteoporosis

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Published Papers (1 paper)

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Review

21 pages, 2697 KiB  
Review
A Molecular Troika of Angiogenesis, Coagulopathy and Endothelial Dysfunction in the Pathology of Avascular Necrosis of Femoral Head: A Comprehensive Review
by Monica Singh, Baani Singh, Kirti Sharma, Nitin Kumar, Sarabjit Mastana and Puneetpal Singh
Cells 2023, 12(18), 2278; https://doi.org/10.3390/cells12182278 - 14 Sep 2023
Cited by 11 | Viewed by 2823
Abstract
Avascular necrosis of the femoral head (ANFH) is a painful disorder characterized by the cessation of blood supply to the femoral head, leading to its death and subsequent joint collapse. Influenced by several risk factors, including corticosteroid use, excessive alcohol intake, hypercholesterolemia, smoking [...] Read more.
Avascular necrosis of the femoral head (ANFH) is a painful disorder characterized by the cessation of blood supply to the femoral head, leading to its death and subsequent joint collapse. Influenced by several risk factors, including corticosteroid use, excessive alcohol intake, hypercholesterolemia, smoking and some inflammatory disorders, along with cancer, its clinical consequences are thrombus formation due to underlying inflammation and endothelial dysfunction, which collaborates with coagulopathy and impaired angiogenesis. Nonetheless, angiogenesis resolves the obstructed free flow of the blood by providing alternative routes. Clinical manifestations of early stage of ANFH mimic cysts or lesions in subchondral bone, vasculitis and transient osteoporosis of the hip, rendering it difficult to diagnose, complex to understand and complicated to cure. To date, the treatment methods for ANFH are controversial as no foolproof curative strategy is available, and these depend upon different severity levels of the ANFH. From an in-depth understanding of the pathological determinants of ANFH, it is clear that impaired angiogenesis, coagulopathy and endothelial dysfunction contribute significantly. The present review has set two aims, firstly to examine the role and relevance of this molecular triad (impaired angiogenesis, coagulopathy and endothelial dysfunction) in ANFH pathology and secondly to propose some putative therapeutic strategies, delineating the fact that, for the better management of ANFH, a combined strategy to curtail this molecular triangle must be composed rather than focusing on individual contributions. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Bone Diseases)
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