Infections and Bone Damage

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: 30 November 2024 | Viewed by 788

Special Issue Editors


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Guest Editor
Instituto de Investigaciones Biomédicas en Retrovirus y Sida (INBIRS), Universidad de Buenos Aires (UBA), Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires 1121, Argentina
Interests: bacterial and viral pathogenesis; Brucella sp.; HIV; hepatitis viruses; SARS-CoV-2

E-Mail Website
Guest Editor
Instituto de Investigaciones Biomédicas en Retrovirus y Sida (INBIRS), Universidad de Buenos Aires (UBA), Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires 1121, Argentina
Interests: viral pathogenesis; HIV; hepatitis viruses; SARS-CoV-2

Special Issue Information

Dear Colleagues,

Infectious diseases significantly affect bone health through various pathways, posing a multi-faceted threat.

Direct attack: Certain pathogens can invade bone tissue, causing osteomyelitis, a condition marked by inflammation, bone deterioration and impaired healing. Untreated, it leads to chronic problems, deformities and persistent pain.

Inflammatory-mediated damage: Many infectious diseases trigger chronic inflammation, disrupting normal bone formation and promoting excessive breakdown. This, seen in HIV/AIDS, tuberculosis or hepatitis, increases the risk of weaker bones and conditions such as osteoporosis.

Nutritional deprivation: Severe infections often lead to malnutrition due to reduced appetite, impaired nutrient absorption or increased energy demands. These deprive bones of vital elements such as calcium, vitamin D and protein, weakening them and increasing fracture risk.

Medication double-edged sword: Some medications used to treat infections can have unintended bone-related side effects. Corticosteroids, used for inflammation control, can suppress bone formation and accelerate its breakdown, increasing fracture risk. Antibiotics and antivirals may also have similar effects.

Hormonal disruption: Infectious diseases can disrupt hormone production, negatively impacting bone metabolism. Hyperthyroidism speeds up bone turnover, leading to osteoporosis, while hypogonadism weakens bones and increases fracture risk. These hormonal imbalances exacerbate bone loss and compromise bone integrity.

This Special Issue will cover a wide range of topics aiming to enhance current knowledge of pathogens and their respective diseases impacting bone. By acknowledging the complexities of this interplay, we can better protect bone health in the face of infectious challenges.

All types of articles will be considered for publication, including short reports, primary research articles and reviews.

We look forward to your contribution.

Dr. María Victoria Delpino
Dr. Jorge Quarleri
Guest Editors

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Keywords

  • infectious diseases
  • bone
  • osteoclasts
  • osteoblast
  • osteoimmunity
  • mesenchymal cells
  • osteomyelitis
  • osteoporosis
  • antimicrobial therapy

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Published Papers (1 paper)

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Research

14 pages, 2977 KiB  
Article
HIV Modulates Osteoblast Differentiation via Upregulation of RANKL and Vitronectin
by Rosa Nicole Freiberger, Cynthia Alicia Marcela López, María Belén Palma, Cintia Cevallos, Franco Agustin Sviercz, Patricio Jarmoluk, Marcela Nilda García, Jorge Quarleri and M. Victoria Delpino
Pathogens 2024, 13(9), 800; https://doi.org/10.3390/pathogens13090800 - 15 Sep 2024
Viewed by 556
Abstract
Bone loss is a prevalent characteristic among people with HIV (PWH). We focused on mesenchymal stem cells (MSCs) and osteoblasts, examining their susceptibility to different HIV strains (R5- and X4-tropic) and the subsequent effects on bone tissue homeostasis. Our findings suggest that MSCs [...] Read more.
Bone loss is a prevalent characteristic among people with HIV (PWH). We focused on mesenchymal stem cells (MSCs) and osteoblasts, examining their susceptibility to different HIV strains (R5- and X4-tropic) and the subsequent effects on bone tissue homeostasis. Our findings suggest that MSCs and osteoblasts are susceptible to R5- and X4-tropic HIV but do not support productive HIV replication. HIV exposure during the osteoblast differentiation process revealed that the virus could not alter mineral and organic matrix deposition. However, the reduction in runt-related transcription factor 2 (RUNX2) transcription, the increase in the transcription of nuclear receptor activator ligand kappa B (RANKL), and the augmentation of vitronectin deposition strongly suggested that X4- and R5-HIV could affect bone homeostasis. This study highlights the HIV ability to alter MSCs’ differentiation into osteoblasts, critical for maintaining bone and adipose tissue homeostasis and function. Full article
(This article belongs to the Special Issue Infections and Bone Damage)
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