ReviewFrontiers in cellular and infection microbiology2013
Apoptosis-associated uncoupling of bone formation and resorption in osteomyelitis.
Review in Frontiers in cellular and infection microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 82 citations in OpenAlex.
- A novel mouse calvarial defect model of osteomyelitis induced by Staphylococcus aureus (ATCC 6538).Laboratory animal research · 2026Article
- Combined analysis of host immune response, biofilm genes, and 16S rRNA detection in fracture-related infection: an observational cohort study.Journal of bone and joint infection · 2026Article
- HIF-1α at the intersection of hypoxia, ferroptosis-associated stress, and cell death crosstalk in osteomyelitis.Frontiers in cell and developmental biology · 2026Review
- Adaptive hydrogel platforms for infected bone defect repair: microenvironmental responsiveness, osteoimmunomodulation, and regenerative remodeling.Frontiers in bioengineering and biotechnology · 2026Review
- Intracellular survival ofVirulence · 2025Review
- Raman Monitoring ofInternational journal of molecular sciences · 2025Article
- Complete Clavicular Resorption after Clavicular osteomyelitis with no functional deficit at 13-year follow-up: A Case Report.Journal of orthopaedic case reports · 2025Article
- A microenvironment responsive nanoparticle regulating osteoclast fate to promote bone repair in osteomyelitis.Materials today. Bio · 2025Article
- Antioxidant scaffolds for enhanced bone regeneration: recent advances and challenges.Biomedical engineering online · 2025Review
- Exosomes derived from bone marrow mesenchymal stem cells induce the proliferation and osteogenic differentiation and regulate the inflammatory state in osteomyelitis in vitro model.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
- Integrative gene expression analysis and animal model reveal immune- and autophagy-related biomarkers in osteomyelitis.Immunity, inflammation and disease · 2024Article
- Use of Biomaterials in 3D Printing as a Solution to Microbial Infections in Arthroplasty and Osseous Reconstruction.Biomimetics (Basel, Switzerland) · 2024Review
- Comprehensive Gene Analysis Reveals Cuproptosis-Related Gene Signature Associated with M2 Macrophage inJournal of inflammation research · 2024Article
- A Review on Pathophysiology, and Molecular Mechanisms of Bacterial Chondronecrosis and Osteomyelitis in Commercial Broilers.Biomolecules · 2023Review
- Efficacy of Silver Nanoparticles-Loaded Bone Cement against an MRSA Induced-Osteomyelitis in a Rat Model.Medicina (Kaunas, Lithuania) · 2023Article
- Effect of Enterococcus faecalis OG1RF on human calvarial osteoblast apoptosis.BMC oral health · 2022Article
- Structural Analysis of Mitochondrial Dynamics-From Cardiomyocytes to Osteoblasts: A Critical Review.International journal of molecular sciences · 2022Review
- Recent Advances in Research on Antibacterial Metals and Alloys as Implant Materials.Frontiers in cellular and infection microbiology · 2021Review
- Inflammasomes in Alveolar Bone Loss.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms underlying the destruction of bone tissue in osteomyelitis are only now being elucidated. While some of the tissue damage associated with osteomyelitis likely results from the direct actions of bacteria and infiltrating leukocytes, perhaps exacerbated by bacterial manipulation of leukocyte survival pathways, infection-induced bone loss predominantly results from an uncoupling of the activities of osteoblasts and osteoclasts. Bacteria or their products can directly increase osteoclast formation and activity, and the inflammatory milieu at sites of infection can further promote bone resorption. In addition, osteoclast activity is critically regulated by osteoblasts that can respond to bacterial pathogens and foster both inflammation and osteoclastogenesis. Importantly, bone loss during osteomyelitis is also brought about by a decline in new bone deposition due to decreased bone matrix synthesis and by increased rates of osteoblast apoptosis. Extracellular bacterial components may be sufficient to reduce osteoblast viability, but the causative agents of osteomyelitis are also capable of inducing continuous apoptosis of these cells by activating intrinsic and extrinsic cell death pathways to further uncouple bone formation and resorption. Interestingly, bacterial internalization appears to be required for maximal osteoblast apoptosis, and cytosolic inflammasome activation may act in concert with autocrine/paracrine death receptor-ligand signaling to induce cell death. The manipulation of apoptotic pathways in infected bone cells could be an attractive new means to limit inflammatory damage in osteomyelitis. However, the mechanism that is the most important in bacterium-induced bone loss has not yet been identified. Furthermore, it remains to be determined whether the host would be best served by preventing osteoblast cell death or by promoting apoptosis in infected cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.