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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Bone Disorders01:29

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Updated: Oct 21, 2025

Improved Enzyme Protection Assay to Study Staphylococcus aureus Internalization and Intracellular Efficacy of Antimicrobial Compounds
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Staphylococcus aureus internalization impairs osteoblastic activity and early differentiation process.

W Mouton1,2, J Josse3,4, C Jacqueline5

  • 1CIRI - Centre International de Recherche en Infectiologie, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.

Scientific Reports
|September 4, 2021
PubMed
Summary
This summary is machine-generated.

Staphylococcus aureus internalization into bone cells impairs early differentiation. This bacterial invasion causes bone loss in a strain-dependent manner, impacting chronic bone and joint infections.

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Area of Science:

  • Microbiology
  • Orthopedics
  • Cell Biology

Background:

  • Staphylococcus aureus is a primary cause of bone and joint infections (BJIs), often leading to chronic or relapsing conditions.
  • Bacterial internalization into osteoblasts is a key factor in staphylococcal BJI chronicity and associated bone loss.
  • Previous research focused on extracellular bacterial effects, necessitating investigation into intracellular impacts on osteoblasts.

Purpose of the Study:

  • To elucidate the intracellular effects of Staphylococcus aureus on early osteoblast differentiation.
  • To determine the role of bacterial internalization in osteoblast dysfunction and bone parameter changes.
  • To compare the effects of reference and clinical strains of S. aureus on bone health.

Main Methods:

  • In vitro infection model using osteoblast lineage cells and S. aureus strains (8325-4 and 8325-4∆fnbAB).
  • Murine model of osteomyelitis to assess bone parameters (trabecular bone thickness) at 7 and 14 days post-infection.
  • Infection with clinical isogenic strains from initial and relapse BJI phases to evaluate their impact on osteoblast differentiation markers and bone parameters.

Main Results:

  • Internalized S. aureus 8325-4 significantly affected RUNX2 and COL1A1 gene expression in vitro compared to non-internalized bacteria.
  • In vivo, S. aureus 8325-4 reduced trabecular bone thickness at 14 days post-infection, while 8325-4∆fnbAB showed no significant effect.
  • Both clinical strains impaired bone parameters in vivo; in vitro, they affected alkaline phosphatase activity, with the relapse strain further decreasing bone differentiation gene expression.

Conclusions:

  • Staphylococcus aureus internalization into osteoblasts impairs early osteoblast differentiation in vitro.
  • S. aureus infection leads to impaired bone parameters in vivo in a strain-dependent manner.
  • Bacterial internalization is a critical mechanism driving osteoblast dysfunction and bone loss in staphylococcal bone and joint infections.