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Related Experiment Videos

Osteomyelitis and intraosteoblastic Staphylococcus aureus.

Lawrence X Webb1, William Wagner, David Carroll

  • 1Department of Orthopaedic Surgery, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. lxwebb@wfubmc.edu

Journal of Surgical Orthopaedic Advances
|June 27, 2007
PubMed
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Chronic osteomyelitis, a bone infection, can have dormant periods. Researchers found Staphylococcus aureus can live inside host osteoblasts, offering a new explanation for this dormancy in bone infections.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Chronic osteomyelitis presents with intermittent symptomatic episodes and periods of clinical quiescence.
  • Quiescence has been linked to host defenses and pathogen sequestration.
  • A novel hypothesis suggests intracellular pathogen incorporation within host osteoblasts.

Purpose of the Study:

  • To investigate the potential for intracellular pathogen localization within osteoblasts in chronic osteomyelitis.
  • To demonstrate the facultative intraosteoblastic location of Staphylococcus aureus in osteomyelitis.
  • To characterize the microscopic features of this intraosteoblastic pathogen localization.

Main Methods:

  • Establishment of a human osteoblast cell culture.

Related Experiment Videos

  • Infection of the cell culture with a Staphylococcus aureus isolate from osteomyelitis.
  • Microscopic examination of infected osteoblasts to identify pathogen location and features.

    • Main Results:

    • Successful osteoblast cell culture was established.
    • Demonstrated facultative intracellular localization of Staphylococcus aureus within osteoblasts.
    • Observed and documented microscopic features of intraosteoblastic Staphylococcus aureus.

    Conclusions:

    • Staphylococcus aureus, a pathogen in chronic osteomyelitis, can reside intracellularly within host osteoblasts.
    • Intracellular localization within osteoblasts presents a potential mechanism for pathogen persistence and clinical quiescence in osteomyelitis.
    • This finding opens new avenues for understanding and potentially treating chronic bone infections.