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Staphylococci planktonic and biofilm environments differentially affect osteoclast formation

Elisabeth Seebach1, Franziska V Kraus2,3, Tabea Elschner2,4

  • 1Department of Infectious Diseases, Medical Microbiology and Hygiene, Heidelberg University, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany. elisabeth.seebach@med.uni-heidelberg.de.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]
|June 17, 2023
PubMed
Abstract

Insights

Bacterial biofilms in chronic bone infections do not directly increase osteoclast formation. Instead, the inflammatory response to planktonic bacteria drives pathological osteoclastogenesis, potentially worsening bone destruction.

Area of Science:

  • Microbiology
  • Immunology
  • Orthopedics

Background:

  • Chronic implant-related bone infections involve increased osteoclast activity and bone resorption.
  • Bacterial biofilms contribute to infection chronicity by protecting bacteria and impairing immune cells.
  • Macrophages, as osteoclast precursors, link inflammation and bone destruction.

Purpose of the Study:

  • To investigate the impact of Staphylococcus aureus (SA) and Staphylococcus epidermidis (SE) biofilms on macrophage-mediated osteoclastogenesis.
  • To analyze the effects of planktonic and biofilm bacterial environments on osteoclast formation using RAW 264.7 cells.

Main Methods:

  • Utilized RAW 264.7 cells and conditioned media (CM) from planktonic and biofilm cultures of SA and SE.
  • Investigated osteoclastogenesis by priming cells with RANKL and adding CM.
  • Assessed the impact of simultaneous CM and RANKL stimulation on osteoclast formation.

Main Results:

  • Priming with RANKL before CM addition promoted osteoclast differentiation, with the strongest effect from SE planktonic or SA biofilm CM.
  • Simultaneous stimulation with CM and RANKL suppressed osteoclast formation.
  • Formation of multinucleated giant cells (MGCs), associated with inflammation, was most pronounced with SE planktonic CM.

Conclusions:

  • The biofilm environment, despite high lactate levels, does not actively promote osteoclastogenesis.
  • Inflammatory immune responses to planktonic bacterial factors via Toll-like receptors are the primary drivers of pathological osteoclast formation.
  • Immune stimulation or biofilm disruption strategies must consider the potential for enhanced inflammation-mediated bone destruction.
Keywords:
BiofilmImmune responseImplant-related bone infectionsMacrophagesOsteoclastogenesisStaphylococcus

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