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Rethinking Bacterial Osteolysis: Translational Evidence From a Porcine Model and Fracture-Related Infections.

Anton A N Peterlin1,2, Nicole L Henriksen1, Julie M Birch1

  • 1Department of Veterinary and Animal Sciences, Experimental Pathology, University of Copenhagen, Frederiksberg C, Denmark.

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|January 27, 2026
PubMed
Summary
This summary is machine-generated.

Bone and joint infections cause significant bone loss, traditionally blamed on RANKL. However, this study shows RANKL inhibition did not prevent osteolysis, suggesting multifactorial causes beyond the RANKL-osteoclast pathway in implant-associated osteomyelitis.

Keywords:
RANKLfracture‐related infectionosteoimmunologyosteolysisosteomyelitis

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Area of Science:

  • Orthopedics
  • Infectious Diseases
  • Immunology

Background:

  • Bone and joint infections (BJIs) are severe conditions characterized by interosseous bacteria, biofilm formation, inflammation, and osteolysis.
  • Osteolysis in BJIs has been primarily attributed to RANKL-mediated osteoclast activation, based on limited evidence.

Purpose of the Study:

  • To investigate the mechanisms of bone loss in bacteria-associated osteolysis using a translational approach.
  • To challenge the traditional view of RANKL-osteoclast pathway as the sole driver of osteolysis in implant-associated osteomyelitis (IAO) and fracture-related infections (FRI).

Main Methods:

  • Utilized a porcine implant-associated osteomyelitis (IAO) model and analyzed clinical fracture-related infection (FRI) data.
  • Inhibited RANKL signaling with Denosumab in the IAO model.
  • Performed mRNA in situ hybridization on human FRI patient samples to assess gene expression (MMP1, RANKL, C3).
  • Quantified active osteoclast numbers and correlated them with osteolysis severity.

Main Results:

  • Denosumab treatment did not alter pathological or radiographic osteolysis in the IAO model.
  • Local RANKL mRNA expression and active osteoclast numbers did not correlate with bone destruction.
  • MMP1 expression was significantly higher in osteolytic FRI cases compared to non-osteolytic ones, while RANKL expression showed no difference.
  • Active osteoclast numbers did not correlate with osteolysis severity in patients.
  • A patient with chronic osteomyelitis on Denosumab experienced significant bone loss, further questioning the sole role of RANKL.

Conclusions:

  • Bacteria-associated osteolysis is a multifactorial process, not solely driven by the RANKL-osteoclast pathway.
  • Inflammatory and osteoimmunological interactions, proteolysis, neutrophil activity, and impaired osteogenesis play significant roles in bone loss during infections.
  • These findings necessitate a broader understanding of osteolysis mechanisms for effective treatment strategies in BJIs.