Cutibacterium acnes invades submicron osteocyte lacuno-canalicular networks following implant-associated

Mina Botros1,2, Karen L de Mesy Bentley1,2,3, Derek T Schloemann1,2

  • 1Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York, USA.

Insights

Cutibacterium acnes can persist in bone for 28 days and invade the osteocyte lacuno-canalicular networks (OLCN), potentially explaining why chronic prosthetic joint infections are challenging to treat.

Area of Science:

  • Orthopedics
  • Infectious Diseases
  • Microbiology

Background:

  • Cutibacterium acnes (C. acnes) is a normal skin bacterium increasingly implicated in prosthetic joint infections (PJI).
  • The pathogenesis of C. acnes in PJI remains poorly understood, with limited research available.
  • Chronic PJI caused by C. acnes are notoriously difficult to eradicate.

Purpose of the Study:

  • To investigate the pathogenesis of C. acnes in an implant-associated osteomyelitis murine model.
  • To explore C. acnes persistence, dissemination, and interaction with bone tissue.
  • To identify potential mechanisms contributing to treatment resistance in C. acnes PJI.

Main Methods:

  • Development of a murine model involving transtibial implantation of contaminated titanium or stainless-steel pins.
  • Assessment of bacterial load, bone osteolysis (micro-CT), abscess formation (histology), and biofilm formation (SEM) at 14 and 28 days post-surgery.
  • Transmission electron microscopy (TEM) to visualize C. acnes within bone microstructures.

Main Results:

  • C. acnes successfully formed biofilms on implants in vitro and persisted in murine tibias for 28 days.
  • Dissemination of C. acnes to internal organs was observed.
  • C. acnes infections showed reduced osteolysis and abscess formation compared to Staphylococcus aureus.
  • TEM revealed C. acnes invasion into the osteocyte lacuno-canalicular networks (OLCN).

Conclusions:

  • The osteocyte lacuno-canalicular network (OLCN) serves as a potential reservoir for C. acnes.
  • Invasion of the OLCN may represent a novel mechanism contributing to the recalcitrance of C. acnes chronic bone infections.
  • This study provides crucial insights into C. acnes pathogenesis in PJI, paving the way for improved therapeutic strategies.