The in vitro model to study S

AO Trauma


S. aureus induces chronic fracture related infection (FRI) by forming biofilm, infecting bone cells and surviving intracellularly, but also by invading the osteocyte lacuna-canalicular network (OLCN). To date, animal studies and a single human patient with infected diabetic foot ulcer showed S. aureus colonization of the bone canaliculi. This mechanism allows the bacteria to escape from the immune system and persist inside the bone causing increasing the failure rate for the treatment of FRI. 




Establish a new in vitro model to study S. aureus invasion of the OLCN and understand the mechanisms and treatments to target it.