Physiopathologie des infections ostéoarticulaires

Abstract

Bone and joint infections gather heterogeneous clinical situation according to the infected site, the presence of orthopedic device and the infection chronicity. Their pathophysiology implicates complex interactions between the infectious agent, host immune system and osteoarticular tissue. It involves virulence factors at the initial phase of tissue invasion and destruction, and persistence mechanisms leading to chronicity and relapse. Infection can arise from three different pathways: direct inoculation during and invasive procedure or an open trauma, extension of a contiguous infection, or hematogenous spread during a bacteremia. Then, bacteria adhesion and the initial development of infection induces an inflammatory response that unbalances bone homeostasis resulting in bone lysis. Conversely, persistence mechanisms allow bacterial escape from the host immune system and the action of most antimicrobials. They include: (i) biofilm formation, a bacterial community adherent to the osteoarticular tissue and/or orthopedic device and organized in a self-produced matrix, that regulates bacterial survival in hostile growth conditions; (ii) bacterial internalization and persistence within bone cells constituting intracellular reservoirs; and (iii) phenotype switching to small colony variants characterized by a reduced metabolism and a tolerance to antimicrobials.