Intracellular Staphylococcus aureus in osteoblasts and osteocytes and its impact on bone homeostasis during osteomyelitis

Abstract

Osteomyelitis is a severe infection of bone tissue that can lead to bone loss and even osteonecrosis. This condition is mostly caused by Gram-positive bacteria, with Staphylococcus aureus being the most common etiological agent. Among the pathophysiological mechanisms involved in osteomyelitis, the ability of S. aureus to be internalized by osteoblasts or osteocytes and to survive within these cells, is particularly noteworthy. Infected osteoblasts and osteocytes not only serve as reservoirs in chronic cases of osteomyelitis but also play an active role in the osteoimmunology process, notably by producing mediators that promote the bone resorption activity of osteoclasts, thereby disrupting bone homeostasis. The present review explores both historical and recent literature on the internalization of S. aureus by osteoblasts and osteocytes, its intracellular behavior following internalization, and its mechanisms for inducing cell death. Additionally, it examines how S. aureus affects bone formation activity and promotes the production of inflammatory and pro-osteoclastic mediators. This review aims to highlight the limitations of current findings and outline key questions for future investigations.

Keywords: Bone and joint infection; Bone homeostasis; Osteoblast; Osteocyte; Staphylococcus aureus.