A review of bacterial and osteoclast differentiation in bone infection.

Abstract

Bone infections are characterized by bacterial invasion of the bone microenvironment and subsequent bone structure deterioration. This holds significance because osteoclasts, which are the only cells responsible for bone resorption, are abnormally stimulated during bone infections. Multiple communication factors secreted by bone stromal cells regulate the membrane of osteoclast progenitor cells, thereby maintaining bone homeostasis through the expression of many types of receptors. During infection, the immunoinflammatory response triggered by bacterial invasion and multiple virulence factors of bacterial origin can disrupt osteoclast homeostasis. Therefore, clarifying the pathways through which bacteria affect osteoclasts can offer a theoretical basis for preventing and treating bone infections. This review summarizes studies investigating bone destruction caused by different bacterial infections. In conclusion, bacteria can affect osteoclast metabolic activity through multiple pathways, including direct contact, release of virulence factors, induction of immunoinflammatory responses, influence on bone stromal cell metabolism, and intracellular infections.