Abstract
Bone infections, also known as infectious osteomyelitis, are accompanied by significant inflammation, osteolysis, and necrosis. Osteoclasts (OCs) are the bone-resorbing cells that work in concert with osteoblasts and osteocytes to properly maintain skeletal health and are well known to respond to inflammation by increasing their resorptive activity. OCs have typically been viewed merely as effectors of pathologic bone resorption, but recent evidence suggests they may play an active role in the progression of infections through direct effects on pathogens and via the immune system. This review discusses the host- and pathogen-derived factors involved in the in generation of OCs during infection, the crosstalk between OCs and immune cells, and the role of OC lineage cells in the growth and survival of pathogens, and highlights unanswered questions in the field.
Highlights
As in other sites, the presence of pathogens in bone first elicits an innate immune response in which mature neutrophils and macrophages surround the invaders to form abscesses [1].Staphylococcus (S.) aureus is the leading causative agent of infectious osteomyelitis for most of the skeleton, except for iOM of the jaw related to periodontal diseases, where Porphyromonas (P.) gingivalis predominates [1,2]
If the infection is not cleared by the immune system or medical treatment, with time, vascular compromise in infected tissue leads to necrotic areas of bone called sequestra that serve as a niche for chronic infection and incite further osteoclastic bone resorption [6]
Protein can form IgG immune complexes that act on the Fc receptor of pre-OCs to promote osteoclastogenesis through a TLR2/MyD88-dependent mechanism that signals to NFATc1 and NF-κB [44]
Summary
The presence of pathogens in bone first elicits an innate immune response in which mature neutrophils and macrophages surround the invaders to form abscesses [1]. The combined actions of the pathogens and host cells lead to high levels of many inflammatory cytokines, which expand the pool of osteoclast (OC) precursors and mature bone-resorbing cells. If the infection is not cleared by the immune system or medical treatment, with time, vascular compromise in infected tissue leads to necrotic areas of bone called sequestra that serve as a niche for chronic infection and incite further osteoclastic bone resorption [6]. As the site of hematopoiesis, bone is home to stem and progenitor populations as well as mature effector cells. This review focuses on OCs as a specific node of host–pathogen interaction that has largely been overlooked except as a source of tissue damage and highlights this cell’s potential to modify disease progression
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