Staphylococcus aureus vs. Osteoblast: Relationship and Consequences in Osteomyelitis

Abstract

Bone cells, namely osteoblasts and osteoclasts work in concert and are responsible for bone extracellular matrix formation and resorption. This homeostasis is, in part, altered during infections by Staphylococcus aureus through the induction of various responses from the osteoblasts. This includes the over-production of chemokines, cytokines and growth factors, thus suggesting a role for these cells in both innate and adaptive immunity. S. aureus decreases the activity and viability of osteoblasts, by induction of apoptosis-dependent and independent mechanisms. The tight relationship between osteoclasts and osteoblasts is also modulated by S. aureus infection. The present review provides a survey of the relevant literature discussing the important aspects of S. aureus and osteoblast interaction as well as the ability for antimicrobial peptides to kill intra-osteoblastic S. aureus, hence emphasizing the necessity for new anti-infectious therapeutics.

Bi-functional titanium-polydopamine-zinc coatings for infection inhibition and enhanced osseointegration

“…Osteoblast infection by S. aureus can lead to reduced bone formation activity and osteoblast death. 58 Osteoclasts infected by S. aureus can enhance bone resorption activity, and the aggregation of osteoclasts in the infected areas is mediated by the pro-inammatory and pro-osteoclastogenic factors resulting from immune responses, 31 which is consistent with the results of histological sections and immunohistochemistry staining in our research. Taken together, the results from the animal model of implant-related infections demonstrated that the Ti-PDA-Zn coating possesses both excellent antibacterial properties and improved osseointegration capability in the presence of S. aureus in vivo.…”

Diminished bone regeneration after debridement of posttraumatic osteomyelitis is accompanied by altered cytokine levels, elevated B cell activity, and increased osteoclast activity

“…It is well accepted that bone infections, especially by S. aureus, cause bone resorption. More precisely, proliferation and mineralization of infected osteoblasts is altered and osteoclast activity is increased in a RANKL‐dependent (Receptor Activator of NF‐ κB Ligand) manner …”

2018 International Consensus Meeting on Musculoskeletal Infection: Research Priorities from the General Assembly Questions

“…It was also clear from the robust and passionate discussion at the ICM 2018, that the time has come to address the need for a scientifically and clinically functional definitions for: “acute versus chronic” infection (https://www.ors.org/wp-content/uploads/2019/01/Question-1.pdf), “implant colonization versus implant‐related infection” (https://www.ors.org/wp-content/uploads/2019/01/Question-2.pdf), and “persistent wound drainage” (https://www.ors.org/wp-content/uploads/2019/01/Question-3.pdf). These new definitions must incorporate our current understanding that the management of bone and implant‐related infections is inextricably intertwined with the biology of biofilms, infection of osteoblasts and osteocytes, and invasion of the osteocytic‐canalicular network by the bacteria . Thus, the challenge to define treatment protocols is dependent on defining biologic metrics, such as when persister cells become inaccessible to phagocytes, and when antimicrobial levels (and durations) needed to eradicate persister cells are not achievable systemically (minimum biofilm eradication concentration [MBEC]), as discussed by the https://www.ors.org/icm-2018-biofilm-workgroup/ .…”