Abstract
In the skeletal system, inflammation is closely associated with many skeletal disorders, including periprosthetic osteolysis (bone loss around orthopedic implants), osteoporosis, and rheumatoid arthritis. These diseases, referred to as inflammatory bone diseases, are caused by various oxidative stress factors in the body, resulting in long-term chronic inflammatory processes and eventually causing disturbances in bone metabolism, increased osteoclast activity, and decreased osteoblast activity, thereby leading to osteolysis. Inflammatory bone diseases caused by nonbacterial factors include inflammation- and bone resorption-related processes. A growing number of studies show that exosomes play an essential role in developing and progressing inflammatory bone diseases. Mechanistically, exosomes are involved in the onset and progression of inflammatory bone disease and promote inflammatory osteolysis, but specific types of exosomes are also involved in inhibiting this process. Exosomal regulation of the NF-κB signaling pathway affects macrophage polarization and regulates inflammatory responses. The inflammatory response further causes alterations in cytokine and exosome secretion. These signals regulate osteoclast differentiation through the receptor activator of the nuclear factor-kappaB ligand pathway and affect osteoblast activity through the Wnt pathway and the transcription factor Runx2, thereby influencing bone metabolism. Overall, enhanced bone resorption dominates the overall mechanism, and over time, this imbalance leads to chronic osteolysis. Understanding the role of exosomes may provide new perspectives on their influence on bone metabolism in inflammatory bone diseases. At the same time, exosomes have a promising future in diagnosing and treating inflammatory bone disease due to their unique properties.
Highlights
Bone homeostasis is a balance of osteoblasts and osteoclasts constantly acting on the bone to renew the body’s bone mass
Chronic inflammation caused by various stressors can to disrupt this delicate balance between osteoblasts and osteoclasts by secreting various inflammatory factors, such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin6 (IL-6), and prostaglandin E2 (PGE2), leading to disturbances in bone metabolism [1]
Some of the pathogenic processes associated with the development of inflammatory bone diseases in exosomes include the delivery of miRNAs, lncRNAs, inflammatory cytokines, chemokines, proteases, and other proteins; activation of macrophages; activation of Toll-like receptors; intercellular communication; and degradation of the extracellular matrix
Summary
Bone homeostasis is a balance of osteoblasts and osteoclasts constantly acting on the bone to renew the body’s bone mass. Chronic inflammation caused by various stressors can to disrupt this delicate balance between osteoblasts and osteoclasts by secreting various inflammatory factors, such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin (IL-6), and prostaglandin E2 (PGE2), leading to disturbances in bone metabolism [1]. These osteolytic lesions caused by chronic aseptic inflammation include aseptic loosening of the prosthesis [2], osteoporosis [3, 4], and rheumatoid arthritis [5]. Reversing inflammatory osteolysis by designing the effects of different types of exosomes on macrophage function and bone metabolism, and cell-free therapy, is challenging, which will provide a new perspective for researchers. We discuss the possible applications of exosomes in inflammatory bone diseases in clinical diagnosis and treatment
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