Application of platelet-rich plasma in traumatic bone infections.

: Traumatic bone infection represents a clinical challenge for orthopedic surgeons. Traditional treatments include surgical debridement and antibiotic, but prolonged use of antibiotic may lead to colonization of resistant bacteria and other adverse reactions.: Platelet-rich plasma (PRP), a biological product extracted from the peripheral blood of patients, has been widely used in the field of tissue repair in recent years.

New perspectives on traumatic bone infections.

In this paper, we review the results of previous studies and summarize the effects of various factors on the regulation of bone metabolism in traumatic bone infections. Infection-related bone destruction incorporates pathogens and iatrogenic factors in the process of bone resorption dominated by the skeletal and immune systems. The development of bone immunology has established a bridge of communication between the skeletal system and the immune system.

Dendritic cells-derived interferon-λ1 ameliorated inflammatory bone destruction through inhibiting osteoclastogenesis.

Bone infection contributing to inflammatory osteolysis is common in orthopedic surgery. The dynamic balance between bone formation and bone resorption is destroyed due to excessive osteoclast fusion and differentiation, which results in severe bone matrix loss. Many therapeutic approaches that restrain osteoclast formation and function act as efficient ways to prevent inflammatory bone erosion.

Platelet-rich plasma loaded with antibiotics as an affiliated treatment for infected bone defect by combining wound healing property and antibacterial activity.

To be faced with an infected bone defect and the need to accelerate bone union while controlling infection is a welcome challenge for orthopedists. Platelet-rich plasma (PRP) has been applied in tissue defects given their composition of growth factors however the weak antibacterial effects have limited the use of PRP in the clinical setting. Therefore, the aim of this study was to explore the feasibility of using PRP in a local antibiotic delivery system (PADS) with the characteristics of promoting wound healing of bone infection.

Metacarpal tuberculosis with Nocardia infection: A case report.

Introduction: Isolated metacarpal tuberculosis is rare in orthopedic surgery. In the case of poor efficacy of traditional treatment methods, such as debridement surgery and anti-tuberculosis treatment, it is necessary to consider whether there is a special type of infection. We describe a case of metacarpal tuberculosis with Nocardia infection in a patient.

Diallyl disulfide alleviates inflammatory osteolysis by suppressing osteoclastogenesis NF-κB-NFATc1 signal pathway.

Skeletal homeostasis is closely effectuated by the regulation of bone formation and bone resorption. Osteoclasts are multinuclear giant cells responsible for bone resorption. Overactivated osteoclasts and excessive bone resorption result in various lytic bone diseases, such as osteoporosis, osteoarthritis, periprosthetic infection, and inflammatory aseptic loosening of orthopedic implants.

Streptolysin O derived from Streptococcus pyogenes inhibits RANKL‑induced osteoclastogenesis through the NF‑κB signaling pathway.

Streptococcus pyogenes (GAS) is a clinically significant bacterial strain that causes bacterial arthritis, osteomyelitis and implant infections. Infection complications can lead to serious bone destruction. Osteoclasts, the only type of cell with bone resorption function, participate in this process.

Interleukin-37 inhibits osteoclastogenesis and alleviates inflammatory bone destruction.

Excessive osteoclast formation is one of the important pathological features of inflammatory bone destruction. Interleukin-37 (IL-37) is an anti-inflammatory agent that is present throughout the body, but it displays low physiological retention. In our study, high levels of the IL-37 protein were detected in clinical specimens from patients with bone infections.

Inhibitory effect of vanillin on RANKL-induced osteoclast formation and function through activating mitochondrial-dependent apoptosis signaling pathway.

Bone matrix homeostasis associated diseases such as osteoporosis and erosive arthritis were caused by the imbalance of osteoclast-mediated bone-resorption and osteoblast-mediated bone-formation. Suppressing the fusion and differentiation of osteoclast from osteoclast precursors are an essential way to maintain the dynamic balance of resorption and formation. Recently, some natural products were discovered to inhibit osteoclast formation and function for potential treatment of osteoporosis.