Effects of systemic Anatolian propolis administration on a rat-irradiated osteoradionecrosis model

ÇOLAK, Sefa; ERDIL, Aras; GEVREK, Fikret

doi:10.1590/1678-7757-2023-0231

Cited by 1 publication

(1 citation statement)

References 32 publications

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“…There are approximately 20,000–30,000 new cases of osteonecrosis in the United States every year and approximately 150,000 cases in China [ 2 , 3 ]. Numerous risk factors, such as the use of glucocorticoids and excessive alcohol consumption, as well as certain disease states, like sickle cell disease and systemic lupus erythematosus, and treatment approaches, like radiation, chemotherapy, and hip surgery, can cause osteonecrosis to progress [ 4 , 5 , 6 , 7 ]. Hip preservation surgery (such as core decompression, bone grafting, and osteotomy) and a combination of medications (such as anticoagulants, fibrinolysis-enhancing drugs, vasoactive agents, and lipid-lowering therapies) can be utilized to treat early ONFH [ 8 , 9 , 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Unraveling the Role of Endothelial Dysfunction in Osteonecrosis of the Femoral Head: A Pathway to New Therapies

Shao,

Wang,

et al. 2024

Biomedicines

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Osteonecrosis of the femoral head (ONFH) is a disabling disease characterized by the disruption of the blood supply to the femoral head, leading to the apoptosis and necrosis of bone cells and subsequent joint collapse. Total hip arthroplasty is not optimal since most patients are young. Multiple risk factors contribute to osteonecrosis, including glucocorticoid (GC) usage, excessive alcohol intake, hypercholesterolemia, and smoking. Continuous stimulation by many variables causes a chronic inflammatory milieu, with clinical repercussions including endothelial dysfunction, leading to thrombosis, coagulopathy, and poor angiogenesis. Immune cells are the primary regulators of inflammation. Innate and adaptive immune cells interact with endothelial cells to hinder the regeneration and repair of bone lesions. An in-depth examination of the pathological drivers of ONFH reveals that endothelial dysfunction may be a major cause of osteonecrosis. Understanding the involvement of endothelial dysfunction in the chronic inflammation of osteonecrosis could aid in the development of possible therapies. This review summarizes the role of endothelial cells in osteonecrosis and further explains the pathophysiological mechanism of endothelial dysfunction in this disease from the perspective of inflammation to provide new ideas for the treatment of osteonecrosis.

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