The role of dyslipidemia and obesity in the pathogenesis of osteonecrosis of the femoral head

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Abstract
The review focuses on current concepts of the role of obesity, the chronic systemic inflammation it induces, and lipid metabolism disorders in the pathogenesis of osteonecrosis of the femoral head (ONFH) in order to substantiate new approaches to its prevention and treatment. This review analyzes modern fundamental and clinical studies focusing on the relationship between metabolic disorders, chronic inflammation, and osteonecrosis. Specifically, we examine research investigating the molecular mechanisms of adipose tissue dysfunction, lipotoxicity, oxidative stress, and their impact on bone tissue homeostasis.The analysis established that obesity acts as a systemic risk factor for ONFH development, functioning not merely as a source of mechanical load but also as an initiator of a pathogenic cascade. Dysfunctional adipose tissue leads to chronic low-grade systemic inflammation and oxidative stress. Together, these factors provoke endothelial dysfunction, impair perfusion of the femoral head bone tissue, and induce lipotoxicity in the bone marrow. Consequently, at the local level, this cascade suppresses osteogenesis, simultaneously enhances bone resorption, and triggers osteocyte apoptosis.Systemic metabolic and inflammatory disruptions initiated by obesity underlie impaired bone remodeling, ischemia, and necrosis of the femoral head subchondral bone. Therefore, the correction of body weight and associated metabolic disorders should be considered an integral part of a comprehensive strategy for treating ONFH and preventing its progression. This integrated approach may improve the outcomes of joint-preserving interventions and delay the need for total hip arthroplasty in young patients.

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