Abstract
Metabolic syndrome is a multifactorial disorder characterized by obesity, insulin resistance, dyslipidemia, and chronic low-grade inflammation, all of which can negatively influence skeletal metabolism and fracture healing. The present study examines the characteristics of osteogenesis in closed diaphyseal fractures of long bones under experimental metabolic syndrome. Particular attention is given to alterations in bone regeneration, callus formation, vascularization, and osteoblastic activity during the healing process. Experimental observations indicate that metabolic syndrome delays the inflammatory and reparative phases of fracture healing, resulting in slower mineralization and reduced mechanical stability of newly formed bone. Histological findings demonstrate decreased osteogenic cell proliferation and impaired angiogenesis in affected subjects compared with healthy controls. These changes emphasize the importance of metabolic homeostasis for effective bone repair and highlight the need for targeted therapeutic strategies in patients with metabolic disorders. The findings contribute to a better understanding of the relationship between systemic metabolic abnormalities and skeletal regeneration.

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