The Role of SIRT1 in Mediating Bone Marrow Edema and Its Interface With Bone Remodeling
Abstract
Background: Bone marrow edema (BME), a common magnetic resonance imaging (MRI) finding characterized by increased fluid signal, is associated with pain and structural deterioration in conditions such as osteoarthritis and avascular necrosis. The pathophysiology of BME involves a complex interplay of vascular leakage, inflammation, microdamage, disrupted bone remodeling, and increased marrow adiposity. Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, is a critical regulator of bone homeostasis, promoting osteoblastogenesis, inhibiting osteoclastogenesis, and suppressing bone marrow adipose tissue (BMAT) formation.
Materials and methods: This review synthesizes existing experimental, preclinical, and clinical evidence concerning SIRT1 in bone homeostasis and examines its potential relationship with mechanisms implicated in BME. Particular attention is given to endothelial integrity, inflammatory signaling, oxidative stress, bone remodeling, BMAT, and mesenchymal stem cell fate.
Results: Current evidence supports a biologically plausible role for SIRT1 dysfunction in the development and persistence of BME. Reduced SIRT1 activity may contribute to vascular permeability, prolonged inflammatory signaling, oxidative stress, impaired osteoblastogenesis, enhanced osteoclastogenesis, and increased marrow adiposity. Although direct evidence linking SIRT1 specifically to BME remains limited, converging indirect evidence suggests that SIRT1 activation could mitigate several core drivers…
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