The Pathophysiology of Osteoporosis after Spinal Cord Injury

The Pathophysiology of Osteoporosis after Spinal Cord Injury

Spinal cord injury (SCI) affects approximately 300,000 people in the United States. Most individuals who sustain severe SCI also develop subsequent osteoporosis. However, beyond immobilization-related lack of long bone loading, multiple mechanisms of SCI-related bone density loss are incompletely un...

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Bibliographic Details
Main Authors: Ramsha Shams, Kelsey P. Drasites, Vandana Zaman, Denise Matzelle, Donald C. Shields, Dena P. Garner, Christopher J. Sole, Azizul Haque, Narendra L. Banik
Format: Article
Language:English
Published: MDPI AG 2021-03-01
Series:International Journal of Molecular Sciences
Subjects:
bone loss
RANKL
Wnt
Osteoprotegerin (OPG)
Estrogen (E2)
neurodegeneration
Online Access:https://www.mdpi.com/1422-0067/22/6/3057
Description
Summary:Spinal cord injury (SCI) affects approximately 300,000 people in the United States. Most individuals who sustain severe SCI also develop subsequent osteoporosis. However, beyond immobilization-related lack of long bone loading, multiple mechanisms of SCI-related bone density loss are incompletely understood. Recent findings suggest neuronal impairment and disability may lead to an upregulation of receptor activator of nuclear factor-κB ligand (RANKL), which promotes bone resorption. Disruption of Wnt signaling and dysregulation of RANKL may also contribute to the pathogenesis of SCI-related osteoporosis. Estrogenic effects may protect bones from resorption by decreasing the upregulation of RANKL. This review will discuss the current proposed physiological and cellular mechanisms explaining osteoporosis associated with SCI. In addition, we will discuss emerging pharmacological and physiological treatment strategies, including the promising effects of estrogen on cellular protection.
ISSN:1661-6596
1422-0067

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