Bone health in Parkinson’s disease: a comprehensive review of bone involvement and its pathophysiological mechanisms

TL;DR

This paper reviews how Parkinson’s disease affects bone health, leading to issues like osteoporosis and fractures due to various physical and medication-related factors.

Contribution

The paper provides a comprehensive review of the pathophysiological mechanisms linking Parkinson’s disease and bone health.

Findings

Individuals with Parkinson’s disease have low bone mass and increased fracture risk, particularly hip fractures.

Osteoporosis in PD is linked to factors like vitamin D deficiency, weight loss, and muscle weakness.

Dopamine depletion and chronic inflammation may disrupt bone remodeling in Parkinson’s disease.

Abstract

Parkinson’s disease (PD) is a frequent neurodegenerative disorder that combines motor and non-motor features, including impaired balance, gait disturbances, and progressive loss of mobility. Bone involvement is well established, with low bone mass and elevated fracture risk- especially hip fractures- being common findings. Because of impaired balance, gait disturbances, cognitive dysfunction, and autonomic failure, individuals with PD experience a markedly elevated risk of falls. Osteoporosis in PD likely results from a convergence of nutritional deficiencies, vitamin D insufficiency, weight loss with sarcopenia, and progressive muscle weakness. Anti-Parkinson medications such as levodopa may also contribute through hyperhomocysteinemia. In addition, dopamine depletion and chronic inflammation may further disrupt bone remodeling. This review summarizes current evidence on bone mineral density, bone quality, falls, and fractures in PD and discusses the pathophysiological mechanisms underlying this comorbidity.

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