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Parkinson’s disease and osteoporosis: basic and clinical implications

ABSTRACT Introduction: Parkinson’s disease (PD) is the second most frequent neurodegenerative disease. Lewy bodies, the hallmark of this disease due to an accumulation of α-synuclein, lead to loss of dopamine-regulated motor circuits, concomitantly progressive immobilization and a broad range of nonmotor features. PD patients have more hospitalizations, endure longer recovery time from comorbidities, and exhibit higher mortality than healthy controls. Although often overlooked, secondary osteoporosis has been reported frequently and is associated with a worse prognosis. Areas covered: In this review, we discuss the pathophysiology of PD from a systemic perspective. We searched on PubMed articles from the last 20 years in PD, both clinical features and bone health status. We discuss possible neuro/endocrine mechanisms by which PD impacts the skeleton, review available therapy for osteoporotic fractures and highlight evidence gaps in defining skeletal co-morbid events. Expert opinion: Future research is essential to understand the local and systemic effects of dopaminergic signaling on bone remodeling and to determine how pathological α-synuclein deposition in the central nervous system might impact the skeleton. It is hoped that a systematic approach to the pathogenesis of this disease and its treatment will allow the informed use of osteoporotic drugs to prevent fractures in PD patients.