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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.

SUBMITTER: Figueroa CA

PROVIDER: S-EPMC7250483 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Low bone mineral density and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Inflammatory bowel disease (IBD) has been associated with an increased risk of osteoporosis and osteopenia and epidemiologic studies have reported an increased prevalence of low bone mass in patients with IBD. Certainly, genetics play an important role, along with other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in IBD and other lifestyle factors. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD are known to enhance bone resorption. There are genes influencing osteoblast function and it is likely that LRP5 may be involved in the skeletal development. Also the identification of vitamin D receptors (VDRs) and some of its polymorphisms have led to consider the possible relationships between them and some autoimmune diseases and may be involved in the pathogenesis through the exertion of its immunomodulatory effects during inflammation. Trying to explain the physiopathology we have found that there is increasing evidence for the integration between systemic inflammation and bone loss likely mediated via receptor for activated nuclear factor kappa-B (RANK), RANK-ligand, and osteoprotegerin, proteins that can affect both osteoclastogenesis and T-cell activation. Although glucocorticoids can reduce mucosal and systemic inflammation, they have intrinsic qualities that negatively impact on bone mass. It is still controversial if all IBD patients should be screened, especially in patients with preexisting risk factors for bone disease. Available methods to measure BMD include single energy x-ray absorptiometry, DXA, quantitative computed tomography (QCT), radiographic absorptiometry, and ultrasound. DXA is the establish method to determine BMD, and routinely is measured in the hip and the lumbar spine. There are several treatments options that have proven their effectiveness, while new emergent therapies such as calcitonin and teriparatide among others remain to be assessed.

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Parkinson's disease and osteoporosis: basic and clinical implications.

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