Post-stroke osteoporosis: Mechanisms, treatments, and recent advances

 We've known of this problem for over a decade, why haven't you figured out how to prevent it?

Osteoporosis (3 posts to November 2013)

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Post-stroke osteoporosis: Mechanisms, treatments, and recent advances

Liu, Zezhong MM^a; Liu, Xiaoguang MM^a; Wang, Congcong MM^a; Sun, Quanxiang MM^b; Zhang, Lan MM^b; Wang, Jun PhD^c

Author Information

Journal of Aging and Rehabilitation 1(3):p 59-67, September 2024. | DOI: 10.1097/jagr.0000000000000015

• Open

Abstract

Post-stroke osteoporosis (PSO) is a common complication encountered in patients after stroke, characterized by a rapid decline in bone mass and disruption of bone microarchitecture, which significantly elevates the risk of fracture. The pathogenesis of PSO is multifaceted, encompassing factors, such as oxidative stress, inflammatory responses, neurological damage, extended immobilization, and hormonal imbalances, culminating in a dysregulation of bone metabolism. Treatment strategies encompass pharmacological interventions, nutritional supplementation, physical exercise, and rehabilitative training. Emerging therapies, such as stem cell therapy and exosome therapy, are being explored for their potential to promote cellular regeneration and modulate inflammatory responses in the treatment of PSO. Future therapeutic approaches should integrate a comprehensive understanding of the multifactorial pathogenesis of PSO to develop tailored treatment plans, aiming to optimize treatment efficacy and improve patients’ quality of life.

Introduction

The current state of stroke

Stroke, as one of the leading causes of death and disability worldwide, poses a significant challenge to public health that cannot be overlooked. In China, it is particularly prominent, ranking first in terms of disease burden.¹ Stroke is primarily categorized into hemorrhagic and ischemic types, with ischemic stroke being the focus of research and treatment due to its higher incidence rate, accounting for ∼85% of cases.² The occurrence of ischemic stroke is a complex process involving various factors and mechanisms, including inflammatory responses, apoptosis, changes in extracellular ion concentrations, and alterations in the permeability of the blood-brain barrier.

Currently, the main methods for treating ischemic stroke include thrombolytic therapy and endovascular thrombectomy. Thrombolytic therapy, which utilizes recombinant tissue plasminogen activator, is considered one of the most effective treatment modalities available.^3,4 However, the efficacy of thrombolytic therapy is limited, with studies indicating that up to two-thirds of patients do not benefit from it,⁵ and ∼10% of patients experience hemorrhagic transformation.⁶ Endovascular thrombectomy, although an effective treatment method, is also constrained by time window limitations and scope of application restrictions.

In recent years, stem cell therapy and exosome therapy have emerged as hot topics of research. Stem cell therapy has shown therapeutic potential by promoting cellular regeneration and inhibiting post-stroke inflammatory responses. Exosomes, as nanoscale vesicles containing various bioactive molecules, play a key role in intercellular communication due to their low immunogenicity, no risk of vascular obstruction, and ability to cross the blood-brain barrier, providing new insights for the treatment of ischemic stroke.

The occurrence of post-stroke osteoporosis

Post-stroke osteoporosis (PSO) is a frequently overlooked but highly significant clinical issue. It is a distinct type of osteoporosis characterized by an impact on both bone mass and quality.⁷ Compared with age-matched individuals without stroke, the risk of femoral neck fracture in stroke patients is increased fourfold.⁸ This type of osteoporosis can lead to disability and even death, becoming one of the major causes of mortality in stroke patients.⁹

The occurrence of osteoporosis is associated with an imbalance in bone metabolism. Under normal conditions, bone resorption and bone formation are in equilibrium, maintaining skeletal health. However, after a stroke, this balance is disrupted, leading to bone loss and a decrease in bone quality.¹⁰ Changes in bone metabolism in stroke patients may be related to neurological impairment, prolonged immobilization, malnutrition, and endocrine disorders.¹¹ These factors not only promote excessive activity of osteoclasts but also affect the function of osteoblasts, resulting in decreased bone quality and increased bone fragility.

Currently, the treatment and prevention of PSO, in addition to routine treatment for stroke, also include proper nutritional supplementation, appropriate physical exercise, and necessary pharmacological interventions. Particularly for patients who are bedridden for extended periods, the prevention and treatment of osteoporosis should be emphasized to reduce the risk of fractures.¹²

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