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)

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem?

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

More at link

Oral Anticoagulant Choice Matters in Bone Health, Study Finds

So ask your doctor VERY SPECIFICALLY  why your anticoagulant was chosen. I just got rat poison(warfarin) because that was the only thing available at the time except for a couple of lovenox shots. 

So good to know your doctors know nothing specific about this and are just guessing in the dark.(suggest, propose, theory) Aren't you happy that there seems to be NO PROTOCOLS anywhere in stroke?  Stroke survivors are just guinea pigs in unregulated experiments.  And you are paying your doctor for that privilege.

Oral Anticoagulant Choice Matters in Bone Health, Study Finds

Investigators compare direct oral anticoagulants with vitamin K antagonists

Did your doctor do anything with this from November 2013 regarding prescribing intravenous bisphosphonates?

Falls, Fractures, and Osteoporosis After Stroke

 

• by Nicole Lou, Contributing Writer, MedPage Today October 21, 2019

Bone fractures are a risk to be considered when choosing the oral anticoagulant for a patient with non-valvular atrial fibrillation (Afib), a study suggested.
The risk of poor osteoporotic outcomes was significantly lower with direct oral anticoagulant (DOAC) compared with vitamin K antagonist (VKA) therapy, as follows:

• Any fracture: 3.09% vs 3.77% (adjusted HR 0.85, 95% CI 0.74-0.97)

• Major osteoporotic fractures: 2.29% vs 2.82% (adjusted HR 0.85, 95% CI 0.72-0.99)

• Initiation of  medication: 2.44% vs 3.14% (adjusted HR 0.82, 95% CI 0.71-0.95)

• Any fracture or starting osteoporosis medication: 5.21% vs 6.43% (adjusted HR 0.84, 95% CI 0.76-0.93)

"Because of a more favorable skeletal health profile, DOAC treatment could be preferred to VKA in patients with Afib with strong risk factors for osteoporotic fractures," said Casper Binding, BMedSc, of Copenhagen University Hospital Herlev and Gentofte in Denmark, and colleagues.
As the team noted in the study online in the Journal of the American College of Cardiology, VKAs like warfarin (Coumadin) have been widely used for stroke prophylaxis for decades. The newer DOACs have been shown to have efficacy similar to that of warfarin in preventing stroke in Afib and do not require international normalized ratio (INR) monitoring, Binding and colleagues explained.
Using data from the Danish National Patient Register, the investigators identified 37,350 people with non-valvular Afib as having had no prior use of osteoporosis medication and having undergone 180 days of oral anticoagulation with a VKA or a DOAC, including dabigatran, rivaroxaban, apixaban, or edoxaban.
Two-thirds of the cohort received DOAC rather than VKA treatment. The DOAC group was significantly older; included more women; and were more often on hormone-replacement therapy and to have had previous fractures, stroke, or a diagnosis of alcohol abuse.
"Studies suggest a link between warfarin and undercarboxylated osteocalcin, which is associated with low bone mineral density," the researchers wrote. "These results correlate with findings that propose a connection between warfarin and an increased risk of osteoporotic fractures."
Then there is the theory that dietary restrictions around VKA treatment could lead to low folic acid intake and a resulting risk of hyperhomocysteinemia, which can reduce bone strength, the researchers continued, adding that in the end, the main results are in line with those of a smaller study of Chinese patients.
"The results of our study not only support what other studies have suggested, but also more importantly they show that the risk reductions apply to nationwide data from a Western society and persist when all DOACs are analyzed and compared with VKA," the investigators said.
They noted that their analysis may be subject to residual confounding from unmeasured variables such as INR, body mass index (BMI), hemoglobin, and renal function.
Writing in an accompanying editorial, Brian Gage, MD, MSc, of Washington University in St. Louis, Missouri, said: "Because patients with low creatinine clearance or low BMI are both more likely to have an osteoporotic fracture and to be prescribed a VKA rather than a DOAC, residual confounding could have exaggerated the association between VKA and fracture."
"Thus, at least for patients who have Afib and no prior osteoporotic fracture (the population studied), the decision to prescribe a VKA or a DOAC should depend on the risks of ischemic stroke, hemorrhage, need for monitoring, and affordability rather than on the risk of osteoporotic fracture," Gage argued.
In summary, he said, the researchers "had a strong biochemical basis to search for a link between VKAs and osteoporotic fracture. Their well-done observational study provides additional evidence of this link, but residual confounding may have exaggerated the association."

The study was funded by an institutional scholarship awarded to Binding.
Binding and Gage disclosed no conflicts.

• Primary Source

  Journal of the American College of Cardiology

  Source Reference: Binding C, et al "Osteoporotic fractures in patients with atrial fibrillation treated with conventional versus direct anticoagulants" J Am Coll Cardiol 2019; DOI: 10.1016/j.jacc.2019.08.1025.

• Secondary Source

  Journal of the American College of Cardiology

  Source Reference: Gage BF "Warfarin-induced fractures in atrial fibrillation?" J Am Coll Cardiol 2019; DOI: 10.1016/j.jacc.2019.08.1026.

 

Missed osteoporosis screening puts stroke survivors at fracture risk

Once again addressing a secondary issue rather than fixing the primary problem, reduced mobility, which is addressed by getting survivors 100% recovered.

Missed osteoporosis screening puts stroke survivors at fracture risk

Stroke survivors are at risk for osteoporosis, broken bones or falling. Yet many aren't screened for such dangers, which may increase the odds they'll suffer fractures, a new study says.
Stroke survivors often have to cope with reduced mobility, which decreases bone mineral density, making bones more fragile. The risk of someone suffering a fracture within a year of having a stroke is up to four times greater than for someone without a history of stroke.
In the new study, published Thursday in the American Heart Association's journal Stroke, researchers looked at data from 16,581 stroke survivors age 65 and older who either had visited the emergency department or had been hospitalized for strokes between 2003 and 2013 in Ontario, Canada.
Only 5.1% of those people received bone mineral density testing. One year after their stroke, only 15.5% of them had been prescribed medications to prevent fractures.
"This study offers more evidence that there is a missed opportunity to identify people with stroke at increased risk of fractures, and to initiate treatment to prevent bone loss and fractures," the study's lead author Dr. Moira Kapral, professor of medicine and director of the division of general internal medicine at the University of Toronto in Canada, said in a news release.
The authors noted their study was conducted in a province that provides payment for osteoporosis testing and treatment, so the results may not be generalizable to places without similar health care coverage.
Previous research has shown that, at most, only about one-quarter of older women in the United States are screened for osteoporosis, with treatment rates as low as 30% even in high-risk groups.
Osteoporosis is a disease that weakens bones to the point where they break easily. According to the National Institute on Aging, osteoporosis can strike at any age but is most common among older people, especially older women.
Weak bones mean that a simple fall can cause a break, which can require surgery or, in the case of a hip fracture, result in a lengthy period of immobility.
If you have questions or comments about this story, please email editor@heart.org.

Falls, Fractures, and Osteoporosis After Stroke

This must not have affected me too much considering  my epic failure at bike stroke therapy  My doctor had 4 years to read about this and never told me to watch out for this.
 http://stroke.ahajournals.org/content/33/5/1432.short

Time to Think About Protection?

1. Kenneth E.S. Poole, BM, MRCP;
2. Jonathan Reeve, DM, BSc, FRCP;
3. Elizabeth A. Warburton, MA, DM, MRCP

+ Author Affiliations

1. From the Department of Stroke Medicine (K.E.S.P., E.A.W.) and Medical Research Council Bone Research Group (J.R.), Addenbrooke’s Hospital, Cambridge, UK.

1. Correspondence to Dr Elizabeth A. Warburton, Department of Stroke Medicine, Department of Medicine, University of Cambridge, Addenbrooke’s Hospital, Box 83, Cambridge CB2 2QQ, UK. E-mail eaw23@medsch1.cam.ac.uk

Abstract

Background— Osteoporosis is a significant complication of stroke. The clinical course of hemiplegic stroke predisposes patients to disturbed bone physiology. Sudden immobility and unilateral loss of function unload the skeleton at key areas such as the affected hip. This is manifest by an early reduction in bone density at this site. Stroke patients may also have motor, sensory, and visual/perceptual deficits that predispose them to falls. These factors result in an early but sustained increase in hip fractures after stroke.

Summary of Comment— Potential bone loss is often overlooked in stroke treatment. Morbidity and mortality from hip fractures might be reduced by preventing bone loss at an early stage. In the crucial first year after stroke, bone loss seems to be due to accelerated resorption. Bisphosphonates are the drugs of choice in preventing osteoclastic bone resorption, but oral administration soon after stroke may be impractical. Potent new intravenous bisphosphonates have been used in postmenopausal women with osteoporosis with good preliminary results. Effective dosing regimens for osteoporosis have included a single annual or semiannual injection of bisphosphonate as well as weekly oral dosing. This article reviews the current literature on osteoporosis and hip fractures after stroke, making a case for a trial of intravenous bisphosphonates early after stroke.

Conclusions— Hip fracture after stroke is an increasingly recognized problem. Measures to prevent bone loss and preserve bone architecture have not been part of stroke management thus far. Because rapid bone loss is a risk factor for fracture, we believe that a randomized, placebo-controlled trial of intravenous bisphosphonates given in the early phase of stroke rehabilitation is indicated.