Yes, Parkinson’s disease significantly increases the risk of osteoporosis. Research shows that osteoporosis and osteopenia affect up to [91% of women and 61% of men](https://pubmed.ncbi.nlm.nih.gov/19346153/) with Parkinson’s disease, making bone health a critical but often overlooked concern for this population. A systematic review and meta-analysis found that Parkinson’s patients have [2.61 times higher odds](https://pubmed.ncbi.nlm.nih.gov/24620034/) of developing osteoporosis compared to healthy controls. Consider a 68-year-old man diagnosed with Parkinson’s five years ago who assumes bone health is only a concern for postmenopausal women.
A DEXA scan reveals osteopenia, putting him at risk for a hip fracture that could dramatically reduce his mobility and independence. The connection between these two conditions involves multiple pathways: dopamine deficiency directly affects bone metabolism, reduced mobility accelerates bone loss, and common Parkinson’s medications like levodopa may contribute to decreased bone density through elevated homocysteine levels. This convergence of falling risk and weakened bones creates a dangerous combination. People with Parkinson’s face a [four times higher risk](https://www.apdaparkinson.org/article/bone-health-and-parkinsons-disease/) of hip fracture compared to the general population. This article examines why Parkinson’s disease leads to bone loss, how dopamine and medications affect bone health, practical screening recommendations, treatment options, and strategies for reducing fracture risk.
Table of Contents
- How Does Parkinson’s Disease Affect Bone Density?
- The Role of Levodopa and Parkinson’s Medications in Bone Health
- When Should Parkinson’s Patients Get Bone Density Testing?
- Treatment Options for Osteoporosis in Parkinson’s Disease
- Why Falls and Fractures Are Particularly Dangerous in Parkinson’s
- Exercise and Lifestyle Strategies for Protecting Bone Health
- Bridging the Bone Health Treatment Gap
- Conclusion
How Does Parkinson’s Disease Affect Bone Density?
parkinson‘s disease undermines bone health through several interconnected mechanisms that operate independently of age-related bone loss. The most direct pathway involves dopamine itself. [Research demonstrates](https://pmc.ncbi.nlm.nih.gov/articles/PMC6760231/) that dopamine receptors are expressed in both osteoblasts (bone-building cells) and osteoclasts (bone-resorbing cells), meaning the dopamine deficiency central to Parkinson’s directly disrupts bone homeostasis. Studies in animal models show that dopaminergic degeneration results in accelerated osteoclastogenesis and suppressed bone formation, even without any reduction in physical activity. Reduced mobility compounds this problem substantially.
Many people with Parkinson’s become less physically active as the disease progresses, and weight-bearing activity is essential for maintaining bone strength. The mechanism parallels what happens during prolonged bed rest or space travel: without mechanical stress on bones, the body reduces bone maintenance. A Brazilian study of 107 Parkinson’s patients found that [42.1% had osteopenia and 34.6% had osteoporosis](https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2024.1326212/full), with lean body mass playing a significant protective role. Vitamin D deficiency is widespread in this population for practical reasons. People with Parkinson’s often spend less time outdoors due to mobility limitations or freezing episodes that make walking outdoors feel unsafe. Combined with potential nutritional issues from swallowing difficulties and reduced appetite, vitamin D levels frequently drop below adequate levels, further accelerating bone loss.
The Role of Levodopa and Parkinson’s Medications in Bone Health
Levodopa, the gold-standard treatment for Parkinson’s motor symptoms, appears to have a complicated relationship with bone health. [Research published in Scientific Reports](https://www.nature.com/articles/s41598-019-50336-4) found that high-dosage levodopa treatment is associated with low bone mineral density due to the deleterious effects of homocysteine, a toxic metabolite produced during levodopa metabolism. This creates an uncomfortable paradox: the medication that best controls motor symptoms may simultaneously contribute to bone weakness. However, the picture is not entirely negative, and stopping levodopa is not the answer. The same research shows that levodopa and dopamine receptor agonists actually inhibit osteoclast formation in laboratory settings.
The relationship is dose-dependent and varies by individual. Clinicians increasingly recommend weight-based levodopa dosing and early use of adjunctive therapies to limit total levodopa exposure, particularly in women during and after menopause when declining estrogen already exacerbates bone loss. If you have been taking levodopa for many years, this does not mean your bones are inevitably compromised. What matters is getting screened and taking protective measures. [The American Parkinson disease Association recommends](https://www.apdaparkinson.org/article/bone-health-and-parkinsons-disease/) proactive screening for osteoporosis regardless of medication history, because the disease itself carries significant bone risk independent of treatment choices.
When Should Parkinson’s Patients Get Bone Density Testing?
The straightforward answer is earlier than current general population guidelines suggest. Standard recommendations call for DEXA scans starting at age 65 for women and when risk factors are present for men. But Parkinson’s disease changes this calculus significantly. A [study of male Parkinson’s patients](https://movementdisorders.ufhealth.org/2012/04/25/get-a-bone-scan-to-treat-your-parkinsons-disease-even-if-you-are-a-man/) found that 72% had osteopenia or osteoporosis in at least one bone site, with reduced bone mineral density present in 58.8% of those with disease duration of 0-5 years. This means bone loss begins early in the disease course, not just in advanced stages.
Yet an [Australian audit from 2025](https://pmc.ncbi.nlm.nih.gov/articles/PMC11735546/) found that around half of Parkinson’s patients do not have their bone health assessed following specialist clinic appointments. This represents a significant treatment gap with real consequences: undiagnosed osteoporosis means untreated osteoporosis, which means preventable fractures. The DEXA scan itself is simple, painless, and takes 10-30 minutes. It measures bone density in the hip and spine, the areas most vulnerable to fracture. Results come as T-scores: anything above -1.0 is normal, between -1.0 and -2.5 indicates osteopenia, and -2.5 or below means osteoporosis. For Parkinson’s patients, [updated guidance from the National Osteoporosis Guideline Group](https://academic.oup.com/ageing/article/54/3/afaf052/8086520) now recommends that a Parkinson’s diagnosis should trigger a fracture risk assessment.
Treatment Options for Osteoporosis in Parkinson’s Disease
Bisphosphonates remain the first-line treatment for osteoporosis in Parkinson’s patients, and the evidence supports their effectiveness in this population. A meta-analysis found that [risedronate treatment reduced hip fracture risk by 75%](https://pmc.ncbi.nlm.nih.gov/articles/PMC7250483/) in patients with neurological diseases including Parkinson’s. Importantly, these medications do not interact with levodopa or other Parkinson’s treatments, making them safe to add to existing regimens. The tradeoff involves practical administration challenges. Oral bisphosphonates like alendronate must be taken on an empty stomach, early in the morning, with the patient remaining upright for 30 minutes afterward.
For someone with Parkinson’s who may have swallowing difficulties, morning stiffness, and a complex medication schedule already, this regimen can be difficult to maintain. Dysphagia affects many Parkinson’s patients and creates both adherence barriers and potential safety concerns with oral medications. The alternative is intravenous administration. [Zoledronic acid](https://parkinsonsblog.stanford.edu/2022/06/bone-health-and-parkinsons-disease-webinar-notes/), given once yearly for three years, has demonstrated approximately 75% reduction in spine fractures and 40% reduction in other fractures. An ongoing NIH-sponsored trial called TOPAZ is specifically studying whether zoledronic acid reduces fracture risk in Parkinson’s patients, with the added benefit of home administration without extra medical visits.
Why Falls and Fractures Are Particularly Dangerous in Parkinson’s
The combination of increased fall risk and decreased bone density creates a perfect storm for fractures in Parkinson’s disease. [Estimates show](https://parkinsonsnewstoday.com/columns/monitoring-bone-health-crucial-parkinsons/) that 90% of fractures result from falls, and 68% of people with Parkinson’s will experience at least one fall per year. Unlike a fall in someone with normal bone density, a fall in someone with osteoporosis frequently results in fracture rather than just bruising. Hip fractures carry particularly serious consequences. They often require surgery, extended hospitalization, and prolonged rehabilitation. For someone already managing Parkinson’s motor symptoms, immobilization during recovery can accelerate disease progression and muscle loss.
Many patients never regain their previous level of function. A [2025 Korean population study](https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2025.1552381/full) found that while osteoporosis alone was not an independent risk factor for mortality in Parkinson’s patients, hip fractures served as a mediating factor that significantly increased mortality risk. One limitation of current fracture risk assessment tools is worth noting. The widely used FRAX calculator does not directly incorporate falls frequency, despite falls being an independent risk factor for fracture. This means [fracture risk is likely underestimated](https://academic.oup.com/ageing/article/54/3/afaf052/8086520) in Parkinson’s patients, where 60% experience falls and 39% experience recurrent falls. Clinicians should consider this underestimation when making treatment decisions.
Exercise and Lifestyle Strategies for Protecting Bone Health
Weight-bearing exercise provides dual benefits for Parkinson’s patients: it helps maintain bone density and improves balance to reduce fall risk. [Strong evidence from randomized controlled trials](https://jneuroengrehab.biomedcentral.com/articles/10.1186/1743-0003-7-50) shows that regular strength and balance training can reduce fall risk by 15-50% in older adults. For someone with Parkinson’s, exercise also helps maintain muscle mass, which has an independent protective effect on bone health. The key is choosing appropriate activities. Walking, dancing, and tai chi provide weight-bearing benefits while being adaptable to different ability levels. Resistance training with weights or bands stimulates bone formation through the mechanical stress it places on the skeleton.
A physical therapist familiar with Parkinson’s can design a program that accounts for individual limitations while maximizing benefits. Many communities offer Parkinson’s-specific exercise classes that address both bone health and motor symptom management. Vitamin D and calcium supplementation remains somewhat controversial. Recent guidance from the U.S. Preventive Services Task Force found [no net benefit](https://www.aarp.org/health/drugs-supplements/vitamin-d-calcium-falls-fractures/) from these supplements for preventing falls or fractures in the general older adult population. However, experts note that correcting deficiency remains important, and deficiency is common in Parkinson’s. The recommendation is to have vitamin D levels tested and supplement if levels are low, rather than taking supplements automatically.
Bridging the Bone Health Treatment Gap
Despite clear evidence that Parkinson’s patients face elevated osteoporosis risk, a significant gap exists between what research supports and what happens in clinical practice. [A 2025 systematic review](https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mdc3.14311) found that most osteoporosis management recommendations for Parkinson’s patients are based on research conducted in the general population, raising concerns about their applicability to individuals with unique clinical needs. The BONE PARK 2 protocol, published in early 2025, represents an effort to address this gap by creating a specific algorithm for assessing and managing bone health in Parkinson’s disease.
This type of disease-specific guidance is needed because Parkinson’s adds complexity that general osteoporosis guidelines do not address: medication interactions, swallowing difficulties, balance impairment, and cognitive changes that affect treatment adherence. Patients can advocate for themselves by requesting bone density screening at diagnosis and periodically thereafter, asking about vitamin D testing, and discussing fracture prevention as part of routine Parkinson’s care. The good news, as [the American Parkinson Disease Association notes](https://www.apdaparkinson.org/article/bone-health-and-parkinsons-disease/), is that low bone density can be successfully treated in people with Parkinson’s. The challenge is ensuring that screening happens so treatment can begin before a fracture occurs.
Conclusion
Parkinson’s disease substantially increases osteoporosis risk through multiple mechanisms: dopamine deficiency directly affects bone metabolism, reduced mobility accelerates bone loss, vitamin D deficiency is common, and medications like levodopa may contribute to decreased bone density. With up to 91% of women and 61% of men with Parkinson’s experiencing osteopenia or osteoporosis, bone health deserves attention equal to motor symptom management.
The practical steps are clear: request a DEXA scan early in the disease course rather than waiting for standard age-based screening recommendations, have vitamin D levels tested and correct any deficiency, engage in weight-bearing exercise appropriate to your abilities, and discuss osteoporosis treatment options with your healthcare team if screening reveals bone loss. Bisphosphonates are effective in this population, and intravenous options exist for those who cannot tolerate oral medications. Preventing fractures protects mobility, independence, and quality of life in ways that make proactive bone health management worthwhile.
