Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder after Alzheimer’s disease (1, 2). It manifests with a wide range of motor and non-motor symptoms that substantially burden patients. The key motor manifestations include resting tremor, rigidity, and bradykinesia, often accompanied by disturbances of balance and gait. These features arise from progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, where abnormal accumulation of α-synuclein (Lewy bodies) disrupts neuronal survival and function. As dopamine signaling diminishes, corticobasal ganglia circuits become dysfunctional, producing the hallmark motor features. PD is now understood as a complex neuropsychiatric disorder, with non-motor features such as mood and behavioral changes, autonomic dysfunction, and in later stages, cognitive impairment and axial postural abnormalities including scoliosis, camptocormia, and Pisa syndrome (3, 4). These complications, together with nutritional deficits, muscle weakness, and body weight changes, contribute to falls and loss of independence, significantly reducing quality of life for patients and caregivers (5). Accumulating evidence indicates that PD is also complicated by osteoporosis and skeletal fragility (6–9). Compared with individuals without PD, patients show lower bone mineral density (BMD) (10) and an increased risk of falls, leading to higher rates of fragility fractures, especially hip fractures (8, 11). Such fractures carry serious consequences, including disability, hospitalization, and higher mortality (7). This review aims to summarize evidence on bone involvement in PD, focusing on BMD, bone quality, falls, and fractures, and to discuss mechanisms that may underlie these complications.

A comprehensive literature search was conducted in the Medline database. The search terms included “Parkinson’s disease” combined with “osteoporosis,” “fracture,” “fall risk,” “bone mineral density,” or “bone quality.” The search was restricted to articles published in English. Eligible studies included original research articles, epidemiological studies, systematic reviews, and meta-analyses. Case reports, case series, editorials, conference abstracts, and full-text articles published in languages other than English were excluded. The literature search was performed in June 2025 and covered articles published from 1990 up to the search date.

Compared with age- and sex-matched controls, individuals with PD consistently exhibit reduced BMD (6, 8, 9), as demonstrated in both cross-sectional and longitudinal studies (12–17). Smaller case–control cohorts have shown lower BMD across multiple skeletal sites, with evidence of progressive decline during follow-up (17). In large prospective cohorts, such as the Study of Osteoporotic Fractures (16), hip BMD was initially lower in PD patients, although differences diminished after adjustment for confounders. Data from the Osteoporotic Fractures in Men study indicated that men with PD experience an accelerated decline in hip BMD relative to non-PD men (age-adjusted mean annualized total hip bone loss: 1.08% vs. 0.36%) (15). Another study found that lower lumbar spine BMD in PD was related to the severity of the disease according to Hoehn and Yahr stage, although this study was limited by the small patient sample size and by the use of dual photon absorptiometry for BMD measurements, rather than the reference method of dual X-ray absorptiometry (DXA) (18). Other studies have suggested that reduced lumbar spine BMD is associated with more advanced disease severity. A large Japanese cohort further linked lower BMD to higher fracture risk, greater disease severity, longer duration, lower body mass index (BMI), and vitamin D deficiency (19). Meta-analyses confirm a consistent pattern: PD is associated with lower BMD at several skeletal sites and an increased prevalence of osteoporosis, though the magnitude of risk may differ by sex. A first meta-analysis reported that PD patients were at a higher risk of osteoporosis than healthy subjects, with an Odd Ratio (OR) of 1.18 [95% CI: 1.09–1.27]. The results showed that PD patients had lower BMD in the hip, lumbar spine and femoral neck than healthy subjects. In addition, the risk of osteoporosis was higher in male patients than in female patients (OR: 2.44 [95% CI: 1.37–4.34] vs. 1.16 [95%CI: 1.07–1.26], respectively) (20). A second meta-analysis reached similar conclusions, finding a higher risk of osteoporosis in PD patients than in healthy controls, with an OR of 2.61 [95% CI: 1.69–4 0.03]. However, unlike the previous study, the risk was higher for female patients. Patients with PD had lower hip, lumbar spine and femoral neck BMD than healthy controls (21). These results were in agreement with a third meta-analysis on BMD in PD patients, which reported lower total body, total hip, total radius, lumbar spine, total femur, femoral neck and hand BMD than in non-PD controls (22) (Table 1). Overall, BMD was lower in patients with Parkinson’s disease compared with the control population, and this reduction was observed at multiple skeletal sites. Whether the decrease in BMD in PD differs by sex remains a matter of debate.

Most studies of bone involvement in PD have relied on DXA, which does not capture microarchitectural features of bone. Trabecular Bone Score (TBS), a surrogate marker of bone microarchitecture, has been shown to improve fracture risk prediction in other populations but has only rarely been applied in PD. In smaller clinical studies, results have been mixed: some reported alterations in TBS despite preserved BMD (23), while others found differences more evident when muscle performance was impaired (24): a first study conducted in Ukraine reported TBS evaluation in a series of 38 male patients with PD and 38 without PD. Patients with PD had osteoporosis according to total body BMD measurements, but BMD at the lumbar spine and femoral neck did not differ between the patients and the controls. The TBS assessment showed significantly higher results in the PD group than in the control group (23). Another study from Italy compared 13 patients with PD in the early stages of the disease to 13 age-matched controls. While there was no decrease in BMD among the patients, TBS significantly decreased in the PD group, as determined by the muscle performance assessment using the short physical performance battery (SPPB). Indeed, patients with lower SPPB scores had lower TBS scores despite having normal BMD values (24). These findings suggest that microarchitectural deterioration may occur earlier than measurable BMD loss. Other techniques such as calcaneal ultrasound have also indicated poorer bone quality in PD, with significant differences observed particularly in women (25). Overall, bone quality parameters are altered in PD, as evidenced by trabecular bone score or ultrasound assessments.

Because of balance instability, gait impairment, autonomic dysfunction, and cognitive decline, patients with PD have a markedly increased risk of falling (11). In a prospective cohort of more than 200 patients followed for 8 years, over two-thirds experienced falls, with prevalence rising steadily over time. Factors such as freezing of gait, higher levodopa exposure, and axial motor impairment were identified as predictors (26). Retrospective analyses confirm that around one-third of patients are recurrent fallers, with risk increasing in older individuals, those with more advanced disease, or with prominent rigidity and postural deficits (11). In a large survey, more than half of PD patients reported at least one fall over a two-year period, particularly in the presence of atypical Parkinsonism or dementia (27). Meta-analyses indicate that nearly half of PD patients experience a fall within 3 months, and that a history of recurrent falls (two or more falls in the previous year) is the strongest predictor of future events (28). Patients with PD presenting with postural instability and gait disturbances were more likely to experience falls than those with tremor-dominant symptoms. In a prospective cohort study of 113 patients with PD, the postural instability and gait difficulty subgroup experienced a higher number of falls related to freezing of gait, balance impairment, and falls occurring at home (29). Overall, these studies consistently report a markedly increased risk of falls among patients with PD.

Multiple retrospective and prospective studies have consistently shown that individuals with PD face a higher burden of fragility fractures compared with age-matched controls. In a population-based study in the USA (Olmsted County, Minnesota), patients with PD were more likely to have a history of fracture than control subjects, with fracture rates of 59 and 44%, respectively, at 10 years. Fractures of the femoral neck accounted for 23% of the fractures in PD patients (30). A retrospective analysis of 200 PD patients and 200 control subjects revealed that fractures were significantly more frequent in the PD group (15% vs. 7.5%). The most common fracture site for PD patients was the femur. Vertebral fractures were also higher in the PD group (31). In long-term population cohorts, fracture incidence in PD exceeded that in non-PD groups, with hip fractures disproportionately represented. Case–control analyses likewise demonstrate that fractures, particularly of the femur and spine, occur significantly more often in PD. The effect of comorbidities on fracture risk was evaluated in the multinational GLOW cohort, which included 52,960 women. This large multinational cohort identified PD as one of the strongest comorbid predictors of fracture risk, even after accounting for other chronic diseases (32). Meta-analysis evidences indicate a roughly two- to threefold increased risk of both hip and non-vertebral fractures, with men appearing especially vulnerable to hip fractures (33–35) (Table 1). Importantly, fractures may occur during the prodromal phase, as patients who later develop PD already show higher fracture rates in the years preceding diagnosis (36). Overall, fracture risk is increased in patients with PD, particularly at the hip, while vertebral fractures are also overrepresented in this population.

As a systemic neurodegenerative disease involving multiple comorbidities, the mechanisms explaining bone loss and fragility in PD are complex and multifactorial (Figure 1).

Robust evidence indicates that PD impacts bone integrity from early in the disease course. Patients consistently exhibit lower BMD than non-PD individuals, and when combined with frequent falls, this markedly increases hip fracture risk. Skeletal fragility in PD arises from multiple mechanisms, including vitamin D deficiency, body composition changes, sarcopenia, reduced mobility, medication effects such as levodopa-related hyperhomocysteinemia, and systemic inflammation. Nevertheless, osteoporosis screening is not standard practice in PD, and clinical guidelines remain inconsistent. There is a clear need for dedicated recommendations and proactive management strategies to improve bone health outcomes in this vulnerable population.