CHARACTERISTICS OF BONE AND MINERAL METABOLISM IN PARKINSON’S DISEASE AND OPPORTUNITIES FOR ITS MODIFICATION
Keywords:
Parkinson’s disease; bone and mineral metabolism; osteoporosis; osteopenia; Vitamin D; calcium-phosphorus metabolism; fractures; dopamine; bone mineral density; densitometry; hypodynamia; sarcopenia; homocysteine; physical rehabilitation; osteoporosis preventionAbstract
Parkinson’s disease (PD) is a chronic progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra and the development of both motor manifestations (bradykinesia, rigidity, resting tremor) and non-motor symptoms. In recent years, particular attention has been devoted to the systemic complications of PD, among which disorders of bone and mineral metabolism occupy a significant place, substantially worsening patients’ quality of life and increasing the risk of disability.
It has been established that patients with PD are significantly more likely to develop osteopenia and osteoporosis, accompanied by decreased bone mineral density and an increased risk of fractures, particularly in the proximal femur. One of the key contributing factors is Vitamin D deficiency, caused by reduced sunlight exposure, limited physical activity, and age-related metabolic changes. Additional contributing factors include disturbances in calcium-phosphorus homeostasis, sarcopenia, as well as alterations in hormonal status, including an imbalance of parathyroid hormone and calcitonin.
The pathogenesis of bone disorders in PD is multifactorial. Hypodynamia and postural instability contribute to reduced mechanical loading on bone, leading to suppressed osteogenesis. Neurodegenerative processes and dopamine deficiency may directly influence bone metabolism through neuroendocrine mechanisms. Furthermore, long-term pharmacological therapy, particularly levodopa-based medications, may indirectly affect bone metabolism and homocysteine levels, which are also associated with an increased risk of fractures.
Clinically, disorders of bone and mineral metabolism in PD are manifested by decreased bone mineral density, an increased frequency of falls and fractures, as well as delayed recovery following injuries. Diagnostic approaches include densitometry and assessment of Vitamin D, calcium, phosphorus levels, and markers of bone remodeling.
Current approaches to management include comprehensive therapy aimed at correcting deficiencies of Vitamin D and calcium, the use of antiresorptive agents, optimization of physical activity, and fall prevention. Promising directions include personalized treatment strategies considering the stage of PD, the patient’s age, and concomitant risk factors, as well as the integration of a multidisciplinary approach involving neurologists, endocrinologists, and rehabilitation specialists.
Disorders of bone and mineral metabolism represent an important component of the systemic manifestations of Parkinson’s disease and require timely diagnosis and comprehensive management to reduce fracture risk and improve patients’ quality of life.
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