Pain and Pathological Fractures as Primary Causes of Mobility Impairment in Multiple Myeloma
Abstract
Background: Multiple myeloma (MM) is a malignant plasma cell disorder frequently complicated by skeletal involvement, affecting up to 80% of patients. Osteolytic lesions, pathological fractures, spinal instability, and chronic pain lead to functional impairment, neurological complications, and reduced quality of life. Bone disease in MM results from an imbalance between bone resorption and formation caused by dysregulation of the RANK/RANKL/OPG pathway.Aim: To review current literature on bone disease in multiple myeloma with emphasis on functional impairment, rehabilitation, and the role of orthopedic equipment in patient care.Material and methods: A narrative review was conducted using PubMed, Scopus, Google Scholar, and Polish medical databases. Articles published in English or Polish concerning adult MM patients with skeletal complications were included and analyzed qualitatively.Results: The literature shows that bone pain and pathological fractures, particularly in the spine, pelvis, ribs, and long bones, are major causes of disability and limited mobility. Pharmacological treatment, radiotherapy, and minimally invasive procedures such as vertebroplasty and kyphoplasty reduce pain and improve stability. Rehabilitation improves muscle strength, balance, and mobility. Orthopedic devices, including spinal orthoses, walkers, and crutches, increase safety and support daily activities.Conclusion: Skeletal complications remain a significant source of disability in patients with multiple myeloma. A multidisciplinary approach combining pharmacological treatment, interventional procedures, rehabilitation, and orthopedic support is essential to improve functional capacity and quality of life.
Fields of Study & Subjects
Multiple Myeloma Research and Treatments
Management of metastatic bone disease
Bone health and treatments
Publication details
- Journal / source
- Journal of Education Health and Sport
- Volume
- 88
- Pages
- 68186–68186
- Publication date
- 15 February 2026
- Language
- EN