Multiple myeloma significantly increases fracture risk in aging adults primarily because it disrupts normal bone remodeling, leading to weakened bones that are more prone to breaking. This cancer originates in plasma cells within the bone marrow and causes a cascade of changes that damage the skeleton over time.
Under healthy conditions, bones constantly undergo remodeling—a balanced process where old bone is broken down by cells called osteoclasts and new bone is formed by osteoblasts. Multiple myeloma disturbs this balance by stimulating excessive activity of osteoclasts while simultaneously suppressing osteoblast function. The result is increased bone resorption (breakdown) without adequate new bone formation, causing areas of weakened, porous bone known as lytic lesions.
These lytic lesions are essentially holes or defects in the bones where tumor cells have invaded and destroyed normal tissue. They reduce overall bone density and structural integrity, making bones fragile and susceptible to fractures even with minor trauma or everyday activities. This fragility worsens as patients age because natural age-related declines in bone mass compound the damage caused by multiple myeloma.
At a molecular level, multiple myeloma cells secrete factors such as RANKL (Receptor Activator of Nuclear Factor Kappa-B Ligand) which promote osteoclast differentiation and activation. Meanwhile, they release inhibitors like Dkk1 that block Wnt signaling pathways critical for osteoblast survival and function. This dual effect accelerates destruction while preventing repair.
Additionally, the microenvironment within the marrow becomes altered due to interactions between malignant plasma cells and surrounding stromal cells; this environment supports tumor growth but also fosters ongoing skeletal damage through inflammatory cytokines like IL-6 which further stimulate osteoclast activity.
The cumulative impact includes:
– **Bone pain** from microfractures or structural instability.
– **Pathological fractures**, meaning breaks occurring with minimal force due to compromised strength.
– Increased risk particularly in weight-bearing bones such as vertebrae (spine), ribs, pelvis, hips, and long bones like femurs.
– Vertebral compression fractures can lead to height loss or spinal deformities impacting mobility.
Moreover, treatments for multiple myeloma can influence fracture risk indirectly. Some therapies may improve bone health by promoting osteoblast activity or inhibiting resorption temporarily; however certain drugs like corticosteroids used alongside chemotherapy can exacerbate osteoporosis-like effects if not carefully managed.
In older adults who already face declining hormone levels (such as estrogen or testosterone), reduced calcium absorption efficiency, decreased physical activity leading to muscle weakness around joints—and often coexisting conditions affecting mobility—the presence of multiple myeloma compounds these risks dramatically.
In summary:
Multiple myeloma creates an environment where destructive processes outpace repair mechanisms within bones through complex cellular signaling disruptions involving increased breakdown by osteoclasts combined with suppressed formation from osteoblasts. Aging amplifies vulnerability due to natural skeletal weakening plus comorbidities common among elderly patients. Together these factors culminate in fragile skeletons prone to painful fractures that severely affect quality of life for aging individuals living with this disease.