Disturbi ossei

Vitamin D deficiency reduces calcium absorption from blood, impairing bone mineralization by osteoblasts. In children, this produces weak, soft bones with pain and deformities like bowed legs and soft skull, termed rickets. Adults experience osteomalacia or adult rickets, characterized by hip and leg pain. Understanding the role of vitamins in maintaining bone health is essential for prevention.

Bone homeostasis depends on equilibrium between osteoclast-mediated bone resorption and osteoblast-mediated bone deposition. Any disruption—such as reduced osteoblast activity or increased osteoclast activity—tips this balance, weakening bones. When resorption exceeds deposition, bone mineral density decreases, leading to conditions like osteopenia and osteoporosis.

Women experience earlier and faster bone demineralization due to lower baseline bone mass and estrogen decline after menopause. Women lose approximately 8% of bone mass per decade starting at age 30, accelerating around age 45, compared to men's 3% loss beginning at age 60. By age 70, women may lose up to 30% cumulative bone mass.

In Paget's disease, osteoclasts proliferate excessively, triggering compensatory osteoblast activity to balance resorption. This results in weak bones with abnormally high proportions of spongy bone over compact bone, featuring irregular thickenings. Patients experience pain and deformity from structurally compromised skeletal tissue.

Aging decreases protein synthesis and collagen fiber production, reducing the bone matrix's tensile strength and making bones brittle. Declining growth hormone levels further impair collagen synthesis. Combined with reduced osteoblast activity and increased osteoclast resorption, aging bones become susceptible to fractures even under everyday mechanical stress.

Osteopenia represents moderate bone mineral density loss where resorption begins exceeding deposition, typically from reduced osteoblast activity with aging. Osteoporosis is severe osteopenia characterized by porous, fragile bones with compromised strength that fracture easily under normal stress. Both result from disrupted bone homeostasis.

Sex hormones like estrogen and testosterone promote osteoblast activity and bone matrix synthesis, maintaining healthy bone deposition rates. When hormone levels decline with age, bone deposition slows while osteoclast resorption continues, reducing bone strength. This hormonal shift is particularly pronounced in women after menopause.