Primary Causes & Pathophysiology
Oestrogen loss at menopause (stopping of periods) raises osteoclast activity (bone removal) and shortens osteoblast life (bone building). Resorption outpaces formation so trabecular plates (spongy inner bone) thin and disconnect. Cortical bone (dense outer shell) thins with more porosity (tiny holes). Microdamage accumulates and stiffness falls. Minor load then causes vertebral, hip or wrist fracture. Secondary drivers such as steroids (steroid drugs) with thyroid excess and gut failure speed the same loop.
Oestrogen loss raises osteoclast drive and lowers osteoblast work so breakdown exceeds building and spongy bone is lost fast
Ageing slows osteoblast formation and impairs calcium uptake so microdamage accumulates and density falls
Steroid excess suppresses osteoblast growth and prolongs osteoclast life plus lowers gut calcium uptake so loss is rapid
Excess parathyroid hormone drives osteoclast resorption to release calcium so bone is removed to raise blood calcium
Excess thyroid hormone speeds turnover with resorption outpacing formation so density falls and fracture risk rises
Low sex hormones reduce osteoblast activity and raise resorption so mass falls in younger and older adults
Poor gut uptake lowers calcium and vitamin supply so hardening fails and parathyroid drive removes bone
Failing kidneys disturb calcium with phosphate and vitamin D balance so parathyroid drive rises and quality falls
Chronic joint inflammation with immune signals plus reduced mobility and steroid use speeds bone loss
Toxins with poor nutrition impair osteoblast work and hormone balance plus raise fall risk so fractures increase