26th January 2024

Pathophysiology 

Osteoporosis results from an imbalance in the normal process of bone remodelling by osteoclasts and osteoclasts. Through the process of normal ageing, the breakdown of bone via osteoclasts increases and is not balanced by the formation of new bone by osteoblasts. This culminates in reduced BMD and changes in the composition, architecture, size and structure of the bone. The remodelling of bone is regulated by various cytokines, including interleukins 1, 6, and 11, colony-stimulating factors, and hormones such as parathyroid hormone, 1,25-dihydroxy vitamin D, calcitonin, and oestrogen. Factors such as tumour necrosis factor (TNF), receptor activator of nuclear factor- kappa B (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) contribute to the resorption of bone in postmenopausal osteoporosis. RANKL secreted by osteoblasts interacts with RANK receptors on osteoclasts to promote the formation, function and differentiation of osteoclasts, thereby triggering bone resorption. OPG is expressed by osteoblasts and plays a role in the inhibition of the activation of RANK.