CELLULAR MECHANISMS OF OSTEOPOROSIS: UNDERSTANDING BONE RESORPTION AND FORMATION IMBALANCE

Abstract

Osteoporosis is a progressive skeletal disorder driven by an imbalance between bone resorption and bone formation, resulting in reduced bone mass and increased fracture risk. This study aimed to elucidate the cellular and molecular mechanisms underlying this imbalance by examining osteoblast and osteoclast activity in primary bone cells derived from osteoporotic and healthy individuals. Bone biopsy samples were subjected to gene and protein expression analyses, as well as functional assays to evaluate cellular behavior. Quantitative PCR revealed a marked upregulation of resorption-associated genes—RANKL, TRAP, and Cathepsin K—in osteoporotic samples, while key osteogenic markers such as ALP and OPG were significantly downregulated.The increased activity of osteoclasts became apparent through the elevation of both TRAP activity and resorption pit area while osteoblast functionality suffered from lower ALP activity along with diminished mineralisation capacity.  Protein expression analysis using Western blot reflected the observed changes detected by functional tests.  Analyses from multiple tests indicate osteoporotic people develop a bone remodelling environment which strengthens osteoclastic activity that results in decreased osteoblastic bone formation.  The abnormal configuration of bone tissue accelerates natural bone resorption processes while disrupting the entire skeletal system balance.  Strong evidence obtained from functional analysis with molecular data demonstrates that osteoporosis develops from cellular imbalance during bone remodelling instead of aging or hormonal change alone.  These findings emphasize the requirement to direct therapeutic approaches at suppressing osteoclast activity while activating osteoblasts and establish ground for developing novel treatments that restore remodelling balance in patients with osteoporosis.