Osteoporosis: Pathophysiology and Bone Remodelling

Abstract

Osteoporosis is a skeletal disease characterized by low bone mass and deterioration of bone micro-architecture resulting in bone fragility. Normal bone remodelling in the adult follows a precise sequence of cellular events: activation, bone resorption, reversal phase and then, bone formation. This sequence of cellular activities occurring at a given site on trabecular bone surfaces or in cortical bone is called the bone remodelling unit (BRU). Bone mass results from the sum of focal bone balance at each BRU. After the age of 35, there is a physiological bone loss due to focal imbalance between the resorption and the formation phases at the BRU level. In Type I osteoporosis, observed in postmenopausal women, there is a predominant trabecular bone loss due to an increased number of new BRUs and a more pronounced unbalanced coupling between resorption and formation. This results in thinning of trabeculae but also in irreversible trabecular perforations with subsequent deterioration of the trabecular bone micro-architecture. In Type II osteoporosis, observed in older people, cortical bone loss is mainly due to secondary hyperparathyroidism due to vitamin D and/or calcium deficiency.