Osteoporosis: Molecular Pathology, Diagnostics, and Therapeutics

Abstract

Osteoporosis is a major public health concern affecting millions of people worldwide and resulting in significant economic costs. The condition is characterized by changes in bone homeostasis, which lead to reduced bone mass, impaired bone quality, and an increased risk of fractures. The pathophysiology of osteoporosis is complex and multifactorial, involving imbalances in hormones, cytokines, and growth factors. Understanding the cellular and molecular mechanisms underlying osteoporosis is essential for appropriate diagnosis and management of the condition. This paper provides a comprehensive review of the normal cellular and molecular mechanisms of bone homeostasis, followed by an in-depth discussion of the proposed pathophysiology of osteoporosis through the osteoimmunological, gut microbiome, and cellular senescence models. Furthermore, the diagnostic tools used to assess osteoporosis, including bone mineral density measurements, biochemical markers of bone turnover, and diagnostic imaging modalities, are also discussed. Finally, both the current pharmacological and non-pharmacological treatment algorithms and management options for osteoporosis, including an exploration of the management of osteoporotic fragility fractures, are highlighted. This review reveals the need for further research to fully elucidate the molecular mechanisms underlying the condition and to develop more effective therapeutic strategies.

Keywords: bone homeostasis; cellular mechanisms; cytokines; hormones; models; osteoporosis; pathophysiology.

Figure 1

A side-by-side illustration depicting the stark contrast between normal and osteoporotic bone. The normal bone structure (right) is well defined, demonstrates a thick trabecular architecture within the bone matrix, demonstrates sufficient mineralization and calcium content, and, finally, shows minimal signs of fractures of degradation. The osteoporotic bone (left) shows signs of advanced bone loss and weakening. There is a dramatic reduction in trabecular density and thickness, resulting in a porous and fragile appearance. The pronounced gaps and voids within the bone matrix represent areas of compromised strength.