Pathophysiological Mechanism of Osteoporosis
The pathophysiological mechanism of osteoporosis is reduced bone mass due to increased osteoclastic activity (bone resorption) exceeding osteoblastic activity (bone formation), resulting in an imbalance where bone resorption outpaces bone formation. 1
Core Mechanism: Imbalanced Bone Remodeling
The fundamental pathophysiology involves disruption of normal bone homeostasis through a continuous cycle where:
- Osteoclastic bone resorption exceeds osteoblastic bone formation, leading to net bone loss 1
- This imbalance results in low bone mass, deterioration of bone tissue microarchitecture, and disruption of bone structural integrity 1
- The compromised bone strength directly increases fracture risk 1
Why the Other Options Are Incorrect
Autoimmune attack on bone marrow cells is not the mechanism of osteoporosis. While osteoimmunological interactions exist and immune system dysregulation can contribute to bone loss, osteoporosis is not primarily an autoimmune disease attacking bone marrow 2.
Increased bone formation due to excessive osteoblast activity is the opposite of what occurs. In osteoporosis, osteoblastic bone formation is either normal or decreased, never excessive 1, 3.
Abnormal deposition of collagen fibers describes conditions like osteogenesis imperfecta or osteomalacia (defective mineralization), not osteoporosis. In osteoporosis, the bone that is present is normally mineralized—there is simply less of it 4, 3.
Contributing Pathophysiological Factors
Beyond the core resorption-formation imbalance, multiple mechanisms accelerate this process:
- Estrogen deficiency enhances osteoclastic bone resorption, particularly after menopause 1, 3
- Advancing age further increases the rate of bone resorption, magnifying the remodeling imbalance 1
- Secondary hyperparathyroidism from vitamin D deficiency or chronic kidney disease increases both bone formation and resorption, but with net bone loss due to cortical microarchitectural deterioration 1
- Glucocorticoid exposure suppresses osteoblast function while maintaining or increasing osteoclast activity 1, 3
Clinical Significance
This pathophysiological understanding directly informs treatment strategies: