Bone is remodeled continuously throughout life by two cell types working in opposition. Osteoblasts build new bone. Osteoclasts resorb old bone. In healthy adults, the two are balanced — old bone is removed, new bone is laid down, and the structure maintains itself. Peak bone mass is reached around age 30.
After 30, the balance slowly shifts toward resorption. This is normal, and for many people it never leads to disease. But several factors can tip the balance further toward loss: estrogen decline after menopause, long-term glucocorticoid use, low body weight, smoking, excess alcohol, certain medical conditions (hyperthyroidism, hyperparathyroidism, celiac disease, inflammatory bowel disease), and long-term use of proton pump inhibitors or certain seizure medications.
Osteoporosis is not simply "less bone." It is bone with a disrupted architecture — the trabecular struts that give the bone its strength have been thinned and disconnected, and the cortical shell has become porous. That is why osteoporosis fractures occur with falls that would not break a healthy bone: the internal support structure is gone, even if the outer shell looks intact on X-ray.
This also explains why drugs act in two different ways. Antiresorptives — bisphosphonates and denosumab — slow the destruction. Anabolics — teriparatide, abaloparatide, romosozumab — actually stimulate new bone formation. Understanding this distinction is the key to understanding why some patients need one class, some need the other, and some need both in sequence.