I have been contemplating writing a blog series about this topic but found the task too daunting for too long. For most patients I talk to, osteoporosis boils down to calcium, and biphosonate medications. The development and maintenance of bone mass is complex, the diagnosis of bone mineral deficiency is nuanced, the efficacy of medication treatment is not as clear cut as we would like. No wonder patients (and sometimes myself) have a “deer in the headlight“ look on our face when discussing the topic.

In this first part I simply want to establish a few simple facts about bone biology.

Bones are made of primarily collagen protein and minerals. Of those minerals, calcium is the primary but not the only one. (magnesium , phosphorus, boron etc.)
The resistance of a bone (“strength”) to fracture depends upon not only the total amount of bone (bone density), but also and very importantly the internal scaffolding and architecture of how the bone is organized to resist trauma .
Bones are not static. They are in a constant state of remodeling over time, both in quantity and in architecture. We have cells that specializes in depositing bone (osteoblasts) and cells that take it down (osteoclasts). The latter are the target of most medications, by preventing the resorption of bones.
Our bone mass will peak in early adulthood. However, you can still do a lot to avoid losing bones at an excessive rate over time.