The dental pulp, or root canal system of a tooth, is living tissue with a blood suppy and nerves and untold millions of cells. This tissue is involved in the formation of teeth, and cells in there are responsible for laying down the dentin, the main body of your teeth that lies under the almost diamond-hard enamel:
Primary dentin is the main body of dentin that forms when a tooth develops, up to the point where it erupts into the mouth and becomes fully functional, chomping away at things like cashews and crunchy granola with reckless abandon. The process of forming more hard tooth slows down at this point, and yet the cells continue to produce, very much more slowly, secondary dentin. This is simply dentin that forms after root growth is complete. Of course, it's not as if your pulps switch over at an exact time- like, your lower first molar transitioned from primary to secondary dentin on Tuesday, August 1, 1989 at 2:10 in the afternoon. Still, cross sections of teeth viewed under a microscope do show the transition from primary to secondary dentin, much like the rings of a tree can be seen in its trunk.
Over the course of our lives, secondary dentin makes the pulp smaller, and this can easily be observed on X-rays. Here is an X-ray from a 9-year-old; we can see teeth at various stages of development. In all of her teeth, the pulps are very large and account for much of the inner volume of the tooth:
Our next X-ray shows the teeth of a 28-year-old. Even at this young age we can see that the pulps are smaller due to the deposition of secondary dentin; they occupy less of the internal volume of the teeth:
There is another kind of dentin called tertiary dentin or reparative dentin. This is dentin that is formed a bit faster again, in response to external stimulation like cavities or fractures. Even injuries that do not crack teeth cause damage, as they push teeth around in their sockets and injure the supporting bone and ligament. All of these processes stimulate the formation of tertiary dentin.
The idea behind tertiary dentin from the body's point of view is that it walls off the dental pulp from the source of the injury. Pulps have a delicate blood supply and are very prone to getting infected if overly traumatized by cavities, injury or severe gum disease. This circle-the-wagons strategy is a dual edged sword, if I may be allowed to stew such a gumbo of metaphors. Because you see, as the pulp gets smaller it does recede farther from the cavity, which is laden with harmful bacteria, but the pulp also gets weaker, in part because its blood supply becomes ever more delicate.
It's like running away from a dangerous animal, but running into a canyon with no exit. Sooner or later, we'd have to face that animal- precisely at the point where we're most tired out.
The more fillings, injuries, or gum disease that a tooth faces, the more tertiary dentin gets deposited. Couple that with the secondary dentin from normal aging, like in this 84-year-old, and we see pulps- or, to toss up a non-sequitur, we don't see pulps- that look like this:
That one lower tooth with the white lines in it has had a root canal treatment long ago. I do certainly hope that my patient doesn't come to need root canal therapy on those upper teeth where the arrows "point to the pulps that we can't see", though, because the canals will be awfully hard to find and clean and fill. And the irony remains that these dental pulps are more delicate than ever, as far as they may be from injurious cavities and the fillings that we do to treat them. So there is a risk...
For more on dental pulp calcification, see:
And consider allowing the magnificent Katherine Clark Gray and our clever Caries Clock teach you how to avoid cavities in the first place: