By Trisha E. O'Hehir
I'm sure you've wondered, as an oral health detective, why some people have more periodontal destruction than others. We used to think it was all about plaque, and that some people were just better at brushing and flossing — the more plaque removed, the better. In most cases, this does work. Like the old saying goes: "A clean tooth does not decay." For most people, effective plaque removal prevents periodontal disease, too. However, for some people, there appears to be more going on. It seems these folks suffer from infection and bone loss, despite good oral hygiene. Why do some people seem resistant to infection, while others break down?
The answer you hear most often is the "immune system." But what does that really mean? Is the immune system not fighting the bacteria? Is the immune system weak or ineffective?
According to the definition, immunocompromised describes an immune system that is functioning below normal. In periodontal disease, the compromised immune system actually appears to be working overtime with destruction as the goal, rather than healing.
Our detective work requires an undercover investigation. To get a look at what's happening on a cell level, we'll shrink ourselves, like in the movie "Honey, I Shrunk the Kids." Put on a scuba diving suit and oxygen tank, and slip into a sulcus and around the mushrooms and towers of bacterial biofilm — subgingival plaque. We're actually swimming through fluid channels filled with the toxic waste products of the bacteria in the plaque biofilm. Don't worry, your special diving suit protects you. At the base of the pocket, we approach the epithelial attachment. Normally, this barrier protects underlying tissue from the toxins and bacteria found in the sulcus. However, as the toxins accumulate — specifically volatile sulfur compounds (VSC) that are released when bacteria and cells die — permeability of the junctional epithelium increases. This allows toxins to pass through to the underlying tissue. Let's follow these toxins through the epithelial attachment and see where they go.
As we swim through the epithelial layer, cell by cell, we see the glue that holds the cells together. After passing through the epithelial layer, we enter the connective tissue layer and follow the toxins to the blood vessels. The toxins trigger the immune system, sending signals that the body recognizes and responds to by sending white blood cells, polymorphonuclear leukocytes (PMN), to the area. This is our body's first line of defense against infection. The body sends the PMN to the area through the blood stream. Mast cells around the blood vessels in the connective tissue release histamine, causing vasodilation and slowing of the blood flow, allowing for the release of PMN from the vessels.
This is where we will see the immune system in action and, more surprisingly, the start of connective tissue breakdown associated with periodontal disease. The white blood cells leave the blood vessels in the connective tissue, and move through healthy connective tissue and through the epithelium to reach the sulcus, the source of bacteria and bacterial toxins. This migration is called "chemotaxis." The PMN will phagocytize the bacteria, stopping the production of toxins and thus allow the body to heal. Let's look and see if that's the case in this immunocompromised person.
Watch closely as the impatient PMN begin their journey. They could move slowly, cell by cell, just as we did coming down this far, but they prefer to use chemical machetes to cut their way through the healthy tissue to quickly reach the bacteria. Some of the cytokines they produce include collagenase, prostaglandin, and interleukin, among others. Release of these substances by the PMN destroys healthy connective tissue in order to allow the white blood cells to move quickly to the site of bacteria. If the immune system is healthy, this destruction is a small price to pay for effectively controlling the bacteria in the sulcus. A healthy immune system is able to keep the tissue destruction and tissue repair in balance.
Stay out of the way of the PMN and watch what happens behind them. The glue that holds the cells together is also destroyed, wreaking havoc with the active transport system. Remember when you studied the Krebs Cycle in biochemistry? Ever wonder why that was important to our work, or did you just file it away as interesting, yet useless, information?
Here's where it comes in. In a nutshell, oxygen molecules travel from the blood vessels in the connective tissue, through the active transport system to cells in the area, and out to the epithelial cells. Oxygen is used in the process of glycolysis to produce energy for the cells. As you look around, floating now in big spaces between the cells, you see the oxygen molecules are having a difficult time traveling cell to cell, due to breakdown of the active transport system. The epithelial cells lining the sulcus are not going to get the needed oxygen, and will go into oxygen debt, producing far fewer adenosine triphosphates of energy. We'll soon see granulation tissue in the sulcus — immature epithelial cells.
As we follow the PMN to the sulcus, we see they are not effective in controlling the bacteria, but they really are trying hard. They use their chemical machetes, destroying healthy connective tissue, but they aren't very effective at phagocytosis when they reach the bacteria. They cause connective tissue destruction, but don't effectively get rid of the bacteria. Since they aren't effective, the signal keeps ringing out to the immune system to send more troops. Look back toward the blood vessels in the connective tissue and you will see a steady stream of PMN coming, destroying connective tissue; yet despite their numbers, they are not effectively controlling the bacteria. We're looking at a neutrophil defect — do you recognize it?
This person also appears to have the genetic factor that allows PMN to produce three times the normal amount of collagenase — the chemical machete. That explains why we see lots more destruction of the connective tissue, but no effective defense against the bacteria. The perio infection appears out of proportion to the amount of plaque in this case.
Have you seen enough? It's time to reverse the shrinking and write up our report on this detective work. We've been blaming the bacteria, but it's really the immune system. We've begun to answer the question of why some people have more disease than do others.
Trisha E. O'Hehir, RDH, BS, is a senior consulting editor of RDH. She is also an international speaker, author, instrument designer, inventor, and oral health detective. Her Web sites are www.perioreports.com and www.toothpastesecret.com. She can be reached at (800) 374-4290 or at [email protected].
