So, there are a net where the bacterial growth was detected, and 87% of the periondontally diseased teeth, 59% of the teeth containing bacteria in the pulp sample indicating that the outside from the periodontal had gone into the tooth. This was done quite a bit. You can look at the number 259 to 7000 times greater than the concentration of the corresponding layers from healthy teeth.
So, what we can say is that radicular structures like these serve as bacterial reservoirs from which bacteria colonization of the mechanically-treated root surfaces can occur. In other words, if you’re planning a tooth and you’re doing tooth planning and scaling, you’re opening up that colony, that periodontal pocket to bacteria to come out of the tooth to come back into periodontal pocket.
So, we have a problem here. You definitely need to clean up the tooth, but at the same time, you’re increasing the risk that the bacteria can come back out of the tooth and reinfect that pocket that is treated. So, we have to have intels and probes to treating this type of situation. So, we can address several major questions. This isn’t all of them, but bacteria can come from the periodontal diseased pockets enter the blood stream.
I’m going to show you a publication later where they treat people with heart disease. They treat them with antibiotics, and these people improve. They take away the antibiotics, the infection comes back. That seems to be a normal situation, and what I would propose and something that we said many years ago along with Weston Price is that you cannot stop infection, periodontally infected tooth, you cannot get the antibiotics in there to clean that infection. The antibiotics do not get into the dentine tubules and eliminate that infection.
So, we can ask other questions. Do bacteria cause systemic infection and relevant diseases? We’re going to discuss these and give several examples of recent publications that indicate that. Do infected and vital endodontically treated teeth lead to blood bacteremia similar as proposed for periodontal disease? I can’t believe they don’t think that. It will be up to your decision to make that. We can look at this like this: Do periodontal disease and infected teeth lead to jawbone osteonecrosis, and does jawbone osteonecrosis lead to other systemic illnesses? This is the big argument now with regard to cavitations, etc.
So, what happened? This was an area of argument that seemed to be tested by microbiology and the techniques most of you know about, but about 20 years, new technologies came in. It’s very difficult to detect anaerobic bacteria because they die. If you expose them a little bit to air, they don’t culture very well. So, you have this problem. If you try to show the bacteria in your root canal ended up in your liver, it’s very difficult to isolate that and culture.
As a matter of fact, it’s almost impossible, but they had this new technique. It’s called polymerase chain reaction or PCR. For those of you that don’t follow, that’s when you watch CSI, and when they get a very small drop of blood from a sample. Then, they go back and say, “This DNA came from Joe Smith. So, he’s the killer.” What they do is they have a technique where they amplify the nucleic acid, and that nucleic acid will identify either the human subject or the bacterial species that put the DNA there.
So, what this allows us to do is it allows us to go into a person who has an infected site, pull out that bacteria, even if it dies. We can isolate the DNA, RNA from that bacteria, amplify it, and say, “This belongs to this specific species of bacteria.”
We can then go into the hard tissue, the atherosclerotic plaques, the placenta. We can translate the bacteria fraction from that, take the DNA, amplify it, and say the bacteria from the mouth ended up in this lady’s placenta. Isn’t that interesting when we say is that bacteria toxic? Does it produce toxins? We’re going to show you, yes, that’s probably the way it works.
This was published in Dental Economics, The Perio/Systemic Link, and you can read this. It’s in your handout, but I think the bottom line here, which is in red, is the consensus in the medical and dental professions at this time is that there is an association between the mouth and the body. 2007. They were finally getting it. I think Weston Price died in 1930 or something like that. The level of causality is still up for debate among some researchers and clinicians. This kind of comment is what led me to tell people who make the comment that I felt like I was in an eight-year argument with the Count Drunk [16:32] with regards to certain things in dentistry.
I mean, you can always have a difference of opinion. I mean, me and my hunting dog disagree every now and then, but I think that that doesn’t really prove much of anything. I think we can now look at this and say what’s the research showing? The point I’m making is that almost all the data I’m going to talk about now was published before this gentleman wrote this article. This was in Oral Microbiology and Immunology, 2006. They’re not in the same order as you have them because I tried to concentrate a little bit on heart versus the other diseases. It says here that ”the present study shows that maintenance of inflammation may be enhanced by the presence of periodontopathic bacteria.” Again, they’re looking at things in atherosclerosis. Much of this research will show you that if have atherosclerotic plaques, one thing that you will find there is a bacteria that invariably came out of the mouth. It’s hard to imagine swallowing that and getting in. It’s going through the blood, through the periodontal disease, or through some other problem.
Again, they take about Bacterial Diversity in Aortic Aneurysms Determined by 16S Ribosomal RNA Gene Analysis. That’s where they use the PCR to amplify this gene and identify what bacteria is in the aortic aneurysm. “A wide variety of bacteria, including oral bacteria, was found to colonize aortic aneurysms and may play a role in their development.” I don’t think I have to explain to you what happens in aneurysm if you have it in your aorta. Once the system gets weakened, the production of toxins at this site by these bacteria would prevent this injury that might have started from being repaired.
Another one here is Serum Antibody Response to Periodontal Pathogens and Herpes Simplex Virus in Relation to Classic Risk Factors of Cardiovascular Disease. Again, not done in the United States, and when we go down here, it says, “The infectious burden comprising HSV and periodontitis may increase the risk for CVD by clearly decreasing HDL cholesterol concentrations.” HDL is supposed to be the high density or the healthy cholesterol. Whether you want to believe that or not, I don’t know, but it does point out the bacteria are involved in this particular disease response.
Periodontal Disease in Patients with Ischemic Coronary Atherosclerosis at a University Hospital done in Brazil, not in the United States. If you look at this, it says, “Periodontal disease was very prevalent in the groups studied with a higher degree of severity in those with ischemic heart diseases. The elevated prevalence of risk factors found indicates that intervention strategies are required.” I think this is something that’s a good take-home lesson for people in dentistry. You have to attack the problem with periodontitis because you not just saving the person’s tooth, you’re enhancing the health. You’re enhancing this person’s ability to live to reach the average age that most of us die. If they don’t have that, they’re going to have severe problems, and they’re going to die early. They’re going to be a burden on the medical industry and our insurance premiums and everything else.
Bacterial Profile and Burden of Periodontal Infection in Subjects with a Diagnosis of Acute Coronary Syndrome, again not done in the United States. It says, “Is it possible that the stimulation of host responses to oral infections may result in vascular damage in the inducement of blood clotting?” The conclusion of this: “The oral bacterial load of S. intermedius, S. sanguis, Streptococcus anginosus, T. forsythensis, T. denticola, and P. gingivalis may be concomitant risk factors in the development of ACS.” I think all the works we’re looking at, I haven’t yet read a paper where they didn’t find this. When does something become so overwhelming and the data become so overwhelming that you begin to believe it.
Again, this is 2005. Early Carotid Atherosclerosis in Subjects with Periodontal Diseases. “The present results in indicate that periodontal disease is associated with the development of early atherosclerotic carotid lesions.” The problem that you have when your scientists when you’re proposing that oral bacteria cause a problem, the one question that you have to ask is what else could do it. Is there evidence that that what else exists there. That’s what I would propose to you and for you to propose to the people who think that periodontal disease and infected teeth aren’t involved. What else does it, and what’s your proof? There comes a time when you have to stop and say that there is nothing else that does this. What else could be causing this infection and the tissue breakdown at this site?
This, here, is the Evaluation of the Incidence of Periodontitis-Associated Bacteria in the Atherosclerotic Plaque of Coronary Blood Vessels. Very distinct. Again, not done in the United States. What they were looking at, unstable atherosclerotic plaque is a dangerous condition, and I think we all know that. I don’t know what they mean by unstable atherosclerotic plaque, but I think they’re talking about plaque that breaks off and can clog arteries. They come to a conclusion: “What is important is the presence of an active inflammatory process expressed by a significantly higher bleeding index in those patients in whom the examined bacterial species were found in atherosclerotic plaque.” I would tell you, when you start breaking down tissue, the bacteria present there is not an energetic thing going out. It’s chemistry. Do the pathogenic bacteria release toxins that cause the tissue to start breaking down when the tissue and the cells start dying? The body responds with an inflammatory response reaction, washing certain types of proteins called inflammatory proteins into that site. Later on we’ll show you what those proteins are.
This one involves Antibodies to Periodontal Pathogens and Stroke Risk. They say the “evidence on the association between periodontal pathogens and stroke is lacking.” That means that they haven’t done the research. It probably will not get funded by the NIH. The conclusions: “The present prospective study provides serological evidence that an infection caused by major periodontal pathogens is associated with future stroke.” In other words, if you’re putting toxin-producing bacteria into your bloodstream, if they settle in the wrong places, you are susceptible to stroke. I think all of you know how important stroke is to the elderly or people in this country.
Here’s another one, Endotoxemia, Immune Response to Periodontal Pathogens, and Systemic Inflammation Associated with Incident Cardiovascular Disease Events. Again, not done in the United States. It says, “In periodontitis, overgrowth of Gram-negative bacteria may caus endotoxemia and systemic inflammation leading to cardiovascular diseases.” Their conclusions: “Our results suggest that the exposure to periodonatal pathogens or endotoxin induces systemic inflammation leading to increased risk for CVD.” I put this on for one thing because they talk about endotoxins. These are lipopolysaccharides, etc. What I’m going to show you, the most severe toxins produced by bacteria, anaerobic bacteria, are small toxic molecules that can go wherever they want. They pass into the hydrophobic aspects of the body and can cause very severe breakdown of the tissue. So, while I believe in endotoxins and I know what they are. I know they’re very toxic, I think because you can buy antibodies and most labs can measure this, they don’t want to talk about hydrogen sulfide metaphile and other compounds because they’re a little more difficult to work with because they’re so small.