This one is an Evaluation of the Incidence of Periodontitis-associated Bacteria in the Atherosclerotic Plaque of Coronary Blood Vessels. Again, published in 2007, General Periodontology, not done in the United States. “In patients with the severe form of chronic periodontitis, it seems that clinical attachment loss is not associated with bacterial permeability into coronary vessels. 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.” I think the more that you have toxic response around the capillaries that surround a tooth in the gum line, the more likely it is to bleed.
I think this is one of the more important ones. This is the Correlation Between Atherosclerosis and Periodontal Putative Pathogenic Bacterial Infections in Coronary and Internal Mammary Arteries. What they did was they looked at the effect and the infection levels in the mammary arteries versus the coronary arteries. The conclusion was, “The absence of putative pathogenic bacteria in internal mammary arteries, which are known to be affected rarely by atherosclerotic changes, and their presence in a high percentage of atherosclerotic coronary arteries support the concept that periodontal organisms are associated with the development and progression of atherosclerosis.” In general, what they’re saying is mammary arteries don’t become infected with periodontal bacteria. Those in the coronary arteries do, and that’s where you get the atherosclerotic plaques build up.
The pressure in your blood system is more near the heart. If you look at it, almost all the plaques that you’ll see there build up are where the heart pumps and you have bending in the artery, and that’s where you have the major blockages with the formation of atherosclerotic plaques. So, it makes sense that the pressure of the heart beating as we age and other problems we might have, if we form a break in the artery, if we have bacteria floating around from our mouth, they set up housekeeping in that site. They prevent that site from repairing normally because of the toxins they’ve produced.
This is Antimicrobial Prophylaxis in Oral Surgery and Dental Procedures. It talks about “transient bacteremia is a known risk factor following oral surgery and invasive dental procedures in patients with altered immune system response and those with a susceptible site of infection like patients with heart valve prostheses or recent joint replacements.” Essentially what they found in here was that anaerobic bacteria were found in 64% of the blood cultures, and they found it also in the plaques that they were looking at this time.
This is Osteomyelities with Proliferative Periostitis, an Unusual Case. This was a single person. They said, “We present and unusual case of chronic osteomyelitis with proliferative periostitis affecting the mandible of a 12-year-old patient. This source of infection was related to the developing lower left third molar which had apparently no communication with the oral cavity.” So, I would wonder, where would the lower third molar get a bacterial infection if it had no communication with the oral cavity? How would the bacteria can into that and get into the jawbone of this patient? That’s something that I think if any of the dentists had an answer for this I’d sure like to hear it because this was one that really confused me, a paper that I did not understand. It does point out that all bacteria get into the mandible of certain patients and create a severe problem which someone might call cavitations or jaw bone infections.
Now, we get into the part that I think is different than a heart disease, which is being studied quite a bit. It’s the Evidence of Periopathogenic Microorganisms in Placentas of Women with Preeclampsia. For those of you who don’t know this, “Preeclampsia is a pregnancy-specific hypertensive disorder that often leads to maternal morbidity and mortality.” It is not to be taken lightly. The conclusion is “the significant presence of periopathogenic microorganisms of their products in human placentas of women with preeclampsia may suggest a possible contribution of periopathogenic bacteria to the pathogenesis of this syndrome.” I would go back and say this is classic academic double talk, may suggest and sometimes they say may possibly suggest, or possibly, may possibly suggest. There’s a time when you say there’s no reason why you should have pathogenic bacteria in the placenta of a mother carrying a child. It just shouldn’t be there, and it doesn’t may suggest. It does suggest. As a matter of fact, some people would say that it would prove there’s a definite problem with this person if it doesn’t exist in the placenta of people who don’t have this problem.
Taking it a step further, the Isolation of Commensal Bacteria from Umbilical Cord Blood of Healthy Neonates Born by Caesarian Section. Again, this was not done in the United States. This study suggests “that term fetuses are not completely sterile, and that a mother-to-child efflux of commensal bacteria may exist.”
They isolated bacteria from the breast milk of a healthy woman, E. faecium, and they injected this into mice, I think intrapatellar. The labeled chain could be isolated in polymerase chain reaction detected from the amniotic fluid of the inoculated animals. In other words, they could take bacteria that went from a mother’s mouth into her breast milk. They isolate that. They amplify it. They inject it into a mouse. They find out that when they injected it into the mice who are pregnant that that bacteria ends up in the baby mice, the ones that are in utero at that time. So, these bacteria have the ability to spread throughout the body without any help. Even if they’re not killing the animal, they can do it. In contrast, it could not be detected in samples obtained from a non-inoculated control group.
When people tell you that bacteria from the mouth can’t get, by injection, into the bloodstream, affect certain organs or get into the babies or into the uterus, etc., or into the blood, they’re totally wrong. The research says they’re wrong. This was a very complete study. Again, it’s referenced here. This was done in 2005.
This is something that should be of interest to all the medical doctors here. Is Periodontal Infection Behind the Failure of Antibiotics to Prevent Coronary Events? This was published in 2007 and in atherosclerosis. It’s a complex study, but you can read it in detail and you can read the rest of it. It says, “This paper presents the hypothesis that periodontitis is behind the failure of antibiotics to prevent coronary events. We discuss the systemic effects of periodontal infection and consider studies to test our hypothesis, which offers a novel viewpoint for discussion of antibiotics in coronary-disease prevention.” I want to tell you how novel this is. If you read Weston Price back in the 1920, is he saying this? There were things, and you cannot cure somebody of certain infection as long as you keep an infected tooth in that person’s mouth. This is hardly novel, but it is novel for people today, perhaps.
What they’re saying is no matter how much the antibiotics would enhance the killing of a bacteria that’s in the heart tissue and save that person, if you are reinfecting that person with bacteria that are coming out of dead tooth or severe periodontal disease where the antibiotic doesn’t work, it’s because it doesn’t get there. You’re just beating a dead horse. You may help the person for a time, but if you don’t tie medicine and dentistry together, join them at the hips so they can’t be separated, you will not cure these people, none of the infections that cause these illnesses.
I’m not going to go through this much, but it says, “The bacteria recovered from these infections are often of oral origin and involved mixed aerobic-anaerobic oral flora.” This is another one. I’m going to skip this, but you can read. It talks about the influence of an endotoxin on mice, but the “experiments indicate that the pathogenicity of a mixed gingival flora may depend on the decrease of the local and systemic disease mechanisms induced by endotoxins derived from Gram-negative oral bacteria.” I believe this. Endotoxins would do this to you, but they are totally ignoring the fact that these pathogenic bacteria make chemical toxins that are relatively lethal.
This is one that might be of interested to the mothers. Distribution of 10 Periodontal Bacteria in Saliva Samples from Japanese Children and Their Mothers. If we read this, “Our results indicate a correlation between the presence of periodontal bacteria in children and their mothers, while the presence of red complex bacteria (this is the bad set of bacteria for periodontal disease) in children was highly associated with that in their mothers.” In other words, mother who kiss their children, who feed their children from the same spoon are actually infecting their children with the same microorganisms. For those of you guys that like to make out with strange ladies, you’re getting the same treatment.
So, the thing is that these infections do transfer, and there is something that you really need to take into account. What we’ve come down to is we need a study of the toxicants with avital teeth and osetonecrotic materials. If periodontal disease causes any systemic illnesses, then teeth harboring microbes should also contain potent toxins. This is where I think my research has come into play, and it’s not novel with me.
Long ago, they would talk about people with bad breath. If you have death breath, you had periodontal disease. You’re producing hydrogen sulfide, methylphile, putrescene, cadaverin, a lot of small chemical toxins. I would almost tell you that the entire dental community with the except ion 0.01% of researchers, are totally ignoring the effect of these toxins on human health. I want to show you the results of what we’ve done. I would like to point out that I started doing this because of the people that are sitting in this audience. There were a whole load of you that would talk about the problems that came along with this.
This is research that we did in my department in my research lab to start with. It’s now done. For those of you who send us toxic teeth, we send them back and tell you the tooth extracted was toxic. This is how it’s done. We take the tooth, we add 1 mL of water. Then, we shake it for one hour. We remove that extract and save it. We don’t do anything with it. We then put it in another mL. We stick it again for another hour, and we remove that. We don’t do anything with it except research. Then, we do the third one. We take this 1 mL extract. For those of you keeping context, a mL is 1000 microLiters. It’s a 3000 microLiter wash in three sequential things. That’s what an analytical chemist does. Three washes gets almost everything, and this is not just on the outside. This one has to be coming through. We’ll show you the amount of protein and the amount of toxin that comes through.
This is where we do the work. We don’t do it over here. We do it over here. Most of the teeth we test would be toxic. With this one, we find out about 20-25% of the teeth don’t display toxicity. So, it allows us to put things in a scale of quarters. Very toxic, moderately toxic, slightly toxic, and nontoxic. You just saw that we did. You see several here. They’re all underlined. If they’re underlined, this is the number of washes, the first wash, the second wash, the third wash. Put it in between.
This is the first wash. See how toxic, how much protein, albumin is out here? If you go to the second wash, it decreases. If you go to the third wash, it’s minor, but there’s still some proteins there. If we look at this, and here’s really an infected tooth. Keep this in mind because when you do the topaz when you’re doing the blue color, you look at the protein level. You look at the level here versus the level over here, and which one of these teeth is the most toxic? We’ll show you in just a second how this tooth, the toxins in this tooth, totally inhibit the photolabeling of these four enzymes that we have here, and that washing it from the first to the second to the third, we get the proteins down dramatically. This is early research.
This is not what we do today, and we have new technology. There’s no way I could explain this technology. It’s called nucleotide photolabeling. Suffice it to say, the NIH funded me to develop this for 25 or more straight years. Let’s take this tooth. This one has the most protein, and I’ll just go back a second. We’re going to be talking about this one and the three washes that go along with it and compare it to the others over here that have less protein.
Here’s the control protein. Here’s the one you should be looking at the saying, “Here’s the level.” If you go over here, that first wash, which is incredibly toxic, wipes it out. Even the second wash wipes out most of it. The third wash does less because we’ve diluted the toxins that are associated with that, but if you look at all the proteins here, you’ll see that there’s an increase of protein. When we have an increase of protein, we generally have a big increase of toxicity.
The concept of this is as these bacteria that invade this site release toxins, your body fights it. It’s similar to when you get a spot of poison ivy. You get that liquid blister. That’s because you’re getting all of these inflammatory proteins such as serum albumin rushing into that site. The water follows it. You get the swelling, but the proteins will bind the toxin to prevent it from going into your body causing the destruction elsewhere. You can see that this one was really toxic and wiped it out.
Over here where we have the less toxic tooth, there’s the first wash, second wash, and third wash. You can see that while the protein is still there, it’s toxic because there’s the decrease in the activity of the enzyme. The less intense the black , the more toxic, the more the proteins are in here.