Today’s first speaker is Dr. Boyd Haley. Dr. Haley is a research scientist and international lecturer with a degree in biochemistry and chemistry from Washington State University, and he has numerous research studies published in peer-reviewed medical scientific journals. Aside from being the former chairman of the Department of Chemistry at the University of Kentucky, his published research includes The Effects of Mercury on Neurologic Tissues, Specifically Tubulin, Simulating the Pathology Found in Alzheimer’s Disease. Not too long ago, he addressed the United State House of Representatives Committee on Government Reform and Oversight. Please give a warm welcome to Dr. Boyd Haley.
As the slides talk about here, we talk about Dr. Micheal Ziff, and most of you would remember him. He was absolutely fundamental on leading a part of this academy. He was the first one to contact me at the request, I think, Robert Reaves [0:55] when I first reported mercury causing the same biochemical effects you see in Alzheimer’s Disease. Mike was incessant. I can’t tell you how many semi-unpleasant conversations we had on the phone, and some of the very pleasant. He never gave up, and I never gave up.
He came up with this mantra: “Show me your science” because I told him I wasn’t about to get involved with people that were flipping about research and what might cause diseases and just taking wild guesses based on emotion. There were a lot of things when I first came into this academy. First of all, I didn’t believe the FDA would allow somebody to put something in my mouth that could leak micrograms of mercury every day. We had some severe discussions about this along with David Kennedy, as I remember. David’s the one that brought me down to the ground with his famous philosophical statement, “Boyd, they lie.” I really didn’t really believe him at that time, but when somebody says something with straight conviction, looking at you straight in the eye, you go check them out.
You’re right, David; they lied. So, I’d like to dedicate this to Mike Ziff. I really miss him. He was a good friend. Mike wasn’t trying necessarily to be my friend as he was trying to get something accomplished, and that’s to help this academy grow and to get the science involved in dentistry. As we do the talk today, you’ll see that it’s improving, but it’s still not there.
This is something that came out, and I don’t know why thing is showing up. It’s a focal infection theory. When I came in, this was really a hot topic, and so today, I want to start out right away with a disclaimer. I’ve only looked into one person’s mouth intently for more than three seconds. I didn’t like it, and I’ve never gone back there. So, I’m not a dentist, but I do understand the biochemistry and the microbiology that’s associated with this. I’m going to try to keep my talk within that aspect.
When you read the dental literature and I do love reading it because it makes a lot of sense. There’s a lot of good research published in dental journals. They had a thing called focal infection theory, and it had been disproved according to the American Dental Association and the Organization of Endodontics, etc. So, when we look at this, it is not a fact. You don’t hear them saying, “Oh my god. We were wrong”. When you look at the publications, which we’re going to go through a large number today, and they’re in your handout, there’s not doubt that most of the infections that end up in your body, affecting certain organs, comes from the oral cavity, from periodontal disease, or infected teeth. We talk about these toxicant producing microbes reside within the dentinal tubules of vital but periodontally diseased teeth. Are they doing some problems? If so, what about non-vital, endodontically treated teeth? Another question. In other words, are periodontally diseased teeth and endodontically treated teeth infected?
We’re going to show you that they are. We’re going to show you that the primary research done by dentists today are way off track. They’re looking for endotoxins. They are looking for endotoxins, but the toxins that are released, they cause the local disruption of the tissues that are infected, are small molecule toxins. They are reactive biocompounds. So, we can talk about this, and this is something that will be brought up, root canals, infected versus toxic, because every root canal tooth, trust me, is infected. Whether it’s toxic or not depends upon the nature of the bacteria in the infection.
We can talk these are clinical or subclinical. We’re going to present data that addresses this, if it’s acute or chronic. Does the infection constitute a foci of infection that can become systemic? I think I’m going to give you convincing evidence from other people’s laboratories that this is the case. I would point out to you the vast majority of this research is not done in the United States. It’s not done here. We’re practicing third world dentistry at the research level in the United States. We’re way behind the people in Finland, Norway, Sweden, Germany, Japan, etc.
If you’re going to have to address all these things with me as a scientist, I go to the very bottom. Are extracts prepared from extracted avital teeth toxic to mammalian enzymes in vitro? If this doesn’t happen, you don’t have an argument or anything to measure.
To get an overview, this was published in 1994 by Debelian, and he lists that were affected. Systemic diseases, he’d proposed was caused by oral microorganisms, and if you look at them from heart infections, brain scan, eye, lung, hematological, implant infections, and jawbone osteonecrosis is mine. I put the question mark. Why? Because I think that’s one of the serious illnesses that comes up, and medicine or American dentistry totally ignores it. As a matter of fact, they don’t ignore it: They tell you it doesn’t happen, and they’re totally wrong.
The one thing that we really can address, it gets to people right away, is the increase in the correlation between periodontal disease and preterm births. This caused the medical establishment or the medical insurance companies in this country hundreds of millions, if not billions, of dollars a year. There’s a direct correlation, the risk of preterm low birth weight babies, and every disease that goes on with that for the infants increases with the severity of periodontal disease in the mother.
We’re going to show you now the biochemical evidence that shows that the bacteria from the mouth into the placenta infected and caused these problems. We’re going to show you the toxicity that’s associated with this. We need to do an evaluation of vital versus avital teeth, and we can look at clevicular fluid next to teeth because it should give us some meaningful way of looking. Are we helping these patients when we treat their mouths? Can we get the infection, the periodontal cavities down and the avital teeth down? Can we tell if they’re there? What I’m going to present to you is a way to identify the proteins and the toxins and the clevicular fluid. We can tell whether or not that site is infected. I can’t tell you a lot about that tooth or that test, but what I can tell you is that there are toxins there.
Now, I was given a paper to read, but I forgot about it. I am associated with Affinity Labeling Technologies or Biosciences, as it is called, and we have developed a test that I will talk about here a bit for you to use. So, I do have some commercial interest in what’s being presented here today, but we don’t have a booth here today because we decided to do that because of the talk. It would look like I was trying to promote or sell something. So, you can’t buy anything from us.
This is first one, “Occurrence of Invading Bacteria in Radicular Dentin of Periodontically Diseased Teeth: Microbiological Findings”. Again, if you look at the names here, it was not done in the United States. What they did was a simple thing. They pulled teeth from people with periodontal disease and people without periodontal disease. They stripped off the cementum, and then they took a dentin sample. What they were trying to find out was if there were bacteria in these dentin samples. To do this, they cultured this sample using an extract of this without crushing the dentin sample. After, they crushed it, thinking if there were dentin bacteria inside, it would be released. You’d get more colonies formed.
If you look at the data, down here at the bottom, these were the test samples, and these were the levels in the infected teeth, which was 501 before they homogenized the sample to break it up. It was 500 versus 12 in the controlled samples, the teeth that were pulled from people without periodontal disease. After they crushed them or after they homogenized them, this went from 500 to 3462, where this one went from 12 to 13.
So, what we’re seeing is that, indeed, if you have your teeth, and you have periodontal disease (the teeth are still alive), the bacteria are invading that teeth. They’re going in through the dentin tubules, and they can go in through the cement. They don’t have to duck when they go through. If you look at the electron microscopy, there’s plenty of room for them to get in, and that’s how you get an infected tooth and a tooth that “needs a root canal” because you form an abscess at the bottom because they come in from the periodontal pocket, down to the tooth into the end. The body responds to it, trying to fight it off, and it develops this type of infection. You’ll notice, everything I have in here, I have in blue, the relevant journal that this was published in.
So, we take the next step, and this was the “Ultrastructural Observations on Bacterial Invasion in Cementum and Radicular Dentin of Periodontally Diseased Human Teeth”. This was done by Walter Loesche. He’s a prominent research at the University of Michigan School of Dentistry, and I think he got hammered on quite a lot early on. We’ve had him talk in this academy. A very good researcher, but these other folks were from University of Gent in Belgium.
This is the electron microscopy. If you look, that’s a dentin tubule hole right there, and you see the filamentous bacteria invading it. If you look here at the bigger picture, you see the bacteria up in the dentin tubules.
When I first got into this, I remember reading a paper where they were attacking Weston Price who said that teeth that got infected were invaded by a bacterium. The argument from the opposition was there wasn’t enough room in these dentin tubules for them to get in, and the cementum kept their mouth.
This paper is living proof, this and others, that Weston Price were right and the other people were wrong. These teeth do become infected. They carry the infectious material back to the tooth, and you can’t get rid of it by any easy means. So, we look at this paper, and you can read this as well as I can, the “Bacterial Invasion in Root Cementum and Radicular Dentin of Periodontally Diseased Teeth in Humans: A Reservoir of Periodontopathic Bacteria”. What they did was, if I can get you this study, they started on the inside of the tooth. That’s were the plaque was for the periodontal diease. So, they tookthis part of the tooth, and they layered it. They were looking for the amount of bacteria that would be from the outside to the inside, in the pulp area of the tooth.
In measuring this, they looked at the colony stimulating factors of the healthy tooth versus a diseased tooth. The healthy tooth is in blue, and you can see its 5.4, 7.6, 0, and 2.3. In contrast, going from the pulp side, in the infected tooth, it was 1399, 2263, 1464, and 16000 on the outer edge next to the periodontal cavity. So, what you can say is that the source, the bacteria’s going from the outside in, getting in the pulp and is going to infect this tooth. So, if you have this number of colonies going from 16000 down to 1400 whereas with this one here you are going 2 to 5, you can see that bacteria are constantly invading the tooth. It can go from the outside into the pulp, and that seems to be the major direction it is going. In other words, it’s not coming from the pulp in. It’s coming from the pulp out. So, you are having an invasion.