We’re going to get started here in about five minutes, and for those that are early, thank you for being on time.  I’m just going to run through housekeeping items as the group assembles here.

First, a few calendar items.  We’re going to be talking today about really fascinating medical science that has to do with periodontal disease and overall health.  A lot of just fascinating information today.  On the calendar, let me just mention a couple things.  One, the end of this month, September 28 and 29, is the Nomar Hygiene Seminar featuring Tommy Nabors and myself and members of the Tops team.  That will be in Nashville.  In December, we are looking forward to our year-end roundtable, and if you’ve never attended a Tops Crown Council Roundtable event, it is a must-do, and you can get more information about that by calling the toll-free service (877) 399-8677.  So, that is the first Saturday, the end of November to December.  We’re really looking forward to the Crown Council annual event, January 24-26, 2013, in Nashville as well.  This appears to be the biggest annual even ever, and great enthusiasm.  The enrollment is over-the-top.  We’re very excited.  If you have not signed up for that, contact the Crown Council office today because hotel space is very limited now at this point.  There will be never-done-before and maybe never-done-again events at this one.

Of course, everyone is aware we’re going to kick off the annual event Thursday with a big event at the Ryman Theater, home of the country music and the Country Music Hall of Fame. It’s the mother church of country music with an All Star lineup of some of the biggest names in country music.  Celebrate smiles for life, and we’re very excited about that.

Speaking of smiles for life, we just wrapped up the 2012 Smiles for Life campaign.  Total money raised was $1.3, and thanks to everyone who participated and made that really a continuing miracle.  Over the last 13 years, we’ve raised over $31,250,000 dollars for children’s charities.  So, thanks for everything you do every year to make that possible and make a difference in children’s lives.

For those that are anxiously awaiting the checks for your local charity, they are being mailed today.  The check is literally in the mail.  They are being mailed to the doctor.  Just a reminder, the reason why we send the Smiles for Life checks to the doctor in the name of the local charity is so that you can organize a check presentation ceremony where you can make that official, instead of dropping it in the mail.  We hope that you’ll use the check opportunity as a way to get additional publicity for your office and your community.

A few housekeeping items.  For those of you that may not have joined us before on a webinar, we have record attendance today, and we are very excited about that.  There is a high degree of interest in this topic.  So, you are aware, you are in listen only mode.  You can hear us, but cannot hear you so we can have a clear broadcast and everyone can hear our guests today.  There is, in your control panel, on your computer screen, there is a question box.  You’re welcome to submit questions anytime during the presentation.  We will have a question an answer period near the end of the hour, and we will take those questions on a first come, first serve basis.  Again, you’re welcome to submit those at any time, and we will address those on a first come, first serve basis and hopefully get through all of the questions.

With that, let me introduce today’s topic.  I am very excited about this. This webinar today has been long in the making.  I sat down several years ago, here in Dallas, with Dr. Tom Nabors whom everyone knows as dentistry’s expert when it comes to periodontal disease and bacterial testing.  He is the pioneer in the industry in bacterial testing.  If I’m overstating, Tom, I’m sorry, but he has done the whole industry in America a whole lot of good.  He’s with us today, and we’ll be presenting along with Dr. Bradley F. Bale.

Dr. Bale who is an MD, it would take me a half hour to read you his biography of everything he has done in the medical world.  So, I’m going to sum it up with this:  This is a man who is constantly presenting to medicine and health care professionals all over the world.  He is one of the most sought out experts in terms of heart disease and the topic we’re going to talk about today.  He is the only physician that we know of in America who guarantees his patients that they will not have a heart attack if they remain under his care.  We don’t know of anyone else that does that.  He talks about it.  He just shrugs his shoulders, “Of course.  I don’t know why everyone shouldn’t do that.”  When you understand the science of what he talks about today, it really becomes pretty common sense.

So, I’m very excited to have the two of them today to share this joint venture between dentistry and medicine and how the two professions can work better together in helping cure one of the prevalent diseases in chemistry and to be able to screen for one of the most prevalent problems we have in healthcare and medicine.  With that, welcome Dr. Bale, Dr. Nabors.  Thank you for being our guests for today for our Crown Council webinar.

Dr. Bale:              Thanks, Steve.  Dr. Nabors, why do you go ahead and say a few words first.  Then, I’ll take over.

Dr. Nabors:         Sure.  Let me thank Steve and Greg Anderson.  Thank you so much for the good works that you have done in the dental profession.  Let me also thank the Crown Council listeners.  This is a special brew, and we are so proud to be a part of this presentation today, so privileged to be a part of the Crown Council on continuing education. Congratulations on all of the good works that you continue to do.  With that, I’ll turn it over to Dr. Bale.

Dr. Bale:              Okay.  Great.  I appreciate the opportunity, Steve, to address your Council because I know addressing oral medicine individuals who realize the important of maintaining excellent oral in terms of also maintaining cardiovascular health.  It’s always been a pleasure to address and share information with individuals who we can partner with in our efforts to keep people from heart attacks and ischemic strokes.

So, I just want to give you the overall outline of what we’re going to cover today.  The first thing we’re going to do is give you a sense of the overall burden of cardiovascular disease and periodontal disease.  Then, we want to share with you some of the information that links periodontal disease with cardiovascular disease.  We’ll a bit about the recent American Heart Association conclusions about the systemic connection.  Then, we’ll tell you about a course that’s available now in dental economics that I have a pleasure of creating along with Dr. Nabors and my partner, Amy Doneen.  I should mention, Amy knows this subject as well or better than I do.  She’s sorry she can’t be on this webinar, but she’s traveling to San Antonio where I am right now because we’re getting ready to give a two-day course to health care providers.  So, she gives you her best, and hopefully you’ll get to meet her sometime.

Then, we will end with a bit about a course that we’re going to deliver November 2^nd in regards to the oral systemic connection.

So, in terms of periodontal disease incidents, we have excellent, very recently published information published online on August 30^th.  That’s pretty hot off the press, and it was the best assessment that’s ever been done for the incidents of periodontal disease in the United States.  They actually did full mouth exams that’s never been done before.  They based the definition of periodontal disease on attachment loss and pocket depth.  What they found was shocking to some people, that’s for sure.  I don’t think I was that shocked because Dr. Nabors already informed me how prevalent periodontal disease is in this country.

This study shows that basically half of Americans aged 30 or older have periodontal disease, and about 60% of that periodontal disease was classified as moderate.  About 20% is mild, and about 20% is severe.  Individuals 65 years of age or older, 70% of Americans have periodontal disease.  That’s huge.  I mean it’s got to be ranked up there as the top chronic disease in the United States, and as you know, it’s highly associated with cardiovascular risks as well as type II diabetes.  A lot of individuals with periodontal disease are not aware of it.

In terms of cardiovascular disease, it remains the number 1 killer in this country.  Every 39 seconds, someone dies of cardiovascular disease, and that’s an endpoint nobody can argue with.  In terms of the age for cardiovascular death, about 150,000 in this country die of cardiovascular disease for the age 65, which robs the mat least 13 years of life.

So, the issue is huge with cardiovascular disease as it is with periodontal disease.  A study was published in July looked to see is an adult more likely to have a noncardiovascular death or are they more likely to have a cardiovascular death, fatal or nonfatal?  The study showed that American adults are 2 to 3 times more likely to suffer cardiovascular death, fatal or nonfatal, than to have a fatal noncardiovascular death.

So, we need to enlist the help of all health care providers, certainly the dental community needs to be very involved in the effort to eradicate this unacceptable cardiovascular risk to the American population.

In the year 2009, the American cardiologists along with the American periodontists certainly recognized this issue, and they confirmed the connection between cardiovascular disease and periodontal disease.  They have outlined the known mechanisms by which they are related, and they specified some treatments that could be delivered.  They called for the collaboration of the two fields of health care to work on reducing cardiovascular risk.

In 2010, the European Society of Cardiology basically stated the same thing that oral health does influence cardiovascular health and that we have to start working together in order to reduce the unacceptable risk.

Our method, the Bale/Doneen method in which we do guarantee our results, and I should mention the guarantee may shock you.  Our patients understand it.  It carries no malpractice connotation.  So, we just feel we have evolved to the point where you can, with reasonable assurance, make a guarantee that the patient won’t have a heart attack.  We haven’t had a patient have a heart attack in over 10 years, but if you’re going to do that, you’re going to have a comprehensive approach.  That approach certainly has to include oral health.

We now have Level A evidence showing independent association between periodontal disease and cardiovascular risk.  So, all prevention programs for cardiovascular disease have to include the oral/systemic connection.

So what is the evidence that periodontal disease could impact cardiovascular risk factors?  Well, there are numerous risk factors we know about periodontal disease.  The impacts I’m just going to share with you.  In one study published not long ago, they looked at over 650 healthy subjects who were 35 or older, and they were tested for periodontal bacteria, the four bacteria that are known to carry significant cardiovascular risk.  That’s A.a, Porphyromonas gingivalis, Tannerella forsynthensis, and Trepnoma denticola.

What they found was very interesting:  The individuals who had the highest tertile of burden of these bacteria had significantly higher blood pressure, 9 mmHg for the systole and 5 mmHg for the diastole.  That increase in blood pressure creates very significant increase risk for ischemic stroke and heart attack.  They found the patients in that highest tertile were three times more likely to be hypertensive, and they did make a lot of adjustments before they came up with that figure.

So, the study was interesting in that it was a concentration of bacteria as opposed to the clinical diagnosis of periodontal disease that carried the risk of increased blood pressure.  So, this is certainly evidence that subclinical periodontal disease can have significant cardiovascular impact, and perhaps we need to think of a diagnosis of periodontal disease that includes bacterial burden.

There are lots of other known cardiovascular risk factors periodontal disease is associated with such as the cholesterol issues, the blood sugar involved in type II diabetics, and, in particular, associations with biomarkers that we know indicate arterial inflammation.  If you come to the course we’re going to deliver in November, we’ll be showing the recently published data published in the journal Lancet that actually demonstrates inflammation is causal of cardiovascular disease.  That’s a huge statement.  To show something that’s causal is difficult, but this data indicates that indeed arterial inflammation is involved in the formation of build-up of plaque along the walls of the artery.  It’s involved in the triggering of events, the heart attacks and the ischemic strokes.  We do have evidence that periodontal disease impacts, in an unfavorable way, all of the biomarkers we use in our work to tell if the artery’s hot, if it’s inflamed.  If it’s inflamed, the patient is in peril.

We’re also going to be discussing toll-like receptors in the course, which gets into the nitty-gritty science about how the inflammation is triggered, and we’ll relate that to periodontal disease.  So, there is evidence that periodontal disease is associated with the formation of disease in the wall of the artery.

In 2008, the United States Services Task Force certainly concluded that was the case.  They did a very extensive review of the literature, excellent studies, and concluded that periodontal disease is an independent risk factor for coronary heart disease.  There are lots of other evidence in that regard, and we’ll be presenting a lot of that data in our course in November.  Certainly, it’s fascinating that the data about their demonstrating the presence of these periodontal pathogens within the plaque that’s in the wall of the arteries.  We’ll answer that question, how can it happen, how can it get in there.  We’ll talk about that in our November course.

Later, we’ll show you a study where we took out the proteins.  Look at this.  This is the albumin levels in humans, and this is where it runs.  In this one that is toxic, look at this albumin.  It’s running very abnormally.  It doesn’t run like regular albumin.  When we go to jawbone cavitation material, there’s a lot of people that do osteonecrosis or cavitation surgery, and they send it in.  Almost all the protein that’s in those cavitations, it’s almost all albumin, and it’s albumin that’s linked to other albumin molecules like it’s been to a place where there’s a lot of rigorous chemical activity.  At the same time, that material will be very high in mercury, silver, cadmium, iron, etc.  So, those jawbone cavitation materials are toxic.  They’re high in metals.  They don’t have normal cell proteins.  They have proteins that look like they’ve been char-broiled.

So, we want to study the small molecule toxicants associated with avital teeth and osteonecrotic materials.  It’s important to remember that this site contains both small molecule toxicants and proteins, and we can separate these rather easily.  Doing so proves that the toxins produced by oral anaerobes are small molecules like hydrogen sulfide and methyl thiol.

Here’s the second step we do.  When you send your tooth in, we take that third wash, from the tooth extract, and we put it in what we call a centricone.  There’s a filter.  Here, then it filters out all the proteins, and you put it in the centrifugation.  You spin it down.  What you get is a protein-free ultrafiltrate of a tooth extract containing just small molecules.  Big molecules don’t go through this.  you can’t find any protein in this material.

This is what we test.  We do this for several reasons, one of them being that we look at the literature about pathogenic bacteria, we found out that the toxins in there were not proteins, not endotoxins, the things that cause other cells to die are small molecules.  This is how we set up our test.  We took all of these proteins, phosphoglycerate mutase, pyruvate kinase, phosphoglycerate kinase, creatinine kinase, [40:54] and a synthetic fibroblast growth factor.

The reason these were selected is they all bound to ATP. They have different molecular weights, so we can separate them on the gel and look at the effect of the toxins and proteins at one time.  At this one we screen them by doing this.  We did nothing or we added hydrogen sulfide, which we know is very toxic at high levels, 2 millimolars.  That’s how high it is in a periodontal pocket.  You can see, it totally inhibited every one of these enzymes.  Hydrogen sulfide is lethal.  It will kill you.  If you go near an oil or a gas refinery, you’ll see these little sticks out there.  They’re measuring hydrogen sulfide because if it builds up, it will kill the population.  So, they have warnings for these.  It is an incredible toxin, and it is produced in your mouth, as we’ll show later.

This T is the toxin from the tooth.  So, here’s with nothing.  Here’s with the tooth extract, and here’s with hydrogen sulfide.  You can see these toxins are as every bit toxic as hydrogen sulfide, but I’m here to tell you it’s not hydrogen sulfide.  When we use hydrogen sulfide, it smells like rotten eggs.  If I were to open it up, a vial, 2 millimolar, and set it here with the top open, everybody in the room would be complaining about the small.

These teeth, they have a smell.  Trust me, they’ll turn you green, but they don’t smell like hydrogen sulfide.  Some of them that are toxic, they don’t have a smell at all.  So, we’re dealing with a compendium of toxins that we don’t fully understand.  One of them we know about is called gliatoxin, and it’s at the end of my talk if I get there.  It doesn’t smell, but it’s more toxic than the rest of them put together.  It’s produced by Candida.  So, what we can say is that the toxicity extracted from teeth are not large proteins but rather small molecules.

Also, this toxicity is most absorbed by charcoal but not by cation or anion exchange resins.  What does this tell you?  I know a lot of you guys carry charcoal tablet when you go to Mexico, and when you start feeling a little sick you take them.  Why do they work?  They soak up the toxins produced by the bacteria that have infected your intestinal tract.  They also soak up vitamins so don’t take them too long.  This tells you that these toxins penetrate.  They’re hydrophobic.  Things that bind to charcoal are more or less hydrophobic.  In other words, they would penetrate the hydrophobic tissues in your body very effectively.  They would go through cell membranes, and they cause a lot of problems.

We’ve talked about a compound I’m making, and this is part of the rationale behind getting something that would go in there and pick up these toxicities.  What we’ve shown here is that the presence of this type of toxicity of hydrogen sulfide and similar compounds can be detected in a radiodiagnostic assay using binding to viable enzymes.  This is nothing but hardcore science.  I mean, this irritates a lot people, as you might imagined, but they haven’t done this and said I’m wrong.  This has been now 12 years.

Here’s the study as we do it today:  We have these enzymes that we use that are abbreviated here.  We can see there are no other proteins here because we filtered them out.  Everything we’re looking at in these studies is just nothing but small molecule soluble protein.  We have two controls, and these are the proteins we add.  These are the enzymes we add to the mixture.  Then we can compare three root canals.

Everything you see here, they’re all root canals.  They’re the same color because they’re from the same mouth.  These three are all from the same person.  Ca means cavitations, and we’ve got a control (+) and a control (-), which is where we have to show what we get without toxin and what we get hydrogen sulfide.  When we evaluate this, what we can see.  The two outside lanes are our controls.  You can see that these proteins interact and become radioactive very quickly.  If you have root canals like these three here, this first one here is not nearly as toxic as the other two next to it.  The two green ones, the outside one is incredibly toxic, and the one next to it isn’t toxic at all.  The person in the light color here, he had the least toxic of the root canals in his mouth.  Now, why is that?  The type of infection, and possibly the person who had this root canal probably practiced really good oral hygiene.  Probably gargled with hydrogen peroxide and treated his mouth carefully.  Probably didn’t eat a lot of sugars, etc. There’s a lot of variability in somebody’s root canal and how much toxins it will produce.

We’re doing an experiment now with one of my people that has a periodontal site, a very nice one that I can get into with microbrush, and he can get into it.  He tested it himself.  It’s amazing how the level of toxin production changes with what he eats.  It’s just a one-person thing, but hopefully it will bring up some interesting information someday.  That pocket is incredibly toxic, and the next day it’s not depending on what he eats.

Let us talk about cavitation materials.  We have tested people who do jawbone cavitation.  We’ve never found one that wasn’t reasonably toxic, if not incredibly toxic.  I would tell the people here that might get attacked on this.  I represented or was an expert witness, and helped a dentist that was being attacked for doing jawbone surgery.  We took nine of his samples, and I did mass spectrometry on every protein that spread out on a gel like this.  Every protein that we tested turned out to be human serum albumin.  Even if it were a higher molecular weight or a lower molecular weight.  You break it down in mass spectrometry, and what it says is the material that you get out of the jawbones that are infected is you’ve had a lot of inflammatory processes.  Albumin’s been rushed to that area, and that place for jawbone surgery totally disrupts cross links and breaks down protein albumin.  We could hardly find.

We found a lot of blood clotting proteins there also.  It was blood clotting proteins and albumin were the major proteins that we identified in the cavitational material from this person.  That eliminated the argument that the person from Temple Dental School was saying that he was removing normal tissue.  It’s not normal tissue.  We also took that same tissue and did ICP mass spectrometry to identify the metals.  What you find when you do that is the metals aren’t consistent with it being normal tissue either.  It’s high and heavy metal such as mercury, iron, silver, copper, and other compounds similar to that.

The material in these jawbones, it’s not normal tissue.  There’s probably something that needs to be removed.  I think it’s something that we need to consider.  I think 12 years from now, if I’m still here alive and talking, this will be something accepted such as the focal point theory. This is the bottom line:  Osteonecrotic materials do not have the metal content of normal tissues nor do they have the normal proteins.  To back up the chemistry, and just to show you where the products come from and a lot of the studies we haven’t done.  When we look at the breakdown of L-cysteine, desulfhydrase is the enzyme that’s in these anaerobic bacteria.  Why did they produce hydrogen sulfide, and why, if you don’t brush your mouth regularly, you start stinking.

We look at this.  It produces hydrogen sulfide.  It also produces ammonia.  What we’re finding is maybe the hydrogen sulfide plus the ammonia together are what perhaps make these sites so toxic and so susceptible to breakdown of the tissue.

This tooth was sent to me by Hal Huggins.  There as a time in my life when I found Hal Huggins a major pain in the rear end.  There’s some things about him that I like and some things I don’t like.  You can’t talk about his intensity.  When he found out I was visiting you guys and talking about mercury toxicity, he sent me some teeth, called me, wrote me.  In general, he harassed the living daylights out of me until I said, “We’ve got to do something for this guy so I can shut him up.”  I thought he was wrong, just to be blunt.  I didn’t believe that a tooth could be as toxic as mercury.

This tooth came from him and it was extracted from a person with multiple sclerosis.  We did the same things that we talked about.   We washed his tooth three times, let it set there, and after the 3000 microLiters, we started adding.  This is a pretty homogenous, by the way, labeled with ATP.  Here’s what happened after we added 5 microLiters of that last thousand microLiter wash.  It just totally abolished the activity of the proteins in the brain.  This was something coming out of a well-washed tooth that had been extracted from a person who was sick.  Now, I am not saying that infected teeth cause multiple sclerosis.  It might be that these people have a lower immune system, and their teeth just become infected.  The person with the tooth needs some dentistry, some good advice.  We need to be studying this area.  There’s absolutely no doubt that this tooth is more toxic than hydrogen sulfide. It might be because of the ammonia that’s in it also.  It might be because of the toxins. We don’t have the answers, but we need to be pushing our government and the National Institutes of Dental Research to have research in this area and not have people from Brazil, Chile, Japan, Sweden, Germany, and every place else do research that we could probably do better and more effective in this country.

To say these teeth do not have an effect on human health, whether this game after or before this person developed multiple sclerosis, it shouldn’t be in their mouth, not this level of toxicity.  This is incredible toxicity.  I give full credit for Hal Huggins for pushing this issue.  I also say Dr. George Manning because coming to one of your talks, I didn’t listen to Al very much until I listened to Dr. George Manning give a talk on root canal coverup.  When I listened to him, it was sensible science he was talking about.  Sensible science is what wins this game.  That’s the reason the academy today is winning the fight with dental amalgams.  Show me sensible science.  Go back to Mike Ziff’s mantra.

So, if we say, “Is there anything else that ties this together?”  This is the research that some of you know brought me into this fight.  This is a polyacrylamide gel.  We’ve separated proteins after grinding up the brain of a normal person and treating it.  We see what goes down in the pellet and what stays soluble.  In normal brain, like here on the side, here’s a pellet and here’s a supernatant.  Tubulin stays in the soluble aspect, and I would point out in a normal brain, tubulin, creatine kinase, and glutamine synthetase all stay soluble.  If you do the same thing with an AD brain, certain tubulin and creatine kinase all go down in the pellet.  It’s an abnormal partitioning that anyone can observe.

People have said I’m right, but it’s ignored.  What makes tubulin and creatine kinase soluble proteins, go down in the pellet?  It’s because they’re abnormally affected by some toxicant in the brain, which renders them to bind to particular material.  If we take a soup and a pellet with no treatment, we look at the supernatant.  There’s the tubulin.  As we increase the addition of the toxic material, that’s 2.5 micromolar, 5, 10, and 20.  If you go across here, when we get to the grey end, here, it’s gone. If we go here, you can see that the tubulin has gone down in the pelette fraction , and you can see that it’s gone here.  Not effected.  So, hydrogen sulfide does not cause the apparent biochemistry that we see in an AD brain, but an extract from an infected tooth does.

I think that this is something that’s very important.  Even if you don’t want to say it causes Alzheimer’s disease, would you want something floating in your blood stream that cause your tubulin to abnormally partition that was very hydrophobic?  The things that do cross into the blood brain barrier and cross into the brain are hydrophobic materials primarily.  If we look at the photolabeling activity, the hydrogen sulfide does not seem to have much effect on brain tubulin, but this toxic material from this tooth with multiple sclerosis and other things totally abolishes the photolabeling and has no effect on this protein.  This is exactly what you see in Alzheimer’s Disease.  That’s exactly the profile.

So, we can say that Alzheimer’s Disease probably has something to do with toxicities coming out of the oral cavity as well as anything else.  So, these were the results.  These were also observed in Alzheimer’s Disease brain and brain tissue exposed to mercury.  This has been published a long time, and nobody has said I’m wrong about it.  They just ignore it.  This is the same situation that’s in your mouth just looking at your mouth by a chemist.

That’s what you have, amalgam fillings that release elemental, as well as Hg2+.  You can have an avital tooth, doesn’t have to be the same tooth, that releases hydrogen sulfide plus methyl thiol plus other compounds.  When these compounds react with mercury, you get the HgS.  You can even get silver sulfide, but this is what precipitates in the tissue.

This is what causes an amalgam tattoo.  If you don’t believe me, excise it from one of the gums of your patient, send it to doctors and have the measure the mercury content or the metal content.  It will be sulfides and other heavy metals in amalgams.  It’s probably not all that toxic to that tissue although it’s ugly.  If you look at this, hydrogen sulfide and you make this from the thiamine, these two organic mercury compounds.  We made them in our laboratory.  We tested them, and what we can tell you is they’re incredibly toxic. The toxicity of mercury compounds is based on their hydrophobic ability or their ability to penetrate cells.

Hg2+ is toxic to the kidney, but it’s not to toxic to the central nervous system because it can’t get it.  Methyl mercury and dimethyl mercury are incredibly toxic to the central nervous system because they’re hydrophobic and they partition into the fat layers, the fat tissues, and they penetrate the body.  They can get into places where we don’t expect, and we can talk about toxicity. We can talk about the synergistic toxicity, and we can say this is a major problem.  We have to look at the ability.

Getting amalgams out for no reason to prevent them from reacting to periodontal disease toxins which we’re not going to stop is a good argument.  You are manufacturing toxic organic mercury compounds in your own mouth if you amalgams and periodontal disease.

Mr. H.B. Wallace, who funded a lot of my research is now dead.  He was the son of the vice president of the United States, Senator Truman.  He was a person who though his father and other people suffered from mercury toxicity .  I have to say I steal a lot of it from people, but on this one particle talk, Weston Price, I read all of his work.  I listened to Dr. George Manning talk, and of course, HHal Huggins was the tack that I had to sit on.  I have a lot of friends in the IAOMT.  A lot of you guys, I can’t tell you how many times I’ve sat and talked with you and how much dentistry I’ve learned and the problems you have.  I really appreciate that.  Like every husband, I’m hard to put up with.  I’m very intense, and I have a very tolerant wife.

I would like to present the Ziff Memorial Plaque to Dr. Boyd Haley.  In Michael’s honor, I’d like to thank you for your research.  He really appreciated your research on the dental mercury issue.  Thank you very much.

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.

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.

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.

Dr. 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.