Archive for October 2013 | Monthly archive page
Then, we come on to the situation with Entamoeba gingivalis. Entamoeba gingivalis is an amoeba. It looks, morphologically, almost identical to Entamoeba histolytica, and in fact, it takes an expert to tell one apart, and the differences are very slight. They are purely in the construction of the nucleus. The type of movement they have is identical. They both may move around very, very rapidly in a slug-like motion, looking for all the world as they slide themselves in their elongated body sliding across the slide, and both of them, in my opinion at least, are pathogenic.
Entamoeba histolytica binds onto the gut wall. You get a node of parasites grouped together. It is assumed they secrete exotoxins, which are presumably what’s responsible for breakdown in the connective tissue and epithelium and also is formed with typically described overhanging edges. Then, it becomes secondarily infected by bacteria.
Entamoeba gingivalis, on the other hand, will be found in the mouth, and when we take plaque and look at it, we find them typically, if there’s an area of parasites, they’re grouped together. In other areas of the plaque, there won’t be parasites. So, the same kind of node formation seems to occur.
Host: So, it is common effectively for parasites Entamoeba gingivalis and Entamoeba histolytica that they’re both seen clustered together or grouped and have a focal point?
Dr. Lyons: Yeah, I think this would be a pretty apt way of describing it. When they’re clustered together, we assume that toxins are being secreted, and of course, this concentration of parasites will lead to an increase concentration of this toxic material which will have a much more profound effect because of its concentration. Then, you get that tissues breakdown. So, in the gut, we get the ulceration of the gut wall, and in periodontal disease, we get an ulceration of the gingivae where it is resting the neck of the tooth. So, we have this sort of band-like color of ulcerated tissue, and then from the evidence which we have been able to elicit so far, it’s highly suggested that Entamoeba gingivalis then invade the tissue.
We have recovered them from pus, from apical abscesses. We’ve recovered them within granulation tissue, from apical granuloma. We’ve recovered them from pus from tonsils, and other researches from periodontal pockets have also recovered them from tonsilar pus and also from bronchial secretions.
When the parasites get into the upper respiratory and lower respiratory tract, they can set off infection, which in some cases, can be extremely severe, and of course, Entamoeba histolytica does not able to cause an infection in a bacterially sterile intesting.
Host: So, it’s possible, then, that Entamoeba gingivalis relates to a host of diseases, one of which seems to be periodontal disease, in terms of attacking the tissue aggressively around the tooth itself in a pocket that’s 2mm or 3mm deep. Can you tell me about the criteria of getting established around the tooth?
Dr. Lyons: Yeah, let me answer that question by giving you a typical art line of what might happen to the average patient. The average patient would possibly be in their mid 20s to the early 30s. The oral hygiene would be relatively good, but for one reason or another, they would have a fair amount of neglecting their mouth. There we be a certain amount of inflammation due to bacteria in the plaque in the gingival margin. As a result of that, if they catch or contact the parasite, then the environment within their mouth is conducive to the survival of the parasite. At that point, the very small parasites cannot survival without motile bacteria because the small parasite feds on motile bacteria such as the Lactobacilli, which one finds in plaques so frequently.
The next phase of the disease there is basically there would be a slight increase in pocket depth. There would be very little sign of inflammation. There really wouldn’t be any cause to be alarmed about the patient’s general periodontal condition, and there’s no disturbance, in other words, of either their general or their dental health.
Phase two of the disease is they would go into a series of flu-like symptoms, which will be protracted or repetitive. So, they’ll have something like the flu or a cough or a cold or sore throat with the usual symptoms that go with that, headache, itchy eyes, running nose, fatigue, and sometimes they’ll complain of either bleeding gums or halitosis.
The important point is regardless of what periodontal disease it is, the one common denominator is the presence of oral parasites in destructive periodontal lesions, and since recent research has shown a wide variety of different bacteria in different periodontal disease, we know one strain common to periodontal disease. The important point is the common denominator is not bacterial but protozoan parasite.
Host: Now, if you take myself as an average 33 year old dentist, what are the chances of myself having contracted or come in contact with Entamoeba gingivalis?
Dr. Lyons: Well, I think the chance is fairly high in a dentist who’s been in practice for two or three years. The dentist will have had his fair share of aerosol mists kicked up by high speed instruments, and within these aerosol mists, it almost certainly will have been oral parasites. So, they may have contracted the disease in the first few years of practice, but the progress of the disease beyond the first stage will be slowed down tremendously with good oral hygiene and by good dental care.
So, the end of the first phase of the disease is that the patient will slowly go into a state of diminished state of health where they’re not as energetic. They’re more fatigued. They go to bed earlier. They get more frequent headaches, but they slowly acclimatize to their diminished state of health.
Stage two of the disease. This is basically periodontal disease, and thy run the full range of periodontal deterioration. I’m sure we’ve all seen patients, some with subgingival calculus, some with none, some with good oral hygiene, some with poor oral hygiene, some with an occlusal problem superimposed over this, and some with none. This will give us basic definitions.
So, to reclassify periodontal disease, I would suggest that periodontitis simplex is an infection with parasites with a superimposed infection of bacteria, given the inflammation, and no occlusal stress. Periodontitis complex is the same condition but occlusal lateral stress thrown in, and periodontosis, which is that inflammation of the periodontium, would be oral parasites with little or no bacteria. Those are the classifications of disease which I understood, and those are my clinical observations of plaque as it relates to those conditions.
Host: What would be the finals stage or stage three, then, Dr. Lyons?
Dr. Lyons: The stage three of the disease is an overlapping stage, and what we’ve heard is there’s complete periodontal breakdown. We have abscessing occurring, excessively mobility migration of teeth, teeth falling out or being removed, and at the same time this is happening, there seems to be common with periodontal patients, much more serious disturbances of their general health, which were not present before they developed periodontal disease, and seems to follow down in sequence from there.
In the past, we’ve tended to regard these as an indication of creeping senility, and this would include hypothyroidism, diabetes mellitus, various arthritic changes, cardiovascular diseases, possibly, and perhaps, some central nervous system disorders.
Host: Fine. Then, you see the infestation of the digestive tract by Entamoeba gingivalis as a progressive lifetime battle between the host and the parasite?
Dr. Lyons: Yeah, we have to limit the digestive tract there to being the mouth and the pharynx, because after the pharynx, Entamoeba gingivalis will be found basically in the respiratory system, and for the appearance of Entamoeba gingivalis as a multinucleated giant cells, I am becoming increasingly suspicious that many of those serious pathologic disorders were in multinucleated giant cells are present.
What we may be looking at is not multinucleated giant cells but a section through Entamoeba gingivalis where the section has missed the nucleus of the amoeba that has gone through all the nuclei of its digested food because Entamoeba gingivalis ingests, as its primary food source, leukocytes, so that when you see a section through Entamoeba gingivalis, seems to have a lot of human nuclei in it. It does, but this is partly digested food and not a human cell with many nuclei.
So, yes, a lifetime battle with usually the patient on the losing end of it because Entamoeba gingivalis does not seem to engender any marked antibody response. As a result of that, we just do not seem to have any basic defenses against the disease. So, it’s a disease that we can contract and get treated for and re-contract and get treated for, and the unfortunate thing is many of the things which patients do to try to eliminate periodontal disease and many of the things which I was taught to do to eliminate periodontal disease, by disturbing the tissues, actually spread the disease deeper and further. What one needs to do with a parasite infection is the least amount of instrumentation coupled with the maximum amount of medication until the disease is eliminated and most of the instrumentation becomes unnecessary.
Host: Tell me, a little bit, what has to be done to prove this a pathogen, and tell me about the type of study that should be done or conducted to re-evaluate, on a broad scientific basis, the pathogenicity of Entamoeba gingivalis in periodontal disease and other associated upper respiratory tract illnesses.
Dr. Lyons: First of all, the original observations, which were done from 1913 to 1929, and the experimentation, which was done from 1926 to 1929, was pretty conclusive that Entamoeba gingivalis is pathogenic. The point has been proved. In order to reinforce the point, I have treated approximate 700 patients now with it, oral parasites and periodontal disease. Some of these were reinfections. So, we have got confirmatory slides now in over 500 cases where the patients had periodontal disease and parasites, and subsequently, they were treated for their parasites, their periodontal disease just healed up and went away. So, that was very nice.
What does one need to do further from there? Really, what we need is anything from 50,000 to 150,000 case reports. Unfortunately, I can’t do that by myself.
Host: A hundred thousand case reports, roughly.
Dr. Lyons: I think that a thousand dentists across North America should be able to have Entamoeba gingivalis investigated. On a clinical study basis, it would only take 75 cases for dentists, and we have a very conclusive argument.
Host: To put it very simply, Dr. Lyons, could you just tell us how we diagnose, in clinical dentistry, the parasite Entamoeba gingivalis?
Dr. Lyons: That’s a very good question, Paul. What needs to be done now is the laboratories and their technicians across the country have to be trained on how to process dental plaque, how to stain it, how to read the slides that they get so that they can recognize Entamoeba gingivalis, and dentists have to learn or be trained in the use of a phase contrast microscope and the recognition of Entamoeba gingivalis on a wet mount. Then, we’ll be getting somewhere.
Right now, nobody’s trained to do it. I’ll do what I do with a typical patient. A typical patient comes in, and they get a very brief clinical examination. We check oral hygiene, gingival condition, the amount of plaque, the pocket depths, the amount of inflammation, whether or not they have halitosis, and if they have a submandibular lymph adenitis. An eighth point, which is sometimes recorded, is whether their salivary production is normal because low salivary production is very often diagnostic.
Then, plaque is taken from the deepest periodontal pockets. Now, before plaque can be taken, the patient must be instructed not to brush or floss for preferable 24 hours but certainly not less than 12 hours beforehand. Having done that, one then needs a special fixative, and it’s an SAF fixative kit. The SAF is sodium acetate, acetic acid, and formalin, and this fixative was developed by Dr. Shelton. The importance about SAF is its low toxicity. It’s non-damaging to dental instruments. It has an indefinite shelf life, and once the parasites are placed in it, they are preserved indefinitely until they can be processed in the lab. It does not need refrigeration. Other fixatives are more hazardous and less effective.
Host: In the past few months, it has been brought to my attention, through discussions with Dr. Trevor Lyons, Ottawa, Canada, and reading several research papers that, perhaps, periodontal health cannot only be achieved with good diet, good home care, and good restorative or periodontal care, and the reason why this is not possible is maybe an etiologic agent involved in the periodontal disease, which is an oral parasite, it’s called Entamoeba gingivalis. To give you a little bit of a background on this concept of related to his experiences the past couple of years, I’ve asked Dr. Lyons to speak to us about his general experiences in treating periodontal disease in regard to Entamoeba gingivalis. Dr. Lyons?
Dr. Lyons: Well, up until about the end of 1977, I firmly believed that the principles of good home care and good dentistry were quite sufficient to control periodontal disease and quite sufficient to control caries as well, and it had been in the hands of myself and my patients and practice. Up until that point, very effective in controlling caries, and towards the end of 1977, I began noticing an increasing number of patients who seemed to be developing a periodontal degeneration.
In February of 1977, one of my patients, a 35 year old woman, presented, complaining that her right upper center was moving and her gums felt itchy. She had very good oral hygiene, and she had most of her gingival calculus. I was at a lost to understand exactly what was happening in this particular case. So, I did the usual things, which I think the average dentist would do under these circumstances. I re-instructed her on her oral hygiene and chided her gently for not having been working hard enough around it, and we cured that around the margin of the upper right one although there was no calculus or anything else around there that was an irritant. I felt that this would be some benefit. We followed this and the usual things that one does for periodontally-involved tooth.
About two weeks later, she was back in. The condition around the upper right center was now a lot worse. The pocket depth had increased from 2.5mm to 5mm. The tooth was still mobile and still moving labially, I smeared her plaque and examined it using a phase contrast microscope. Now, I’d been examining plaque constant with a phase contrast microscope since 1971, and my technique had always been to take it from the medial of the lower left six because I felt that this was going to give us statistically significant comparison patient-to-patient.
Well, at this point in time, I decided to diverge from my usual technique, and I smeared the plaque long her upper right center. I found within her plaque, a large number of protozoan parasites, which were later identified as Trichomonas tenax and Entamoeba gingivalis. At this point in time, I believed that protozoan parasites were nonpathogenic and had no causation in any kind of periodontal disease or disease in the mouth, but both myself and the patient were somewhat concerned. So, the decision was taken to eliminate the parasite before embarking upon further extensive periodontal care.
At the end of her first course of treatment to eliminate parasites, we had successfully eliminated parasites, and to everybody’s surprise and pleasure, we’d also eliminated the periodontal defects. The tooth was no longer mobile. It was no longer drifting, the pocket depth had returned to 0.5mm to 1 mm around the upper right central. Subsequent to that, we used grass line to bring the tooth back in to its proper position in the arch but adjusted the occlusion so that the lower teeth weren’t banging it out labially, and it remained stable from that time to this, which is a period of just over two years.
This sort of set me on a path looking for oral parasites, which I didn’t necessarily been doing before. I’d just been examining plaque, and I had noticed some oral parasites in some people’s plaque. I just disregarded them because they were not supposed to cause disease. All the patients who had had oral parasites discovered in their plaque went on to a periodontal deterioration.
So, I now changed my technique and started examining plaque from the worst area in the mouth, and what I found was patients with periodontal deterioration, which was, generally speaking, pockets in excess of 3 mm, a generalized mauvish discoloration of the tissue, which was flaccid and had lost its tone, contour, and stippling, and bled easily, and very often, they had a halitosis that was faintly reminiscent of garlic. These patients, all from these periodontally involved pockets, gave parasites, usually Entamoeba gingivalis. Less than 10% of the parasites that we found were Trichomonas tenax.
So, during this period of time, which was the following winter, now, we’re getting into 1978, what I did was to treat patients with parasites for the parasites, and sat back and noted, with a great deal of pleasure from myself and my patients, that periodontal deterioration disappeared and their tissues returned to a normal, healthy color, tightly bound, no longer bleeding. The halitosis disappeared, and the tissue resembled that one would expect to find in the mouth of a child.
Host: Now, Dr. Lyons, since this concept runs contrary to accepted periodontal therapy, at least in North America, I’d like to ask you if there’s any other people doing or research in this general area throughout the world.
Dr. Lyons: The answer to that is yes, and perhaps, if I give you a very brief historical background, I can tell you at the same time how we found out some of this information. Well, before I started finding out oral parasites, I turned to people who I thought would be considered experts, and finally, I was directed to Dr. Ted Shelton of the Ontario Ministry of Health’s Parasitological Service. It was thanks to the hard work of Joe Palmer and Dr. Shelton that we made positive identification of type IV parasites that I was finding and also developed a test kit and a simple way for any dentist to take any plaque and send it into any laboratory so that a plaque search can be made for oral parasites by laboratory using staining techniques, which would either augment or supplement or by instead of having a chairside microscope.
As a result of the number of cases that I began to turn up, showing 100% correlation between periodontal and the presence of parasites, Dr. Shelton conducted a search and review of the literature. In the process of that, we found cases reported. For example, by Brump [7:40], as early as 1913, where they found 100% correlation between oral parasites and periodontal disease and many other researches at the beginning of the century had similar results. They called it “pyorrhea alveolaris” at that time which I think is still a very good term because it dispenses a lot of the latter definitions of what kind of a periodontal disease we have.
One thing that I have found constantly through all kinds of periodontal disease, whether it periodontitis simplex or periodontitis complex or periodontosis, is that oral parasites were always present. The type of parasites sometimes varied. The type of destruct seldom varied, but the amount and type of variation varied according to whether or not there was a bacteria super infection or supra infection, which was imposed over the parasite infection, and whether or not there occlusion appearances which would alter the pattern of bone loss.
As a result of the literature review, we finally came up with a very definitive article, which had been published in the Journal of American Dental Association in August of 1929, and it had been published by some American protozoological researchers. Charles Crawford was the chief of these, working out of Berkeley, California, and they had a 100% correlation between periodontal disease and the presence of oral parasite and had further go on to experimentally induce periodontal disease in experiment animals, which initially were free of periodontal disease and parasites. They did this simply by infecting them with oral parasites.
So, the situation became very, very clear just at the time of the great Wall Street crash and immediately prior to the depressions.
Host: What was the problem at that time, Dr. Lyons, that they didn’t pursue this line of treatment?
Dr. Lyons: Well, at that time, they didn’t have any drugs that were suitable for the treatment of the disease. The only things that they had used were derivatives of ipecac, which they had gotten some success with, and emetine hydrochloride. The problem with emetine hydrochloride is it’s a very dangerous drug and had the tendency to cause fatalities. Of course, during the Depression, it was important to hang on to your patients and get rid of periodontal disease.
So, that method of treatment, which was medication approach to periodontal disease, largely fell by the wayside, pending the development of new drugs. These new drugs were developed during World War II and basically fell into a range of antiprotozoan drugs. Malaria, of course, is also caused by protozoan parasite.
By 1962, one drug in particular, which was metronidazole, had been developed. It was in the market, and it was very effective in the treatment of certain kinds of oral infection. It’s also been used for vaginal trichomoniasis, also used for intestinal infections, particularly giardiasis and amebiasis.
Host: Could you tell me a little bit of both the protozoan parasite group and a little bit about the metronidazole?
Dr. Lyons: Well, starting with protozoans, protozoans is a group of one-celled animals, and they can be subdivided to those which are free living and those which are host dwelling, in other words parasites. Now, some of the free living protozoans are also opportunistic parasites. That is to say, they will live in a host if they find that the environment is suitable.
The main groupings of the animals according to their morphology is the ciliates, and in the free living ciliates, we find paramecium. In the parasitic ciliates, we find Balantidium coli. There are no ciliates that live in the mouth. In the flagellates, we might consider, for example, euglena, as one of the free living flagellates. Gardia lamblia would be one of the parasitic flagellates, and this one lives, as does Balantidium coli, in the gut. In the mouth, a flagellate is Trichomonas tenax.
Of the amoebae, the soil amoeba, of course, are free living amoebae, although they may occasionally be opportunistic parasites. Entamoeba histolyitica is probably the best known parasitic protozoan of the amoeba group, and it, of course, lives in the gut and causes dysentery. Entamoeba gingivalis is its first cousin and lives in the mouth, and we believe now, or at least I believe, that it is the cause of severely destructive periodontal disease.
Now, of course, there are many other protozoans which parasitize the human race. We have, for example, the malarial parasites, Toxoplasma, Entamoeba coli, Entamoeba hartmanni, Dientamoeba fragilis, Endolimax nana, Chylomastix mesneli, and on and on. Now, some of these are pathogenic. Some of their role is unknown, or it’s at least being re-evaluated. Some of them are already suspected of being pathogenic. An example of one of the protozoans whose role as a pathogen has been recently re-evaluated is Giardia lamblia. It was once considered commensal. It is now considered sufficiently pathogenic and sufficiently serious that it has become a reportable disease. This has nothing to do with dentistry, but it does show that protozoan parasites, generally speaking, are being re-evaluated in their role in disease.
Trichomonas tenax, very loosely similar in appearance, perhaps, to euglena. They’re very small. They’re less than the size of a leukocyte. They’re usually about the size of a rather elongated erythrocyte, and they’re very difficult to find in a phase contrast examination. They’re also difficult to find in any of the staining techniques that we have done so far. We really don’t have a good test for these, but they only form about 8% of the infections that have been noted more recently, particularly in Russia. In Kiev, for example, they have thousands of cases with oral parasites in periodontal disease, treated with metronidazole to remove the parasites and successfully eliminating the periodontal disease, but I digress.