Periodontal Disease

Oct
2013
24

posted by on Gum Disease Prevention

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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.

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