Pulp autonomies can now be done without having to use former, to be opened up and be treated with the laser, dropped inside of the pulp chamber with the laser. We use a little MTA on top of that and then go ahead and place our restoration. When we talk about indo terbium chromium YSTG laser uses the radial firing tips and they are much provisioned for removing bacteria form the root canal system and also removal of the smear layer. As you can see on this photograph look at the dental tubes they’re wide open. 15% of root canals that GPs do each year require retreatment and generally it’s because of reinfection. 99.7% reduction in bacteria count is when a canal is sterilised with a laser.
The radio fire tips as you see into his photograph here have a unique being because of the angle on the tip it disperses the energy laterally at an angle and if you notice it comes to a very exact point. When the tip comes to a point like that no energy is omitted thrush the end of the top. At this case we do want it to go laterally. If it goes out the end it ocean gout the end of the root ad stimulate some apical bleeding.
Here you see an indo tip , one that’s a brand new one and one that’s been used one too many times. As you can see in the photograph it’s blunted and if we use one too long and it becomes too blunted like this then the energy can travel out the end of the tip, out the end of the root of the tooth and cause an apical bleeding. There are two different sized tips at 200 and 300 micron they fit east [toy down inside the canals. Here you see a tip in use and we can set working length by the rubber stop that you see on the tip.
Down on the canal you admit their energy on the way out to remove the smear layer and to get rid of any bacteria that may be present. When we look down in the canal after that this is what we see. You will see that the canal are really frosted looking, very clean and a wonderful environment. It gives us a better seal between the [Inaudible] and the tooth. We can actually open the tooth up for indo using the laser if we need to. Other times if it’s a really hot tooth and you go in with your hand piece you know that the vibration that you get from hand piece, woven though you have good anaesthesia the patients still feels it. If you have a really hot tooth like that one of the best thing you can do is to open the tooth and get you access with you laser.
We use conventional instrumentation after that and then we turn to the laser for cleaning. It removes the smear layer, only takes about 2-3 minutes and also we get micro agitation tip to help clean out the cancel. From this photograph you can see with the laser it in water as laser energy has admitted it, it cause bubbles and squeezes down inside the canal. I see little particles falling out all the time as it cleans. It does a wonderful job of cleaning the root canal system. Then we can turn to the laser drive for disinfection. It reaches out into the dental canals and destroys the hidden bacteria that might there. Reamer we are using a radio fire tip.
Let’s talk just briefly and give another examine of another thing we can use the laser for and in endeavonance for an apectomy. Teeth 9 and 10 and on the radiograph we see a rather large lesion inn association with the apices of 9 and 0 and in kHz radio graph you can see that we’ve complete the indo on both of those two teeth . We just measure up from the incision edge to locate the approximate apex of that teeth and we will make out incision using the laser. Once we have the incision and woe open up the indoor of the bone using the same laser tip and then once the window is complete us clean out the legion area and wee amputate the apex with a little slight beble for access.
After we do that we can use the laser to go to the end of the root of the teeth and take out the gutter putura or the material it might be using at the very end and then we can do a retriivabatye field using MTA. Following that we can use a brine graph, seek though the area and then we are finished. With the laser we’ve made our access with an incision, we’ve amputate the root, we’ve opened up the root at the end of the tooth. It’s just a great tool and here you eel postoperatively our legion as it started and post operatively here is the lesion after we did the apical.
This is one week later, six week later and 12 months later. One thing that I mention about this particcualr case is that this patient was an extreme diabetic so healing was even compromised by that fact and I think you can tell that we got wonderful healing in this case.
Now let’s talk a little bit abs tout soft tissue. The treatment of a respective legation, we could also use the same treatment for an after ulcer. you want to get to the legion why it is still in the vesicular state before it gets into the vesicular stage , when the patient can first feel it coming on this time to treat it .We treat the herpetic legion with the laser. We just fire around the outside and work our way to the centre covering all of it. We want to be sure when you do a good high volume suctions system and one of the better quality mass.
You can also treat an after sulphur inside the mouth with the sane techniques. We do quite a few biopsies in our offices. This a biopsies for the removal of a fibroid, it’s a very large none. We use soft tissue pick up forceps and soft tissue tip on the laser and an incision to remove the entire fireman and after tan we use chisel tip to go back and do the laser band aid. It says here to put a little oxy fresh gel on top of the legion and here it is 6 days post operatively.
One of the things that you see with the laser is that healing is just wonderful after using a laser, much better than if you use a blade or an electro surge. By the way the patient that you saw in the photograph here was 86 years old at the time this was done so I think that was pretty good healing for someone off that age. A Paloma on the tongue , again using soft tissue pick up forces and soft issue tips on the laser , we just go around and remove that and if you notice the absence of one thing here., the absence of bleeding . Even though we are working on the tongue which is just full of blood vessels we have little to no bleeding and these are not touched up photographs one we didn’t blot the tongue just before we made the photographs to impress you. This is the we way it really looked immediately after we removed the papilloma.
The laser candid, we put socket gel, oral pain gel on top of that and here it is 6 days later and you can see that it has healed up so well .It really a little difficult to even tell where the pap lama was before we took it off. I don’t know if you have this in your practise, I just want to mention it to you. You can purchase this through Henry Schein dental, it uses The Dental Pie 300, it’s a multi oral cancer screening device. We use it in urn I office it has a wide wave length that just helps to eliminate the mouth. The violet with speckle glasses will show up any kind of legions as a dark spot in the tissue and then you can help to differentiate it by the green amber light and it shows you the vasculature to the area that you are concerned about. A very concise vasculature probably means it so and a very diffuse vasculature is something that concerns.
This is a wonderful tool and I know that it goes hand in hand with laser se and we use it in our office routinely .We did do a training video for them and you can see that at abystintrimera.net.
Again remember every day , very way dentistry we see people come in all the time with a Lowe attach phrenic or a diasoma between 8 and 9 and were phrenectomy is necessary and remember we see the problem if we have a solution to that problem . Here’s an ortadontist case, a very; low attached perineum removed with the laser. Again look at we do not see, bleeding. We do a pretty aggressive phenectomy and we have very little bit of bleeding when we do this. Post operatively several weeks after the fact look at what our attachment reoccurred I’m going to show you in the next series of slides how you determine where you can place your reattachment of the phrenic and we can put it exactly where you want it to reattach.
Here’s that phrenctomy step by step, also with the distraction of kea legion. Low attach premium again, soft tissue pick up forces in the laser. We do an aggressive phrenectomy. We’re going to take the entire little muscle out. Very little bleeding here. Turn it over and do the other side. Now we’ve removed the perineum and then we go back between the central insiders and actually cleanout. There is always that little area between the teeth where there is a lot of tissue attachment and the bone just sort of invigilate there. We’re cleaning that out there really good to make sure that we have all the fibres.
Then a very important step is to score the periostum. The way that we determine how we do that so we look at the junction of the removable and the attached tissue and where we scored the perisotuium there we will have a scar band and that scar band will determine where the phrenum reattaches. If you’ll just lock that in your in as we got through these remaining slides you wills eye that the phrenum actually goes back and reattach exactly to that spot. With these you could probably leave them open. I think we get better healing and also by placing sutures it prevents any kind of reattachment in there of the tissue.
Now it’s healed up from that but you still see that we have a little legion of here to the right and we will go in and remove this legion using the ablation process. Thad is a chisel tip and instead of sizing it and cutting it out we’re just going to ablate it away. The tissue is just taken down cell layer by cell layer until it’s gone and here it is a few weeks after that when it is healed up completely. Remember in your mind where we score court pereostum and this is where our attachment will go back to.
If you didn’t see this wonderful article in Dental Economics recently by Rodger Levin , the march edition I would encourage you to take a look at that and when you’re Dental Economic issue arrives this month be sure to take a look at our upcoming article, The $250 000 Smoked Ham. In the article it talks about the fact that we a general dentist refer out of our offices each ear, approximately $250 000 in production that we can do under our roof. It’s not the exotic, its everyday destroy that we are referring. In December the UPS guy comes and brings us that wonderful smoked ham and we are so excited because we have a $95 ham while we spent $250 000 of our practise.
I got this information from Charles Blair very recently. There’s 500 dental procedures that you and I do .The referral dentist does only 60 of those 500 procedures. Joe’s average dentist does 90 of the 500 procedures. The decathlon dentist does 120 of those 500 procedures so what I want to challenge you to do tonight is to go back and look at the number of procedures your routinely doing and if you are under that 120 mark by adding a laser into you practise you can became a decathlon dentist. So you’re training starts today. Also in the Dental Economic the September issue please look at my article don’t be a Sheep. We talk about how to differentiate your practise, how to separate your practise form others. When we come out of dental school sometimes we tend to follow the practise that is right in front of us and we do what they do. Let’s differentiate ourselves and laser is a great way to do that.
Perhaps in the Orthatribune you saw our article that talks about how lasers relate to orthodontist cases and things that we can do and upcoming in the fall there will be an article and LVI Vision The impossible is nothing which will cover a lot of the information that we talk k about tight . That was co-authored by Lorne and myself.
When the lark goes off in the morning are you really excited to get up and go to your office air would you rather just hit the alarm clock like you see in the picture? Do you feel you need direction for you practise? Lasers might just be the driving force that you need. I will honestly tell you that before 1998 when we purchased out first laser dentistry had really become really boring and I was experiencing burn out from it , the same thing all day long , every day .
In the 1998 we purchased out first laser which was Boa Lays laser and later on we purchased a Delight and a Versa wave and then the laser that we currently use which I think is the finest laser on the market is the Boa Lady MD Turbo . When you look at this picture GD black just think about all the changes that has occurred in our profession since these days. These are antique pieces that are in our witting area. Things have really come a long way since the old singer sewing machine, foot pedal driven hand pieces and belt driven hand pieces and then along amen air driven high speeds and now the modern appotoires that we have today and we can now take it one step further by the addition of a laser.
As we start tonight I want you to open your minds and erase any pre conceived notions you may have about lasers and dentistry whether good or bad. Just open up your mind to the concept tonight. The things that we say here could change your practise forever in fact they can possibly change your life.
I want you to differentiate your practise by jumping out of the dental fish bowl, not like every other practise that is out there. We want you to catch the concepts that we will present here and run with them and for those of you that choose to do that the rewards for your effort will be great. During the next 45 minutes we’re going to talk about nothing but lasers and more lasers. Lasers are all about solutions for everyday problems. You knee every day when you and I go into the office we are faced with one problems after the other, our patients bring us those problems and from those problems we have to be problem solvers, we have to have solutions. One of the problems we battle each and every day on almost each and every patient is bacteria and one of the things that you will learn tonight is that bacteria is every susceptible to laser energy .
You just don’t see the problem if you don’t have a solution. What if all you had in your armentary was to set up forces. What would you see on every [patient? Of course you would see extractions but what if you wades a hand piece and then maybe threw in lights and some instruments and some filling material then we can see a lot more problems because we have a lot more solutions. Then if we added an indo cabinet to our raptor now we can actually think about saving teeth by doing root canals. If we added a soft tissue laser, just think of the soft tissue procedures that we can do now. All of a sudden we more problems because we have more solution and ultimately if we added an YSGG laser, an all tissue laser now we can really see solutions to all the problems that priest present to us.
Did you know that only 5 % of general dentist routine lead to osseous and soft tissue procedures? Don’t limit your practise. Rumanian chromium YSGG laser is juts the tool kin the dental tool box but what a fantastic tool it really is and who would have thought that you just couldn’t run dental practise without a laser. There are three things that will shut my laser in my office down and one is loss of air, once is loss of vacuum and the other is loss of laser. Our patients are so oriented towards laser that they just would not want to have procedures done without one.
Let look very briefly and I do mean briefly at physics tonight. Abler Einstein certainly understood that the impossible was nothing. He talked about laser mathematically woven before there was laser. The word laser is an acronym for light amplification by stimulated emission of radiation. In the room that you are sitting right now you probably have some lights in, some ordinary visible light that is multiple wave lengths, non-directional and non-focused. With the laser it monochromatic and its collimated and its coherent light. It’s a single wave length of light.
The light energy that travels from the laser itself travels via fibre optic delivery system to a hand piece and then the energy is admitted at the end of a tip .When the laser energy leaves the tip it comes in contact with the tooth and it would either reflect , transmit , hit and scatter or be absorbed and the thing that you and I care about the most is the absorption . The 2780 anatomy of wave length is the peak absorption in water and hydroxyl appetite sow when we aim the laser at the tooth it’s looking for water. In enamel there is 3%-5% water, dentin have has 10% – 12%, carouse has 16%-18%. Maybe sometimes as high as 40%.
The more water that the tooth structure has or the tissue or the bone the faster the laser cuts. The more water it has the faster the laser will cut. That’s why soft tissue cuts faster than any other tissues. When the tip is aimed at the tooth it’s looking for the water molecules. The water molecule that highly absorb that wave length and as it absorbs it expands and eventually that water molecule will explode and when it does it blows off everything that surrounds it.
One blast from the laser will leave a crater that’s about 30 – 50 microns deep into his diameter of the tip that was used. Now let’s move unto some cases. Let’s look at operative dentistry. As we go through this bear in mind problems that you see each and every day in your office. Anybody ever see an area like this? Probably saw one today? The carious extends under the tissue, we have to move the tissue back. We can think about electro surge, we can think about retraction cord door we can think about a laser.
In this case without any anaesthesia we were able to move the tissue back, access the decay, remove the decay and place the restoration in a dry environment. All without anaesthesia, without packing cord in a comfortable four hour patient.
This patient fell on the asphalt in school. You can tell by the asphalt that is still left on the initial edge there. The mother brought this patient in unscheduled and we were able to clean the tooth up, prep it with a laser without anaesthesia and then send the child back to his mom. Unscheduled patient so we sent that young patient out looking just like they hid right before the accident and you don’t think we were a hero that because of what the laser was able to do for us and for our patient .
A class three
Take the amalgam out with a hand piece and turn to the laser for a nice prep. By the way we get a 50% stronger bond when we prep with the laser than we would if we prep with just burg
We see class ones all day, every day in our practise and it’s so nice to be able to go in and do these without anaesthesia. Our patients really appreciate the fact from allusions such a and they can return to work or school or home without a numb lip.
I don’t know how many of you may use a diagnodent in your practise but a diagnose is also a laser and its works wonderfully hand in hand with the Boa Lays laser. We like early detection of the decay. 80% of the decay occurs in in the inclusion surfaces and with visual and bite wing we probably diagnose about 50%. In our practise anything that measures 20 or above on our diagnodent we fill. We like to fill it early that meets it a lot easier for us to do it without anaesthesia. By the way being even very conservative we do 80% of our restoration without anaesthesia.
When you are working on a class two you make sure you protect the adjacent tooth with the matrix band. This sis showing the Boa Lays turbo hand piece as it preps a class two. We are able to go through and do this without anaesthesia in most cases.
Now let’s talk briefly abound indo .Lets start by talking about direct pulp exposure, mixed incision and we receive a direct pull exposure in this case. As all of you know when you get a direct pupil exposure we can do a pulp cap but we usually expect in about 6 months, 12 months it will be going back and then variably do an indo on a tooth like that. With laser we can treat a direct pulp exposure a little differently. When we get the red pinpoint we can tune it brown using the laser. What this does is to sterilise the environment. Then we can place on top of that some MTA and then go ahead and place our restoration. You can see in the radiograph how deep the restoration was that we placed here. This has been two to three years now, post operatively and the tooth is doing very well.
Now why if we get a pulp exposure and we treat it with a laser is that going to be different than what we’ve done in the past .When we get the mechanical exposure we have no way of getting rid of the bacteria. Remember we talked about it in the beginning that lasers are problem solvers and so with the laser we can actually sterilise that environment before we seal it up with our restoration. That h why we see almost assuredly when we do a pulp exposure we will see success.
Lorne: We are going to go ahead and get started. Greetings to everyone .Thank you very much for attending. I want to thank you all of you for joining us this evening. We’ve had over 250 registrations as of this morning so I’m glad that I’m seem to be hitting on some topics that are of interest to many of you out there. For those of you that have been on our webinars in the past with me this one is just going to be a little bit different because we have just a ton of great info. We are going to speak for about an hour this evening. We’re going g to have at least 15 – 20 mixtures for questions.
I was talking with Don earlier and really neither one of us has to be done right at hall past the hour so we can probably go a little bit past that if we have more questions. Each of one of you should see a little box on your go to webinar control panel where you can ask questions. Just type it in , feel free to ask , make them throughout the lecture as you think about them but we’re really not going to have time to get to the questions until after we are done speaking .
By tomorrow I’m going to be sending you all a number of things you’re going to be getting a short survey as soon as you log out of this webinar .Please indicate on that survey if you want to be contacted for more information. I will be putting the webinar on the website so if you have to leave early don’t worry about it, you’re not going to miss anything. Also Amanda from my office will be sending you links to that for those of you who are on the call, you can get an hour and half of education credits as well.
I’m sure most of you know who I am already. I did practise as a periodontist for ten years, People know me as a digital dentist, I work with offices all over the country to help them make technology decisions and certainly lasers fall into that category. As many of you know when I’m put together these webinars I try to find topic that I think would be of interest to dentist . I get a chance to interact with many of my colleagues at trade shows and when the topic turns to lasers I find that many dentists out there are worried that laser just really have very limited uses. In my experience though and I have a lot of clients that are using lasers they’re telling me just the opposite , that their lasers get use pretty much every single day . One of the goals do for today was to dispel this notion that lasers are only useful for high-end procedures by highly trained dentist. In my experience probably a third year dental student can easily handle a laser.
We want to look at that, we want to look at the great h return on investments that you are going to get with lasers, look at some of the pricing as well because this really is a very affordable price. I really wanted to thank Henry Schein and Boa Lays from partnering with us tonight .They’ve really been a leader when it comes to dental laser treatment. At this point I’m going to go ahead and introduce Matt Hunt who is the director of laser sales of Hennery Schein Dental. He’s just going to say a few words.
Matt: Thank you very much Lorne. To follow up on certainly your comments earlier we are very excited and we would like to thank all of you on behalf of Hendry Schein and certainly Boa Lays for certainly taking the time to learn more about using lasers in your everyday dentistry. As Lorne said I think in the past these have been perceived as maybe some kind of gadgets and or elite type of practise that are integrated them . That certainly not the case and we have very excited, Henry Schein again and Boa Lays to have Dr Wilson share a lot of his everyday application and or procedures that he uses. Thank you again for joining and I look for award to an exciting filled hour to go over all the everyday application that the lasers can do for you. Lorne?
Lorne: Thank you Matt I appreciate that. I’m absolutely thrilled to introduce Don Wilson who is going to be presenting the bulk of the webinar tonight .It will probably be safe for me to say that Don has begotten more about lasers Thant I’ll ever know. He has graduated for the University School of Alabama School of Dentistry. He holds both a standard and advance participant certification as well as educator status through the academy of laser dentistry. He is also an associate fellowship within the World Clinical Laser Institute. He has conducted about 300 laser seminars and is the director of laser education at the National Institute in Charlotte. I’m going to turn the screen over to the Don and have him take it away.
DON: Thank you very much Lorne and welcome to all of you tonight and it’s a pleasure to be with you. I appreciate the time that you are giving us tonight out of your busy schedule. I realise that all of you have lots of things that you need to do and it’s just an honour to have you on the webinar tonight. We will be talking about the impossible, it’s nothing, the reality of lasers for everyday dentistry and I would like to thank Henry Schein. It’s a pleasure to be associated with him and with my good friend Matt Hunt. Even though Matt lives in California he’s a great Alabama fan. He’s coming down this fall to be with me for the Florida game and it’s just a pleasure to be associated with him. Thank you Lorne for allowing us to be on the program and to Boa Lays. It’s a wonderful company and appreciate the fact that we are associated with such a fine laser company.
Also a commercial for the National Institute, we do teach laser education along with cosmetics at the Laser Institute and we invite you to come and share with us. You can look at the programs that are available at national instuitute.com.
Let me give each of you a pat on the back for joining and participating in the program tonight. Your practise is about to change if you take the things that we are about to present tonight and employ them into n your practise. Thank you for seeking out this knowledge. Whether you attest use it or not you are at least looking at laser education for your practise.
In 2010 we designed a new program the impossible is nothing the reality of laser and everyday dentistry and we are going to cover portions of that thigh. We have limited time but we are going to cover just a little bit of physics and then we will cover all the procedures that you see listed there and then we will talk finally about the return in investment.
Boa Lays is really the most complete family of dental layers and featuring the new I-Lays, the pocket sized personal laser that is production right now. The Easy Lays which I use every single day in my practise or soft tissue procedures we’ll talk about that tonight. The Water Lays Sing 100, which is an economy entry level hard and soft tissue laser and of course the Water lays in the turbo which is the one that we will focus on tonight. It’s for basic and beyond dentistry.
It only lasted 12 seconds and it only flew 120 feet on December 17th 1903 at Kitty Hop, North Carolina because until that moment flying with power was impossible but on that very day it became possible and you know what has happened since that point. If we determine something to be impossible out vision for the future is blind. Orville Wright was quotes as saying “isn’t it astonishing that all these secrets have been preserved for so many years just so that we can discover them “and that’s kind of the way I feel about lasers. What a wonderful addition it has been to our profession.
Lasers are not only used or a fad or off the radar or a just a niche in dentistry. We have just seem to tip the ice berg. There will be over 4000 lasers purchased this year by dentist .It is a very rapidly growing facet of our profession. Five out of a hindered dentist now routinely use the laser. Lasers are part of everyday, every way dentistry. We use our lasers all day long every day. It’s a fact dentist who own a laser produce 25% more than dentist who do not own a laser. For those of you who would like to get in touch with me and ask any questions following tonight’s webinar, you see my email there firstname.lastname@example.org. If you would just put in the subject line “reference something to laser” I will be glad to respond to you.
Our little part of the world is in the north west corner of the state of Alabama, Florence Alabama, the home of W.C Andy the popular blues, Helen Keller the first lady of all times with disability of not being able to hear or to speak , the famous Fames Studio that was the hit recording capital in the world in the 60s and 70s and Stewart Saint who many of you know because of his fame and Goth and went into British Open last year.
We are along the beautiful Tennessee River, it’s a very important part of our culture here and this is our office and I just wanted to share this with you so that you get a concept of the guy that’s talking to you tonight about lasers. We are just in my option an ordinary practise. We practise in a rural area and I think I’m a common everyday dentist. I don’t think we have anything that’s especially exceptional in our abilities so I want you to know that I’m an in the trenches dentist just like you guys .
Our newest practise is Signature Smile. I’ll talk about the fact that later on we have had various practises through the years.
Everyday dentistry with the Boa Lays laser. We’re going to talk tonight about getting more patients, keeping more patients and growing more patients in our practise. I want you to understand this is not star was technology. I think through the years us as educators have kind of made lasers a little out there like it’s kind of an elite kind of thing. It’s really not, it’s something that every dentistry can do. This thing is not a laser sword.
Lasers do not make a bad dentist good but it will make a good dentist great. I would like you to ask yourself do you believe that doctors are really taking a serious look at laser technology these days. In dental town recently there was a survey and it was determine that 77% are treating pockets greater than 6 mm. Then it was determine 78% believed laser could be used for periodontal surgery but then it was discovered that only 18% reported actually using laser to treat perio. That means that there are 60% of the doctors out there who are seriously thinking about adding laser to their practise and I’m sure because you are on the webinar tonight you are in that 60%
Alcohol has the same effect on them directly when it’s taken in a form of cherry. We know that alcohol will penetrate the plaque. We know that it’s a wetting agent. We know that it penetrates, therefore, into the parasite, and by dissolving the acroflavein in it, we can take this protoplasmic poison straight into the body of the parasite.
The important thing about acroflavein 1 in 50,000 as a preventive used one to three times daily is that it’s not a tissue irritant, and it’s not, to a great extent, bacteriostatic. It has to be stronger than 1 in 33,000 in order to be bacteriostatic. The method we have our patients use it is to take one teaspoonful at the mouth at full strength, rinse it around the mouth for five minutes, spit out, and then don’t eat or drink or rinse for the next 55 minutes. Again, for the Torrens powder, pat it on the gingival margin, spit out all the excess, and then don’t drink or rinse for the net 55 minutes.
Other drugs that can be used for the treatment of parasites. Apart from metronidazole, tetracyclines are weakly antiamoebic. The dosage regime that we employ is two 250mg capsules twice a day, no milk products at the same time, obviously. This is continued for two weeks. At the end of two weeks, we usually examine to see if there’s parasites in the plaque. If there are parasites in the plaque or if the patient isn’t completely healed or if it’s been a very severe infection, then tetracycline 1g bid for another two months.
Another drug which is not yet completely proven is ativrin, another antimalarial, is effective most of the intestinal protozoa. We’ve used it in a couple of cases of resistant infections. In fact, ativrin, 1 tablet 3 times a day is more effective than metronidazole over 11 days with the paste. So, ativrin by itself seems more effective than metronidazole and metronidazole paste, but ativrin has unpleasant side effects.
One of the things we’ve tried to get rid of these protozoans is to go on an overkill and then to try to prevent reinfection during the convalescent phase which can last for a matter of weeks up to nearly a year.
Anybody who’s going to be prescribing any of these things should remember two things: One is the importance of a sound medical history and consultation with the physician if necessary. The second one is to be totally familiar with the drugs they’re prescribing. A compendium of pharmaceuticals is essential in this point of view.
Host: I’d like to have a little summary, again, of step-by-step process of handling a new patient. A new patient comes in, obviously the periodontal situation is very active. So, the first thing we’re going to do is tell the patient of a little bit of both the concept of parasites and say we should not prescribe anything without doing a proper testing. We could either test by using a microscope, a phase contrast microscope, to observe the amoeba, or else, we take a SAF kit to do the sampling. We take the sample, send it off to a lab. That comes back positive, you being highly suspicious, put the patient on a preventive mouth rinse. Tell me a little bit about your choice of rinse here, and the progressive treatments, maybe the mild case or the severe case just to summarize it one more time.
Dr. Lyons: Yeah. Okay, well, if we’re waiting for the results to come back, we put them on modified Torren’s powder once a day and a pretreatment rinse, which they use four to eight times a day. The reason for the fluctuation in time is sometimes they can’t keep it in their mouth for five minutes. Sometimes, they have to eat within the 55 minutes.
Modified Torren’s powder, of course, is the salt and baking soda combination which has been finely ground up. Some patients like to add flavoring to it like cinnamon. The preventive rinse is 1 in 50,000. The pretreatment rinse is 1 in 10,000. The pharmacist has a bottle of concentrate and just mixes it up using alcohol form the liquor store, which is diluted so that it’s 16%, and then he adds the flavoring.
Once, we have gotten our positive diagnosis or in the case of a severe infection, we use a pretreatment rinse to get the numbers down. We then go ahead and watch as the patient is being treated with the drug and with the paste. We got to continue with the modified Torren’s powder.
Sometimes, the patient will develop a severe reaction medically, and because of their general symptoms, they have to discontinue treatment. Very occasionally, the worst complication that we get is basically a herpetic stomatitis. If the patient develops a herpetic stomatitis and I think we have three cases in 700, what we do there is we take the patient off all medication. We get them to continue with the rinse frequently, to use modified Torrens powder (to take 3 teaspoonfuls in 4 ounces of hot water and use that as a rinse), to stop toothbrushing entirely, and to use modified Torren’s powder on their finger.
After about 5 days, it will subside, by which time the patient will have developed some sort of skepticism for the treatment so they need a little bit of hand holding. Then, they retake treatment, and when they retake the treatment, surprisingly, another herpetic stomatitis does not recur.
We’ve had one or two problems with urticarial. Generally speaking, the urticarial response ceases immediately when medication is discontinued, and this can be controlled with the use of antihistamines. However, with antihistamines, because we think they affect the metabolism of the parasite, will also slow down the rate of uptake of the drug, and therefore, prolong treatment.
In one case with urticarial, we suspect that there might be something like Endolimax nana in the patient’s system, and this is why he’s developing the responses that when he took the metronidazole, the other parasite was not as affected by the metronidazole as Entamoeba gingivalis. Therefore, this other parasite overgrew, and it therefore, developed this problem as a side effect of treatment but not as a side effect of the drug.
Host: That summarizes the treatment. After the treatment has been done, what do you follow up?
Dr. Lyons: As far as follow up is concerned, the most important aspect is home care on the part of the patient, and this involves the usual regime of home care which is effective for that patient coupled with the specific antiamoebics that we’ve previously mentioned, the modified Torren’s powder, and the acroflavein 1 in 50,000 mouth rinse. We have patients in the high risk category group using the mouth rinse anywhere from four to six times daily, normally one to three times daily and using the modified Torren’s power once daily or as they feel they require it.
The medical implications are largely speculative, but they’re based upon clinical obsevations of dental patients where there is a correlation oral parasites and systemic disease and a clue as to what parasites may be related to other diseases and an indication that this demands much more careful investigation. As far as dentistry’s concerned, I really do feel, from the research that has gone on in Russia, in France, and Germany, Spain, and Italy, and in the United States back in the 1920s and the early part of the Depression, that the case has been proven for the pathogenicity of Entamoeba gingivalis, and that many of the cases that we see in the mouth should really be classified as oral amoebiasis.
My last patient this morning actually just returned from a cross country skiing trip in the Rockies, and he’d been treated the second time around for reinfection. In January, he was clear, and by the middle of January, he goes off to the Rockies, he gets some skiing in. Everybody’s passing food and water bottles and so on and so forth around, and in spite of the precautions he endeavored to take, he knew he had the disease back again. Within five days of this, he noticed his gums getting sore and bleeding. He got back to Ottawa. He came down with a protracted and lengthy flu-like illness. He was pronounced not to have mononucleosis. It was one of the many other case reports I have labeled as a “virus”, and he would have to sweat it away.
When we found out he had the protozoan parasite, we prescribed, and I’m quite confident once he starts on this medication, the remaining of his flu-like symptoms and his extreme tiredness and frequent headaches, which he’s still experiencing, since March, will all go.
Host: This has been the pattern that has repeated itself patient after patient after patient?
Dr. Lyons: Yup. I have another interested case, a young lady. She’s 27 or so. She’d had a severe facial pain due to an occlusal problem. The slide she had had been a problem. The balancing slide interferences have been eliminated. She balanced in centric. She was balanced in lateral excursions back, and now she has severe facial pain. It seems to be centered around the center of Messina, approximately where the proglottid is, and it’s going right up her head and back up into the occipital region and down her neck and even down her left arm.
Her ECG was negative. Her plaque examination was positive for oral parasites. She started medication. No other treatment was done to relieve her pain. Within two days, she’s free of pain.
Host: You’re suggesting the proglottid was infected with the oral parasites. Is this possible?
Dr. Lyons: Yes. Now, I had another interesting case presented. About a year ago, a patient came in with her husband who had broken a tooth. At the end of the appointment, I looked at her and said, “What’s the matter with you?” She said, “I have this vague infection in my salivary gland, and I have to go see the ear, nose, and throat surgeon next week, and he says I might have cancer. They’re going to do a biopsy. It may be an infection. I’ve been really worried, and I’ve been really tired. I’ve been sick, nauseous, that is, and I’m off my food. I’m losing weight, and I’ve been really feeling worse and worse over the last two years”.
She had some of the most active amoebae that I have seen. She started treatment that night. The following day, the salivary glands were no longer tender to palpation. Salivary production returned to normal. The salty taste she complained off disappeared. Her energy and her vitality returned, and she said, when she finished her medication, that she felt better than she had in four or five years.
Host: This is over a period of a 10 day course of medication?
Dr. Lyons: This was over a period of a 10 day course of medication. Now, there were the other patients. I had a patient sent to me by a periodontist. This lady was 57. She was unable to keep her mouth clean. She said she was brushing three to six times a day and still the plaque was forming, and she complained her gums were very itchy and sore. She said, “They’re driving me crazy,” and clinically, she had a 3mm pocket. So, the generalized deterioration of the tissue and her plaque was 3+ despite the fact that she brushed quite recently, and she had amoeba present in her plaque quadruple plus.
Post-treatment, she complained of nothing in her mouth. The periodontist said she couldn’t believe how good patient’s mouth looked, and of course, the patient’s pocket had returned to half millimeter and no inflammation. The tissue looked firm, and it was firm and healthy and pink and stippled and no more symptoms. She said, again, she felt better than she’d felt in many years.
Acute ulcerative gingivitis presents in the usual way. Plaque examination reveals fusiformis, spirochetes, Entamoeba gingivalis, and large numbers of bacilli. One of the interesting clinical observations, microbiological observations, is that when we give patients local antiamoebics which reduce the viability of the amoeba, we find that spirochetes are able to penetrate the amoeba wall to get inside the amoeba, to swim around inside the amoeba, and then to exit the amoeba.
So, spirochetes would seem to be the natural enemy of amoeba, and apart from being a cause of periodontal disease, I think they’re possible out last line of defense. Fusiformis like the hyena is a scavenger. Amongst the amoeba, it has been destroyed, for example, using Torren’s powder, causing the cell membrane to rupture. Then, fusiformis will start swimming inside the carcass, scavenging it.
Host: As we know, with any infection, it is considered good policy to test the type of bacteria or whatever organism is involved and then prescribe accordingly. With a patient’s periodontal disease, it is not considered prudent, I would imagine, just to prescribe metronidazole and the adjunctive paste. How would you caution us on that?
Dr. Lyons: Yes, I would certainly caution everybody not to go jumping in to any periodontally involved patient with metronidazole and the metronidazole-Mexiform paste. Make a positive diagnosis of oral parasites first because then, when you’re asked about treatment at any point in time, you can say you’re treating for oral parasites and you proved they’re there, and there is the adequate documentation. There’s enough of the documentation, I feel, to be ample justification to treat patients for oral parasites. Then when you’re treating them for oral parasites and suddenly the disease is gone and they don’t need surgery and they only need a quarter of the scaling they needed, then you say, “We don’t have to treat you for the periodontal disease anymore because we got rid of the parasites, and obviously they caused the disease.”
Now, sometimes, when the patient has got a yeast present in their mouth as well, the yeast will overgrow and clinically, the tissue will almost look identical with a yeast infection as they will with parasite infection. So, the microscope really becomes all important, and if they have got a yeast infection, prescribing metronidazole and the paste will eliminate all the microorganisms except the yeast. The yeast will overgrow and make the patient worse.
Under those circumstances, one needs an effective antifungal preparation in order to eliminate that disease. The thing that I found that most is when oral parasites are present, we have an aggressive, osteolytic response occurring with an apical migration of the periodontal membrane, and all the typical parameters of active, destructive, deteriorating periodontal disease. It can be slowed by home care, slowed by dental care, but generally speaking, not arrested.
With medication, when we have a positive diagnosis, we can eliminate and cure the disease and get healing, which previously has been thought of as impossible. If there’s yeast there, it simply stops healing. It does not progress, but it doesn’t get any better either.
Host: Dr. Lyons, I want to ask you about again about trification. If you could just clarify your approach to them and how patient handles them with these water-soluble creams and products that you’re using to inject in the trification.
Dr. Lyons: Sure. Well, once the pocket depth has returned to normal and all the irritants over hanging margins have been removed, if there’s a persistent trification present, the important thing is it must be kept clean, and if it’s kept clean, then generally speaking, there won’t be any more deterioration. My particular pet way of keeping these clean is to use a pipe cleaner, and during the treatment, we’ll have the patient, when they’re using the paste, take the pipe cleaner and smear it in the paste through there.
So, they’re going to be smearing the paste through the gingival margin, and trification and bificaiton involvements. They’ll use the paste through there with the pipe cleaner. Once they are clear of disease, then the next important thing is prevention. Now, the routine thing we’ve done to prevent periodontal disease just doesn’t work. So, what we’ve done is to develop two reasonably effective preventive aids.
One is the modified Torren’s powder, previously mentioned, which can be used in perpetuity, at least once a day, and it should be used on a finger and not on a brush. It works by reverse osmosis, and by keeping the bacterial population down, it makes the mouth a nonconducive place for the establishment of parasite colonies.
The other active preventive, which requires no patient dexterity, is a mouth rinse, which is basically acroflavein. Acroflavein, from 1926 to 1929, was investigated along with the other essential dyes. Acroflavein was found to be the most effective amoebicide and would kill amoeba at dilutions down to 1 in 200,000. We formulated a mouth rinse which is acroflavein, 1 in 50,000, in 16% alcohol with an orange flavoring. For alcoholic patients, it’s set up straight in water. The reason for putting it in 16% alcohol is alcohol, like the barbiturates, narcotics, and particularly antihistamines, all seem to affect amoeba making them much less active and motile. They become much less active and dormant and wound up, and they seem to have a much lower rate of metabolism as a result of these drugs.
So, taking plaque, then, from the deepest periodontal pocket, I use a number six straight ended probe, and it’s moved around from the medial lingual to the medial. The plaque is lifted out and immediately deposited into the fixative, and the instrument is agitated rapidly to detach the plaque. I’ll take plaque from all quadrants of the mouth, from the worst areas, and then, the container is tightly resealed. When the form is filled out, it must be marked “dental plaque”, otherwise, at the lab, it might be mistaken for an empty container and simply thrown away.
If one is fortunate enough to have a phase contrast microscope, and in my opinion, all dental offices should have a phase contrast microscope and personnel adept at using it, then the situation becomes somewhat easier. What one needs to do is take a drop of the patient’s own saliva, not sterile bruff [31:12], not artificial saliva, not normal saline. These fluids will not provide reliable results. We must have homeogenic liquid which will not cause any distortion of the parasites.
Then, again, take drop of the saliva, put it on the slide. Take plaque from the deepest periodontal pocket, and from the base of it, deposit it down on the slide into the saliva, that is. Drop on a cover slip, and then press that cover slip down in order to squash the plaque out into the thinnest possible film. I use a double pipe cleaner, and I press it really, really hard. Sometimes, when I got too much saliva or too much plaque, it will come oozing out of the edges of the cover slip, and I just wipe it off.
Then, I make my lower power search. Now, when I do my low power search, instead of using the phase contrast condenser, which is matched to the low power phase contrast objective lens, I use the condenser which is actually matched to the high power phase contrast objective. So, on my microscope, I have 100 times low power, 1000 times high power, and that addition of one additional zero from 100 to 1000 times is important. It could be 125 to 1250, but it must be a 10 times factor. Then, you can use the high power phase contrast condenser with both the low power and the high power objective lenses. Then, on the low power, using that setup, you’ll get an apparent dark field illumination, which makes the Entamoeba easier to see, and on the high power, you’ll get a bright field phase contrast, which will make the positive identification possible.
The protoplasm is clear and non-granular. The movement is typically ameboid. Sometimes, it will be sluggish, just putting out a pseudopodium and retracting it, and at other times, it would be moving rapidly across the slide. Occasionally, they would be dormant, just sitting there and not moving. There would be a number of occlusions within the endoplasm, which are wound and look like nuclei. They are the nuclei of leukocytes, and then, the identifying factor is the Entamoeba nucleus. The Entamoeba nucleus is smaller than an erythrocyte. It’s about 4 microns across, to my recollection. It has an outer chromatin ring on which one can sometimes see the thickening of the three or four chromosomes. It has a central karyosome so that the whole thing looks like a bicycle rim with a halve, and the halve is sometimes a dark spot. Sometimes, it’s another second circle inside this outer circle.
Sometimes, one can see strands of chromatin material, which join the outer ring to the central karyosome, and it’s the identification of the nucleus of the parasite, which is diagnostic.
Host: Now, how are we going to treat this disease if the phase contrast microscope result is positive or if they report, “Yes, we found parasites in your specimen”?
Dr. Lyons: Well, here we just take a leaf out of the book of gastroenterologists and gynecologists, and parasite infection of both these body cavities are treated in basically the same way. The organism is considered to have invaded the wall of the body lumen and also to be present in the lumen itself. So, if one gives medication, which is entirely parenteral, the systemic medication will eliminate the parasites from within the tissue but will not affect the parasites within the lumen, and if one uses a local antiseptic, it will eliminate parasites within the lumen but not within the tissues. So, we need to use both.
I have used, with most success, metronidazole, and a metronidazole-based paste. The unfortunate thing about the paste is the taste. Sorry about the alliteration. So, the routine treatment that we follow is metronidazole times 30, and to minimize the side effect of the medication, the following should be employed: On the first evening, with food, one metronidazole. On the second day, again, one with breakfast and one with the evening meal. Now, the reason for bringing up the dosage to the third day, which is the full dosage, which is one of the 250 mg pills every 8 hours, is that as the parasites are destroyed by the medication, the disintegrating parasites seem to release a lot of antigenic material, which can cause quite a severe system reaction to the patient. We try to minimize these side effects.
It’s important for the patient to realize that most of their side effects are due to the destruction of the pathogenic parasites, and we’re fortunate, with Entamoeba gingivalis, that the release of antigenic material during treatment does not cause as severe are reaction as occurs with some of the treatment regimes for some of the other parasites.
The patient should be instructed that if they do become very ill, they should decease medication. They should also be instructed that they should phone in if they get any side effects. There’s two side effects that we see due to the medication alone: One is slight and transient headache, and the other one is an altered state of taste. These both disappear when the medication is discontinued.
One drug interaction which must be avoided is metronidazole and alcoholic beverages. They interact very badly. The patients don’t die if they take them both at the same time, but they’ll sure wish that they could.
Host: Could your treatment be for very bad periodontal condition and perhaps describe a case history that you’ve done, and then we’ll talk about a mild case.
Dr. Lyons: Sure. Before we do that, I think I’d better finish the pace that we use. What we have taken is 1 ounce of metronidazole vaginal cream. Then, we take 6 Mexiform tablets, which is an intestinal antiseptic and also antiparasitic, and both a drugs are antibacterial.
The Mexiform tablets are finely crushed and mixed in with the paste in order to stiffen it up, and due to the extreme bitter taste of the paste, we’ve disguised the taste by using a very strong anise flavoring. The patient will still have a bitter aftertaste, but at least it’s tolerable. The paste is applied to the gingival margin with a toothbrush, finger, pipe cleaner, but preferably with a toothbrush at least twice a day. This is done at the same time that the medication is taken. When the paste is applied, it should only be applied very sparingly. The excess can be spat out, and then, the patient does not eat or drink or rinse, of course, for the next 55 minutes. The important thing is if too much paste is used, it can be nauseating. The patient salivates excessively, and all the good which you’re trying to do is undone.
So, we can come on to sever cases. That’s how we treat a severe case, and we sit back and wait and see, how many pockets heal and at what depth they remain. After approximately 6 weeks and during the 6 weeks, they would continue with the paste and they will also have been using adjunctively, modified Torren’s powder, which is basically 6 parts baking soda to 1 part salt. Again, it has to be finely ground, and an ordinary house blender will do this.
A patient will take about a teaspoonful of this, and just pass it on the gingival margin with a saliva-wetted finger. This ideally should be done once a day. Patients on a salt-free diet should use baking soda by itself. The effect of the powder will help to keep the teeth looking with, help tooth keep the members of bacteria down, and help tissue to respond normally. Also, it will act as a partial preventive because when oral parasites come in contact with the power, they’re destroyed by reverse osmosis.
What do we do now if we’ve treated the patient and they’re back in 6 or 8 weeks later and they still have deep pockets? Well, the first thing that we do is go back again and check for parasites. If there’s parasites, they’ll then go back to medication, and before they finish the medication, they come back in and they have all the subgingival calculus removed. When I remove this, I use very fine curettes, and I always dip the instrument in the metronidazole-Mexiform paste prior to each movement with the scaler or curette. This will minimize the chances of any post-operative infection or soreness. At the end of the appointment, I’ll carefully apply a little of the metronidazole-Mexiform paste into dental areas to give us a sterile wound, which would then heal.
Now, having done all those things, one will still find that there’s a very deep periodontal pocket. They’re still on a five or a six, a triplication involvement or something like that, and it’s still wound. Take a 5 cc syringe with a 20 or 18 gauge needle, blunt the needle, and put it through at about 110 degrees. Then, fill it with metronidazole-Mexiform paste. Instruct the patient on how to inject the paste to the depth of the periodontal pocket, slowly pulling the syringe out as they fill the pocket. They should do this for a period of time until the pocket is healed, and they should do this at least twice a day and continue, during this period of time, in using the paste.
Sometimes, during this period of time, the patient will recontract the disease. The disease is contagious. It is spread by mouth to mouth contact which can be direct, which needs no explanation and indirection which can include any object which goes into the patient’s mouth which may have been contaminated with someone else’s saliva.
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.