Keystone Pathogens of the Human Mouth & Systemic Inflammatory Pathways
Keystone Pathogens of the Human Mouth...The Systemic Inflammatory Pathways That They Cause
April 7, 2022
Members: View full video here FOR CE
Our topic for this month is periodontal disease, and of course, we have no one better to start this month off than Dr. Tom Nabors he has spent over 40 years researching and developing a clearer understanding of a medical-grade definition of periodontal infections and how these infections are directly related to chronic systemic diseases.
He has many firsts in his career as well as numerous scientific awards and honors he is a nationally recognized authority on the use of DNA PCR as a critical component in both oral and general health. He is most recently the Chief Oral Systemic Officer at Direct Diagnostic Labs.
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Keystone Pathogens of the Human Mouth
I am very interested in this topic and have been for a very long time. Our topic is keystone pathogens of the human mouth. Interestingly enough, that came from a recent textbook I purchased called "the microorganisms of the human bowel." I'm going to reference that as we move into our presentation. I changed it around to discuss the keystone pathogens of the mouth because that's what we need to be looking at relative to diagnosing and treating periodontal disease. The added component is the systemic inflammatory pathways and co-morbidities that they cause.
Systemic Inflammatory Pathways
We're all concerned about the concept of systemic inflammation and all of the sources that cause systemic inflammatory pathways. I am the chief of the oral-systemic division of Direct Diagnostics.
Two Roads of Periodontal Infections
- Lost in 1936
- Causation and inflammation: Keystone pathogens and understanding the inflammatory reactions they cause
- The oral-systemic connection: IS IT REAL?
- Bringing it all together: Under the concept of collaboration cures
I asked myself a question,
"Why is it true that 80 of the American population has some form of infection in their mouth that would cause some form of periodontal disease"
So I began research that and I came across this article written in 2013 called nature yeah from nature genetics, from the Australian Center for ancient DNA [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3996550/] and what they did is they looked at 34 ancient skulls and if you look at this one here you'll notice that the teeth of this deceased individual from thousands of years ago actually look very very good. You don't see carries and you don't see periodontal disease.
Why is that true? The conclusions from their study were that hunter-gatherers had really good teeth because of the things that they ate. Yet, what we see is huge amounts of gum disease and cavities occurring throughout the next thousands of years. This conclusion we're still waging and often losing our war against oral disease. Why is that true? Because when the farming populations began to arrive there was a massive change in the foods they ate. It's true today. Our diets change shifting from meat and vegetables to carbohydrates and sugar. As a result of that so did the composition of the bacteria in our mouths.
Also made by these particular researchers: by saying we brush our teeth and we floss and we think we've got good oral hygiene but we're completely missing and failing to deal with the underlying problem. This was written in 2013 it says 10 years from now we're going to find out that the microbiome is a key part of what you get monitored for and treated for.
....well my journey started in 2001 around this particular topic. In my own practice I realized we needed to look at the differences between individuals that were healthy and those individuals had that had disease. Even in those that had disease, we've discovered that there was a major difference in the pathogenic quality of their disease.
So let's look at what the human microbiome project is telling us about the human microbiome.
We know that all of these 10 areas of our body from the outside to the inside have been mapped relative to to the types of microorganisms that we are living with. It's estimated the average person has a hundred trillion microbes as opposed to 10 trillion human cells in other words that our human cells are outnumbered by the number of 10 relative to the number of microorganisms and interesting too the majority of the microorganisms that live on us and in us are bacteria another interesting part of this discovery is that the large intestine contains the largest diversity of microorganisms and guess what the human mouth and oropharynx has the second largest diversity of the microorganisms that live in those particular areas so as we look at the mouth and oral pharynx we now know today that there are at least 770 species and again they are all designed to be beneficial and when we look at the mouth again we see that bacteria dominate even though we know they're viruses and fungi other forms of bacteria are the forms of microorganisms we also know that relative to the topic today that there are keys to understanding this infection we call periodontal disease and they're called keystone bacterial pathogens and these are the ones that cause the dysbiosis and we understand this concept where a normal flora is misarranged or created or actually goes into a different direction based on the types of pathogens that are there so they don't function properly so let's look a little closer so i've created this two road path relative to where we are and where we need to be and i say that as a profession meaning that the ada and the aap and adha tend to be lost lost in 1936 and why do i say that because we'll realize that there are two paths and the path that we're on actually originated in 1936 so our educational system today for whatever reason tends to ignore the microbiological influence on systemic inflammation and so what's the real key point here 1936 was the date that dr charles williams invented the periodontal probe the periodontal probe measures past damage but it in no way can determine the differences between health and disease it can no way determine the differences between disease patterns irregardless of pocket death and if you notice here i have a phrase an end of an error and it's certainly true it's i'm not saying we should throw away all our probes but we should make sure that the probe is not our most sophisticated biological or diagnostic tool that we use in measuring these types of inflammatory infections there are many errors that we have had in dentistry per se and most many of us have lived through them we could name them as an example one would be dental amalgam when i started practice that was the main focus of restoring teeth or gold crowns we didn't have the aesthetic capability that we have today and we could go through many areas of error ending either dental materials or the technology that we use so i'm suggesting that that the literature today says the periodontal probe as a diagnostic instrument is over and we'll discuss that so where did these phrases come from that are still used today when they came from 1936 we can't cure periodontal disease one superior patient always imperial patient i showed these illustrations here because these come from actual ads that occurred during that time frame even today when we graduate from dental hygiene school or from dental school these are the type things that we are hearing and that we're being taught it's not real periodontal disease unless the patient has at least four to five millimeters of pocket depths and in fact we're told we can't treat periodontal disease as a true infection unless we have alveolar bone loss and oftentimes we're trapped not only by the periodontal probe in 1936 but we tend to be trapped by dental insurance companies that say show us x-rays of our build of bone loss and then we may or may not actually pay you for doing these types of services again this era of these types of statements has ended based at the scientific level we just need to realize that there is another road so let's talk about keystone for a moment if you notice in the beginning we talked about keystone pathogens and it's important that we have an illustration when we look at this roman arch here we notice at the top that's the keystone what does the keystone do it locks the other pieces in place and it's a stone in which that the associated stones depend for support so as an example when we look at periodontal disease the way that we diagnose it today we look at bleeding on probing we look at pocket depths these are part of the stones in the arch and part of the things that we should be doing attachment laws staging grading history all of these are important parts components relative to a good periodontal exam the one thing that is missing and has been missing until we were able to develop clinical laboratories is this the keystone what is the keystone around all of the other stones see the keystone here is the pathogenic microorganisms that actually cause the disease and thus we connect the keystone pathogens to all of the associated sp stones that are depending on the keystone pathogens for support so let's look for relative to the literature this is a a study from microbial in 2021 so why are keystone pathogens so important in the management of chronic periodontitis and here's a simple statement and that is successful management of chronic periodontitis relies heavily on the elimination or at least control of known pathogenic consortia that is keystones associated with the disease so that changes our thinking relative to our goals the periodontal treatment and periodontal diagnosis again when we look at the literature relative to defining periodontal disease and defining periodontal therapy our first goal should make sure that the patient that we are seeing the patient that we're diagnosing and treating that we make sure that our therapy abrogates systemic inflammation this comes from a study a number of years ago by dr stephen offenbacher dr beck and others called changing paradigms in the oral disease systemic disease relationship certainly everything i've said today relative to the periodontal probe relative to keystone pathogens relative to abrogating systemic inflammation as our primary goal are certainly paradigm changes relative to our thinking in the subject of diagnosis and treatment and thus it is important for us that we recognize the importance of keystone pathogens and that we recognize our ability today to test for these the another let's say paradigm shift in this thinking is that when we are only using a probe and we're really basically measuring pocket depths and bleeding we find that these individuals have different keystone mechanisms or actually keystone pathogenic complexes they're not all the same nor are they saying based on concentration nor are they same based on inflammatory pathways so it's important that we have at least a beginning grasp that testing for pathogens is an important part of abrogating systemic inflammation when we look at this study which was a controlled trial looking at periodontal therapy and relative to good responders and poor responders the art the authors of this study came to the conclusion that we must promote a shift from predominantly pathogenic microbiata to a host compatible one what are they really saying and this is what we are saying too another huge paradigm shift and that is we must heal these infections the only way that we can really do that is to know what drives alveolar bone loss the systemic mechanisms that are associated with that because those are the same chronic systemic inflammatory mechanisms that are connected with the systemic inflammatory diseases that we are attempting to collaborate with and thus another reason that we have to be testing for keystone pathogens the conclusion of that particular trial that i made reference to said that we need to achieve clinical and microbiologic stability those of us who have been in dentistry who have treated periodontal disease particularly identical hygienists who primarily have accepted that responsibility observe they know what clinical stability looks like and we also need to recognize we need to understand what microbiologics stability looks like so why did they say that in this particular trial because they concluded after 16 months of treating these patients that roughly 35 of those patients failed relative to reducing the rate of disease in other words the disease progressed and or came back and the conclusion statements were that all of our failure relative to our treatment was due to microbiologic instability again another reason for us to test they concluded finally by saying regardless of your chosen treatment model and we do have many other treatment models out there that all therapy options will have to be validated by these parameters i may make a statement there in that oftentimes we are somewhat misled by manufacturers by saying
that this product or this procedure uh will all always achieve well i would just say to you that that is not necessarily true after having reviewed over 40 000 case samples of every form of periodontal therapy
that we do have good technology we could have do do we do have good medications but they don't always work exactly the same way for every patient so it's important that we be able to test before and after so again let's look at the literature relative to what we're doing we've had multiple studies around this as we are looking at what we are doing and comparing that to what we could be doing and should be doing and this basically is saying what all of us has have observed and that our traditional model of probing deaths attachment levels forcation mobility occlusal abnormalities habit pattern staging and grading and so forth are inaccurate in other words we need a better approach jurgen slots dr slides spent 40 years studying this particular topic and what he said is what happens by using this traditional model we end up under treating serious disease we end up over treating not so serious disease or we end up not treating at all and none of those are acceptable relative to what our end goals should be that is making sure the mouth is not a source of systemic inflammation and another particular article called the immunopathogenesis of periodontal disease that talks about treatment planning again it references what we are doing relative to what we should be doing in other words treatment planning should be based on the etiology and pathogenesis of the disease not the periodontal probe why is that true because we understand today that it's the specific puritan periodontopathic complexes that drive both the innate response as well as the adaptive response so it's important that we understand the differences in the biofilm impact that we are treating because if we understand that we'll understand more about the concept of innate response and also adaptive response again as we look at this relationship of periodontitis to one particular disease and risk for atherosclerosis and we look at an update on intervention trials what we have learned is that some periodontal treatment does attenuate systemic inflammation and endothelial dysfunction but it's go it's dose dependent what does that mean it means that the better we can eliminate the cause of systemic inflammation in other words control the dysbiosis biofilm and reverse that to a harmonious relationship between all of these microorganisms in the mouth then we will actually observe that periodontal treatment better periodontal treatment will be more associated with a higher rate of change in systemic parameters important statement there the better we do there the more effective it is relative to endothelial dysfunction and also the course of systemic inflammation so here's a study so relative to let's say the traditional model of periodontal probing and the traditional model of just using scaling and root planing how well are we doing in that and are there trials that will give us other information let's say platforms that we can base our belief systems on this particular study was called pocket closure and residual pockets after non-surgical therapy a systematic review and random effect meta analysis and so the primary aims of this particular medical analysis were to prevent tooth loss and secondly to arrest progression of periodontal disease or periodontitis i put in here not healed in other words we've been satisfied with not healing the disease if we just quote arrest the progression why is that true well we didn't know that our goal should be to make sure that the mouth is not a source of systemic inflammation but in our collaboration cures model when we are collaborating with other health care providers we need to know for sure what our goals are certainly preventing tooth loss is an important goal but we can prevent tooth loss and still have systemic inflammation so just the arresting of progression of periodontitis is not sufficient in our goals today relative to systemic inflammation when we look at this study further they looked at forty six hundred and ten papers the trials that they looked at were relative to greater than ten months follow-up they were all randomized clinical trials in systemically healthy patients i looked at all of these very very famous journals that we should all be familiar with and here are some of the conclusions so despite non-surgical treatment being considered quote ideal for treatment of parentitis we observe a remarkable percentage of pocket depth remains after therapy they could have included bleeding on probing as well and so they go on to say that whether periodontal uh pocket depths less than three millimeters is ideal for a threshold to distinguish between health and disease is still debatable let me assure you that is not debatable and you'll see one slide i have many others that we can't depend on a probe depth of less than three millimeters to assume that that area is healthy and we can prove that not only in the literature but we can also prove that by testing so let's go a little bit further based on these paradigm thoughts that we are talking about and it concludes by saying if pocket depth greater than or after non-surgical treatment in other words we haven't cured the infection is considerably unsatisfactory treatment outcomes making non-surgical treatment alone unable to achieve treatment goals well gosh you know that's what we've been taught non-surgical periodontal treatment reduce the pocket depths reduce the bleeding but it's okay to leave so how did these what was the final conclusion relative to how well we are doing based on looking at probe depths and looking at non-surgical treatment just with non-surgical treatment that is basically um you know curating and uh using removing biofilm with ultrasonics and so forth but no medications what do we find that we end up leaving one half to two-thirds of the site still infected and thus we have a consistent proportion of our patients that will be in need of additional therapy so with that as a background looking at the subject of inflammation and some of the paradigm shifts in the literature are changing relative to what we should be doing and what our goals are i've created this little model here because there are two roads and i want us to kind of look at this robert frost's point because i think that it is poignant relative to our illustration of this particular two-row example so two rows diverges in the road and i i took the one less traveled by and that has made all the difference well we were all taught to take the road most traveled and what is that road that is the road where we diagnosed with a probe and we use a classification system our design is quote our our goal is to control infection not let's not particularly cure it and in many cases we have 67 percent of our patients still infected even though they look better and there's there's zero link to trying to compare the periodontal probe and a classification system to any oral systemic relationship but what's the other road here it is it's the road of understanding dysbiosis that is driven by keystone pathogens and the inflammatory pathways that they cause this is the way we determine a true medical grade diagnosis with our goal of stopping inflammation with zero of our patients in other words all of our patients are well not infected and this is how we connect the infection that occurs in the mouth to the oral systemic world so i'd like for us to recognize that this road less travel is the road in our particular road forward in the in the subject of paranatology that is making all of the difference and testing does that well i made reference to this particular book that i um indicated in the first few statements that i had recently purchased and i wanted to introduce you to dr willoughby dayton miller dr miller was a doctor of medicine he lived from 1853 to 1907. his textbook has been reprinted because of the importance of what he did and i would also say the importance of what he continues to do well dr miller went back to dental school why'd he do that because he was so concerned about his his patients that had oral infections and he became both a dentist as well as a doctor of medicine i say that dr um miller was the first collaborator he collaborated with himself he knew the medicine side but he also knew the oral medicine side he became the first oral microbiologist and here's some statements that he made that i think are critically important relative to starting the second road the second road around microorganisms of the human mouth not the periodontal probe and here's what he says microorganisms are responsible for diseases of the teeth in contiguous part they give rise to other local and general disorders of a most serious nature it's been my endeavor to bring about a better understanding of the nature and extent of bacteritis in the human mouth of the disastrous effects which they are capable of producing and a more proper appreciation every dentist and different dental hygienist should stand up and clap appreciation of the importance of dental surgery and dental hygiene as a branch of general medicine that history is very important it almost happened the ada and ama almost joined in the early 1900s that's a different story as to why it did not happen but it's very interesting and here's the final thought in my opinion it is utterly impossible for anyone what's he saying any clinician whether you be a dentist a hygienist or a doctor of medicine or nurse practitioner or idea whatever it's impossible for us to obtain a proper understanding of the action of microorganisms in the mouth without a knowledge of at least the elementary principles lying at the foundation of the science of bacteriology we saw that microbiology today and i'm quite sure today that dr mueller would say the action of specific microorganisms in the mouth relative to the subject of systemic inflammation and that's where we are today this is the second road it's very interesting to know too this textbook was written in 1889 and dr miller started this second road long before the periodontal probe was actually invented so here's what i want to say sort of in conclusion of the two roads first of all we need to bridge them together we don't need to throw away everything that we are doing i'm not saying that at all but imperial probing is periodontology's past periodontology's future is testing because that connects us to the subject of systemic inflammation yes there's a purpose for protein to understand the history to understand how deep we need to go to understand recovery i get that but it doesn't bring us to this particular subject and the most important subject of inflammation and so i compare paradontologies past to the automobile that you see automobile was very early and i compare testing in the subject of inflammation to a tesla that's what testing is compared to the periodontal probe and we let's bridge these relationships let's use the good that we know and that's also let's add the better that we are learning so testing how do we bridge it we need to understand how testing defines causation of inflammation a little bit of microbiology and immunology and autoimmunity but more importantly what are our targets for therapy so a couple of statements here that we want to make relative to the whole subject of inflammation meaning from latin to set on fire and when we're talking about our particular subject even though there are many reasons for inflammation we're talking about invading pathogens are opportunistic microbes and that's our subject relative to periodontal disease acute inflammation is of course the good and it's designed to promote healing lasting a few days or weeks designed for protection and but in the case of invading microbes and that's what these keystone pathogens are our immune system might not be sufficient to kill or control the microorganisms that are infecting the human so that then leads us into the bad and that's the subject of chronic inflammation as we look at that in the uh the subject we see that that chronic inflammation is always out of proportion to the threat is directed against inappropriate targets it can last for years and the result is that there's more damage to the body than the causative agents we've observed that in cardinal disease haven't we and that is we've learned that it's not so much the microorganisms that cause the damage but it's the microorganisms when they stay there that create this systemic inflammatory burden that causes the alveolar bone loss that causes the endothelial dysfunction that causes these inflammatory mechanisms that are rampant when we have a source like this with millions of microorganisms from the mouth entering the bloodstream whereby that can create systemic inflammation thus causing damage to other organs as well from a biological stand point of view chronic inflammation ends up with a progressive shift in the types of cell and that chronic inflammation from any source can lead to a host of other diseases and here's an important thing for us to remember and that different microbes in the mouth create different inflammatory patterns relative to the components of inflammation there are three there's the clinical phenotype or the display there's the biological phenotype and we could define that based on the inflammatory media media mediator cytokines mmps and so forth and then there's the genetic phenotype as well all of these we can define but let's really focus on where we are today today we're focused and i always have been focused on the display in other words the clinical phenotype and if i showed these all of these are patients of either mine or my son's practice relative to defining infection if we looked at these and looked at the x-rays we would all disagree as to whether these are infected or not it would only take a one result report using saliva to confirm to us which of these infections are true infections creating systemic inflammatory pathways creating systemic inflammation that is detrimental to the host and it would it would guide our therapy regardless of pocket depth so as we look at defining periodontitis i think this is the very best the definition of periodontal disease i've ever seen it was written in 2013 but it's called it says gingival and periodontal lesions are the result of bacteria-induced inflammatory mechanisms involving dna and adaptive arms i've created a little model up there i'm gonna go through this rather fast i can see that my time is running uh kind of fast and so when we talk about lesions or wounds sometimes they're mild we see them in this orthodontic case sometimes they're very severe but the point is they're bacteria induced and if you look at the top of that slide you will see that there are virulence factors there are specific bacterias there's time and there's dose all of that's important relative to creating these inflammatory responses that are recognized by the innate response we look at molecular patterns in a minute we look at prolact receptors this is part of the innate response and we look at the adaptive arm through inflammatory pathways very very quickly uh this is just designed to say that yes we know the mechanisms that are involved and we understand this at the scientific level not that you need to understand all that but at the same time we need to recognize that diabetes doesn't cause periodontal disease smoking doesn't cause it body mass doesn't cause it all of these are background that's good background information that might change the severity of the disease but doesn't cause it neither do does genetics cause periodontal disease so let's look for a moment about cell to cell communication and the inflammatory reactions so here we have on the right side we have a defensive cell let's call it a leukocyte and we do a cross-section and we see these little projections on the outside of the cell part of it is sticking out part of it and sticking into the cytoplasm and if we look a little bit closer we can also see some of these same little projections inside the endosome here and here we see the nucleus but each one is numbered they have a different number these down here are numbered these are designed to recognize dna based on the types of microorganisms that are there these are designed to detect rna in other words viruses primarily and if you notice these red lines these red lines represent inflammatory initial inflammatory pathways leaning to leading to the nucleus of the particular cell and what is very unique about all of this is that each one of these little antenna we call them actually they are microbial sensing proteins that recognize the threat and what do they do well they transform the response by recognizing a particular bacteria or another particular bacteria they re they transform the severity of the response of the infection through the tissue and into the vascular tour and so we look at that a little bit closer based on molecular patterns these are called pathogen associated molecular patterns so there are particular molecular signatures that our cells recognize and here's an example of that so we have these pamps recognized as this column on the left then we have pathogen recognition receptors all different numbered and these are the types of pathogens that they recognize again let's look at that a little bit closer so here is a pamp in other words if we circle this here this is the molecular pattern of this specific pathogen here and here we have our molecular sensing protein and so at the end of that is called the pattern recognition receptor and if you notice this molecular pattern and this recognition receptor fit much like a key and lock mechanism so this receptor will recognize the let's say the endotoxins or exotoxins of this particular pathogen based on its knowledge of this bacteria that is innate by the way and thus it then will determine the type of inflammatory response if this is a gram-positive microorganism that is not pathogenic it will simply bring the organ or it will encircle the organism and it will kill it through the normal process but in these types of microorganisms it can't kill these because of the ability of these particular pathogens to escape the uh let's say the killing property of the particular defensive cell or this pathogen can actually invade that cell and actually live inside that cell for periods of time here's another example of let's say h pylori the other example could be let's say lps as represented by let's say pg so the point being is different numbers of total like receptors recognize certain aspects or certain um pathogenic properties of certain bacteria and create inflammatory response so as we made reference to the ability of microorganisms to be killed or not killed what we've recognized is that microbes that invade are the ones that create the most problem and they always win and how do they do that by degrading deregulating inflammation by raising inflammation and by the level of symptoms we know today that there are certain pathogens in the mouth that are called keystone that do the same they deregulate inflammation level of inflammation rises and the level of symptoms rise and we've recognized that these are primarily either gram-negative or in in one particular case a facultative organism that actually becomes the most serious relative to the most aggressive immune responses and what are they called well we originally knew them as red complex and that being aapg and tf we've grouped these together by calling all four of these red complex aapg tf and td and they are the major keystone pathogens all of us should recognize these four as the most important relative to creating an innate response that can't be stopped that can't be killed unless we control these particular microorganisms again as we look at the literature historically this is 2016 red complex as a whole should be considered as targets in the prevention and treatment of periodontitis here we look at 2022 in medical microbiology looking at actually 65 years of microbiology research and again they say these known punitive pathogens apgf and td regulate and here's the real answer to why these are so important and why the others are not and you say well tom gosh weren't you the one that bring brought out an 11 pathogen tests i say absolutely because that's what we knew in 2006 and 2008 but what we've learned today is that these regulate the empathogenicity or the inflammatory nature of the entire subgingival community so here's how that happens through crosstalk between bacterial species and the immune response per se so here's some ways crosstalk occurs between red complex bacteria and even health associated with it doesn't matter whether how many types of organisms are in the pocket it's the red complex that regulates the pathogenicity of everything that is in there even if it's considered harmless it becomes harmful because of cell signaling which is a communication from welsh one cell group to another in other words the pathogen tells the other cell or informs the other group of cells of what to do and also signal transduction a very similar model here's one that's really important too these red complex bacteria share their genetic virulence with everything that is there through horizontal gene transfer either through conjugation or transduction or through transformation what's really important i guess in all of this conversation relative to red complex is how they transfer their virulent properties to the entire flora that is there and so in a sense everything that's in the mouth or close to these red complex bacteria become pathogenic but what we also know is that can be reversed when we reverse the red complex complex either by killing them all or reducing them to a host acceptable level quorum sensing when we have uh biofilm uh quaran since extension is a very unique way platonic bacteria have a difficult time doing that through nutrient exchange if you look at this uh very high powered microscopic view you see these nanotubes where these bacteria share even food to keep them alive and then of course the epigenetic factor these bacteria can invade any type of cell whether it's an endothelial cell whether it's a colorectal cell whether it's an epithelial cell whatever these microorganisms are invasive and so when they live inside these particular cells they create an inflammatory network so other things we need to know about red complex is it down regular down regulates the biological processes of blood coagulation and hemostasis thus to secure some of the nutrients such as iron that are important relative to keeping this biofilm alive that it wants to survive but here's the real key thing that we really need to recognize and that is when we remove red complex this genetic transfer stops and those microorganisms that are present now convert back to health associated species that's really important that's really what we want to have to happen another thing that reference to a paradigm probing in less than three millimeters a really important study and there are many others relative that and that is pathogens may be present in high levels and proportions in shallow crevices of paradise patients challenging the notion that they should not be treated during therapy also goes on to say this data shows systemic antibiotics had positive effects by reducing pathogens in both shallow and deep sites now i want to say a point here unfortunately in our profession there have been some that is saying never use systemic antibiotics let me just say that's not scientific truthfulness there those are individuals that are trying to sell products it is true using inappropriate antibiotics that don't target these specific pathogens are trying to use antibiotics alone does not work but when you use an appropriate therapy based on planktonic microorganisms research clearly shows not only does the systemic antibiotic remove the pathogens in the deep pockets it does it in shallow pockets as well and more importantly it reaches the systemic world there's nothing else that we can do that can reach the systemic world like systemic antibiotics now having said that i'm not saying that every patient should have systemic antibiotics if you can treat them without systemic antibiotics and you have a before and after test that shows you've removed the harmful red complex bacteria then that's great but please do not believe that that you should never use systemic antibiotics as i'm saying that is not scientifically accurate so let's look at the gold standard for what we should be doing and that is we should be using microbiological analysis and antimicrobial therapy that's not me saying that the literature has been saying that since 2002 for the past 20 years and yet we see practitioners traditionally have chosen treatment based on personal bias i'd also say based on manufacturers also based on our educational system our educational system did not give us this type of information so using microbiologic studies that have been verified by rigorous clinical trials is the reason that we use microbiological analysis now i'm going to go through this rather quickly because i realize that my time is getting short i do want to leave a few minutes for um questions but if you don't this is so important i hope that you take a picture of this this is from nature reviews immunology february 2021 and it's important relative to local and systemic mechanisms that link periodontal disease and inflammatory co-morbidities and i apologize for not being able to go through all of this but i think it's important that we recognize that the review aims to substantiate that the mouth body link is not simply a consequence of common risk factors that's very important and i think that we need to recognize unfortunately our ada and rdha and the aap are looking at periodontal disease in the periodontal or oral systemic relationship as common risk factors literature clearly says it is not a consequence of common risk factors but it's in fact driven by multiple microorganism-induced inflammatory or immunological mechanisms that converge to increase the susceptibility of patients with periodontitis to non-communal chronic inflammatory diseases and so i'm going to go through this sorry i apologize time wise so how do these bacteria get to the rest of the body through the blood through or digested through oral pharyngeal to reach extraoral sites and as a result of that the inflammatory nature of the entire body changes and thus we have to understand that we understand most of the mechanisms now around periodontal comorbidities as a modified risk factor for life-threatening disorders built all around this subject of inflammation now this is important but i'm sorry i don't have a lot of time to spend on that please pull that article but it's very true that successful treatment of periodontal disease can reduce the risk or incidence of epidemiologically associated disease but the literature is lacking why because we rarely treat periodontal disease successfully in these clinical trials what are they doing they're using scaling and root planning to compare systemic inflammatory markers and other mechanisms around an unsuccessful periodontal treatment model we have known this for years so we need further improvement in our treatment so testing is not just about learning the cause of systemic inflammation and the cause of alveolar bone loss but it's important that we recognize that we need to treat periodontal disease on a personalized basis and we have ways to do that again look at what they say here at the bottom targeted therapies against specific periodontal therapies such as p-gingivalis and and fusobacterium nucleotides are their key virulence factors see that's what we have been recommending now those of us who have been following this research now for a long time so why because it's beyond the power of mechanical therapy alone to eradicate these pathogens so as we look at this a little bit further what we realize is that the physical removal using curettes and ultrasonics and so forth without appropriate medications whether they be local systemic whether they be trays or whether it be lasers whatever your choice
in many cases is only a brief reduction in the colonizing organisms and the total bacterial mass and thus these can be restored in three or two to seven days in conclusion from another study published in late 2021 scaling in root planning fails to eliminate the tested pathogens so what are we trying to do today when we're trying to link periodontal disease again you'll have to look at this little illustration a little bit closer as we look at the types of diseases and the source of periodontal disease connecting and we tried to in the literature connect the clinical signs of periodontal disease to breaching the blood-brain barrier through bacterium through oral digestive but it's not clinical signs it's testing that links all of this it's these bacterial links that not the clinical presentation so let's use what we are doing relative to periodontal probe for getting information but let's test because this creates truly the world of difference and understanding the subject of the inflammation let's stop seeing patients that like this every six months let's be able to here's a uh a a a an example just very quickly and i look at my time here very quickly how we can target infections this patient had been treated three previous times unsuccessfully two times in a general practice one time in a periodontist office and it was determined they could not heal this they would have to remove this tissue and do a graft so all we're going to target and if you'll notice this is 11 pathogen test but we're not worried about all the rest of them the orange or the green at all why this is our target right here a a that's our primary target we're going to target tf and td secondarily but here's the patient literally two weeks later look at how targeting those pathogens in very minimal non-surgical treatment no grafting no surgery and look what happens to the entire micro floor not just the red complex but look what happens to the orange by targeting the red we control the orange as well the pathogen burden is almost eliminated when we eliminate the red here she is one year later three years later four years later and here's our first and second report and all she had basically was trophies for the first year of every three months then she was moved to every six months she didn't need to be seeing a dentist or a periodontist every three months diabetic patients one of my patients i can't show you the entire case but we need to be looking at this patient as a potential heart attack or potential stroke same thing is true here implants i was asked to confer with that this was the infection this patient's already had a heart attack we need to co-manage these patients and sadly we're just now starting to test and what we're learning here over the past year is that it really has been a real revolution an evolution in those that want to start testing many people now in many offices are testing so here's an older test that i started with out of germany and look how we are able to eliminate these red complex bacteria it reduces risk we can tie this into cimt we can tie this into systemic inflammation we can tie this this is one of the very this was 2005. one of the very first tests a patient been in had been sick for for 35 years we finally recognized she was infected with aaa by testing so just briefly we need to understand that it's just not this local inflammatory reaction that we are really looking at we're looking at systemic pathways particularly to like receptor four that connects us to the io17 pathway why is that important because il-17 cells do damage to endothelial cells epithelial cells fibroblasts macrophages dendritic cells chronicites and osteoblasts creating many different paths of inflammation creating different types of cytokines and mmph's a and pg are the worst of that and when we look at setting in motion periodontal disease sets in motion the most dangerous uh inflammatory pathway that we have called the il-17 pathway and it's associated with pathology in all of these diseases from autoimmune diseases to r.a to multiple sclerosis psoriasis crohn's systemic lupus asthma and hyper immigration e immunoglobulin e so the point is we can stop in the ielts 17 pathway there are drugs for blocking that that some of our medical colleagues are using and there's been talk about creating drugs for blocking inflammatory pathways for predominantly but we don't need to do that all we need to do is block these keystone pathogens we don't need to give patients different medications to interfere with their inflammatory pathways we need to just kill these pathogens out so here's sort of my ending here let's move periodontal medicine away from 1936 from this left side to the 21st century let's stop inflammation target causation let's heal these diseases and so here's the takeaway know what the keystone pathogens are and that that they drive aggressive inflammation they are the causative agents of periodontitis these ones link to the systemic comorbidities the periodontal probe has a place but it's a classification system it is not a medical grade diagnostic system only through a clinical laboratory salivary test can you get a medical grade diagnostic so please consider start testing so here is my information dr tom neighbors gmail.com here's my phone number 615-879-3739
it has been a genuine pleasure for me to be presenting tonight i wish i could meet all of the wish i could see all of you one of these days let's um let's meet each other please give me a telephone call if i can help you or email me in any way so again thank you very much for attending tonight
thank you so much for coming here tonight we do have quite a few questions um okay with you i'll go through a few of them and the ones that we don't get to um i will work with dr neighbors this week to get those answered and we will send out an email with the recording of this and the answers to all of your questions um so let's go with this one real quick is how do we find out how to treat these specific red pathogens without scatter therapy a very good question and i would just give our team a very very big big shout out because along with our laboratory we recognize that we needed to create a model where we are targeting these microorganisms and we could we can actually use practically any model that you are using all we want you to do is use a first test and a second test and then in the second test if you haven't achieved the end result then we'll guide you through a a model that can help you achieve that result so contact me or contact directdiagnostics.com
and then we'll make sure that we can help you in every way achieve an end result that achieves the goals that we are trying to achieve um and then i'll do one more what are practices using to test the pockets and the bacteria well of course salivary diagnostics is the key we started out using subgingival in other words gingival curvicular fluid back in 2001. the studies clearly show that saliva is as accurate and even more so than sub g at times but for those that are using subgingival and you want to use a saliva test all we do is is we we gather one milliliter of saliva in the tube but if you want to also put some paper points in there from the gingival curvicular fluid that's fine too so we can test both ways we just need a little bit of saliva so our laboratory of course is the most modern one and we have achieved some let's say real breakthroughs in that there are other laboratories out there that are doing that but i'd be happy to help you with that if you would like and what are your thoughts on the period trade delivery system perio protect trade delivery system prayer protect trades are a great delivery system the problem that we are confronted with is the subject of testing and what we have learned is that there is no perfect model uh for treating every patient we have certainly seen good
a lot success that has to do of course with the individual it has to do with compliance it has to do with other issues that are facing the patient so yes we support as a as an individual i support and as a laboratory we support all the models out there we're not saying that there's only one way to treat what we are saying is use a person second report and when you discover that some particular patient isn't responding as well we can certainly help you with that