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Transcribed by Anam Khalid Monday, November 3rd, 2014

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Clinical Assessment and Epidemiology of Periodontitis by Dr. Steven P.

Engebretson & Periodontal Therapy I: Treatment Planning and Diagnosis

Diagnosis and Treatment of Oral Disease

[Slide #1] [Health, Periodontitis, Gingivitis]

[Dr. Engebretson]Aright, lets get started. So, we have a double-header today.Theres me now and were going to talk about risk factors and epidemiology ofperiodontitis. And well go into a little bit of depth about what is a risk model andwhy risk factors are important to know about and how that can help healthcare. So

the real question is how do you go from, you know why do about half of the adultsin the country have a healthy periodontium? Almost everybody gets gingivitis from

time to time and why do the ones who get advanced periodontitis get advanced

periodontitis? Is it something that they can do something about? Or are there

certain traits that are associated with this disease?

[Slide #2] [Risk Factors and Epidemiology of Periodontitis]

[Dr. Engebretson]So again, heres my email down [email protected] youhave any questions about the material today.

[Slide #3] [Study question:][Dr. Engebretson]So one of the fundamental questions is who gets it? Who getsperiodontitis? Does everyone get it equally or are there certain subgroups that are

more prone to developing periodontal disease. And periodontal disease, keep in

mind, thats, gingivitis, periodontitis combined. Were going to talk primarily aboutperiodontitis today.

[Slide #4] [Wilson and Kornman 2nded]

[Dr. Engebretson]Heres some things to read about if you like to read. Wilson andKornman is a great chapter I dont know if theres a new edition of this out. I thinktheres a 3rdedition. Carranza almost any textbook that you choose to purchasewill have a nice chapter on epidemiology of periodontitis.

[Slide #5] [N/A][Dr. Engebretson]So just a review, you know, everyone starts out healthy.

[Slide #6] [N/A][Dr. Engebretson]Then develop some sort of a change in the subgingival microflorausually from a gram-positive to a gram-negative type.

[Slide #7] [N/A][Dr. Engebretson]And I like this slide because it shows you what is going on underthe pocket. But this is a nice book its really expensive but it has nice pictures in it.Rateltschak published this in the Thieme in Germany. But anyhow, these subgingival

microorganisms release toxins that can activate your immune system. Certain white

blood cells become activated and release cytokines that can tip the balance in favor

of bone resorption so the osteoclasts become active and youve heard a lot about
mailto:[email protected]:[email protected]:[email protected]:[email protected]

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[Slide #9] [N/A][Dr. Engebretson]Its easier to see when you get in clinic, you can see it from acrossthe room practically on the viewboxbone loss. Heres a healthy person. Heres aperson with bone loss.

[Slide #10] [Fundamental concepts ][Dr. Engebretson]So were going to talk about epidemiology. I know some of youhad some of it and others have had less of it so well all get on the same page. Welltalk about risk and what we mean by risk. The epidemiologic term risk rather than

some other field.

[Slide #11] [Epidemiology, epi (upon) ][Dr. Engebretson]Then specifically what are the risk factors for periodontitis. Sowhen you get into clinic, your antennae will go up if a patient, in their healthy

history, that leads you to believe that theyre going to be at increased risk for

periodontitis.

So what does it mean? You know its a Greek work, I guess. Epi is upon, demos, thepeople study of the disease distribution within the population. Its reallyimportant for lcinicals to understand what risk factors are for any given disease

when we meet patients and assess patients. And were readingthis is probably alittle old now but its a really well-written chapter on the epidemiology ofperiodontitis. Much more exhaustive then we could ever cover today. Its about 36pages. And you can find it in the Annals of Periodontology, Volume 1, No. 1. You can

buy it online on Perio.org. Or find your friendly local graduate student who may

have a copy he can lend you.

And theoretic epidemiology, and you want to go beginner textthis is commonlyused in pH programs around the countryGordis, Epidemiology, second edition. Itsonly about this thick and it costs about $35 and its really, really good.

[Slide #12] [Definition][Dr. Engebretson]So anyway, epidemiology is the study of the distribution and thedeterminants of health-related states or events in specified populations and the

applicationthis is importantand the application of this study to the control ofhealth problems. So all the studies in the world wont make any difference unless weapplied what was learned to the population in terms of interventions and health

management.

[Slide #13] [Objectives of epidemiology][Dr. Engebretson]So, heres the objectives. First, identify that the causes or theetiology of diseaseso thats important. And second, to determine the extent of thedisease found in the community. What kind of disease are we dealing with? Do many

people have it or a few? And then thirdly, its important to understand the naturalhistory or the prognosis of a disease. and fourth, evaluate existing and new

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preventive and therapeutic measures and modes of healthcare delivery. So, knowing

who has certain etiologic factors can help us to design therapies and preventive

measures and then finally, all of this informs public health policy and decision-

making. And some of you may go on to become policy makers yourselves. So watch

out you may have to this may becomes very important to you someday.

[Slide #14] [Incidence][Dr. Engebretson]So just some fundamental concepts, what is incidence? Incidenceis the equation of the number of new cases in the numerator that occur during a

specific time. Divided by all the persons at risk of developing the disease during that

time period. And its usually expressed as new cases per 100,000 persons per year.

Okay, thats incidence. The number of new cases that occur over a time.

[Slide #15] [Prevalence][Dr. Engebretson]Versus prevalence. Which is the frequency or a number of cases

of a disease that can be identified within a specified population in a given point intime. So prevalence is like a snapshot of how many people have the disease in a

given population at that time. Okay?

They always ask these questions no matter what exam youre taking whether its aboard exam or a NERB or a so people get tripped up on that. So

[Slide #16] [Mortality][Dr. Engebretson]Mortality we dont usually think of mortality in dentistry but,just for your education, the mortality rate is the number of deaths in the population.

Its sort of the disease burden and when you read when you pick up the Timesand

you read about some new outbreak whether its SARS or Ebola, theyll often talkabout deaths over the number of people exposed. And they call that a case fatality

rate. So, does anybody know the case fatality rate for Ebola currently? Anybody?

Anybody? Theres a hand down here. Seventy. Yeah, in the United States orwhatever area so. Has to do with a lot of things: access to care, and things likethat. But yeah, mortality rate of about 70% so yikes. Thats a dangerous disease.

[Slide #17] [Risk Factor][Dr. Engebretson]Okay, so what is a risk factor? Its an aspect of personal behavioror lifestyle so its something you can do to yourself or something that happens toyou while youre out and about. An environmental exposurecould be something

you have no control over. Or it can be something youre born with. Inherited,genetic. Any of these things can become risk factors for disease.

[Slide #18] [Criteria for Causality][Dr. Engebretson]As opposed to causality, we talked a little bit about this last time,heres what needs to happen for something to become causal. And by the way, aword of caution, causation in epidemiology, there are strict criteria to say that this

causes that. And you really have to go through the hoops to be able to establish

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causality. Does anybody remember when they finally determined that cigarette

smoking causes lung cancer? You guys think that everyone knows that, right? But it

took decades for that causative pathway to be established. But obviously there

needs to be so these are the things that are criteria for causality that you appliedto anything in even when you think about what are the causative factors of

periodontitis. There has to be a strength of association. That is the more of theexposure of this risk the stronger the association needs to be. And, in other words,

the more of this exposure that occurs, there should be more of the disease occurring.

And the exposure to whatever factor that is should have happened before the

occurrence of the disease.

Finally, studies from different populations should show consistent findings.

Also estimate biological sense. So there has to be some sort of plausibility to this

causation. And then finally it has to be specific. So, if removing that factor lessens or

mitigates the association of the event, which is one of the powerful things aboutrandomized clinical trials where you can isolate a particular factor through

randomization, modify only that factor and if the outcome of interest is mitigated

then thats a strong evidence of a causal relation.

[Slide #19] [Risk Factors for Periodontal Disease][Dr. Engebretson]And Ill give em to you right now. We dont need to draw this out.Theyre pretty well-known. Microbes and certain microbial factors--and youll haveother lectures about thatare strong risk factors for periodontal disease. Microbescause periodontitis but were talking about specific microbes. And there have beensome publications that declare certain of the pathogens to be causative for

periodontitis, although that can be debated.

There are genetic and heritable factors. So when you get into clinic and you get a

patient that has periodontitis and you ask does your mom and dad have bad teeth or

wear dentures at are early ageyou know, invariably, you hear this, it runs infamilies. Do we have a genetic test, no. I wish we did to find out who is at more risk

and this is an area of active investigation for those of you that have that

investigative bent. Fruitful ground for future discoveries.

Smoking. Do smokers get more periodontitis than the non-smokers. The former

smokers have more periodontitis than the never-smokers. So, smoking and the

neat thing about smoking well I dont know if its the neat thing but smoking is amodifiable risk factor and well talk more about that.

Diabetes. People with diabetes have more periodontitis than people without

diabetes on average. Both type Is and type IIs.

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And then what about age? Older persons seem to have more periodontitis. Is that

caused by age or is age a risk factor for it? And I have a little question mark there

because well talk about that in more detail.

[Slide #20] [Historic Overview]

[Dr. Engebretson]And so, the idea of talking about etiology and certainlyepidemiology of periodontitis, I think I mentioned this last time, its a moving target.Fifteen years from now, it might be a different lecture. Fifteen years ago it certainly

was a different lecture. So, back in the 60s, in this very room, people learned things

that if you have poor hygiene, youll get periodontitis. And if you get periodontitis,you will lose your teeth and you will get a denture. And thats it. Its sort of a factorof age and oral hygiene.

Longitudinal studies done in Sweden in the 80s show that thats not necessarily thecase. That even if you have periodontitis, many of the areas in the mouth are not

active. That is, just because an area had a pocket doesnt mean its going to always

progress to a deeper pocket. So and then relatively few of the sites in the mouthactually progress in a given period of time. So not everyone who gets it gets worse

and not everyone who has poor oral hygiene automatically finds that they break

down. And then studies done by Sid Sokransky, who was a famous oral

microbiologist that did a lot of really highly regarded science in his career. He

passed away about He did some longitudinal studies that showed that it tends tooccur in bursts and it was episodic. So patients will go and itll be very quiet andthere will be no progression of periodontitis for a long time and then unknown

triggers occur and new pockets develop, new attachment loss occurs. So the idea

that its not a continuous disease, its episodic in nature has changed the way welook at it.

Also depends much on the methodology and how we measure periodontitis in the

population that determines what the prevalence is.

[Slide #21] [U.S. Prevalence of Periodontitis: 1999][Dr. Engebretson]So, for example, this is the National Health and Nutritionalstudies that are done periodically are meant to sample the population so that it

could be generalized to the nation. So its supposed to be a representative sample ofthe population which you want because this data sort of tells you about whatshappening in the country. Of course, its going to depend on what part of the countryyou live, what kind of community you practice in But in 1999, in adults over the

age of 30, the prevalence of advanced periodontitis on average was about 3%.Doesnt sound too menacing, right? 3% of the population. How about 10% atmoderate periodontitis and about 21% had mild periodontitis. So, that leaves 65.5%

with no periodontitis at all. So thats a good thing, right?

Well, there were issues with this particular sample and this was from the basis of

what we say and what we think and, like it or not, the way third-party is paid and

the way peoples refer patterns occur, so but this type of survey had important

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issuesthat is, there was sampling of the mouth so that the entire mouth wasntexamined, only index teeth in specific quadrants. So, theyre big studies, I forget howmany but theres usually 4 or 5 thousand examinations that need to occur. If youcould do only half the mouth and then extrapolate that thats the way it is thatsgoing to save you time. Its very expensive to get all these examiners together and

get them to examine all these people. And so these sampling methods have beenused in the past. However, theyve always been criticized as not being entirelyaccurate. And so a group sort of rallied and petitioned that the NHANES should

include a full mouth of periodontal examination. So every tooth in the mouth

present, six sites per tooth, probing depth, recession, you know, bleeding score and I

think they did a calculus measure.

[Slide #22] [Table 2][Dr. Engebretson]So about 10 years later, this was published. And you can look thisup. Its in the Journal of Dental Research 2012. So the citation is down here for you.Interesting detail about the population of the country that has periodontitis, and by

age group, and it only samples adults over the age of 30 and for dental reasonswhyperiodontitis is very, very infrequent under the age of 30. But broken downby gender, race, ethnicity, education level, poverty level, marital status, and smoking

status. So, another thing to think aboutprevalence depends on how you define thedisease. so, if you define periodontitis with a very low level of loss of clinical

attachment, relatively more individuals will be positive. For example, here, if youreover the age of 65 and the criteria for disease is attachment loss greater than or

equal to 3 mm, in more than 96% of adults, over the age of 65 had periodontitis by

that definition. If, on the other extreme, you define disease as presence of

attachment loss greater than or equal to 7 mm, and it doesnt seem like much but onthe periodontal probe thats a long distance to jump, then only 25% have

periodontitis as defined by the 7 mm jump.

[Slide #23] [Table 1. Prevalence of ][Dr. Engebretson]Lets look at this in a little more detail. These are distributed soyou can look them up on your own and see the little numbers but down here dontforget to check out smoking. So if youre a current smoker, 64% of adults haveperiodontitis compared with non-smokers, 39% have periodontitis. And when the

whole mouth was probed, as opposed to the exams I showed you before, 47% of

adults over the age of 30 had periodontitis, which is very different than what I

showed you beforesomething on the order of 20 to 30%. So, this study made bigheadlines in the periodontal community and it really changed the way we think

about prevalence of periodontitis in the country. And you can go through some ofthese risk factors.

Turns out males get it more often than females. There are some ethnic contributions

here. Seems that blacks get it more than whites. Mexican Americans have it more.

Education level has something to do with it, you know, more than high school39%have periodontitis. Less than highschool, 67% have periodontitis. Poverty level has

something to do with it. Etcetera, etcetera. Marital status, I couldnt figure this one

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out but if youre married you have less periodontitis and if youre widowed you havemore. If youre divorced you have aboutbreak even. If youre separated, you havethe most. And of course, the smokers. So, I guess, if youre divorced, smoking,Mexican, male you can see where this goes. On the other hand if youre rich,educated, married and white and the rest of it so everyone that walks through

your door is going to be a little different.

[Slide #24] [Prevalence by age][Dr. Engebretson]This is a nice graph from that paper. I like it because it just puts itout for you. Heres over the age groups, 30 to 80. Heres with a low diseasethreshold, by the end of life, virtually everyone would have it at a low disease

threshold than a higher disease threshold. It peaks out at about 20% or so. But look

at this one herethese are overall rates of classically defined mild periodontitis,moderate periodontitis and severe periodontitis. And the severes, you have very few

30-year-olds have severe periodontitis. Its still very infrequent but by the timeyoure in your 50s and 70s, about 10% of the population has advance periodontitis.

And when you see these cases youll understand why its significant. If you haveadvanced periodontitis, you need generally a lot of treatment, a lot of dentistry.

Whereas the moderatesmost people are moderatesthey wind up with moderatedisease and they stay with moderate disease, so interesting table.

So thats the most current epidemiology of periodontitis in the United States. About10% have advanced, about 30% have moderate and about another 10% have mild.

So about a half of adults over the age of 30 have some form of periodontitis.

[Slide #25] [Early Onset Periodontitis in the United States of America][Dr. Engebretson]And I mentioned the kids the data on juvenile periodontitis or

early childhood periodontitis is difficult because the rates are so lowbelow apercent. So, you know, on average you can probably think of children as being at

very low risk or its very, very infrequent for children to have periodontitis. But ifyou ever go on pediatric rotations or hospital rotations, wherever you get the

chance to see a case of early periodontitis in a teenageryou do see it. It can bequite dramatic. But its very infrequent in the population and unless you work in ahospital or in a pediatric, large group practice, youre unlikely to see these casesoften.

Of course, if youre anorthodontist thats one of the reasons you get per-operativepanoramic on a kid because if you get one and you need to know if the patient has

bone loss around the teeth before you start having mom and dad start paying ahundred dollars a month for the next 4 years for those braces.

[Slide #26] [NHANES III][Dr. Engebretson]So what about age? Back to this. What happens withperiodontitis over time? You know, remember we talked about hard outcomes and

clinical research? Well, tooth loss is a hard outcome. What happens to teeth in

patients with periodontitis over time? They lose teeth. If you lose the tooth, its no

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longer at risk for periodontitis. So the incidence rate could actually drop. You see the

relationship? Prevalence goes up over time because periodontitis is largely, mostly

irreversible. So once you have loss of clinical attachment, you have it. And if you get

it again, you get more. So, it accumulates over time, generally. Whereas tooth loss, as

it occurs, mitigates some of this because if you lose a tooth, your attachment levels

go down. So the bottom line is age, in and of itself, is not a risk factor forperiodontitis. And so its been shown with the incidence of periodontal attachmentloss over the age groups is relatively consistent. The only reason you see it in older

age groups is because its cumulative. So theres a if the incidence is constant, andteeth are not lost, the prevalence increases. You know some teeth are lost so the

prevalence doesnt go up dramatically. But thats why age is thought to be a riskfactor but its not a true risk factor in that sense. Are you recording that?

Age is inevitable, by the way. I dont think you can get out its not a modifiable riskfactor.

[Slide #28] [Risk Assessment][Dr. Engebretson]Unless you go to one of those Swiss clinics where they inject youwith stem cells and whatnot. Okay, so what about risk assessment? How do we

assess risk in the population. And first of all we have to identify the risk factors.

Then you develop a risk assessment model. You assess the population. And that

allows you to target these populations for treatment.

[Slide #28] [Odds Ratio][Dr. Engebretson]And youve got some common things that you can note is theodds ratio. Often, risk is expressed in terms of odds. So, lets take a hypothetic groupof patientstheyre either diseased or not diseased. And theyre either exposed or

not exposed to the risk factor. And if you take the ratio of all the diseased or exposedversus all the diseased and not exposed, it gives you an equation of something like

this. In other words, its ad over bc. So its a cross product. That gives you a numberand thats called the odds ratio.

[Slide #29] [Odds ratio][Dr. Engebretson]And so, just plugging in some hypothetical numbers here where300 individuals, 155 are exposed to the risk factor and have the disease and 80 are

not exposed to the risk factor and do not have the disease. and if you multiply by

these two and divide by these two, you get a odds of about 12. So what that means is

that if you are exposed to the given risk factor, in this model, your odds are about 12

times as high to have a disease.

[Slide #30] [Odds Ratio][Dr. Engebretson]And sometimes its a cohort study where they follow it over timeand thats an odds that an exposed person develops the disease. lets say you took athousand smokers and a thousand non-smokers and you followed them for 10 years

and you measured periodontitis and tooth loss over time. And the exposure in that

kind of situation would be smoking. Okay?

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In a case control study its the odds that a case was exposed case control study canbe done as cross-sectional studies, cohort studies are populations that are followed

over time.

[Slide #31] [Identify ][Dr. Engebretson]So, basically it helps you to understand whether a disease Israndomly distributed or there are certain factors associated with the disease

occurrence.

[Slide #32] [Develop a Risk Assessment model][Dr. Engebretson]And in the end, once you know all these risk factors so I was we were giggling about what if youre a rich, white, female whos well-educated andyou have all these kind of risk factors you can come up with a model where itllgive you something called the r-squared coefficient. That is, its a way to explain theoccurrence of a disease in a population using these risk factors. And so each of these

factors, x1, x2, and x3would be explanatory for, say, smoking economic factors, sex,and so on. So thats called a risk assessment model. And risk assessment models canbe very powerful because they can help you to devise tests for risk.

[Slide #34] [Assessment of the model][Dr. Engebretson]And the assessment of a model allows you to screen thepopulation for a disease that may have these particular risk factors. So Ill give youan examplepeople with diabetes have a 2 to 4 fold risk for having periodontitis. Soyou might think that screening for patients in a periodontal clinic could be an

effective way to assess for undiagnosed diabetes in a high-risk population, for

example. Or a smoking cessation clinic, you might see higher occurrence or higher

prevalence of periodontitis and that type of thing.

[Slide #34] [Screening][Dr. Engebretson]So, some of the terms. Youre all familiar with screening. Youknow I think Wallgreens has the blood pressure anyone can screening for bloodpressure is an extremely efficient way of helping to intervene on some patients who

are at high risk for heart attach or stroke and kidney disease, among other things. A

blood cholesterol screening can be a very effective means of identifying individuals

at high risk for myocardial infarct. And youll read about the controversiessurrounding mammography for everyone. At certain age groups and whether these

are efficient utilizations of our healthcare resources. So these things youll read

about it all the time. Tuesdays in the Science Times when the correspondents areevaluating this or that study.

Colonoscopyis that an effective means for assessing risk for colon cancer. So,polyps, does that so theres always a cost of a test, accuracy of a test, and what itmeans.

[Slide #35] [Screening]

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[Dr. Engebretson]So, when you screen someone, and they either have the diseaseor dont have the disease, there has to be some kind of gold standard for who has thedisease. And your test, your diagnostic test or your risk test can be positive or

negative. So someone who tests positive with your test could truly have the disease

or they could be a false positive. And in the same token, if you test negative for a

disease you can be a true negative and not have the disease or it can be a falsenegative.

[Slide #37] [Screening][Dr. Engebretson]So you get these terms called sensitivitythat is how good is thetest. Its just a ratio of all the true positives divided by all those with the disease.Thats sensitivity. Is it a sensitive test? And a specific test is all the true negativesdivided by all the non-diseased. So if its specific, it identifies those who dont havethe disease. If its sensitive, it identifies those who do have the disease.

[Slide #38] [Screening issues]

[Dr. Engebretson]Okay, and then theres something else called sensitivity andspecificity of a test. Well what does that mean for your patient and theres acalculation called

[Slide #39] [Positive Predictive Value][Dr. Engebretson] the positive predictive value. And that means whether yourpatient actually the odds that your patient will actually have the disease.

[Slide #40] [Screening][Dr. Engebretson]And, for example, we mentioned that it depends on theprevalence of the disease in the populationif the disease prevalence is very low,

you can have a very high sensitivity and very high specificity. These are nice valuesto have for a diagnostic or a risk test. But the positive predictive value, that means

does my patient actually have it, can be quite low, only 17%.

[Slide #41] [Microbial Factors][Dr. Engebretson]So, in the remaining minutes, lets go over the risk factors forperiodontitis. You can read through these. Youre going to have microbial lecturesbut theres really quite a lot of evidence that links certain microbes to theoccurrence of periodontitis.

[Slide #42] [Microbial Factors]

[Dr. Engebretson]And even World Workshop has gone so far as to declare thatthese three species fulfill all of the criteria for causality. Again, they can be debated

and its microbial sampling has its errors in and of itself. But certainly bacteria arecausative of periodontitis. Whether these particular bacteria are causative agents of

periodontitis, it has been at least suggested by large groups of experts. By the way,

aa,Actinobacillus actinomycetemcomitanshas been renamed toAggregatibacter

actinomycetemcomitans. Tannerella forsythensis was formerly known as

Bacteroides forsythus. And good ol P. gingivalishas kept its name. PG, AA, and TF.

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[Slide #43] [Natural History of periodontal disease in man][Dr. Engebretson]So, what about the heritable factors. So no one can help beingborn to your parents and its too late to change that, right? So, what do we knowabout this? We know a lot about this from studies of populations that dont movearound a lot and they dont have access to healthcare. Or they have all the same

access to healthcare. Norwegians in the 70s studies the Sri Lankan tea workers,guys that pick tea leaves and they live in communities nearby and there are no

dentists. And they all have basically the same thing. They use twigs and a toothpick

is actually a really good way to clean teeth. So and they followed them for a reallylong period of time. What they found was that about 80% of the people had

moderate progression of periodontitis. 11% of the individuals had no periodontitis

at all and about 8% had rapid progression of periodontitis. And this is in a

population where everyone had basically the same access to healthcare and the

same oral hygiene care products.

[Slide #44] [Genetic and heritable factors]

[Dr. Engebretson]So its been considered to be evidence that theres a stronggenetic component in patients who get periodontitis. Michalowicz and others did a

famous twin easy to remember, its the Minnesota twin study in University ofMinnesota. They collected large groups of monozygotic and dyzogtic twins, reared

together and reared apart as well as siblings. So you can take all the environment

versus genetic and, to make a long story short, theyre interesting studies. You oughtto go and read these. Genetics accounts for about 50% of whether or not you have

periodontitis, on average. And specific genetic tests have been looked at over time

and some of them are promising in some populations but then not promising in

other populations. So these investigations are underway and so this is one of those

things thats going to be different fifteen years from now when someone gives this

lecturewhat are the genetic factors and whether genetic tests I wish I had one. Iwish I had a genetic test for kids so I would know which ones are in that 47% that

are going to have periodontitis. Especially I wish I knew the 10% that are going to

have advanced periodontitis. And if half of that determination is genetic, wouldntyou like to know that up front?

Or, on the other hand, if youre only going to be mild, I wish I had a test for mildperiodontitis. If somebody was 32 and had mild attachment loss, do they need the

same kind of follow-up care and treatment as someone who might be lining up to

have advanced disease? anyway, just throwing that out there.

[Slide #45] [Smoking][Dr. Engebretson]Smoking, theres tons of evidence that smoking is associated withperiodontitis. Lots of rationale for that, you know, toxic byproducts, cyanotic

gingiva, etcetera, etcetera. We wont go through that but smokers and formersmokers have, on average, two to four times the amount of periodontitis as someone

whos a never-smoker. What about pot? Someone asked what about pot? Well, wehavent had big enough studies to say something about that but were talking abouttobacco.

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[Slide #46] [Smoking][Dr. Engebretson]And interesting, that this is you guys are all going to learn howto do smoking cessation. And every now and then youll be able to convince apatient ways to stop smoking. By the way, that nicotine replacement therapiesthey work. Theres even medications that can help you to not crave nicotine. And so

during a period of withdrawal, someone whos ready they have real tools. And therates of cessation you know, smoke-free at one year, if thats your outcome withmedications and nicotine replacement, theyve achieved smoke-free rates of 60% inclinical studies. Who knows the old way of cold turkeyyou wake up and say Imgoing to quit. Thats it. Throw the cigarettes in the garbage. Im a free man or awoman. Smoke-free at one year, cold-turkey: 7%, 8%. So, if we can get somebody to

be smoke-free for a year as a dentist in the clinic using tools you have learnedthatcould be a really good thing.

[Student]Could you prescribe that medication?

[Dr. Engebretson]-Yeah, if youre a licensed dentist in New York State, yes. Or underthe supervision of a faculty in dental school clinic, yes. So yeah, all good stuff.

[Slide #47] [Periodontal Disease and Diabetes][Dr. Engebretson]So diabetes we talked about last time but

[Slide #48] [Diabetes][Dr. Engebretson] pretty much, across all age groups, 2 to 4 times the prevalenceof attachment loss.

[Slide #50] [Aging]

[Dr. Engebretson]And aging. Aging we talked about

[Slide #51] [Aging][Dr. Engebretson]So, aging is not a true risk factor because the incidence ofattachment loss over time has not been shown to be affected by age. So, age is not a

true risk factor.

[Slide #52] [Model of Periodontal Disease][Dr. Engebretson]And just to put it all together, these are models people have usedbut its sort of gives you a way of thinking about a patient in these terms. So youassess the patientare they a smoker, is there a family history, is there poor oral

hygiene, are they susceptible, not everybody is. There could be other virulencefactors that have yet to be determined that could lead to connective tissue and

breakdown, pocket formation, and bone loss. Well talk about something calleddisease trajectory. So if someones going to remain mild or neverhave periodontitis,thats one thing. But if someone has a very advanced disease trajectory and losesattachment very quickly, and breaks down very quickly, its also something youdlike to know. So I dont show you here but you all heard of the, for example, theFramingham heart study. Now you can go online, the American Heart Association,

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and take a little online test. If you answer some questions about your risk profile it

can give you your oddsyour personal oddsof going on to develop cardiovasculardisease. There is such a company that has an online risk profile test for periodontitis

and its a company called Previser and you can find them at previser.com. Fulldisclosure, I have no financial interest in them. Theyre the first ones that have

started to look at risk profiling and online risk assessments for patients. Of course,its a paid service you sign up for but then you can get a risk profile for a patient.

[Slide #53] [Other Factors][Dr. Engebretson]Things that we didnt talk about today that have been consideredrisk factors for periodontitis are osteoporosis and stress. Evidence for osteoporosis

is not as strong as some of the others. Although some studies show increased risk

for periodontal bone loss in certain populations. Stress is another one. We see it in

practice all the time. Somebody is having a bad recall, plaque, bleeding, breakdown

and, you know, when theyve been doing so well. And what will they sayoh, Imgoing through divorce or oh, my kids are doing this or oh, my house burned down.

So something a stressful life event zaps your immune system, everybody knowsthat but its really hard to assess it objectively. So the data on stress is a little bit less,you know, clearer than that.

[Slide #54] [END!][Dr. Engebretson]So Im going to end there. We have time for questions. If youdont have any ah, a question.

[Student]The study you were talking about, it was 96 I think, it refers to themicrobial population associated with periodontitis. Dr. Craig taught us that

Treponemma denticola is also included in that?

[Dr. Engebretson]TD, yeah.

[Student]Yeah, so should we include that in the list that you have with the

actinomyces and

[Dr. Engebretson]You have TD, Treponemma denticola, I may have an old name inthis slide so thanks for calling that out. Wheres my bug slide? Okay, so addTreponemma denticolato the list for sure. Slide 41, yeah. Add Treponemma denticola

to the list. So, TD. AA, PG, TD. Other questions? Good, so keep some of those

principles in mind. Diagnostic tests come out from time to time. Sometimes theyre

for kids, sometimes its a saliva test. For the brush biopsy for if you dont wanna becutting your patient, you can do the brush biopsy. You wanna know what the

sensitivity and specificity of these tests are and then what the positive predictive

value, negative predictive value of these tests are. Is diabetes a modifiable risk

factor? Thats a really good question. Ill tell you one thing from just having readsome of the diabetes literature, youve all heard of bariatric surgery? You know, thestomach clip and bypass surgery? Bariatric surgery is now being shown to reverse

diabetes and to put someone into remission from diabetes. Medications can stabilize

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diabetes but over time diabetes is a destructive disorder and progressive. But, you

know, for the first time this is the first therapy that there have been isolated casesof transplantation of beta cells from pancreatic stem cells into young people and

having had them produce insulin so this would be a curative, so a modifiable risk.And for diabetes, possibly bariatric surgery could reverse diabetes. So its

modifiable in the sense that it can be stabilized so we speak of good control, badcontrol. But over time, diabetes is a very difficult disease to manage. Its modifiable,yeah but very difficult to modify. Smoking is a modifiable and what about smokersthat youve successfully Ill give you an example. I had a woman, she was a wife tothe French consulate general, very nice woman. And she smoked Galois, you know,

the French with their little cigarettes and finally we talked about cessation andshe agreed that it was a good thing. We put her on the drug Zyban, thats buproprionalong with nicotine replacement patch. A six week period. And she quit. In her sixth

month recall she looked at me, she said, Dr. Engebretson, Im very angry with you.She said I have gained twenty-five pounds. Her appetite returned. She went out to

eat a lot I guess, you know, when youre the consulate generals wife you have to go

out to these functions all the time. She gained weight and guess what she did? Shestarted smoking again. So, you know, what are you going to do? You can have these

victories. You think its a good idea, you know. You just have to keep after people sothat they know that there are tools in place because most smokers have been

unsuccessful quitting and thats common. But its reassuring to know that the firstattempt is not always the one that does it. So, good. Any other questions and then

well let you go for a break? Oh, question.

[Student]Are the microbial factors, risk factors modifiable as well in periodontitis?

[Dr. Engebretson]So, yeah. Right. Scaling and root planing can modify the bacterial

burden. However, studies have failed to show that you can eradicate a pathogenconsistently. So if you have sensitive enough microbial assay, there is a Swedish

study where they tried to do that. Well, if PG is, you know, can be eradicated. And

they used the, you know, DNA test and they had them back week after week if they

had it they got more treatment. You know, more scaling and root planing. And they

could never get it to zero. The microbes are but it may not be necessary toeradicate the organism. If you get the the biofilm is a very complex thing. So if youcan keep the populations down which is what we do in periodontal maintenance

visits. We just knock the populations down and it seems to work. So you dont haveto eradicate it. If you could, that might be a good thing but so, its modifiable, yes.But in terms of eradication, thats probably less realistic. So why dont you take a

break and come back at 4 pm sharp for your next lecture? And thank you very much.

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