Transcribed by Anam Khalid

Monday, November 3rd, 2014

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 of
periodontitis. And well go into a little bit of depth about what is a risk model and
why 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 adults
in 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 there. SPE2002@nyu.edu if you
have any questions about the material today.
[Slide #3] [Study question:]
[Dr. Engebretson] So one of the fundamental questions is who gets it? Who gets
periodontitis? 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 about
periodontitis today.
[Slide #4] [Wilson and Kornman 2nd ed]
[Dr. Engebretson] Heres some things to read about if you like to read. Wilson and
Kornman is a great chapter I dont know if theres a new edition of this out. I think
theres a 3rd edition. Carranza almost any textbook that you choose to purchase
will 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 microflora
usually 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 under
the 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
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[Slide #9] [N/A]

[Dr. Engebretson] Its easier to see when you get in clinic, you can see it from across
the room practically on the viewboxbone loss. Heres a healthy person. Heres a
person with bone loss.
[Slide #10] [Fundamental concepts ]
[Dr. Engebretson] So were going to talk about epidemiology. I know some of you
had some of it and others have had less of it so well all get on the same page. Well
talk 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. So
when 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, the
people study of the disease distribution within the population. Its really
important for lcinicals to understand what risk factors are for any given disease
when we meet patients and assess patients. And were readingthis is probably a
little old now but its a really well-written chapter on the epidemiology of
periodontitis. Much more exhaustive then we could ever cover today. Its about 36
pages. 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 commonly
used in pH programs around the countryGordis, Epidemiology, second edition. Its
only 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 the
determinants of health-related states or events in specified populations and the
applicationthis is importantand the application of this study to the control of
health problems. So all the studies in the world wont make any difference unless we
applied 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 the
etiology of diseaseso thats important. And second, to determine the extent of the
disease 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 natural
history 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 decisionmaking. 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? Incidence
is 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 in
time. 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 a
board 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 Times and
you read about some new outbreak whether its SARS or Ebola, theyll often talk
about 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 or
whatever area so. Has to do with a lot of things: access to care, and things like
that. 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 behavior
or lifestyle so its something you can do to yourself or something that happens to
you 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, a
word 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 applied
to 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 the
exposure 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 about
randomized 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 have
other lectures about thatare strong risk factors for periodontal disease. Microbes
cause periodontitis but were talking about specific microbes. And there have been
some 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 in
families. 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 a
modifiable 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 certainly
epidemiology 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 factor
of age and oral hygiene.
Longitudinal studies done in Sweden in the 80s show that thats not necessarily the
case. 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 mouth
actually 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 to
occur in bursts and it was episodic. So patients will go and itll be very quiet and
there 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 we
look 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 Nutritional
studies 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 of
the population which you want because this data sort of tells you about whats
happening in the country. Of course, its going to depend on what part of the country
you 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% at
moderate 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 wasnt
examined, only index teeth in specific quadrants. So, theyre big studies, I forget how
many but theres usually 4 or 5 thousand examinations that need to occur. If you
could do only half the mouth and then extrapolate that thats the way it is thats
going 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 been
used in the past. However, theyve always been criticized as not being entirely
accurate. 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 this
up. 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 reasons
whyperiodontitis is very, very infrequent under the age of 30. But broken down
by gender, race, ethnicity, education level, poverty level, marital status, and smoking
status. So, another thing to think aboutprevalence depends on how you define the
disease. 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 youre
over 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 on
the 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 so
you can look them up on your own and see the little numbers but down here dont
forget to check out smoking. So if youre a current smoker, 64% of adults have
periodontitis 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 big
headlines 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 of
these 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 have
more. If youre divorced you have aboutbreak even. If youre separated, you have
the 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 it
out for you. Heres over the age groups, 30 to 80. Heres with a low disease
threshold, 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 time
youre 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 have
advanced periodontitis, you need generally a lot of treatment, a lot of dentistry.
Whereas the moderatesmost people are moderatesthey wind up with moderate
disease and they stay with moderate disease, so interesting table.
So thats the most current epidemiology of periodontitis in the United States. About
10% 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 a
percent. 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 if
you 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 be
quite dramatic. But its very infrequent in the population and unless you work in a
hospital or in a pediatric, large group practice, youre unlikely to see these cases
often.
Of course, if youre an orthodontist thats one of the reasons you get per-operative
panoramic 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 a
hundred 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 with
periodontitis 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 for
periodontitis. And so its been shown with the incidence of periodontal attachment
loss 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, and
teeth 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 risk
factor 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 risk
factor.
[Slide #28] [Risk Assessment]
[Dr. Engebretson] Unless you go to one of those Swiss clinics where they inject you
with 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 the
odds ratio. Often, risk is expressed in terms of odds. So, lets take a hypothetic group
of 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 exposed
versus 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 number
and thats called the odds ratio.
[Slide #29] [Odds ratio]
[Dr. Engebretson] And so, just plugging in some hypothetical numbers here where
300 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 time
and thats an odds that an exposed person develops the disease. lets say you took a
thousand 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 can
be 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 Is
randomly 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 and
you have all these kind of risk factors you can come up with a model where itll
give you something called the r-squared coefficient. That is, its a way to explain the
occurrence of a disease in a population using these risk factors. And so each of these
factors, x1, x2, and x3 would be explanatory for, say, smoking economic factors, sex,
and so on. So thats called a risk assessment model. And risk assessment models can
be 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 the
population for a disease that may have these particular risk factors. So Ill give you
an examplepeople with diabetes have a 2 to 4 fold risk for having periodontitis. So
you 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. You
know I think Wallgreens has the blood pressure anyone can screening for blood
pressure 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 controversies
surrounding 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 are
evaluating 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 it
means.
[Slide #35] [Screening]
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[Dr. Engebretson] So, when you screen someone, and they either have the disease
or dont have the disease, there has to be some kind of gold standard for who has the
disease. 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 false
negative.
[Slide #37] [Screening]
[Dr. Engebretson] So you get these terms called sensitivitythat is how good is the
test. 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 negatives
divided by all the non-diseased. So if its specific, it identifies those who dont have
the 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 and
specificity of a test. Well what does that mean for your patient and theres a
calculation called
[Slide #39] [Positive Predictive Value]
[Dr. Engebretson] the positive predictive value. And that means whether your
patient 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 the
prevalence 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 values
to 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 for
periodontitis. You can read through these. Youre going to have microbial lectures
but theres really quite a lot of evidence that links certain microbes to the
occurrence of periodontitis.
[Slide #42] [Microbial Factors]
[Dr. Engebretson] And even World Workshop has gone so far as to declare that
these 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 are
causative 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 actinomycetemcomitans has been renamed to Aggregatibacter
actinomycetemcomitans. Tannerella forsythensis was formerly known as
Bacteroides forsythus. And good ol P. gingivalis has 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 being
born to your parents and its too late to change that, right? So, what do we know
about this? We know a lot about this from studies of populations that dont move
around 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 really
long 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 strong
genetic component in patients who get periodontitis. Michalowicz and others did a
famous twin easy to remember, its the Minnesota twin study in University of
Minnesota. 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 ought
to 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. I
wish 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, wouldnt
you 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 mild
periodontitis. 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 with
periodontitis. Lots of rationale for that, you know, toxic byproducts, cyanotic
gingiva, etcetera, etcetera. We wont go through that but smokers and former
smokers 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, we
havent had big enough studies to say something about that but were talking about
tobacco.
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[Slide #46] [Smoking]

[Dr. Engebretson] And interesting, that this is you guys are all going to learn how
to do smoking cessation. And every now and then youll be able to convince a
patient ways to stop smoking. By the way, that nicotine replacement therapies
they 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 the
rates of cessation you know, smoke-free at one year, if thats your outcome with
medications and nicotine replacement, theyve achieved smoke-free rates of 60% in
clinical studies. Who knows the old way of cold turkeyyou wake up and say Im
going to quit. Thats it. Throw the cigarettes in the garbage. Im a free man or a
woman. 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 learnedthat
could 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 under
the 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 prevalence
of 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 of
attachment 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 used
but its sort of gives you a way of thinking about a patient in these terms. So you
assess 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 virulence
factors that have yet to be determined that could lead to connective tissue and
breakdown, pocket formation, and bone loss. Well talk about something called
disease trajectory. So if someones going to remain mild or never have periodontitis,
thats one thing. But if someone has a very advanced disease trajectory and loses
attachment very quickly, and breaks down very quickly, its also something youd
like to know. So I dont show you here but you all heard of the, for example, the
Framingham 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 cardiovascular
disease. 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. Full
disclosure, 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 considered
risk 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, Im
going 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 knows
that 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 you
dont have any ah, a question.
[Student]The study you were talking about, it was 96 I think, it refers to the
microbial 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 in
this slide so thanks for calling that out. Wheres my bug slide? Okay, so add
Treponemma denticola to 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 be
cutting 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 read
some of the diabetes literature, youve all heard of bariatric surgery? You know, the
stomach 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 cases
of 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, bad
control. 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 smokers
that youve successfully Ill give you an example. I had a woman, she was a wife to
the French consulate general, very nice woman. And she smoked Galois, you know,
the French with their little cigarettes and finally we talked about cessation and
she agreed that it was a good thing. We put her on the drug Zyban, thats buproprion
along 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? She
started 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 so
that 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 first
attempt 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 pathogen
consistently. 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 to
eradicate the organism. If you get the the biofilm is a very complex thing. So if you
can 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 have
to 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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