23/24: Diagnosis of Caries

Transcribed by: Atiya Bahmanyar August 12, 2014
Diagnosis and Treatment of Oral Disease

Introduction to Cariology/Diagnosis of Caries

[mumbling with the AV guys and Dr. Wolff]

Yeah something got tripped. Im powering up right now.
Student: I heard you were handing out candy

[Mumbling]

Dr. Wolff: Whats tomorrow?

Introduction to Caries, Caries Management and Caries as a Public Health Issue
[Dr.Wolff]: The remote is working but the pointer is not. Its not bad, its too weak.
Ummm. So your class is actually the first class thats heard something about caries
as their operative dentistry class, and thats great. Were going to try to build upon
that. So were going to spend a little bit of time working towards that, um, as we go
through the process. Today Im going to talk a little bit about the whole scope of
what this course is going to include as well as some very specific learning objectives.
The very first of which will actually be getting you to understand how to diagnose
caries, whats the physical diagnosis and what process were going to do. Youve
already received, the 14 of you who attended Dr. Ds lecture. Youve already
received presentation on, and for those of you who are listening to the tape, I hope
you listened to his before you got to mine, so that you hear me say only 14 attended,
but neither here nor there. Thatll be my last sarcasm and since you folks were good
enough to be here and eating all the candy that was brought for you.

[Students: Woo]

[Dr.Wolff]: Go get that candy off the table. Umm. But theyre probably sitting in their
living roomoh, nevermind. Im going to concentrate and get you guys out of here.
Umm. Caries we would imagine, so when I entered dental school in 1977, the very
first presentation I received was from an epidemiologist who told me that caries
would be gone by the time I graduated. Sealants had been invented, and fluoride
reached its apex in usage throughout the country. It was all over, and sometime
right around you know 10 years into practice, caries would not be an issue. Were
that only the case. It wasnt even close to being the case. And dental caries today is
actually a growing disease with more and more issues associated with it. Today
were going to, I was going to set up my twitter account and you could tweet me if
you had a question and wanted to ask it.

About the Course
[Dr.Wolff]: This is such an intimate group spread out over a very large area of
listening, normally I would consider this a living room group. Please, raise your
hand, do the speak up thing and ask the questions. If you need to email me a
question, please email me a question. Dont isolate this, um, as most of you know, I
have a daughter who went through dental school. Um, or is going through dental
school right now- in her second year she was studying for an examination in the
DOD course, where as she was studying- she came across an old copy of an
examination through whatever method, um, and the class was arguing in facebook
as whether or not this patient had a high or low caries risk. And it was kind of
interesting, shes busy cursing out her computer while listening to me on tape while
rather than listening to me the original, she did not go to class either. But listening to
me on tape, taking notes, going through the process and cursing the facebook
process thats going on in the class. Theyre all idiots, dan-na-da-na-dah. Now its
interesting because I sit in the evening and my email is always open and running.
Im always working, I love what Im doing, Im always working. Now, the class was
arguing as to whether or not a patient who had caries that was treated a year before
and was restored, and theres now current caries in the mouth is still a high caries
risk patient. And what facebook voted, was that that patient was a low risk because
the patient no longer had caries in their mouth. What Samantha actually new, was
that the rule said if you had had caries in the last 3 years that had been treated,
youre still a higher caries risk patient and no matter what metric you use within the
last year, absolutely youre still a high risk patient. So she votes for the high risk,
everybody comes back and says no, there is no caries in it its low risk. Theyre
arguing back and forth, and I finally go whats going on there, I cant take it. Shes
sitting at the dining room table with this throwing things around and getting
annoyed and she says- I didnt want to tell you but theres a copy of the old exam
floating around and the class has a debate about one of the questions on it- they said
its low caries risk- I said what do you think? And she says I think its high caries
risk. Why do you think its high caries risk? And by the way Samantha, its a brand
new examination I dont care that you have the old exam, you dont have to hide that
from me. They werent supposed to, but it was a brand new examination. So she
types back on facebook, that I have it from a good source that the patient is high
caries risk. And a student in the class answers on facebook hes wrong. So I write an
email to the entire class minutes later, because I dont use facebook nor am I invited
on your facebook page, that the patient is high caries risk because somebody asked
me a question and the answer is and I make a public answer to every one on the
email thread, then it was the class of 2015- the patient is high caries risk because
of

Now its an interesting and bothersome thing to me, because you folks were
studying using facebook, which is great, but you could have gone to the source. A.
you could have gone to the sheet which actually says 1 year, heaven forbid someone
actually pulls out the sheet that says caries risk as part of the course. But outside
that, someone could have asked the question of a course director or a course
lecturer and gotten the right answer. So when you dont probe the faculty, youre
making a mistake. Not all faculty answer their emails all hours of the day and night.
Feel free to send me an email, feel free to ask me questions- and youll get the right
answer. So as we look at this patient, and this is my famous lside, I love this slide, its
got lots of stuff on it.

NYU| DENTISTRY (First caries slide)
[Dr.Wolff]: So we see here the caries right at this spot (arrow) I have to ask this
question, when we do that to this patient and we treat this tooth, have we actually
cured the patients caries? Why?

By restoring this tooth
[Dr.Wolff]: The risk factors are still there. So caries cavitation is the outcome of the
disease, not the disease. And, uh, cavitation I should say, I got that a little messed up.
Cavitation is the outcome of the disease, not the disease. So for many, many decades,
treating this hole was a surgical intervention, and when we finished the patient was
cured, or so it was thought. How many people have ever had a restoration ever
placed in their mouth. Any of your dentists ever given you fluoride after youve
gotten that restoration. Told you that you need to use fluoride routinely as a
preventative factor cause youre at risk for developing caries. Thats the key!

Treatment of the disease requires
[Dr.Wolff]: So upstairs, routinely we have these patients getting all sorts of
restorations in their mouth and dentists make the recommendation, brush, floss,
and cut down on sweets. Weve already had the discussion last year flossing and
cutting down on sweets doesnt reduce tooth decay. Anyone want more of that
chocolate? Yeah, I know its circulating around somewhere up there. If you need
more, go pick some up, your strep mutans needs a good feeding right now. Risk
reduction turns out to be the most important factor, and when we look at this
radiograph we see lots of areas over this radiograph thats telling us that the disease
is in multiple processes.

NYU| DENTISTRY (Second caries slide)
[Dr.Wolff]: Caries was born, the discussion, the early era of caries. How many
treatments did GV Black have to control caries? One. It was restorative therapy, it
was actually amalgam, they did have silicates, cements, um, available, um. But it was
surgical intervention, there were no drug interventions and did they know, when he
first wrote did they even know what causes caries? Were going to talk a lot about
risk assessment, do you do risk assessment or? No, I do risk assessment. The risk
assessment lecture is very important

Risk Assessment
[Dr.Wolff]: and its not mechanical that you need to understand. Its your ability
to discuss this with the patient. Who gets caries and whose fault is it? Its the
patients. Youre there to educate them and guide them and give them the best
methods of preventing it, but they own the disease! And you have to do everything
in your power to make sure that they understand that its in their hands. So if we go
ahead and look at this particular patient, this particular patient has this toothache of
3 days what do we see on this tooth?

35 year old female
[Dr.Wolff]: distal of tooth

NYU| DENTISTRY (Third caries slide)
[Dr.Wolff]: number 30 has caries probably, distal on 28, definitely on 28 and
probably on 29 all have what look likewhen did this start? Is caries a rapid
disease? Not typically. Could be, but when we say rapid, we are talking about
months or years, not days. Thats rapid, is months or years. This is an ongoing
disease process that has the opportunity to do 3 things, get worse, arrest, or get
better. They use fluoride, they brush their teeth 2x a day, and they use dental floss,
yet theyre still developing the disease and we have to understand what the risk
factors are for the patient and how to control them.

Why do I get cavities, but my sister never does?
[Dr.Wolff]: Caries comes from the latin word, um it stands for rot or rotten.

What is Dental Caries?
[Dr.Wolff]: It came out of medieval Europe and it comes from medicine, and it was
actually gangrene that they were referring to. Um, so they used to call it um the rot,
when the bone became infected. Rotten teeth are the signs of a disease which is
called dental caries its a very simple disease. New textbook by Rory Hume and
myself, will be coming out in the fall, well see to it that you have it available on vital
book. Um, we spend a good deal of time talking about the history and understanding
because where you are right now is in the (something) of change in therapy. Before
you finish dental school, there will be therapies to arrest active caries in almost all
circumstances that will be acceptable and viable in dental practices, and this is going
to radically change the way we approach dentistry. Its one of the most common
diseases and they like to refer to this as being more common that asthma and
resulting- you know, the truth is very few people die of dental infections. Lots of
people die of asthma, so we need to recognize the magnitude of the disease is much
much greater. Its the most important cause of tooth loss in adults, or younger
people. 20% of the population has 60% of the decay; where are they on the
socioeconomic strata? Heres lookin at ya.

Disease Distribution
[Dr.Wolff]: I just found out we had a simpatico thing with diet coke. She has that
giant can, we wont go into that. So the lower economics is that is there something
genetically in lower economics that make them more likely to get tooth decay?? I
just had this discussion actually with a director of dental clinics in Brooklyn less
than an hour ago. Anything genetic that we find in lower socioeconomic? Tell me
something else that tracts with that? Diet? Thats true. Now Dr. Caufield likes to
refer to malnutrition, now, malnutrition is a lot of things. What does mal mean?
There ya go. It is bad nutrition. It may even mean a deficient diet in certain areas
and certain items, like vital nutrients. But, its not the malnutrition that we currently
or frequently attribute to, um, starving. Its not that type of malnutrition that we
refer to. SO if it correlates with mal, malnutrition, it correlates with education in all
respects. SO going to a bodega thats selling food in an area thats lower SES we see
processed foods going out of there we see high carbohydrate foods going out of
there, easy items to eat and cook and that influences their malnutrition and their
likelihood of getting caries. But whats interesting is 10% of the population receives
65% of the restorations, but its not necessarily the people with all the caries.

Distribution of Insured Restorative Services
[Dr.Wolff]: Where are the 10% actually residing? They actual reside in a better SES
population thats actually receiving much more of the care and much higher
utilization of their insurance

Distribution of Insured Restorative Services (with graph)
[Dr.Wolff]: So were just in this Medicaid practice or capitation practice in Brooklyn
and he was saying I would love to get my patients in 4x a year for fluoride patients.
We wouldnt worry about that at all. He says I couldnt get them to come in 4x a year
for anything. I have nurses chasing after them to get stool samples, to do blood and
stool because thats an outcome measure that the insurance companies use. I have
people chasing after them to talk about the tobacco cessation. It all stems back to the
education, or the lack there of, that health is something that can be improved by
prevention and that comes back to this risk assessment management. So the
wealthier people are using 65% of the restorative dollars that are spent on delta
dental. They automatically have a job, and its not the low socioeconomic group.
Another problem that we have is that were going to deal with old teeth. Were going
to deal with old people that didnt exist, old teeth that never existed because were
getting better in perio control.

We are getting older!
[Dr.Wolff]: This is an oncoming crisis. Aging and dental health. Were going to talk
about some items related to saliva. Thats going to be, I think thats not for a while.
You know this 1000 medications

Effect of Medications
[Dr.Wolff]: Its actually more than 1000 now. Sreebny was one of my mentors in my
pHd program and what was very interesting it was very simple study. He sat with a
book called the physicians desk reference. It was something with paper inside of it.
He sat with a book and looked at every single medication and just counted up how
many of these had the side effect xerostomia and whats amazing is that in this PDR
there are today using computer searches and medical prescription guides, its
actually measured in the 1000s. Lots of our patients are taking polypharmacy that
results in dry mouth and it coan be over the counter or um prescription in nature.
Weve managed to decrease decay in our young population. Our older population we
have real significant issues, even today, with large amounts of decay.

Caries Scores by Age Group
[Dr.Wolff]: Much less today than we had in the early 80s but we still have a
significant amount of surfaces that are decayed, missing, or filled. Thats really good
news since I understand most of you have a fairly large tuition debt. That means that
you must be able to fix Mr. Cavity. Theres going to be plenty of work out there for
your generation and probably for your childrens generation too. But the problem is,
whats occurring down here is a question of whether or not this continues to grow
as they get older. Unfortunately as weve been able to manage and control in our
younger population, and there seems to have been a little boost, you can actually see
out here that theres been an increase in our most recent time frame in caries in the
younger population, theyre actually seeing a rise now, instead of it being at 6-19
theres a rise in the health programs for preventative; we are now seeing a rise in
the 19-25 yearolds and in fact this may not be so artificial in the future. I cant
imaging 25, 45 surfaces of caries or restorations in the mouth- thats a massive
number of surfaces. Uh, Im sorry 45% of populations having more than 20 surfaces
of caries thats been restored in the mouth. So prior objectives were to just diagnose
and treat the disease, today the decision has been to prevent the disease as a big
portion. Many insurance companies, medical being one of really great examples
have made a tremendous effort

OBJECTIVES OF DENTAL THERAPY
[Dr.Wolff]: to actually pay for prevention and they now are starting to pay for
outcome. So we are going to see medical practices throughout the US and world in
dental practices following shortly that actually pay for outcomes, reduce blood
pressure, reduce number of smoking, and reduce caries will be one of the outcomes
that we need to see, and youll be paid more. As a matter of fact, its being
demonstrated on the west coast in the Kaiser group, if youre group has patients
that have lower DMFS each year incrementally when theyre in your practice, you
receive a 20% higher reimbursement than you would have had if you didnt have
the higher reduction. So, this is a pay for performance modulus. We are seeing it
start to break into dentistry. Kaiser is a large um group that provides dental
insurance to large industry on the northwest in the US. Its just a coming trend thats
going to arrive. We have to remember that restorative technologies are profitable
for manufacturers and for practitioners, so a lot of people actually see no reason to
do prevention.

REPAIR DEFECTS TO RESTORE FUNCTION
[Dr.Wolff]: Im pushing you guys against the salmon stream, the water stream, to try
and get it so you can actually work on prevention as part of your practice. But the
biggest psychologic(al) barrier and I saw it yesterday when it was in practice- my
patient says Dr. Wolff, I have this little thing in my gum over here. It was a little
black spot on the root of their tooth. Black, black, it had been a little bit of loss, and
in fact when I look at my records its been black and its been there for years I dont
know hwy last week they looked at it and said I have an emergency. I looked at it
and said its arrested decay, weve been tracking it for a number of years now. Its
fine, its at the gum line, putting a restoration there is difficult and youll have issues
associated with it. The patient almost begged me, to please drill it. Now, the
interesting thing is, if I dont like what it looks like- its a problem to the patient and
we should treat it. We should treat it. But if theyre coming to me to treat it because
its caries, I can treat it in a different fashion. And in fact for the last decade we have.
Shes on home fluoride, she gets fluoride varnish when she sees us 2x a year in the
office. Despite the fact that shes an adult- thats managing her risk. The comment is
treating the spot is not going to make you greater or less at risk for tooth decay. If
its bothering you visually Ill treat it- but understand, from a medical standpoint
you dont need to treat it. Its a different module and a different method of treatment
but patients are not exactly into that treatment. So our goal is to promote and
maintain an intact dentition throughout life. Whats interesting is if we actually look
at caries historically, we saw this very well, 10 teeth with caries, historically very
high

CARIES MANAGEMENT
[Dr.Wolff]: but 3 or 4 when you go look at the before the common era, before
zero

DECAY HISTORY OF MAN
[Dr.Wolff]: You know it was very rare, and whats the reason for that? Did they not
eat sugar? It wasnt processed- so it wasnt concentrated to a highly compact
fermentable item and there are number of different, and theres an exception to
that- and its honey. Naturally processed by bees, but honey was something used by
royalty- not commonly available, not to mention you had bees around to get it. We
did not, what caused the spike? It was the crusades. Right around the crusades, they
came back through the trade routes and brought sugar to Europe. So we had Europe
now with processed sugars, Europe that rewarded itself, it was worth much more
than gold the first time it was brought to Europe, and very quickly was one of those
things- sugar was one of the main reasons Christopher Columbus set sail to find the
new world quote unquote. In an effort to find a quicker route to bring this stuff into
Europe. So one of the things that was brought back by one of the crusaders was
sugars- through one of the spice routes from south east asia into Europe and caries
went up radically. Now caries has been around for a very long time. It dates back to
the, descriptions date back to the ancient Egyptians. It started out with worms
destroying teeth. The worm destroying teeth actually persisted for quite a while.

HISTORY OF CARIES: ACID FORMATION AND DIET
[Dr.Wolff]: if you ask your friends and family what causes tooth decay theyll tell
you bacteria eating the teeth- bacteria, just small worms. They dont realize that
theres an actual process. Um, its been described as an evil by which teeth become
full of holes and hollow, um which most often effects the back teeth, especially so
when they are not cleaned of food particles which decompose producing an acid
moisture which eats them away and destroys them so that finally with much pain
they rot away little by little. Interestingly they thought it was the decay of food not
realizing the bacteria causes the food to decay and its the process of bacteria eating
the food. So it was not until the 1800s that people started realizing that the natural
process of breakdown generates acids.

Acid produced as a natural process
[Dr.Wolff]: It was Miller in 1890 same time that GV Black was writing that actually
explained the process of fermentable carbohydrate to certain bacteria they eat it,
they produce acids, the acids sit on the outside of the tooth.

Mouth organisms produce lactic acid
[Dr.Wolff]: And it was from 1890 until almost 1980-1990 that every body assumed
that it was a one way path, that demineralization was the eventuality. And in fact as
we describe this eventuality it was always in the direction of fermentable
carbohydrate to demineralization. Now, what interestingly occurred is the
conversations in the early 1980s

Mouth organisms produce lactic acid
[Dr.Wolff]: actually highlighted the concept that there was this

Millers acid Decalcification Theory
[Dr.Wolff]: acid balance that went on, and people started talking early in the 40s
about this being mediated by saliva as one of the items that will control whether or
not you get tooth decay. It turns out a number of factors influenced whether or not
we would get decay. So you start looking at people that have absolutely clean teeth,
they eat lots of sugars and they dont get decay.

DemineralizationRemineralization
[Dr.Wolff]: They were missing plaque was part of the formula. Another word for
plaque is biofilm. As it turned out, you needed a susceptible tooth, and teeth.

Caries: Multi-factorial Etiology
[Dr.Wolff]: What helps influence whether a tooth is susceptible or not? This is the
interactive part of the lecture, so Im going to harass you for a moment then well go
back to the screen to make sure youre awake. Crowding. Okay, so anatomic
alterations that make the capture of plaque easier or the cleaning more difficult. The
location of the teeth? Hmm. What do you think might influence lower anteriors?
Whats that? Saliva. That actually turns out to be the largest mediator. Some other
things, where do we most likely get caries? Its pits and fissures. And what is that?
Well it is the occlusal surface, except unless its the lingual of a lateral incisor in
which case its still a class 1 on the lingual surface. A sneak examination but the term
class I, but were going to eradicate because we dont really want to talk about that.
Its occlusal surface caries. But, so, um, weve got this plaque retained area on the
um, does anybody have pits and fissures that arent sealed? Do you have any caries
in your pits and fissures? Why? Theyre naturally sealed. Right. Theres a
coalescence of enamel in those areas and they dont trap plaque. Dr. Caufield spoke
about another time of location that helps create caries. Malformation of tooth
structure that retains plaque inside it; it acts as a really great, great medium, culture
medium, its a dish that hold the plaque there no matter how you brush you cant
take that out. SO these anomalies or malformations on the enamel at that surface
can actually lead to plaque accumulation that can lead to demineralization in that
area. So thats the tooth susceptibility. So lets talk about the plaque. What influences
the plaque? Hygiene, thats how much is there. Anybody know any cows that brush?
You have a cow that brushes? You always have the one person in class whose cow
brushes. The rest of you have cows that dont brush. I have never personally met a
cow that brushes. Any of you have met a cow that has cavities? How is it possible
that something that has never brushed, never gets tooth decay? Yeah, its actually
what we feed it and what bacteria is in the mouth and has the opportunity to grow.
Were going to talk about this mixed bacteria colony in a moment because were real
advocates of the actual colonies and what they mean(?). Now what they get infected
with is another caufield discussion and that vertical transmission from mother to
child turns out to have some influence in what causes this and what arises there.
Then how we feed it and how we culture it. How thick we allow it to grow, what we
allow to occur, because not all plaques are equal and what you get and what your
brother and sister get may not, so you got the same vertical transmission, but your
grooves and pits and fissures may be better coalesced on you than on a sister. You
may keep a little bit better of the plaque, you may have gotten the same stuff from
your mother, but there could be minor nuances that differ you both. Now sugar
turns out to be the feeder of all this and that is the one that creates- but does any
body know anyone that eats lots of sugar but never gets tooth decay? Its this
something else thats effecting it and thats actually a real common finding. I have
patients that come in and say I dont eat any sugar thats a lie. They may not eat a
lot of sugar, but they dont eat sugar is probably not the truth, and they still get
caries all the time. Its almost impossible if you eat no sugar at all to get caries. As it
turns out, saliva has a giant mediating effect, and Im sorry of this, op, didnt mean to
go that fast; saliva and what goes on- so were going to spend time talking about
saliva and how it mediates this entire plaque environment, the sugar environment
the tooth environment as far as remineralization to determine whether or not you
get tooth decay over time. Now, this plaque turns out to be a very interesting item.
Now everyone tends to call it biofilm in this environment. The term plaque no
longer exists in anything other than dentistry. Plaque is not a description of a
biofilm.

What is Plaque?
[Dr.Wolff]: All a biofilm is, is a very complex community, it has all sorts of methods
of attaching to the surface, at the same time its not a single bacteria. The key here is
to understand that its a mixed bacteria with lots of things going on inside it. But it
gets even wilder. The plaque actually is a place where things occur. The transfer of
ions from the saliva surface into the biofilm, the biofilm acts as a reservoir to save it
there and then it goes into the pellicle, then eventually into the tooth, or it goes out.
This is a slide courtesy of Colgate, I remind everybody I am a consultant for Colgate,
associated with the development of tooth paste. Okay? I helped invent a toothpaste
that Colgate currently is marketing world wide.

Um. It is important for you to recognize that some of the theories that will be spoken
about related to that toothpaste, actually involve modifying the biofilm, not
eliminating the biofilm. My bet is before you retire from dentistry, we will stop
trying to eradicate biofilm with chlorohexidines or iodines, and we will stop
brushing off all our biofilms, but rather help try and maintain a healthy biofilm of
mixed bacteria. There are lots of ways that people are proposing this. We will talk
about a few of them during the course some of these methods of doing this may be
by using probiotics, and others by fertilizing essentially thats the Colgate
technology, if we feed arginine to this bacteria, to this plaque, it goes from being a
plaque that contains lots of demineralizing bacteria to a balanced plaque that has
remineralizing agents inside it. So as things are transmitted from the surface, it
comes from saliva, and controls this flow in and out of the biofilm and heavily
influences what occurs inside the biofilm. We can get a more cariogenic biofilm if we
just put in things that cause acid formation which results in demineralization.

Source of Caries Problem
[Dr.Wolff]: We can go ahead and use saliva to wash away the acids. Anybody heard
any of that theory of washing away the acids? What was that? Its an advertisement.
You see it all around you. Its in the press, you hear about it. Mouthwash? No they
dont talk about mouthwash if you cant brush your teeth, what do they talk about
doing? Chewing gum after eating. What that is, is primarily a dilution and slightly an
attempt to bring more buffering capacity from the saliva to the plaque and actually
modify that plaque. So, saliva controls that plaque environment quite heavily and
were going to talk about the management of the plaque. So we can either result in
demineralizationWhat happens if you brush right after you have a high sugar diet
15-20 minutes after you do that? Because? So the acid has come into the surface, its
resulted in demineralization. Where do the calcium and phosphates go? Where does
the calcium and phosphate go from the tooth? Is it in solution? Or does it go quietly
into the pellicle and the biofilm? It cant get directly into the- because theres
something covering it. You wouldnt have gotten demineralization if there wasnt an
acquired pellicle and biofilm over the top because I can pour all the sugar into your
mouth and if theres no biofilm there for it to eat and produce acids, the sugar
doesnt cause decay. So if we grew you up in a sterile bubble and you had no
bacteria in your mouth at all, is sugar cariogenic? Now Im sounding like iwork for
the sugar industry. Its not the sugar thats bad, or its not the bullets that are bad,
its the guns, or its not the guns its the bullets. You need both together to make this
happen. You need both to make this happen. Sugar alone doesnt cause caries. What
occurs there is the sugar fed to the biofilm now results in the biofilm generating
acids, the acids attack the tooth surface, the acids slowly dissolve, and what can
mediate that? How can I slow the dissolution of the tooth? Well buffering is one, but
theres something very specifically that slows the dissolution of the tooth when
exposed to acids. FLUORIDE! Thats one of the 2 mechanisms of fluoride in working
to prevent tooth decay. It effects the mineral so that it doesnt dissolve as easily and
well go over that also. So the key is, once you get the calciums and phosphates
inside this biofilm, if you were to come and brush it away, theres a net loss of these
calciums and phosphates from the tooth structure, and even the presence of saliva
on the surface, that calcium and phosphate is not easily restored even from the
calcium and phosphate from saliva. So saliva is an exceplent buffer, it washes away
acids and it contains, its super saturated with calciums and phosphates, where do
we see proof that its super saturated with calcium and phosphate? Calculus! So we
get that precipitation, and thats just remineralization; and that just goes to this
balance of whether or not we get remin- or demin- in that item.

Role of Saliva
[Dr.Wolff]: Now this is a very classic drawing by Stephan, he actually did this in
1946 its called the Stephan curve. We go ahead and we feed um, we feed, the patient
some glucose,

At Normal pHpH 7
[Dr.Wolff]: the resting plaque pH, uh, Stephan did this by the way,

Demineralization
[Dr.Wolff]: he took a bunch of dental students who didnt brush for a week

Stephan Curve
[Dr.Wolff]: thats when you can do a lot of research on dental students without
paying them or asking permission. Everyone had to participate. Told them not to
brush their teeth for a week and then had them all swish with sugar, a glucose
solution, then started collecting plaque specimens from each area in the mouth.
Over time what you found is, just before the plaque was near neutral, right after
within 5 minutes the plaque pH drops, it drops rapidly, it drops below 5.5- an
important item because 5.5 turns out to be the critical pH for the dissolution of, of
enamel. Anybody remember the critical pH for the dissolution of dentin? 6.2. Its
important because youll find that patients that have arresting, saliva flow, but that
is subnormal, actually have a resting pH near 6.2 and its why we have older patients
with dry mouth getting rampant tooth decay. Theres no buffering capacity inside
the system. So it drops below 5.5, they start dissolving. If we put fluoride in the
system it actually lowers this bar just a little bit. The pH drops, as it rebounds it
comes back to stop dissolving and eventually it starts to remineralize. So the top is
the repair zone, the bottom is the danger zone, and if we add fluoride to the system
we actually lower the critical pH and decrease the um, the likelihood of dissolving
the tooth and effecting the mineral. So caries management for a long time said- eat
less sweets. And that was the theory. So after a generation of dentists told you to cut
down sweets, it was suddenly discovered that it doesnt reduce tooth decay- not
even a little.

Stephan Curve and Plaque pH
[Dr.Wolff]: Why? How much sugar does a bacteria need to eat to reduce the pH?
Yeah- micrograms. So- 2 teaspoons of sugar in a cup of coffee- thats drank over an
entire period of a day- results in caries because of the repeated diving of the pH
below the critical pH and the rise. So it turned out not to be the actual quantity of
sugar, but how frequently because if we moved this interval closer and closer, you
actually always stay demineralizing the Gatorade with less than 100 calories of
sugar, the coca cola with 100 calories in the big glass thats deadly, not because you
drank it once but because you drank it over the course of a day. So the theory of cut
down on sweets actually changed. Its more cut down on the frequency of sweets.
Big chocolate cake, 2 cups, eat it in one gulp, is one exposure to sugar. Whats the
exception to that rule? Hmm? Diabetes, you die- you know because of all that sugar.
Low clearance- sticky foods. How many of you had sticky chocolate? Im sorry but
its sticking around. The rest of you had one occurrence and your pH is normal
already- its been 45 minutes since your piece of chocolate. Anyone want some more
chocolate? Were going to keep your pH down for a few hours. D4s are going to be
looking for board lesions shortly, it takes a lot of chocolate to make that happen.
Were going to talk very briefly about materials of tooth structure. By the way,
enamel is more resistant to tooth decay than dentin. Anyone want to tell me why?
Hmm. Whats that? Its more mineralized. Theres more mineral in it to start with,
and its highly organized.

What are teeth made of?
[Dr.Wolff]: Dentin comes in tubules. You make tubules- theres mainly air in the
middle of this- tehres more surface area to be exposed to the acids. It dissolves
more rapidly.

Enamel
[Dr.Wolff]: It has less mineral content- less organization- about 1/3 of it is proteins
in one form or another. Theres also collagenases associated with decay and other
things. Collagenases are activated in the acids, wee quicker breakdown in the
surface- we see more rapid decay in dentin. Much more difficult to control caries in
dentin.

Acid Exposed Dentin
[Dr.Wolff]: Well talk about the caries balance, imbalance, it will be a part of our
caries risk assessment. Um, prior to Dr.- um I should have had Featherstone 2006,
Featherstone was here, it should be Featherstone Wolff actually, hes now dean at
San Francisco, um, we had this balance, and he had this triangle right in the middle
here-

The Caries Imbalance
[Dr.Wolff]: and I asked this question, do you believe fluoride and salivary stimulants
and antibacterials can actually reduce decay- or actually reduce the risk. And the
answer was yes, it reduces decay but you can still get decay around it. SO the
problem is- when we have patients that have indicators of decay and decay risk, like
active lesions- those patients very rapidly develop decay, we have to work really
hard on the other side to pick it up. Its not a fair balance, your risk is much greater
once youve demonstrated the likelihood of getting decay and its not as simple as
putting you on a fluoride. We have to work real hard and we have to educate our
patients to understand that. Were going to talk about the classification of caries.
Um. This was not considered caries. I still ask this question of dentists all over the
world as I lecture, is this caries? And they go no. You guys, is this caries? Raise your
hand- yes? PLEASE RAISE YOUR HAND! I JUST NEED TO GET THAT INNER FEELING
THAT WE TAUGHT ONE THING TO YOU FOLKS! Hes a tough sell over there.

Caries classification of the groove
[Dr.Wolff]: Have another chocolate on me. Go ahead.

Caries Classification of the Early Lesion
[Dr.Wolff]: Get fat and have cavities. Its okay. This is the earliest signs of decay. It is
the caries process. Its the same caries process, identical to what is occurring in
cavitation. It just hasnt gotten there yet. GV Black didnt recognize this as caries. It
didnt exist then. Do you know why? You only had one cure. The 1 cure was to drill it
and put a restoration in it. So when he saw demineralization on the margins, he had
to cut it out. He had to drill away and get clean margins to put as amalgam in there,
which by the way had a life expectancy of less than 5 years. Try that on for size if
youre 20 years old and hes putting a restoration in your mouth.

Caries Classification of the Gingival 1/3
[Dr.Wolff]: This is clearly caries. We will talk about caries in the gingival 1/3.

Root Caries
[Dr.Wolff]: Um, theyre both carious lesions arent they? That looks brown and soft,
it is. This is black and soft isnt it. Should they both be treated? Whats the difference
between the 2? Exactly. This ones not active anymore. Its like fallen on top of itself.

Active caries versus arrested caries. So thats a discussion of our activity. Well talk
about classification of lesions and how we deal with the discussion of a lesion.

Is caries still a problem?
[Dr.Wolff]: Is caries still a problem? You bet caries is still a problem. This the the
decay of about 12 year olds , the caries rates for 12 year olds, I want you to look at
Australia by the way which has an incredible public health system as far as the
delivery of dental care. Theyre one of the examples that uses non-dentists to deliver
some prevention. And thats up 12 year olds um, but lets take a look over here

Dr. Poul Erik Peterson
[Dr.Wolff]: at the 44 year olds. They now have 13.9, um, what happened? How do
you go from this picture being a very lowest in the world of decay rates- to being at
the highest in the world? Whats that? They dont seek care at the same rate. They
went from a public health system that was mandatory for children to no public
health system necessarily for adults. Decay rates are sky rocketed they arent a big
fluoride contry even though theres a large amount of fluoride toothpaste available.
The US is in the moderate, but we see much of the world in the older population
with a very significant amount of decay and restored teeth. Thats a major problem-
so decay is still a very very current problem. Were going to talk about the
challenges of poor nutrition and access, and lack of education to see if we can
address some of it. Were going to talk about some of the models of prevention and I
did give you this presentation, but well spend more time talking about how or why
or what we did to control tooth decay. We need to recognize that decay is a
continuum, its dynamic, its multifactorial, and early caries lesions are reversible in
many many many many respects.

Challenges to Oral Health
[Dr.Wolff]: Even late carious lesions may be arrested and left alone. A large number
of very respected caries researchers talks about today about opening up access to a
lesion so saliva can get in there, arresting it with silver nitrate thiamine fluoride, or a
number of ways and leaving it alone.

Summary
[Dr.Wolff]: So I have a question, whats the life expectancy of an 85 year old in a
nursing home? Less than 2 years. How many of those patients actually need to have
a dentist restore their teeth if we can arrest the caries? Probably none. Probably
none. We have a mode a treatment today that doesnt fit the disease frequently and
doesnt fit the disease were treating. Were going to spend a lot of time speaking
about it. Im going to take questions while I boot up the next presentation and I
promise I will speak relatively quickly and be done by 4:30. Is that okay? Sure. I
really do appreciate, um, your being here, and you know what. Im going to ask- who
has a piece of paper- any of you have a piece of paper. You have a piece of paper?
Can you please circulate on that piece of paper your name and net ID have people
sign it. If you are at a point break, I will be happy to see to it that you people get the
point break if you are there. Now there are 32 of you, if there are 33 signatures in
there- no body gets it. Dr. Allen will be the keeper of the paper. Any questions?
I was going to post this but Id probably rather have people listen to the hour and a
half lecture and take notes. So. Yeah isnt that cruel? It is cruel? Not cruel? Oh I
should post it? What if I gave it to you? Just you. I have your net IDs. There you have
it. Well find out who shares it, and Ill copyright it- and then Ill find out which of
you share it AND THEN IM GOING TO SUE YOU FOR EVERY DOLLAR YOURE NOT
WORTH!

Diagnosis and Treatment of Oral Disease

Dental Caries Activity and Diagnosis

Diagnosing dental Caries
[Dr.Wolff]: Were going to talk about diagnosing dental caries here and this is really
important. Were going to look at activity and were going to talk about the concept
of activity and were going to talk about diagnosis. So whos responsible for
screwing all of dentistry and also coming up with all the wonderful things associated
with dentistry? No, not Mark Wolff. No where near as good as GV Black, my hero.
And GV Black was the 1 person that had 1 bullet, 1 treatment, and 1 classificaction
system for caries based on the fact that he only had 1 method of treating it, so Im
going to treat everything, describe everything the same. So when he looked at this
patient- someone please tell me whats the classification of that caries?
Classification Dos- class 2. Hmmmmm.

NYU | Dentistry (GVs pic)
[Dr.Wolff]: Does that classification tell you anything about the depth of that lesion?

G.V. Black
[Dr.Wolff]: Does it tell you anything about what surface that lesion was on? Was it
on the occlusal surface too or was it just on the distal surface.

Image
[Dr.Wolff]: You dont know. So was that a one surface cavity or 2 surface cavity? By
the way, when we count DMFS, how many surfaces is this? TWO! So after patients
see the dentist, their DMFS rises more than their D was before. Because part of the
process we need to go and treat these is to get in there and actually remove some
good tooth structure in the process. It doesnt tell us about depth, location, activity,
it doesnt tell us much other than how to bill a patient, and thats all GV blacks
classification did. It was essentially a billing classification. And were getting away
from that concept of a billing classification. Its still a class II restoration. Were
going to describe the caries to the faculty in different terminology. We are going to
use terminology like I have an active lesion that penetrates 1 level on the proximal
lesion on the tooth number whatever.

Blacks Classification of Carious Lesions
[Dr.Wolff]: Does the system actually tell you about surface of caries, extent of the
caries, I shot that already, and it doesnt make it possible to recognize that the event
of remineralization occurs. So I told you fluoride prevents caries by effecting
minerals. It has an effect, did Dr. Caufield talk to you about the amylase reaction?
Yeah he did. So it interferes with the amylase reaction- it has an effect on the killing.

Blacks Classifications of Carious Lesions
[Dr.Wolff]: It requires some relatively high concentrations. Higher than youd
conventionally see in toothpaste. But when we put fluoride varnish on , part of its
effectiveness is clearly inhibiting the amylase reaction.

Millers Acid
[Dr.Wolff]: But the big thing you need to recognize is that we now have methods of
taking the calciums and phosphates and forcing them back into toothpaste. We have
wide range of products currently available, MI Paste, um, theres a trical phosphate,
theres a number of different products on the market that contain calcium and
phosphate and fluorides, calcium, phosphate and arginine, in an attempt to change
the balance of the equation. As weve already discussed, you know this is a simple
chemical equation. If I put you to bed every night wearing a tray thats stuffed with
calcium and phosphate and you ate sugar just before you put the tray in- are you
going to demineralize or remineralize? Ive got a tray loaded with calcium
phosphate covering your teeth. Youve got acid on your teeth and no ability of saliva
to go in there. Are you going to dissolve the tooth structure? Why? Low pH. Tell me
about your, Hassels- what is it? Yeah that equation. If you keep a solution out here of
calcium and phosphate- even as we drop the pH can we see a mass action pushing in
this direction? No. So what if our strategies for controlling caries is actually to use
calciums to prevent the tooth from deminerlizing as well as to push it into
mineralizing. After a night a demineralizing with all that stuff on the surface, the
minute saliva touches the stuff- itll neutralize the acid, and youll get almost
immediate precipitation into the surface, and thats pretty dramatic. SO we now
start concentrating, not on this one surface here and creating surgical work- but
looking at these demineraliztions early and figuring out how to manage them.
Looking at the aproximal demineralizations. But in order to treat them and say
whether things are getting better or worse- we need to be able to record how severe
the disease is.

(He flipped between a number of image slides)
[Dr.Wolff]:
In 2002 and 2003, a group of cariologists, which I wasnt a part of at this time but
did join them in 2006, looked at a staging of caries that went more than hole or no
hole. As a matter of fact, it eliminated the use of the explorer, and said that we
shouldnt be sticking it in surfaces, because that will take demineralized surfaces
and break them up. It said rather were going to use this on the surface, scratching
across the surface to see if its rough

ICDAS
[Dr.Wolff]: Listening to hear whether its rough, but never pushing into surface to
see if its soft. Thats actually a real critical decision in here. SO we have these sound
tooth structures and at the first visible sign of enamel change its not there when its
wet but when we dry it we see the slightest whiteness and start to chart that. Now
as it turns out we start to calibrate examiners to determine the difference between
an ICDAS 1 and 2 lesion in the presence of saliva versus absence of saliva and it
turns out it takes a very well trained examiner to pick that up. Didnt turn out to be a
very user friendly mechanism, but its an effective way for research. Then we have
all sorts of discussions of occlusal surface and breakdown of surface and whether or
not we have caries of the surface. It turns out to be simple- are we open with the
caries in the dentin or extensive caries to the dentin. Do we have areas of
demineralization and do we see evidence of it on the radiograph, particularly on the
occlusal surface. So tooth 19 has a non-cavitated, ICDAS on the occlusal surface. How
do we decide whether or not to surgically treat this? Whats that? So
radiographically we dont see anything here. Thats a good sign. Clinically we said
its ICDAS 3- which is this ugly surface here, maybe a little breaks in continuity.

List 5 critical decisions
[Dr.Wolff]: But not a giant hole anywhere. Do you surgically treat this? Do we treat
it? So, tell me what our treatment is? Sealant is the most common treatment and
sealant, the good news is, if you have a tooth that has active decay you actually
arrest the decay for a period of time as long as the sealant is in tact. So its not a bad
thing to make the mistake and seal something active so that whole oh should I or
shouldnt I or if I dont treat it its trouble, but how do I decide whether or not to seal
this patients tooth?

ICDAS
[Dr.Wolff]: Do we seal all 6 year molars on 6 year olds? Ah risk, yeah, its a risk
measurement. So if I come in to you and Im 55 years old, oh okay and Im 59 years
old, and I have that tooth surface, and you look around and I havent had a carious
lesion in 10 years in your office. If we looked at it and I said it was an ICDAS 2 last
year but an ICDAS 3 this year what does it tell you? Its progressing. So you have
activity evidence. If its been an ICDAS 3 for the last 10 years should you be treating
it? No, because theres no activity on it. It hasnt progressed, and thats the key.
Thats where activity and diagnosis and visual appearance of the lesion come
together in a synthesized decision on how to treat the patient. Its that collision. You
cant take a single snap shot and know for sure. So I look inside a patients mouth, its
the first time hes come to see me, hes 59 years old, hes never had a restoration and
hes got a mouth full of these. Whats the likelihood that its an active lesion? I told
you the last hour of lecture, how quickly does caries progress? Has there been
enough experience of the tooth at 59 years of age. Yeah its been hanging out for 53
years. Theres no hole in it yet. Whats the likelihood its an active lesion? Very low.
So I get patients that come from my practice, move, I have a very academic practice,
I still practice out by stonybrook university. These guys go from my practice out to
another area, another practice; the guy looks inside their mouth and goes you have
9 cavities. And they go, Dr. Wolff hasnt treated me for cavities I nthe decade that I
saw him. So there are 2 choices of how this can be. Whats that? GV Black is treating
him, in which it gets treated. Or Im just a slouch, a crummy dentist, a slug. One of
the 2, Im glad none of you had the courage to say that to me. The truth is, Im
misdiagnoser or Im a very good diagnoser. In fact if you track this over time with a
category and you know if its getting worse or staying the same you know you have
the ability to say thats a quiescent lesion. Now what happens when he comes in
with the first one of these thats become an ICDAS 5 and I see breakdown into
dentin. Same patient 59 years of age has nothing nothing nothing nothing and all of
a sudden, one of those teeth break down. What do I do? I treat the tooth that broke
down and what do I do? (student says fluoride) well talk about fluoride in a little
while because fluoride on occlusal surfaces isnt highly effective. But sealants on any
tooth that I suspect to be at risk starts to become a different diagnosis, because the
patient has proven risk by virtue of the change in category. Now hopefully I see an
ICDAS 3 then 4 and see the lightest shadow. Theres nothing worse than an ICDAS 3
turning into a 5 because I didnt treat it when it was an ICDAS 3.

So a very complex matrix gets developed with caries classification and were going
to use caries classification in school that essentially says you have a sound tooth,
you have a tooth with initial lesion, and these initial lesions are all non-cavitated
lesions. Can we have a white spot thats an active lesion? What does it look like?
Have any of you done any bonding on any enamel?

Guiding Principles
[Dr.Wolff]: Have any of you done any bonding on enamel? Whats that? Did you do
any live tooth bonding? In school? No? did you excavate caries on an extracted tooth.
Ill make sure Dr. Bucklan has you etch and bond them next year. Well yeah no not
you, but next years class, unless you want to go back to first year again in which case
we can accommodate them. Etching results in what a frosty white area and if you
ran your explorer over it, it feels rough. Why does it feel rough, no not etch, what
occurred? What does the etch do? I think thats me dinging Im sorry. It is me
dinging. Can you do me a favor Kennie and run up to blue stone, (someone) is
looking for me and let her know that Ill be done after 5. Thank you. Okay where
were we? Why does it feel rough? It removes structure- we dissolved mineral ,we
took it away and havent replaced it. The good news is when you etch the tooth if
you dont bond to it, saliva precipitates mineral in the surface and it becomes
smooth again. Thats the earliest evidence of demineralization. So we can have these
initial white spot lesions and we can make 1 of 2 decisions. Its always non surgical,
you dont cut them, but the question is do we need to do something that helps
remineralize or prevents demineralizing or do we just leave it alone and let it take
care of its own fate? And activity helps us make the decision for us. When we see
even the slightest white spot thats rough and chalky, we talk to the patient about
what? Getting the plaque off the tooth. Talking about the fact that our acids start to
demineralized. So even the earliest lesions get treatment, but non surgical
treatment. Now these moderate lesions are lesions that we need more help with.
Sometimes we use diagnostic aids, Ill show them to you in a moment, other times
we look at the caries risk at both at the lesions activity and at the lesion surface but
its clearly at the patients risk, um and we have to decide do we do nonsurgical
therapy or do we do surgical therapy. So if its an active lesion, we take an X-ray we
look at it we dont see penetration into the dentin we are going to use a non-surgical
attitude or a sealant to go into that occlusal surface, or we are going to do something
to come in there do something really early minimum surgery that we can do without
doing major damage to the tooth. Do we choose to do amalgam or deposit. We do
that at the time before the prep not before we start the procedure. We think we are
going to use composite but if we have to use a different material at the procedure
we are capable of using it. Its very simple when we see cavitation to the dentin, or it
used to be. In Europe today D1 lesions are being either sealed or remineralized if on
smooth surfaces. Theyre not even treating D1 lesions radiographically. Were not
there yet, but it does appear that its effective. Standard surgery, minimal
intervention at all times. Were going to be using a sound, initial, a moderate, and an
extensive loss for caries, on roots Im sorry. You absolutely use only 3 classifications.
Totally sound, moderate with a loss of surface but not cavitated, or extensive when
we see cavitated. Yes? (student speaks) Yes. So fluoride will tend to make it less
soluble. I dont like the word harder, it happens to be that it is harder if you do a
micro hardness test, but its less soluble is the real issue.

Root Caries
[Dr.Wolff]: Um, but we actually look at remineralization as capturing more calcium
back into the tooth surface. Measurable amounts of calcium into the tooth surface.
Whats that? Dentin or enamel. And we use calcium products or saliva to go do that.
We see changes in microhardness also just with pure remineralization, not with the
use of fluoride- so we actually get a harder surface with more calcium content. We
see it in microradiography, we see increases, we see actual physical measurements
with some of the research that we actually do here at blue stone. Yeah? (student
speaking). Thats a good question. Can you get enough calcium in there that the
demineralized area suddenly looks normal again? Up until a week or 2 ago, I used to
show pictures of my 30 year olds maxillary premolar which when she came home
from college and was 19 years old all of a sudden she had an early lesion that just
touched the dentin. We went for 11 years without any progression of the lesion, I
guessed her last radiographs were 2 years ago, so 9 years. Last week, she came in
and had radiographs just taken a week ago and had caries so my concept of
remineralization has just been totally shot, hah oh no, in real experimentation we
stop the progress of the lesion and in fact she stopped the home care and things to
prevent the progression of the lesion. Uh, and I wonder if that was a HIPPA
violation, ratting out my own daughter. Its not the one you know so maybe its not a
HIPPA- who cares. What is she going to do arrest me? Fire me yeah, thats a better
idea. Yeah during the summer when we go fishing and vacation, Ill invite you to
come join me ,its okay.

Caries Adjacent to Restorations (CAR)
[Dr.Wolff]: So caries adjacent to a restoration. Has anybody heard of the term
recurrent caries? Thats what every one of my faculty call it. How would you feel
about a faculty member doing a restoration on your tooth and 5 years later saying
we have recurrent caries. Re-occuring caries. Is it because you didnt remove it Dr.
Wolff. No! Its new caries occurring at the margin. Is it recurrent? Or is it caries
around the margin? Now this becomes an important new discussion, because we are
starting to talk about not removing all the decay anymore and there will be a
difference between recurrent and caries around the margin, caries around the
restoration. What we currently call recurrent decay is actually caries around the
restoration. Activity, we talked about it. You can either see it in progress, lesion
either getting worse and worse, you can see it in the ICDAS classification, you can
feel it.

Activity
[Dr.Wolff]: Now one of the interesting things, and I was not a full understanding
about this, if you probe the gingiva, and it bleeds, what does gingival bleeding have
to do with caries? You saw Gregorys tooth, that canine with caries on it, what does
probing that surface, that perio tell you? If it bleeds what does that say? And what
caused the inflammation? Not well, its not really an infection, an infection yes, that
means that theree plaque accumulation there. So bleeding on probing when doing a
perio examination when the patient has caries, the caries is not related other than
its a sign that theres been plaque accumulation the last minute. So you cant cheat
the last minute. The kid brushes his teeth really well right before he comes in and
his gums are bright red and you know he hasnt brushed in 3 months. I see it all the
time, their teeth are perfectly clean and their gums are bright red. I know every
time, because mom got them to brush before they came to the office. I said, you
brushed today? How about yesterday? Really? Because your gums are all red, they
bleed when I touch them. Youll learn a lot about plaque from that. So gingival
bleeding indicates in a large extent whether or not the lesion is active, Because it
demonstrates the plaque accumulation and remember if you see white spots and
theres no plaque there, its probably not from plaque, its from another type of acid
exposure- what would that be? Erosion. So Im drinking my citric acid right now, pH
3.2, a little bath around the tooth. Whats happening to that tooth surface right now?
Im dissolving in the same way Ive taken that sugar and eaten it.

Activity
[Dr.Wolff]: As a matter of fact if I left plaque on my teeth, the plaque tends to
protect against erosive acids associated with oral consumption which is pretty
remarkable. So we use a visual examination, tactile, I like using the perio probe
because I cant put any force or break any enamel, run around the surface you want
to see if theres caries there. Run the perio probe in there feel whether theres a hole.
You can do that you cant put it into tactile, you cant do that. We use radiograph al
lthe time, radiograph is still the gold standard for aproximal lesions. We still havent
come up with new technology that beats it. Laser fluorescence, were going to teach
that to you this year. Have you learned about that yet with Dr. Glotzer yet?
Transillumination is interesting. The probe is dead. Stop sticking it in the teeth. Rat
them out, Ill come get them- Ill stick it right up theirFaculty appointment.

Caries diagnosis
[Dr.Wolff]: I dont need to stick a probe- thats a terrible picture, I dont need to
stick a probe in there. I can dry that tooth, I can look carefully at the surface and I
can determine whether or not theres dentin exposed in it. What I know about these
surfaces is if I take a sharp pointy thing and push it into a deep V wedge its going to
stick. And unless I see visual image that indicates caries the likelihood of that probe
telling you that its caries thats there that I didnt detect is less than 50/50 and since
when do you get to amputate an arm thats almost gangrenes.

Image of occlusal surface
[Dr.Wolff]: Dentists take this attitude well Id rather drill it before it became
carious. Well then lets put restorations on every tooth in the mouth! I know, you
guys think thats a good idea because you have a lot of student debt. But the truth is
theres no rational for ever destroying a tooth with good tooth structure in the hope
its going to prevent decay from occurring. Its just faulted logic. So I hear faculty all
the time. If we dont get it now itll be carious in a few years. Well in a few years your
restoration is going to go bad because we know the average life expectancy of a
restoration is 8 years. Ohhh I forgot. Youre Dr. Perfect, everything you put in the
mouth lasts forever, unless you visit another dentist and looks at your work and
goes dr. perfect didnt do such a good job. We can take it out and do it better. And in
fact- thats the number one determinant of the expectancy of a restoration, Im going
to say it over and over again because youre going to be evaluating someone elses
work. And you will be as criminal as they will be of you if you dont look at it and go
Okay, the margin is ratty it doesnt look, but I dont see any evidence of caries, the
evidence of demineralization, the evidence of breakdown, and the rationale of lets
change it before it goes bad- just bad logic. Talk to the patient, you have a number of
old restorations in the mouth that may not last many more years, but well keep an
eye on them. Much more valuable.
Guiding Principles
[Dr.Wolff]: This is an electrical conductance- theres some faults in this concept this
is a meter thats for sale and available on the market. You actually dry the tooth and
take this and you stick this into the groove and if theres conductivity it means its
going through dentin and that means that if theres caries it gives you a red, yellow,
green indicator on it to say that theres caries. But it overdiagnoses areas that have
no caries. Because conductivity does not directly relate to whether its carious, it
relates to whether or not its communicating with dentin. So if you have a groove
thats malformed open to the dentin its going to read just like caries .You still have
to fall back on your visual identification.

Image
[Dr.Wolff]: Its not a great technique. Then we have these laser fluorescence
devices. You hold them on the tooth, you shine the light in there and they reflect
back and show back the byproducts of caries and give you a physical reading you
use as a measure of whether or not you have tooth decay. Once again- very suspect
to over-diagnosis because stain in groove also increases measure of whether or not
its giving that indication- they detect stain and caries byproduct in the same way. So
its an overestimate. These are great helps, Im looking, Im arguing Dr. Wolff is that
an ICDAS 3 or should that be sealed or is this an ICDAS 4 that should be surgically
treated? Lets take out the diagnodent and take a look at the caries around the
groove not into the groove, around the groove, and if you see elevated numbers- I
agree, lets restore it. These are great adjuncts after youve done the clinical
diagnosis- not substitutes for it. So you go ahead and shine the light on the surface.

Image
[Dr.Wolff]: This is actually a great one that you guys dont use nearly enough in the
clinic. Whats it called? Transillumination. Using energy to go through the tooth and
cause a reading that allows you to see differences in density. Whats another
product that allows you to use the exact same way? Whats that? X-ray! Radiograph!
Were using photons in this one- and thats using high energy. This one doesnt
cause any damage to tooth. It doesnt put you at risk of cancer or anything else. The
other one comes with ionizing radiation it puts you at risk for damage to tissue. You
can shine a light on this look through any anterior teeth totally and actually for the
boards this is an effective method of isolating a tooth that has caries to the dentin.
They accept transillumination. Why doesnt it work in the posterior? Its too thick-
the light wont penetrate through. It doesnt transmit all the way through the
aproximal region. We can go ahead and offer a whole load of other methods to
manage these in a different fashion. What do you do with this? Its dry, its frosty.
Whats that? We first look a radiograph and make sure that theres no evidence that
its into the dentin. If theres evidence that its into the dentin, theres good rationale
for surgery. If theres no evidence that its in the dentin- you seal it. Its frosty- its
active.

Management of Pre-cavitation
[Dr.Wolff]: You know this is a photograph from Dr. Kaim. That little hole in all this
demineralization that you see here when it was open up was this giant carious
lesion. But its still was at minimum an ICDAS 5 this was never a seal this tooth.
Theres a hole in it and should have been judged as having a hole. This decay was
into dentin this area was kind of suspect and as we opened up the tooth we could
see the penetration to dentin in a number of areas but the real question is could this
have been sealed.

Image- J. Kaim
[Dr.Wolff]: This was an ICDAS 4 that was at that breakpoint and you probably could
have sealed this and the person could have done just as well. We tend to surgically
treat that at the school, Im not going to argue this point at this moment. I dont want
you guys surgically treating ICDAS 3s or just touching dentin on the radiograph.

(switches between various images)
[Dr.Wolff]: Abfractions are unique items. DO you know that that is, right there?
Whats that? Tell me what was inside that tooth. That was the pulp chamber. Its
actually the pulp has receded, disappeared, its gone. Pretty incredible. You can have
this loss- its thought to be from occlusal loading and some sort of activity. Why do I
know this isnt from a toothbrush? The adjacent teeth have nothing going on on
them.

ABFRACTION
[Dr.Wolff]: Unless you use a very small toothbrush on only 1 tooth, you couldnt
reproduce that. Its not erosive because what? Im only putting the acid on that one
spot on the tooth. Theres something else functioning there. Erosions tend to be this
shaped, theyre an acid event, they cause sensitivity frequently, theyre relatively
simple- the acids come from 2 sources- extrinsic being from drinks and things like
that- remember sports drinks have lots of acids. Intrinsic is vomiting and internal
items. This is probably caused by regurgitation. This erosion is clearly caused by
regurgitation- this one is caused by pregnancy and this one by bulimia. Not on facial
surface why? Acids coming out.

Chemical Erosion
[Dr.Wolff]: Some key items, brushing your teeth in the shower, brushing your teeth
frequently, throw up and brush immediately, its a common finding.
This what is that?

Dentin Exposure
[Dr.Wolff]: What is this? And what is this? Ahhhh-hahhh. Theyre both caries!

Erosion
[Dr.Wolff]: Whats the distinction between the 2? Stage, activity, this is soft, brown
looking. Its not black or showing signs of remineralized. We get a sense of frostiness
when its dried- its active, it shows signs of an active lesion, do you surgically treat
that? In the US yes you do- we would actually consider that relatively moderate to
extensive caries and should be treated. If you were speaking with Edwina Kid she
would tell you to arrest it and remineralize the caries and leave it alone. That may
work in England but doesnt work in US court.

Image- NYU|Dentistry
[Dr.Wolff]: But surgically treating this tooth would be a real real mistake. The
American dental association held a conference thats come up with an absolutely
wild, so on tooth 19 it has a site 1 initial lesion that would be rated 19.1.1. Yes? Oh I
hate that question, its a really good question. Why dont you seal that surface?
There actually is a product recently, its still illegal, its still not approved in the US,
the truth is its a viable product and Im sure youll using it before graduation- its
called ICON

Further Simplified Format of ICCS
[Dr.Wolff]: Okay It uses hydrochloric acid to etch the surface and it has a plastic
just like our sealant to cover the surface- its a new technology thats out there- the
problem is once you put that in place- He didnt take that bag of chocolate with him
did he? If he took that chocolate wed have a discussion. Is the chocolate over here?
No, I dont really care.

Image
[Dr.Wolff]: If we go ahead an seal that we cant get fluoride or calcium back into the
surface so its a real problem. This is the ADAs method of defining a lesion and its
crazy. So youve got cervical facial lesion on tooth number 6 it will be a 6F3.3.
Cervical, facial surface, 3.3 means its extensive. Cervical is 3- extensive- crazy
system I dont think its going to get any traction.

Further Simplified Format of ICCS
[Dr.Wolff]: But where we are seeing traction is a method of classifying thats
associated with sound, demineralized cavitated severe and moderate cavitation.
And we- this system is almost a variation, but so where we have gone on this at NYU
and we were here actually before the world has actually followed it, its the same
classification taught here for almost 9 years. It talks about looking at the surfaces as
being in tact radiographically, particularly, just penetrating the enamel. Anything
thats less than hitting the dentin is an E2, if its hit in the outer 1/3 its hit the DEJ
but not progressed passed the outer 1/3 thats a D1. If its progressed beyond the D1
to the inner 1/3 thats a D2 and a D3 is the deepest and thats a radiographic
distinction.

Caries Score Legend
[Dr.Wolff]: It also fits the intial caries, looking at the E1 and E2. The moderate
caries being D1 and D2 or the extensive caries being a D3 lesion. WE have now gone
on to what is now known as the international caries monitoring system and its the
ICCMS. Class 2 lesion is not a description of the lesion- you have to go further. You
know, I sent out the police looking for the candy. Did you just stuff it outside in your
locker or something? Thats what it was. Sugar addicts- thats terrible. Radiographs
are still considered a new standard. This is the new computer system that youll be
using to help classify caries um when you hit the clinic in January. Youll actually
take the measures and say you know that its cavitated moderately and its active
and youll actually chart that on the surface that its located. So well be able to
measure severity and progression of lesions as you go do it. Itll be quite simple
youll hit all of the extensive caries- bing bing bing bing bing. All those surface- you
hit add- moderate- ding ding ding ding ding-Demineralized but inactive ding ding
ding ding ding and youll chart it that way. Youll have initial lesions, moderate
lesions, um and caries into the pulp.

-C0000, Caries
[Dr.Wolff]: This would be classified as an initial, this comes from the ICCMS
document- this would be considered and initial lesion, early- its ugly, but its an
early lesion with no evidence radiographically or examination as penetrating. When
we go ahead and look at these we look at the radiograph to determine whether or
not theres been penetration in here. Theres been some penetration. Im sorry this
came out of their monograph it did not um copy over well.

Radiographic
[Dr.Wolff]: These are the extensive lesions and you can see the extensive lesion on
all of these. So we will categorize these as mild, moderate or extensive. Anybody
have any doubt? This is actually an extensive lesion its at the junction of the D2 and
D3- I would call this a D3 lesion- looking at the distance from here to here this lesion
is in the middle third.

Clinically moderate caries lesions
[Dr.Wolff]: And that raises the very end of our presentation- you were a wonderful
audience, I appreciated you coming, I promise to reward each and every one of you
somewhere in the future- I cant promise you the location but youll be happy you
were here- just say August 12, 2014 and its golden. They already know the little
code they have to flash me with their fingers so it wont work for those of you that
arent present. I wish all of you a wonderful day- good luck on that DOD exam- I hear
its terribly difficult- no Im just kidding. Any questions? Thank you!


23/24: Diagnosis of Caries

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23/24: Diagnosis of Caries

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Transcribed by: Atiya Bahmanyar August 12, 2014

Diagnosis and Treatment of Oral Disease

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