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, 2014

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Diagnosis and Treatment of Oral Diseases-- Lecture #25 Saliva and Caries by Dr.
Wolff

[1] [Title Slide: Caries, Plaque and Saliva]
[Dr. Wolff] Are we there? Ok, so we are going to spend some time together now!
[student: sarcastic yaaaay]
[Dr. Wolff] I told you the hearings not gone yet. The memory is fading quick but the
hearing is not. You can hope by the time youre a senior I forget what you look like! Thats
ok ehhh its too late, youre too distinctive! Uh, so this is actually the area I got my, I
received my PhD and was studying saliva and its relation to tooth decay. I get really excited
about it so I presume that you folks will get excited too. Or not. And thats ok. Did enough
people show up that I post the [slides]? Yes? Well post the slides in a few minutes to the
class so you can have the PDF of it. So caries plaque and saliva, as it turns out

[2] [What is a Biofim?]
the theory about what caused caries has changed over the years in multiple, multiple
ways. At one point it was very clear that the tooth worm was eating the outside of the
tooth. Everybody knew it. Then everybody knew that as food rotted, the acids of the food
rot would eventually break down the tooth and cause tooth decay. And it was a rich,
famous person that actually proved that it was the consumption of carbohydrate that
releases the acid that causes bacteria to release acids that dissolve the teeth. It was Miller,
1890. Thats an important step, if I knew anything on an examination, that would be
one of the things that I would keep tucked in the back of my head. So Miller showed
that it was the release of those acids after exposure to carbohydrates that caused this. Now
after that, everybody pursued what bacteria were creating the acids. Miller actually got it
wrong, he thought it was lactic acid produced by lactobacillus, and yes, lactobacillus
produces lactic acid and it does dissolve the tooth. But it turned out, well actually, some of
the best scientists did a really neat experiment. If we take a, if we take a little swab of
plaque and throw it on a plate and make it grow, we can go look at what bacteria grows
faster. So in that particular plate or that particular environment. And everybody found that
people with higher amounts of decay had Strep mutans. Lots and lots of Strep mutans. So
for a very long while, typically the entire 80s and 90s, there was a group of researchers that
swore that a bacteria, if we could come up with a method of killing that bacteria, we could
prevent tooth decay. Now first they looked at injections to kill this bacteria, they looked at
immunologic, they forgot that the mouth is almost outside the body, an amount of
antibodies, immune system response very different inside the oral cavity then it is even
inside the gut which is outside the body as it turns out. Its not fully inside the body. So
that turned out not to be so true. A theory emerged, actually, as I was doing my PhD, my
mentor, Israel Kleinberg, actually was proposing, 1994, that it was a mixed ecology almost
like the grass. Anybody garden? Weve done some grass discussions. If I go ahead and I stir
up the ground, I tear up this grass anybody play golf? Thats probably better. No golfers?
You ever see a weed in the middle of the 16
th
green? Almost never happens. These greens
are particularly not in Florida, in Florida, the greens are terrible but no. In a professional
golf course you get very tight grass that is grown and cropped extremely short. Every blade
of grass on that green is almost identical. And the thing that keeps it that way is actually
the health of the grass. Everything thats there you dont get that giant weed with that
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little dandelion growing up the middle. Anyone have a lawn that has dandelions? No never
mind. That grows where there is opportunity on the lawn. Very hard to get that weed to
grow in the middle of the putting green on the 16
th
hole. Well it turns out that the mouth is
very similar to that. So in the early 1990s Kleinberg and this guy Marsh, one in England,
one at Stonybrook, were making a proposal that it was a mixed ecology, it was a balanced
existence between good bacteria and bad bacteria that lived inside our plaque at all times.
And it was when this balance went off in one direction, what happens if it becomes too
anaerobic, too thick, too anaerobic in existence, what disease do we see pop out? Whats
that? Its not caries. Its periodontal disease. These are facultative these are anaerobes
they actually enjoy living in a shortage of oxygen, they can live deep inside the pockets. As
a matter of fact, if you look at the oxygen tension deep inside the pocket, its almost totally
depleted if not totally depleted. Many of the periodontal pathogens, and were not going to
speak about it, just the simple stirring and adding of air to the surface disturbs periodontal
disease. Thats one of the mechanisms that flossing is so effective. Now caries tends to be a
little bit different. Facultative anaerobes or pure aerobes that like being at the surface, like
thin surfaces, makes it a little more difficult to brush away. So this plaque - which by the
way we call plaque in dentistry but were the only group that calls it plaque, its biofilm to
all others, has this very complex organization both in the molecular structure and actually
in the communication between bacteria and the environment. Now you can get plaques, as
plaque grows thin what do you think is happening at the surface? Are they aerobe or
anaerobe? Aerobe. What do you think it is 10mm into the pocket? [students mumbling,
saying anaerobe] Yeah, so you can get a plaque that is actually mixed ecology with a very
mixed EH (pH? Unclear) and oxygen tension as you go from the surface to the very base of
it. It actually becomes more electronegative, it favors spirochetes, it favors the pathogens
deep inside the pocket. Well, Im a cariologist, Im gonna just cover that upper area, the
aerobe and the facultative anaerobe.

[3] [Why is one biofilm carious and another not]
So we keep asking this question about one biofilm being

[4] [Image]

...no caries there. Redness, periodontal disease, ugly. Ive told you, have you guys met this
physics professor, doesnt brush his teeth? Ok, this is my patient, physics professor,
brilliant, writes formulas down in the middle, on the bracket table cover, sits back down,
comes to the office once a month. Actually, came, he died of cancer, but came to the office
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once a month for us to clean his teeth because he was too lazy to brush. Periodontal
disease all over.

[5] [Image]

But we have this guy over here, pink gingiva, and the teeth are melting away. Absolute
clean, has this very thin biofilm. And it was the contention of Kleinberg and Marsh that the
mediator, the thing that controlled whether this patient got decay or doesnt get decay,
turns out not so much to be the bacteria, because we all come plus or minus some with our
full range of bacteria, but it is the ecologic pressure that pushes us towards caries or pushes
us to periodontal disease or sometimes both. Whats the ecologic pressure on this guy?
Look at his tissues.
[Student: saliva?]
[Dr. Wolff] - No saliva. So the ecologic pressure on this person was a lack of saliva.

[6] [The BIOFILM is where it ALL happens]
We are going to spend some time right now talking about how saliva controls what is going
on in the biofilm and what some of the mechanisms of that actually are.

[7] [Plaque Accumulation]

Plaque builds up very quickly on the teeth. Dr. Caufield is absolutely correct that it is a
niche environment, it builds up quickly, it spreads from defects, it hides in the defects.
Bacteria sit there as a reservoir, they grow, they expand.
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[8] [Role of Dental Plaque in Health and Disease]

Marsh made it very clear that in this healthy environment, it is very hard to take a
bacterium and stick it in here. And that is one of the reasons that this idea of giving you a
probiotic and expecting it to grow and compete appropriately doesnt work so easily.
Because getting a healthy biofilm to grow there when something is already surviving is not
easy to stick another species in. Everything is already functioning. And when we go ahead
and look at these ecologic pressures, it can be anything! Increased carbohydrate, suddenly
eating lots of sugar, what does that favor? I eat lots of sugar. What does that favor in my
biofilm? Are the two of you working that question out over there? No, the ecologic biofilm,
we add more sugar, what does it favor and why? Youve already taken your micro course,
whats the answer? Size 7. We werent looking at shoes? Oh no, Im sorry. Never mind, it
was just a different conversation. Oh you were looking at shoes! Shes turning red! If I add
lots of sugar to a patients diet suddenly, I favor the bacteria that like to eat sugar. So we
take our fermentable carbohydrate consuming bacteria, like Strep mutans, lactobacillus,
actinomyces, any of the bacteria that like fermentable carbohydrate and they start growing.
What does this do to reproduction? How does the ecology change? If I have bacteria that
are producing acid and they produce it constantly, what type of bacteria will want to grow
in that environment? Base-forming bacteria? No, it is bacteria that dont mind acid forming
environment. Favors acid-producing bacteria as it turns out. So even though I may have a
healthy base-forming bacteria in there, it doesnt get a chance to reproduce. It doesnt get
adequate food, it doesnt start to grow, it doesnt reproduce. The colony counts start
moving towards acid-formers. So lactobacillus goes up, and Strep mutans being the big two
players start rising. It means less carbohydrate produces an even greater drop in pH
because there are more bacteria that produce acid. So the minute I start taking this
balance, I got some good guys, I got some bad guys in here, I take the good guys and feed
them, I take the bad guys and I feed them some sugar, they produce some acid, they prevent
the good guys from reproducing, but the bad guys can keep reproducing, they make more
of them, now I add a little more sugar, I get more acid, more acid makes more environment,
we push this pressure in this direction and there are a number of different ways we can do
it! We can stop brushing our teeth. What does this do to the environment? It does two
things. It increases not the biofilm, because increased plaque is increased biofilm, thats
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just the word. If I stop brushing my teeth, I get a thicker biofilm which means I get more
biomass, more bacteria, more. So the counts start to rise on the surface of the tooth. If
theres lacto if theres strep there we are going to get more acid to sugar. What else
happens in that plaque? Right it becomes more oxygen consuming. The base of that now
starts to be more anaerobic. It means I may be favoring redness of the gingiva, difficulty in
the periodontal status, more spirochetes, more anaerobes, more everything will start
developing inside the pockets where it is anaerobic. We deplete the oxygen at the surface
with rapid oxygen consuming bacteria. So that pushes a stress that changes the flora,
decreased saliva changes the flora too.

[9] [Image]
Everything exists in the mouth. Good guys, bad guys, we like to see a balance of it

[10] [Flow Chart]
This is a crop out of his textbook, and each of these things, if I put fermentable
carbohydrates on the top, it produces acid. If it produces acid, I culture things that like to
be low pH, so I get my Strep mutans, my lactobacillus, and in the end product I see
demineralization. And on the other hand, if I can produce a food in there, it makes the
base-formers grow, that makes the base-formers grow, it results in a neutral or a rising pH.
As it turns out that that was the invention that came out of my particular mentor, I dont get
any penny of it, but I am a Colgate consultant so I have to tell you the patent is held by
Colgate, its the new pro-argine technology that feeds arginine to the plaque, trying to take
this environment that is highly acid forming, give the base-forming bacteria some food that
they like, and push the pH of the plaque up. In fact studies that Dr Allen and myself, and dr
Klachani have run here, have demonstrated that we can take a plaque that is acid forming
and by feeding it the pro-argine chemical, which is just and L- uh, a lysine, uhhhh, an L-
arginine, containing food, umm um toothpaste with uhh, um, calcium carbonate in it, if we
take that and feed the plaque that over a period of two weeks, we make a plaque that has a
resting pH of about 6.2, 6.3, 6.4, and push it up to 7.2. We actually change the ecology just
by having the patient brush with a different toothpaste. Same patient brushing with Crest
winds up with the pH staying the same. Feed it the right food, we push it in a proper
direction.
[Student question: If you are brushing to get rid of the biofilm, how would you feed
inaudible]
[Dr. Wolff] You never get rid of biofilm. Its a fallacy. My belief, the belief of my mentor
from literally 20 years ago now, was that were not going to at some point go for total
removal of the biofilm. We are going to go for biofilm management. Ecologic management.
So, biofilm elimination. That was the idea of having you rinse with a chlorhexidine, a
poviodine, taking an antibiotic to kill everything. But what winds up occurring is it doesnt
kill everything whoop wrong button [screen goes black]. Instead, one or two of these
bacteria (back to slide 9) survive, and unfortunately the ones that survive tend to be the
most nasty in what we deal with. If we wipe out the healthy portion of the flora, what
comes back frequently is a flora that we are not as happy with (back to slide 10). It has the
preponderance of the ones that so if you leave the ecologic pressure thats going to want
to make Strep mutans, youre going to get more Strep mutans than when you started, and in
fact a number of studies that have looked at what kills with products like chlorhexidine,
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thats in the outcome. You dont take all the plaque off. You thin the plaque. You reduce
the biofilm. You take most of it and you put it into solution inside your mouth, you spit
some of it out. It recolonizes coming out of the dextrans now start to hold it, it sticks to
the outer tooth, and it starts to regrow. It populates from defects on the tooth and grows
outward like we showed on that ultraviolet photo.

[11] [Breakdown of Microbial Homeostasis]

So when we kill normal diet or diligent hygiene,

[12] [Breakdown of Microbial Homeostasis]

we wind up with either demineralization or inflammation depending upon which direction
and what food were feeding it.










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[13] [The Role of Plaque in Development in Demineralization]

This is decay. If it is dull and matte it is active caries. If it is not it is arrested caries, but that
was or is decay. It is the byproducts of decay. Demineralization. All this is is a cavity, a
cavitation waiting to occur. 6 months, a year, 2 years keep feeding it, the surface breaks
down, you get caries.

[14] [Biofilm is Where it All Happens]
Biofilm is where it happens, but not what controls it. Saliva controls what is happening
inside the biofilm and we will talk about how that occurs right now.

[15 - 17] [Venn Diagrams]
So we know that when we cut saliva out totally we wind up with a patient that is very hard
to resist caries. There is a very high correlation to dry mouth., but dry mouth does not
guarantee that you are going to get caries. It just makes you much more likely to get caries.
If you reduce the biofilm radically, if you control the tooths surface by addition of fluorides
and other items, you can control the risk of caries. That poor patient that had radiation
therapy actually kept his mouth immaculately clean, was using fluoride, he had a bad floor,
he probably would have been a candidate for us to try to go in with a very aggressive
eradication of Strep mutans using any of a number of items. Another study we have
recently run in the school and will be running again is a targeted peptide that attacks Strep
mutans and kills that bacteria alone. Shows a lot of promise because if you can be feeding
the right nutrients to the plaque when you kill that one bacteria, you stand the chance of
shifting the flora in a totally different direction.

[18] [Comic]
I told you all this. Bacteria in your mouth eat sugar and excrete acid, which harms your
enamel. If you eat a candy bar, more bacteria will poop in your mouth and that is all this.
Bacteria do a couple of things. They eat, they reproduce, and they poop acids. Not all
bacteria, the acidogenic bacteria. And that is all they do. And if you think of it in that sense,
and then add the step 2 of the Miller equation which weve already shown you, acid in
presence of tooth makes dissolution, you now understand the entire decay process and
how to manage it.

[19] [History of Caries: Saliva]
We talked about this
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[20] [Plaque pH]
Stephan talked about have we spoken about the Stephan curve last year with you?
Stephan spoke about the fact that when we go ahead and take plaque and add sugar to it,
the pH automatically goes down. What makes this pH come back up? It is saliva. If we take
the saliva away, it takes about four hours which is about this length of time, it goes from 20
minutes to about four hours before that pH rises above the critical pH. What is the resting
pH of a patient that starts out with dry mouth? About 6.2. It means they live very close to
dissolving all the time. As a matter of fact, if they have exposed root structure, dentin has a
critical pH of 6.2. What would effect this line here? How do I change the position of that
line? Below that line, everything dissolves, above that line we get remineralization. Whats
that line called? Critical pH. Below the line it dissolves, above the line it remineralizes.
How can I move that line? [student: Fluoride.] And which way will it move? Up or down,
you cant choose them both. Well, you can, but one is right and one is wrong. It is going to
move it down! What it does is it says the tooth doesnt start dissolving until I get to a lower
pH. And if the tooth doesnt dissolve until I get to a lower pH, I stand a better chance,
instead of it being this long dissolving, it is only this long. So it decreases the amount of
time the tooth is dissolving. That is one of the values of fluoride and the tooth structure.
Thats the critical pH there.

[21] [Caries Rates]
So, Eskimos and the African Bantus adopted sugar containing foods and went from being a
population of no decay to a population with nearly the highest decay.

[22] [Image]
We spoke about these guys already, they made fun of my inability to make fire. But they
also dont get tooth decay.

[23] [In Vivo Plaque pH Responses]
They dont get tooth decay because they have a saliva that buffers the same amount of acid,
the same amount of sugar-causing acid Im sorry. The same amount of sugar the same
amount of acid produced by the bacteria in the mouth, they buffer it back quicker than
other patients with different saliva. They do that by a number of things. They have slightly
higher bicarbonates, they have slightly higher levels of the amino acids associated with
remineralization instead of demineralization. Arginine being one of them. So caries-active
people have lower pHs to start and have pHs that go down and stay down longer. It is
associated with saliva and what causes it.

[24] [Volume of Saliva Produced]
We produce a lot of saliva in our mouth, about a quart and a half a day. Its resorbed by the
gut, it is one of the fluids we use it when we speak when I get dry here. A little water helps
but saliva is what normally does it.

[25] [Protective Functions]
It does a whole load of protective items. You know we talked a lot when we were children
about the digestion with saliva. As it turns out that was just a phony story. You dont need
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the amylase in saliva to digest your food. It breaks some down but it doesnt do a whole lot.
It does carry a bunch of antibodies that we believe give the tissues some protection.

[26] [Factors Affecting Saliva Flow Rates]
Things that effect how much saliva we have. You know time of day, circadian rhythm, turns
out to be a very interesting item. Anybody drool on their pillow at night? You dont need to
confess, it is ok. Some people are droolers, some people are not. Most people decrease the
amount of saliva flow at night, and thats totally normal. And that prevents us from
drowning, choking on our own saliva and things like that. Thats good news, not bad news.
But the question actually goes a step further than just what happens if I give you a cookie
before you go to bed? And what does that Stephan curve look like when youre salivary
flow is naturally slowing down? Its combining the concept of cookie, the concept of saliva
and the concept of circadian rhythm. Whats going to happen? We havent gotten to caries.
The pH will drop, that is because of the cookie, and it will stay down long, it doesnt affect
the critical pH, it just stays down below the critical pH for a longer period of time because
you dont have the natural saliva production. Where do we see this as a tremendous
problem? Early childhood caries with patients that are using nursing bottles. You provide
the sugar during the night, there is no saliva at all to buffer that back to neutrality, it makes
the matter worse. And dont get me wrong I dont say that all childhood caries is from the
nursing bottle, Im saying that nursing bottle can increase the likelihood of childhood
caries. Standing up keeps you dry, drinking makes you dehydrat dehydration makes your
mouth dry. Light, daytime actually makes you salivate more. Smell has an effect on
salivation. Picture does not. I show you this lovely warm cinnamon cookie, and nothing
happens in your saliva. I bring a tray of cinnamon cookies into this room, and everybody
salivates for the next hour. Many medications reduce our saliva. Several thousand at this
point.

[27] [Stimulation of Saliva]
We can stimulate saliva a number of different ways. We can do it with drugs like
pilocarpine. These are stimulants for saliva but they are hard to live with because they
cause palpitations. We can ask patients to chew on things, chew on gum, whether it is
flavored or not, most chewing gums loose their flavor after a few minutes. Now that
chewing gum, does it still stimulate saliva? Actually it does, but not for the entire time
youre chewing, after a while it actually causes you to dry out a little bit. We can give you
citric acid, which actually is a chemical stimulant to saliva.

[28] [Flow rate vs. Concentration]
We know that when salivary flows go up, we get one really great effect and that is increased
bicarbonate flow. Bicarbonate neutralizes acid. So thats where we get this chew gum after
eating meals, to reduce the likelihood of getting decay. It neutralizes the acid, it helps wash
away the byproducts during that time.

[29] [No Title]
This is a Kleinberg graph, and its typical of what we used to get examined on. If you go
ahead and add urea, you actually cause base-formers to grow. If you add short chain
carboxylic acids and serine, we see the pH come back to neutrality. Sugar, we go ahead and
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see the pH drop, below neutrality, but we wont see it drop below neutrality in serine. Ok,
we see arginine, it rises just slightly above neutrality, and then it tops out in its ability to
control the bacteria base or base-form in the environment. So our saliva supplies a myriad
of things that help balance out what the pH remains in our mouth.

[31] [Graph, Mean Whole Saliva Flow Rate]
This is stuff that was actually from my thesis, but what I need you to pick up out of this is
patients that have very high saliva flow are very near neutrality in the acidity. When
salivary flow drops, ok, when whole saliva flow drops below 0.1, which is where we call
people dry mouth, we see pH drops near 6.2. And we did this on several hundred patients,
looking at their salivary flows, and then measuring what their pHs were. Their wetness is
different and their wetness is different and their pHs were different in each case. So pH
drops as we get dry, and our wetness so we get that sense of dryness. As it turns out,
patients dont complain about dryness until they start getting below 0.2 ml/min at rest. So
0.1 turns out to be that critical number.

[32] [pH of Saliva, Brawley]
Brawley in the 1930s sampled thousands and thousands of patients for flow and pH, and
what he found was that the pH of patients, the highest population of patients had a flow of
nearly 6 Im sorry. The pH of patients with the highest flows of saliva were up near 500
of these people had a pH near neutrality. Out in the wings we get people with very high
and very low pHs. So the population tends to be centered around that neutrality, and that
is why the population tends to be balanced as far as decay.

[33] [Hyposalivation]
In the general population hyposalivation is about 15, 20, 30% at most. Elderly are slightly
more, anyone want to tell me why? Whats that? Polypharmacy exactly. Its not that the
acini got old.

[34] [Hyposalivation]
Resting flow rates, you need to know these. Resting flow rate of less than 0.1 or stimulated
flow rate of less than 1.0 ml/min are generally signs of patient dryness. We flip the lip
open, we can go ahead and look at it, it looks dry. Dr. Glotzer, did you do salivary collection
in his laboratory yet? You actually can physically measure it. Stimulated is easier to collect
than resting. Resting you have to actually rest when you do it otherwise you get a higher
flow rate.

[35] [Medication Categories Associate With Dry Mouth]
Lots of drugs cause dry mouth. Were not going to spend much time on it. But what we are
seeing is that if we dont deliver the amino acids, if we cant put the bicarbonate there, we
see patients that actually wind up with higher caries rates, lower pHs in the mouth at rest
and longer term functioning.

[36] [Buffering Capacity of Saliva]
Uh, the ability to neutralize acid

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[37] [Saliva Eliminates Acids in Several Ways]
we dilute, we neutralize, and we make base-forming bacteria.

[38] [Graph]
The stuff, if we were to go ahead and look at a culture of bacteria, if we were to provide that
plaque with sugar, we see the classic Stephan curve. If we just put the hard particles from
the saliva into the patients mouth, or into the culture, the pH drops, stays down and is very
slow to come back if at all. The moment we place in the mixed environment the salivary
supernatant, the clear liquid of saliva, we see this pH start to return back to normal. It was
one of the sentinel experiments that actually showed that it was the saliva that helped
neutralize the acids from the Stephan curve.

[40] [Dental Embryology]
Very quickly, a quick discussion about why we see decay forming in the breakdown of
enamel. Enamel crystals are laid down in a very specific format by the Tomes process they
are arranged in rods. These rods come out from the DEJ to the surface, multiple rods
together. They rotate just slightly as we come back up. They are C shaped in format, they
fill with an amorphous hydroxyapatite in the middle. This precipitation of hydroxyapatite
both in the Tomes process and in the amorphous center of the C shape gives it its color and
its shape. When we see demineralization, we start to lose some of that preformed. When
we remineralize, after the tooth is erupted, we dont have to Tomes process to reassemble
these crystals. At best we can reharden the surface, but we may not be able to return the
surface to its natural color. And that is because of the complex method in which the initial
tooth was actually formed.

[42] [Enamel]
Enamel is a real crystal. There is very little proteinaceous matter inside it. Its somewhat
interesting. Decay in enamel is a pure dissolution process. Whereas decay in dentin, dentin
contains a significant amount of protein, it also involves denaturing of the protein to get the
dentin to fall apart as it dissolves. So theres actually collagenases, elastase, in the caries
process. Its actually mammalian, it comes from us. It is activated by acids, it helps dissolve
the dentin proteins that are holding the tooth, collagens that holds it together. These
organized crystals have tremendous potential for remineralization. Where do we see
remineralization all the time? Theres an oral process that remineralizes, its the other thing
that saliva brings to the table. It was actually in the graph, I didnt concentrate on it. Its
not calculus its calcium. Calculus is what we see. Saliva brings calculus and phosphate to
the table. If we make it high pH, it precipitates on its own. It does not form I dont think
its the next slide (flips through slides).

[44] [Enamel: Calcium hydroxyapatite]
So, hydroxyapatite is a very complicated crystal and youll need to know this formula for
the examination. Youre writing it down? What can I tell you. If we substitute a fluoride
for one of the hydroxide ions, what do you get? Whats that? You dont get fluoride, you get
fluorapatite, which tends to be less soluble. Its also a slightly larger crystal, doesnt pack
quite as nicely as the hydroxide calcium hydroxyapatite. If I go ahead and substitute a
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magnesium in for the calcium, do I have a more or less soluble crystal? It is a more soluble
crystal. So as we see teeth dissolve and get remineralized, they dont always remineralize in
this format. They remineralize in a less mature format that is more likely to dissolve. And
that is a slight problem. It may be more likely to dissolve but its harder than the dissolved
form.

[45] [Image]
So as we get this remineralization, we get these pulses of demineralization,
remineralization, demineralization, remineralization. Calciums are added and eventually
the calcium content grows enough that we wind up with hardness that doesnt let the tooth
fall apart.

[46] [Graph]
We see immature calciums. They come out as a calcium and phosphate ion at very low pH,
at these acid pHs. At the basic pHs, we get very mature calciums and phosphates. When we
go ahead and look at calculus, calculus sits somewhere around here, it its maturity. It is a
very immature calcium based product. That immaturity in the product means that it will
dissolve easier than natural tooth. Lets talk about that basic chemistry in that solution. If I
add acid to a solution, will it hold more or less calcium? Any of you take freshmen
chemistry? None of you did. Youre all getting expelled immediately, how terrible. It was a
prerequisite for getting here. If we add acid to the tooth, we get calcium coming out of the
tooth into solution. Which calcium is going to come out first? The most mature crystal or
the least mature crystal? Because it is more soluble to acids. That becomes an interesting
item. We dont see caries where we see calculus. And that is for two reasons. First saliva is
precipitating lots of calcium and phosphates. Second, if I have to put calcium in solution,
and if I add acid and its below 5.5 in pH, I have to be putting calcium into solution. If I do it
in the presence of calculus, it comes from the calculus. It doesnt come from the
hydroxyapatite of the tooth. So we wind up with this being a surrogate source of calcium,
protecting the tooth from dissolving in tooth decay. And that is a very mature thought. And
that means if we can get calcium species on the outside of the tooth, even if they are less
mature species, we can protect the tooth from dissolution. Thats the principle behind MI
paste, the new tricalcium phosphate paste from 3M. The Sensodyne with novamin paste.
There are a bunch of these pastes that are designed to put an immature calcium at the
surface of the tooth that when placed, when acid is placed on the surface, instead of the
hydroxyapatite dissolving, these less mature crystals come out of the tooth and wind up
filling up the acid contained solution and prevent the tooth from dissolving. It is a
surrogate. Now if you brush it away, rinse it away, and put more acid there, eventually you
will still make a cavity. So you can overwhelm that environment. But you can also balance
that environment such that by putting calcium on there, like wearing an MI paste at night,
you can add the calcium at night, in the daytime you have your acid challenges, balance this
off, and that is part of this balance between remineralization and demineralization.

[47] [Enamel]
Talked about fluoride substitute, carbonate substitute

Transcribed by Erica Manion September 3
rd
, 2014

13
[48] [Enamel images]
...thats hydroxyapatite.

[49] [Enamel calcium phosphate- hydroxyapatite]
Plaque calcium phosphate we talked about, it is amorphous, saliva calcium and phosphate
ions are amorphous, they kind of sit, they dissolve more easily than the hydroxyapatite.
Their precipitation on the surface has the affect of protecting the tooth from caries.

[50] [Salivary calcium and phosphate ions]
Why dont we leave on the sides of teeth? Are there any hygienists in the room? Whats
that? Well calculus is hardened on the sides of the tooth, what else does it do? It is a site for
bacteria that secrete exotoxins and irritants that cause other reactions of the tissue and
wind up breaking down the tissue, so thats not a good thing. And that is why we take
calculus off. From a caries perspective, leaving calculus isnt a bad thing. Its terrible from a
gum disease, from a perio standpoint.

[51] [Salivary Precipitin]
I gave you the more soluble, its a surrogate calcium source.

[52] [The balance between cycling demineralization]
The balance between, this cycling between demineralization and remineralization
determines whether the tooth falls apart. And its this ragged balance that anything that
upsets this ecologic pressure can suddenly result in tooth decay. Is there anything else that
I wanted to cover?

[53] [Enamel Caries]
We gave you critical pH

[54] [Caries Attack on Enamel]
Ion, caries, oh yes we do need to go over this

[55] [Image, same as slide 13]
So initially, when this area is exposed, so what caused the acid to be there? Whats that?
Tell me. [student: Fermentable carbohydrates, bacteria, and environment?] You pretty
much got it right, thats pretty good. You can go graduate now, youre done. So the
presence of fermentable carbohydrates meant that plaque was accumulating there. The
presence of bacteria, and then fermentable carbohydrate provided this environment that
caused the tooth to dissolve. So what happened inside this plaque? Tooth dissolved, where
did the calcium go? I made acid. Where does the calcium go when I have plaque on that
outer surface? Does it get to the tissue? Or does it go into the plaque? It does go into the
plaque. What happens if I neutralize the acid? It precipitates. So we take some calcium out
of the tooth, it precipitates. Does all of it go back into the tooth? Or precipitate? No. A
certain amount of it stays inside the plaque. When we brush it away, eat an apple, do
something, it leaves the surface. And that is forever lost, and that is what we are looking at.
Somebody who has lost calcium from the surface that was not replaced, but the reason why
we dont have a giant hole is we were replacing the calcium.
Transcribed by Erica Manion September 3
rd
, 2014

14

[56] [Enamel Lesions]
And whats happening on a subsurface level, this is a drawing that came from, his name
stars with a C if I remember It doesnt matter. It came out of a textbook from somebody,
its not my drawing Im crediting it to somebody that I didnt put down on the bottom of the
slide, Im sorry. This surface stays intact because we dissolved, take the material away, and
re-precipitate on the surface.

[57] [Image]
We can actually look at a real ground glass, this is from Silverstone, its cut off at the
bottom. This is actually what the surface looks like. When we look inside the center of this,
we get this microscopic picture, its not what we actually see. When we go ahead and look
at it we see the inside of the tooth having lost a lot of its enamel. We see a dark zone. What
is this dark zone around the outside? Precipitation, demineralization, precipitation,
demineralization. Two areas get to neutrality before the rest, what is it? The very deepest
part of the lesion gets precipitation, they very outer part of the lesion gets precipitation as
we go through the process. We have high concentrations of calcium right next to tooth
structure, so we get this precipitation right at the depth of the lesion and we get
precipitation at the surface of the lesion. We can see it here also

[58] [Enamel/Biofilm/Saliva]
this is just a diagram. Calcium and phosphates come out of the tooth in the presence of
acids. They go into the plaque. We can either get it to go out into the surface if we leave it
there long enough, leave the sugars, make the acid. It comes out of the tooth and goes into
the mouth. The moment it goes into the mouth there is a net loss of calcium from the tooth.
If we have a method of forcing calcium and phosphate into the plaque, we get precipitation,
we get calcium, we get remineralization.

[59] [Image]


Transcribed by Erica Manion September 3
rd
, 2014

15
This is from Don Zero, its just a graphic. We see this loss of mineral in the deepest portion,
in the more surface portion, if we add calcium phosphate from here we actually work to
remineralize.

[60] [Image]
This is once again from Silverstone, that we actually see this occurring in the enamel rods
where weve lost it, you can see this histologically. So we see areas of less density inside
here.

[61] [Enamel Lesions]
And if you go touch it with an explorer, you break open that outer surface, and now you
have an area that will retain plaque and actually cause caries. Well, cause deeper caries,
this is caries. Because now you cant brush it and keep it clean, the surface is no longer
intact.

[62] [Image]


And we see this in lots of areas, we can see it in the aproximal region on these teeth.

[63] [Image]


Transcribed by Erica Manion September 3
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16
Why is it disk shaped? If I put a drop of acid on the surface, it doesnt bore straight down, it
bores in a round shape, almost a funnel, because we are dissolving from the periphery. As
we dissolve from the periphery, we loose mineral, and that is exactly what we see here.
When it gets inside dentin, dentin has a higher solubility a lower solubility, it dissolves
more rapidly. So we see a quick spread and once again that same V shape as it gets deeper.
So it comes in, it hits the dentin, at this very narrow V when it breaks into the dentin it
spreads out and engulfs a larger area because it dissolves more rapidly.

[65] [The zones seen before complete disintegration of enamel are:]
We talked about this

[66] [Image]
We talked about this

[67] [Bitewing Radiograph Image]
This is the real type of picture of it

[68] [Blank slide]
And I think we are all done. Any questions? Yes?
[student: The crystal structure, like hydroxyapatite, the alkylinity, is that correlated to the
number of calciums or is it associated with the structure itself?]
[Dr. Wolff] Well, calcium phosphates, the solubility of calcium phosphates is related to the
number of calciums in the crystal, and its organization. So the lesser organized the crystal,
the looser the crystal, the more soluble that crystal is.
[student: On one of the slides it had octocalcium phosphate? Inaudible, more acidic than
tricalcium phosphate]
[Dr. Wolff] It dissolves, yeah I know where it is. [Goes back to slide 46] This is showing
solubility in the presence of acid. Highly soluble in here. Octocalcium phosphate is more
soluble than hydroxy, which is Ca-10.
[student: What about tri vs octo? 8 vs 3 calciums?]
[Dr. Wolff] Its not the pure crystal arrangement that determines the ability. The tighter
the crystal, the more difficult it is to dissolve. That order is correct. Yes?

[student: You said when calcium goes into the plaque then not all of it goes back into the
tooth?]
[Dr. Wolff] Right.
[student: So where does it go?]
[Dr. Wolff] So all items have a solubility for calcium. Even at neutrality a certain amount
of calcium stays in our saliva, doesnt precipitate. It only precipitates when the pH rises
and the solution becomes hypercalcium, and you get crystal formation and spontaneous
precipitation. SO I can put 2 tablespoons of sugar in my coffee, it dissolves in the coffee.
When I put 20 tablespoons in there, eventually it will no longer dissolve in the solution.
[student: But so if you have a net loss of calcium from the tooth it has to go back in
eventually?]
[Dr. Wolff] It doesnt have to go back in. It can get swept up into the saliva.
[student: But to prevent caries..]
Transcribed by Erica Manion September 3
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17
[Dr. Wolff] It has to get back into the tooth.
[student: So where does the extra calcium come from?]
[Dr. Wolff] It comes from either us forcing calcification by using acid fluorides that
dissolve and then get a spontaneous precipitation using the calciums that are in the mouth.
It comes back from us adding calciums in toothpaste, or it comes back naturally from our
saliva putting precipitate in, which contains calciums and amino acids into the plaque.
[student: Dietary calcium doesnt have an effect?]
[Dr. Wolff] Dietary calcium has almost no effect on tooth decay.
[student: And then one more question How does drinking water after eating effect..]
[Dr. Wolff] Drinking water after eating dilutes the acids in the plaque more rapidly.
[student: So, in terms of coming back to neutral pH?]
[Dr. Wolff] Its much quicker. It speeds that process along. Come on in! Its all yours.
Thank you. We were just in our question and answer period, Dr. Moghadam.