Hello. This is episode five of season two. Of course, the topic is the six lessons
approach to Biomimetic Dentistry. The last two episodes we talked
about cracks and we talked about decay and how they were confounding to myself
and are confounding to other dentists that are dealing with these two
major pathologies in dental practice. But after cracks and decay are understood
as the problem. The approach that these six lessons takes
is to try to make an early diagnosis of the teeth
that are at risk of decay and of cracks. And as we talked about last time,
that is always related to gaps underneath restorations
or cracks into teeth. And so what are the symptoms
that we look for in a tooth that has a risk or is developing
cracks or gaps under restoration? I wanted to use the information that I gleaned from studying the actual
anatomy of teeth. There's many, many outstanding books
that have given great detailed descriptions of brittle enamel
and how tough dentin is connected to enamel through a miraculous interface
called the dentino-enamel junction. We also call that
the dentino-enamel complex. But once you understand
this incredible creation of a tooth, to try to mimic it,
we have to understand certain things and the basic foundation
that a tooth is not acting like a tooth. If it has sensitivity to cold, sweet,
or biting. Now, when we say that we have to be
a little more sophisticated. If a tooth is sensitive to cold,
when you eat a very cold ice cream
or any type of cold refrigerated dish that's normal and that normal reaction to higher cold or lower cold temperatures is something that we use
to evaluate the health of the pulp. And so cold testing is something
that needs to be done on every tooth to determine if the pulp is vital or it has some level of inflammation. So that's the first thing
we want to test with cold. And if we have a normal response
it may be high normal or low normal. There is a bell curve and different
people have different sensitivities in their teeth. Some people all teeth are highly sensitive
to cold. Other people, they don't have
any sensitivity in any of their teeth. So that's a very confounding variable
the bell curve of sensitivity. But it's the best we have. But to extreme sensitivity to cold we usually associate a tooth
that has a crack or a gap underneath the restoration
or the crack into dentin. So this is founded on the research from Martin Brannstrom that was published
in the early and mid 80s. He was a very, very prolific researcher
on pulp histology, a very good friend of Charlie Cox,
who passed away last year, and Martin Brannstrom was able to
with some pretty sophisticated testing on vital teeth, understand
exactly how the movement of purple fluid was a response to these thermal stimulus. And then he was able to show
also that a cracked tooth also had an exaggerated response,
and that crack in the teeth indicated that the pulp
was being irritated by an opening and closing of that crack,
and that opening and closing pulled ondontoblasts
in and out of the tubule, and it also caused
circulation of pulpal fluid. And as was later
discovered and documented, actually 25 years later by Charlie Cox,
that there were actually flagella off of the odontoblastic processes
and these little flagella. Charlie called those nociceptors. And so the movement of the nociceptors
stimulated actual nerves that were in the pulp. And then that purple fluid
was the means by which the nociceptors and the nerves
were communicating with each other. The next thing the Brannstrom showed
was that if you have a crack, not only do you have a movement
from opening and closing
the gap under mask to a function, but you also would have a possibility
of having a sensitivity to sweets. How does that work? Again, the theory that has been validated
is that we actually have an osmotic gradient, and most of us have studied
osmosis a long time ago. We have an idea that certain molecules
can get through certain permeable or semi-permeable membranes,
and then that can cause a different gradient of certain molecules
on each side of the membrane. I mean, all that stuff
that cell biologist study a lot. Here's a good example of a paper
that was published that is kind of way over my head, but
that's the only way you can learn things. Pulp biology,
basically to master that takes four years at a PhD level,
13 pages with, about 196 references. could be a start. But again, when I talked to actual cell
and pulp biologists as they understand inflammation
and they understand in this, complex movement, some of it is osmotic,
some of it is just a pressure, and some of it is just a mechanical movement of fluid. If there is a infection in the pulp, meaning bacteria
are now being parasitized in the pulp, then that starts
a cascading of certain cytokinases and the cytokinases communicate
with the general immune system. That is all of our bodies
24 7 365 for as many years as we live. We're not really aware of those,
but the immunologic response and having a prime
or a an improved immune system, these are really hot topics for all people
interested in nutrition and health. But in the teeth,
we have a pretty good idea that if we don't have pain on biting,
there's no crack or gap. If we don't have cold sensitivity, there's no movement,
exaggerated movement of the pulp of fluid. But once we get into the infection,
then that cold sensitivity and the sweet sensitivity,
which is that osmotic, gradient that becomes exaggerated
and all of a sudden we have a pretty good idea
that we have an actual infection in the pulp from either decay or cracks. Cracks are infected. A very nice article from Doctor
Ricucci from Italy was published a few years ago,
showing the infected cracks and how they open about 200 microns,
200 microns or 200 thicker than bacteria. The bacteria
making acids in these infected cracks do cause a decay process. It's been termed occlusal effect caries
by Graeme Milicich and Tim Rainey. But these ideas of
if we have what I call an easy prediction device,
what we call a risk assessment for cracks and a risk assessment for decay,
the inter related symptoms of cold sensitivity or exaggerated cold
sensitivity, pain on biting, and then a sensitivity to sweets which is indicative of this exaggerated,
response in the pulp
when there's actual infection in the pulp. This 1234 system
that I developed for myself, became very,
very useful to evaluating these teeth that before I would just say, well,
the X-ray doesn't show anything, but the first breakthrough
is that question about cold sensitivity. And that was for Martin Brannstrom. And so when I read Brannstrom’s
book in 1995 96, it was already 14 years old. It was published in 1982. And, I was actually introduced
to brand some research from Fusayama that was introduced to Fusayama
by Ray Bertolotti in 1995, and the 1993 book
that Ray had at one of his seminars. I purchased it,
and then, as I would always do, because I have a historical background,
when I quit dentistry, I became a historian full time
for six months. After seven years
of getting a second major in history. But if you're a historian,
you always read the footnotes first. Because if there's any ambiguity
to a document's conclusions in history
is always revealed in the footnotes. In other words, this is what I said,
but maybe I'm not quite sure. So you have to read this
and this and this and these footnotes, these references that historical documents
in professional historical circles really live and die on. You know, my dad was a physicist
and not a historian, but there's certain things in common
with getting a PhD in physics or getting a PhD in history,
and that is that you have to understand that it's an evolutionary process
that builds on the shoulders of former physicist or former historians,
in our case, former dentist. And whenever new information comes out,
it always has to answer questions that previous publications didn't answer. And the questions
usually come in the footnotes. And this is the case in Fusayama’s book. He had a question. And the question is
how long is the ondontoblastic process? And, there were two schools of thought. He felt like it went five millimeters. So you got a cell body
that's, eight microns in length, and all of a sudden it has a process that basically at least a thousand times
longer than the cell body. So the odontoblast is in the pulp,
and it's got this arm sticking off in the pulp. Fluid in the tubule. That's almost a thousand times
longer than the cell body. You know, it's just like you understand these things and you go,
oh my goodness, each my teeth. The reason why they're sensitive
in a normal way or an abnormal way is because there's actual cells
that perceive pain, just like the cells in my skin
or different parts of my body, but they're structured in a very,
very different way. You know,
you just have to shake your head. But Fusayama is taking the scanning
electron microscopy records, and he's documenting near the siege
the day, I should say, the day that there are remnants of these processes
that are being shut down. They get smaller and smaller
as they get closer to the enamel. But, his theory
was they go all the way to the deejay based on the idea
that the actual mineralization of the tooth starts at that DEJ area
and we got amino acid go all the way to the top of the enamel,
and that's about 2 to 3mm in thickness. And then we got odontoblasts that go
the opposite direction of the ameloblast. And they go down farther. They go down about 5 or 6mm. And so the processes that start growing off the cell bodies,
as the cell bodies migrate, as they're producing dentin,
the Donald blast process is there. Or at least a remnant of it
for the whole length? Brannstrom on the other hand, when he looked at the seams,
he didn't see those in the same way. And in his book in 1982,
which was two years after fusion, his first book, 1980,
had a different opinion. He felt like the dinosaurs thought process
has got shorter and shorter, and we're only in maybe the first couple
of millimeters, not the full 5 or 6mm. Well, these discussions
that Fusayama mentioned in his book, and then I would read Brannstrom’s because
Fusayama said this was the discussion. But Brandt's room in his book solved
the problem of where dental sensitivity came from. Cracks and gaps. These are the things that give pain, just like decay,
which is Fusayama’s expertise. created a response, an immune system. So we have these two experts in the 80s, one in Japan and one in Sweden,
who disagree on some things. And a person like me is just like,
I don't know anything. Let me, you know, let's see what they got. You read both. Then you go back
and forth, back and forth. But this is how science works. And so people that don't understand
the healing capability of the Pope probably won't be interested
in pop biology. But every patient that you have, ones
that have teeth that aren't sensitive to the sweet goal or by especially if that's a symptom
that could lead to an early treatment. So the six lessons approach is early
diagnosis using the 1234 method of risk assessment,
look for crack into enamel. Ask about symptoms. Is the cold sensitivity present? Is the biting sensitivity present? is a sweet sensitivity present
that would indicate that this crack that you're visualizing in the enamel
is now past the DEJ, and is into the sensitive
part of the tooth the dentin. That crack in the marginal ridge
usually is always a manifestation of some kind of micro movements that has allowed
the rods in the crack to separate. They can separate and stop the day. Most of them do. But there is a symptom that is shown,
I should say, a sign that can be observed that, particularly in conjunction
with the symptom of sweet tooth, cold or biting
sensitivity, can very easily be related. And this was done again in that period
when Fukuyama in 1980 and brands from 1982. Right between those two years,
Larson and Douglas and guides filled the University of Minnesota
published a landmark paper in 1981. They got 1980 Fusayama
you got last in 1981. You got Brannstrom 82. They're all trying to figure out
how much strength does a tooth need to prevent cracks and infection,
and it related to the isthmus width. And the isthmus with on intact
by customers could withstand 500 pounds of force
before they would fracture. But if you did a GV black preparation
which removed the interconnection between the cusps
which are now termed sub occlusal oblique transverse ridges or Rainey ridges,
after the discoverer of this anatomical structure, then those curves
move in an exaggerated manner and that leads to initiation
of fractures and cracks. So the fracture resistance of a tooth
that had a conservative GV black preparation
taught in dental school of 1.5mm, that was taught by GV black
as a way to prevent decay by eliminating these groups that were prone to decay,
called extension for prevention. One of GV Black's original principles. Only one problem it harmed the tooth. And so Hippocratic Oath. Hippocratic says, well,
if you don't know what you're doing as a physician,
at least don't do any harm. If you've hurt somebody before,
don't do it again. It's like do no harm
becomes pretty common sense approach to trying to fix a body
if it's having problems, which many do. But as we get to
this isthmus width of two millimeters. So we got one look for cracking it,
and we'll ask for symptoms to look for isthmus width. Once we get past two millimeters
we've lost 60% of the fracture resistance of the tooth. According to the Larsen and Mondeli’s
experiments on the extracted bicuspid. The third idea of number
three of measuring the cusp width, because that predicts if a cusp is at risk of fracture,
a thin crust becomes dehydrated because now you have a restoration
in between the cusp and the pulp. So the pulp can't hydrate
the end of the cusp tip. If that happens, that person
is three times as likely to fracture. And that was proved in 2007 by Vedantam
and Kishen out of Singapore. And number four is the box depth. And the box depth. Probably let me know all of these ideas
in the science of dental anatomy and what it's like to have
a functioning tooth without symptoms. Number four is huge because once
I started to investigate this area, all kinds of things became manifest
that the deeper you get into shoes, the more ology
and the more water you have. That gives it flexibility. That's a good thing, except if you're
trying to do restorative cohesively. The more college in the more water,
the less bond able that two structure is. So as soon as you get four millimeters
deep towards the siege, you have all kinds of problems
that have to be addressed as far as the sophistication of your
restoration, these sub gingival areas. If he's silly, I wish it was simpler,
but this works if you understand that the 1234 risk assessment for fracture
and decay gives you the ability to make an early diagnosis of a tooth
and treat it early and early treatments are easier,
less time consuming. They'll cost the patient less. But if the patient is in a proactive first
and just says, well, I don't get my tires changed in my car
until I have one blowout, you know, that's one philosophy
on driving a car, but it's a little risky. Most people will go and have their tires
checked, and when they get low and Fred, then they'll say, okay,
time to get a new set of tires. I would like to be under control. And I'm driving my car in water or snow anyway. So the 123, four risk assessment, these are the the foundations of the six
lessons approach, early diagnosis and early treatment of teeth
that are at risk for fracture and decay. Usually, once you start treating a tooth
that is at risk, you'll see the vast majority of time there. The processes are already in progress and so early crack removal
much easier than late crack removal. Early decay removal,
much easier than late removal. And the exciting thing that we didn't know
20 years ago is that if you get trained in the lesson for stress reduction,
you have a permanent bond. They don't break down ever. In other words, Bob Paxton,
my neighbor, lives two blocks away. I trained them 18 years ago. He's done 10,000 by all bases,
never has had recurrent decay underneath a bio base
because the tooth doesn't have a gap, there's no cracks, and all of a sudden
you have a hybrid layer that's acting like a natural tooth,
which is what biomimetics means. Mimic the natural tooth. All right.
Thanks for letting me talk with you. And until next time,
get bonded, stay bonded.