27: enamel ii

Transcribed by Jazmin Lui April 23, 2014

CRANIOFACIAL BIOLOGY ENAMEL II – DR. WISHE

Good morning. This was our last slide from the previous lecture, and the scene depicted here looks like many of you. You’re about to fall asleep, you’re short of some shut eye, but you’ll eventually catch up. The last topic we discussed was Hunter-Schreger bands.

O-FIG. 3-21 NEONATAL LINE (11th Ed)Now we’re ready to move into incremental lines. You know what the

word incremental means – it’s a depositing or laying down by layer by layer by layer. That’s your appositional layers, we’re talking enamel, dentin, doesn’t really matter. Now we’re going to talk about incremental lines present in enamel. All incremental lines have common feature – they’re all hypomineralized. And what they basically represent are disturbances in the process of growth and mineralization in growth of enamel. Dentin has a similar set of lines. We’ll do a comparison in short while comparing the two types of bands. The first things to discuss happen to be the lines of Retzius

O FIG. 3-15 LINES OF RETZIUS (11TH ED)Oh, I forgot. I ended the lecture and showed you my animal slide. Now we’re where we’re supposed to be. OK. As you look at these two pictures this represents the enamel and these lines that are extending across the enamel represent lines of Retzius. Why they use lines I don’t know, for the most part they have certain thickness, and maybe calling them bands of Retzius would be more appropriate. But these lines nevertheless vary in thickness and depending on the disturbances of growth in the mineral process. They actually start at the DEJ which is this structure here and extend towards the free surface of the enamel. Wherever they touch the free surface of enamel you’ll find structures called perikymata. We’ll come back to that momentarily. As you start cervical region of the tooth you’ll see lots of lines of Retzius. As we move up towards the occlusal end of tooth they tend to spread apart much further. Also as we move up towards the occlusal end of the tooth the lines of Retzius no longer touch free surface of the enamel. So as you look at this particular area, You’ll see likes of Retzius going around not touching the free surface. That means at the occlusal end of tooth you’ll never have perikymata, which actually represent the touch point of the lines of Retzius at the free surface. Also as you look at these lines they have unequal thickness, that’s just related to the length of disturbance.

NANCI TC Fig 7.49 LINES OF RETZIUS (7TH Ed)Here’s another picture again, the arrow is pointing towards the lines of Retzius. You’ll notice this dark patchy area which is located in dentin.


From here to here is dentin and dentin is the major tissue of tooth. This surface should be more like that. It just looks like it’s been chopped off – you don’t really see too much enamel covering the dentin.

So in all probability that enamel was probably worn down after years of masticating food. Enamel does become thinner as you age. It becomes thinner in terms of overall thickness and vertical height. So you’re having a loss of enamel in two different directions. At any rate, there have to have been some sort of lesion in this neck of the woods. It doesn’t show it in this picture, but part of the enamel could have been eaten away by bacteria, once it gets through enamel it could pass into dentin. Once bacteria gets into dentin they’ll open up dentinal tubules which we haven’t talked about yet. The odontic process which is housed in tubules dies if you will and you open up pathway directly to pulp. This is the pulp. So once air rushes into tubules you get darkening effect and these tubules are now referred to as dead tracts. And we’ll come back to that. It’s in this picture so I’m just pointing it out to you.

GH PLATE 13.2 FIG. 1 ENAMEL (5TH Ed)As you look at the enamel over here you can see these lines of Retzius going around and as these are at a different angle, these represent the enamel rods. They both start at the DEJ and go in a direction towards the free surface of enamel. Obviously something is happening in this


region. This is a multi cusped tooth and the other is partially shown on the right. And the enamel has been chewed up like Pacman and Paclady, just munched away. So all this enamel has been dissolved by your bacterial acid and enamel is 96% hydroxyapatite. So the acid completely destroys that tissue. In addition, you’ll notice certain dark regions, over here and here. Once you get this darkening of the enamel something is going on, and that would be the appearance of a carious lesion. You’ll notice something happening over in this area, a darkening of a tissue, this appears to be some sort of structure passing into the enamel [points to crack next to “e”]. This could be enamel lammela or enamel crack. We’ll see some in other pictures. Once you have a hypomineralization effect occurring in the enamel (that’s through the action of your bacterial acid), you’ll find that area is hypomineralized and bacteria find it much easier to attack enamel with less calcium. Less hydroxyapatite. Makes sense. And here we have some darkening of dentinal tubules, again, your dead tracts. This picture also shows you the dentinal tubules, let’s see if I can draw this a little bit better, which are described as being S shaped. It’s not a complete S it’s a partial S, but that’s the appearance of dentinal tubules particular in the crown. In the root the tubules tend to be much straighter, much more perpendicular to long axis of the tooth.

DVD – ADULT CROWNNow here’s another picture again, showing a lot of lesions, where you see these darkened areas. In fact in this area it looks like there’s a hole in there. So somehow bacteria got into the region, it could be where this arrow point is, it could be over here, it could be in another dimension. And you’ll notice the surface enamel seems to be OK, but as you go deeper, the end of the enamel, the part of the enamel towards the DEJ is really being eaten up and is now extended into the dentin. Something is happening over here, it’s a darkening of the enamel tissue right up in this region. The tubules are dark, so that’s your dead tracts. And notice this area right in here [points to end of dead tracts]. This is your own tooth playing dentist. What your tooth tries to do is try to seal up dentinal tubules to prevent any passage of bacteria from tubules to pulp. And this can be done in two ways, we’ll discuss that in much detail later on, one is through formation of tertiary dentin, and one is in the formation of sclerotic or transparent dentin. We’ll come back to that in a while.

O FIG. 3-16 LINES OF RETZIUS (11TH Ed)Cross-section through the enamel. Now this is a good representation of the lines of Retzius. You can see the thickness is highly variable. Then we see some other structures present. This area, and this area, and the picture calls them cracks. Looking at the picture you can’t tell if it’s


a crack or not. It could an enamel lamella which could turn into a crack. In any case the lamella and/or crack are hypomineralized and that part of the tooth doesn’t have as much protection as the rest of the enamel. If we look at the DEJ (which is where I’m pointing to right now) you’ll see some fuzzy structures arising from DEJ, those are known as enamel tufts. So both are sort of representations of geological faults that are happening which caused some sort of event to lead to hypomineralization. With the enamel tuft there is no problem in terms of danger to the tooth. Starts at DEJ and extends up into the enamel, up to 1/3 the thickness of the enamel. When it comes to lamella they do present a problem. The enamel lamella start at the free surface, could extend partially into enamel, could extend all the way through the enamel, and it could even cross the DEJ and extend all the way into dentin. So this represents a weak point in terms of the enamel and could guide the bacteria right into the dentin, knocking out the dentinal tubules. A good explanation of these disturbances would be by my following example. You have an earlier version of a Corvette which had a carburettor, and most of you probably have no experience with a carburettor type of car, but you had to pump the gas, let the gas into the carburettor, push the button or turn the key and start the engine. Say it’s a cold day, you go shopping. Bloomingdales, Macy’s, you park your car and come back hours later. It’s easy enough to put the packages in the car but it’s not going to be so easy to start the car because of the extreme cold. So one pump of the accelerator and turning the key won’t do. You may have to pump the accelerator a few times, but not rapidly cause if you do it rapidly then you’ll flood out the engine, then you have to sit even longer till the gas gets out of the carburettor. Eventually the engine will turn over and you’ll hear – ch, ch, ch, it’s running very rough. After you sit a couple of minutes the engine smooths out and you go on your way to the next shopping centre. And you stay there for a few hours and then it happens again. This doesn’t happen to new type of cars, they don’t have carburettors, they have fuel injectors. They’ll start immediately. So in that case there was a delay in the ability to start the car. And that’s what happened here. Something disturbed the formation of enamel. Mineralization of the enamel. And then to get it going again it takes a while to start again. And as a result you get the appearance of these dark brown type of veins. You can also think of the lines of Retzius as xylem rings. Think of a tree. Cut through the tree stem, cut through a branch you’ll see rings. Same sort of philosophy applies there. There’s a delay in growth of the stem or the tree branch itself.

O FIG 3-21 NEONATAL LINE (11th Ed)OK, We have something that’s called a neonatal line. You can figure out what it is yourself, in essence it’s a line that occurs between pre-natal and postnatal development of the enamel. Here’s your enamel,


you see some lighter tissue, some darker tissue, and here’s your pointer to the neonatal line. In essence the neonatal line is nothing more than an exaggerated line of Retzius, it’s a much thicker band and structure. When you’re born two major things happen. One, you have a change of environment. You’ve just lost your swimming pool. Now you’re in the outside cruel environment. That has a very strong effect on growth process. Number two, the pattern of nutrient changes. You used to get everything from your Mom with the placenta system. That no longer exists. So now you have to adjust to formula, mother’s milk, etc. apparently most children have problem with have to adjust to formula, mother’s milk. Apparently most children have a problem after they’re born with formula and you have to play around until you get the right formula, most children are sensitive to the formula to begin with. Those are the two big differences between prenatal and postnatal development.

A&C PRENATAL/POSTNATAL ENAMEL FIG 7-10Here again is another picture showing you the neonatal line. This is the early enamel, or pre enamel, or prenatal enamel, here’s the layer of postnatal enamel. Just think for a moment where do we find the ameloblast? It’s gonna be out here. So at the apical end of the ameloblast the enamel is gonna be laid down. This is represents the DEJ. So the newest enamel is going to be closest to the ameloblasts. The oldest enamel is going to be closer to the DEJ. That’s the enamel that was first formed, makes sense. And to switch to the dentin side, here’s the pulp, put your odontoblast right here, same story happens. The youngest dentin will be closest to the odontoblast. The oldest dentin will be over here on the other side of the DEJ. Again, that makes perfect sense.

NANCI TC FIG 7-62: PERIKYMATA (7th Ed)Perikymata. So I mentioned before we have lines of Retzius, or in this picture stria which means line, touches free surface of the enamel, you’re gonna get the structures which I’m pointing to, which are perikymata. And the perikymata are transverse, wave-like grooves that go around and encircle the tooth. As you look down towards the cervical region of the tooth you can see much more perikymata than as you go up towards the occlusal end. In addition as you get towards the occlusal end the lines of Retzius don’t touch the surface of the enamel and we see, goes around this cuspal area. This is characteristic. As you get older the perikymata will disappear.

A&C FIG 7-14 PERIKYMATA (3RD Ed)Now here’s a nice picture of the tooth, they lopped off the dark lines of your perikymata. You don’t even need the dark lines, just look to the


right. You get the impression that something exists in this area. But you don’t get a proper view of a groove like structure.

NANCI TC FIG 7-60 ENAMEL (Enamel Rods, Lines of Retzius, Perikymata) (7th Ed)Another picture from your book Tancatti. It does show the presence of your lines of Retzius. So here it touches your free surface, here’s another example of a line touching the free surface. That’s where you get your perikymata. And by the way these lines extending across the enamel happen to be your enamel rods.

O FIG 3-19 PERIKYMATA (11TH Ed)Not the greatest picture but you can see something on the surface of the enamel. Again that represents your perikymata. Now the picture on the right is giving you a more accurate representation. Remember perikyamata are transverse, wave-like grooves. As you look at this SEM picture you see these ridges, and what do you find between the ridges? A space, a groove. That represents the perikymata. And with due time, number of years, these ridges becomes shorter and shorter and disappear so that the enamel itself will appear smoother much later in life. And again the max number of perikymata are towards the bottom of the tooth. And the number decreases as you go towards the occlusal end.


A&C FIG 7-15 PERIKYMATA SEM (3rd Ed)Here is another nice picture, an SEM. These are your enamel ridges and in between would be your perikymata.

O FIG-311 RODS (11TH Ed)Here we have a nice picture of enamel rods, “O” by the stands for the book Ohban’s Oral Histology” that we used many moons ago, it went out of print but there’s nothing wrong with the pictures. They aren’t flaming technicolour but they’re still pretty good. You’ll see these structures extending in this direction. They represent the enamel rods. And then you’ll see little cross- structures more or less perpendicular to enamel rods. We can draw some diagrams, here’s the rod. And here’s those little structures. Almost resembles a step ladder. And these little structures are known as daily incremental lines. And they really represent shorter periods of disturbances. Roughly 4 micrometers of enamel deposited each day and if you have disturbances in it you’ll get these daily incremental lines.

O-FIG 3-18 STRUCTURELESS ENAMEL (11TH Ed)So those are the incremental lines. Let me tell you the names of the equivalent in dentin. Line of Retzius in enamel, contour line of Owen in dentin. Both tissues have a neonatal line. Daily incremental lines in enamel, lines of von Ebner in dentin. And the same explanation is used to explain why they happen, the disturbances of mineralization. What we see in this picture is something called structureless enamel. When enamel begins to form you have your ameloblast but not your ameloblastic processes. As a result the enamel that’s forming doesn’t really have a rod like structure. So you’re going to find structureless enamel in the beginning of enamel formation as well as at the end of enamel formation. So this is more like a surface of the enamel, so why do you get structureless enamel at end of enamel formation? Because your ameloblastic processes die off and although processes are not incorporated into enamel, like the odontoblastic process is incorporated into dentin, it still helps to determine the structure of the enamel rod.

O FIG 3-28 LAMELLA (11TH Ed)Now we come to other hypomineralized structres, which I hinted at before, those are your enamel lamella, tufts, what I didn’t mention happened to be the enamel spindles. Here we have a nice pictures, there’s your enamel, your DEJ, and your dentin. It’s hard to see your lines of Retzius, but the region appears a little darker, so that could be a line of Retzius. More important we see this structure. And this is your enamel lamella. Starts at the free surface and this case goes completely through enamel, across the DEJ into dentin. Again it’s


hypomineralized and occurs because of disturbance in formation and can turn into a crack. It is a potential weak point for bacteria to get into dentin and make it’s way through the dentin and into the pulp. Bacteria will always go towards the area which is less mineralized. At the DEJ we can see these little fuzzy structures. They start there and they extend into the enamel, up to 1/3 of the thickness of the enamel. And as you look at the lamella and tuft, it’s hard to focus on them. That’s because they’re extending into different planes. It’s not like a straight line. In fact if I were to draw a picture of a tuft, it’s going to look like that, almost like you’re pulling grass out of ground. You have a root system and the root system is extending in all directions. So that’s the way the tuft actually looks. No real known significance in terms of tuft except wherever you find enamel tufts the direction of the rods in the enamel go a little crazy, go into all directions. When they do that, that’s what’s known as gnarled enamel.

DVD LAMELLAHere’s another picture of enamel lamella and this one is going through the enamel and actually stopping at the DEJ. Here’s some nice example of a tuft, it looks very fuzzy. Both the lamella and the tuft look a little fuzzy, you can’t get a clearer picture.

DVD TUFTSSome more tufts. And then in the background if you look carefully you’ll see structure like this, and there’s something hidden back there, and here’s another one. These are enamel spindles.

A&C FIG 7-12 TUFTS (3RD ED)We’re still on tufts. Some more fuzziness.

NANCI TC FIG 7-57A DEJ (7TH ED)And before we get into spindles, I’d like you to take a quick look at DEJ. So here’s enamel and here’s dentin. And in your permanent teeth especially, the DEJ is not smooth, it’s scalloped. Something like this. And you have enamel sitting in and fitting into these scalloped areas of dentin. This provides a much better adhesive force for the two tissues to stick together than just having a union like that. The picture on the right is showing the same thing but the calcium has been extracted so all you have is enamel space. Dentin having 20% organic material is still present. Look at DEJ you can see scalloped region very nicely.

NANCI TC FIG 7057 ENAMEL, C: TEM OF DEJ, D: SEM OF DENTINC is a transmission electron micrograph of enamel dentin. And so it’s difficult to see what you’re looking at here, but in this area roughly. Again you’re seeing this scalloped nature of the DEJ. And this is just the scanning electron micrograph, there’s no enamel you’re just seeing a


surface view of the dentin. Remember SEM just gives you surface views, you can’t see cell details

TC FIG 11-22 SPINDLES (OLDER EDITION)Now we come to enamel spindles. When dentin forms you have your odontoblast and your odontoblastic process. This process becomes surrounded by your dentinal matrix and supposedly the process terminates at the DEJ but it is possible for this process to extend across the DEJ so let me just redraw this without my little dashes and let’s make this the DEJ. So this represents your enamel and the process is in the enamel. Think of bone as Sharpey’s fibres. You couldn’t put a fibre into bone matrix once the bone is formed. So in this case, the odontic process has to be sitting where the enamel will form. And then the enamel forms around the process. I’m gonna put a couple of squigglys in here, so that’s your enamel. If I were to draw this differently, I better go back to this one, here’s the shape, roughly, of a spindle, there’s another spindle, and here’s my, got a little messed up down there. And if you look at spindles you’ll see a lot of bumps. This is what I was trying to illustrate with my messy drawing here. But in each case there seems to be a line entering the spindle. That happens to be the odontic processes. If you were able to look at the spindle you would see this process more or less in center of spindle. So the enamel matrix that forms around the process doesn’t mineralize like the rest of the enamel should so the spindle is also hypomineralized. So we have lamellar, tufts, and spindles that are all hypomineralized. This has no relationship to geological faults or anything like that, there is no problem with the spindles per se, in terms of with bacterial attack because it’s incised by the DEJ. The tufts and the spindles, I don’t want to say are problem free, but there is no comparison to the effect you would have with the lamella.

NANCI TC FIG 7-58 SPINDLES (7TH ED)Here are some more spindles

AC FIG 8-16 DEJ-SPINDLES (3RD ED)Here’s a very nice picture, really a good number of spindles. In fact, if we look in this area you can see the odontblastic process crossing the DEJ and going in the direction of the spindle. Same thing is happening in this neck of the woods.

ENAMEL DEFECTSThis we already did when we talked about the enamel crown. You should be aware that enamel defects can be caused by any number of reasons. Could be genetically based, something wrong with the genes, genetic proteins, diseases can affect enamel formation and I used the example of strep infection, and I have some pictures to show you that


illustrate that, we spoke a lot in basic tissues with regard to bone and in craniofacial about tetracycline and why not to use it in pregnant women and young children. And we have two conditions: hypoplasia and hypocalcification/hypomineralization. Hypoplasia is a defect involving the formation of the organic matrix. As result you don’t get a full sized tooth, you don’t get an erupted tooth, part of the tooth is missing. Calcification has no relation to formation of organic matrix, it’s just not as hard as it should be.

C FIG 7.9 FLUOROSISBefore we get to this, I’d like mention enamel fissures. These particularly tend to occur in multi cusped teeth. Here we have two cusps and here’s the region between two cusps. Whether they are going to be ameloblasts all along here, when you get to this narrow part there’s not enough room for these ameloblasts, some ameloblasts just die off, and as a result you’re going wind up with a very thin channel called a fissure because it hasn’t mineralized properly. You can’t even stick a single tooth brush bristle in there. Does represent a potential area of weakness. If it’s hypomineralized, that’s a good area for bacteria to release its acid and actually attack the tooth. So the best that you can do is clean out the area as best as possible without destroying too much of the enamel itself and filling it up say with a resin. You can use an amalgam too but resin works a little bit better. But eventually because of location the resin wears thin and disappears and you have the same old problem. As you get older a lot of things change, not only in the rest of the body, but so does oral cavity. Since we are talking about enamel, one thing that changes is going to be the loss of enamel tissue. With mastication taking place constantly, days, weeks, months and years the overall thickness of enamel wears down. The vertical height of the tooth will wear down. And this is wear and tear, the word attrition is used to indicate what is happening. And let’s say your maxillary lateral incisor gets shorter and shorter, the corresponding mate, the mandibular lateral incisor on the same side of the mouth, “Hey, what happened to my friend? My mate?” will erupt into oral cavity looking for it’s mate. Same thing happens when you have a tooth extracted and the space is empty. This is just a normal every day type of phenomenon. The perikymata will disappear after a certain amount of time. The colouration of tooth could change. If you’ve had endodontic work done, the pulp chamber, canal, no longer has pulp. It’s been cleaned out and filled with gutta percha, and this affects the overall colouration of the dentin. The colour of enamel is direct reflection of the colour of the dentin. Usually when the pulp is gone, the enamel looks a little darker, a little greyer in nature. We described the enamel as semi-permeable tissue, not completely, semi, means partially permeable. Well over the years the permeability is going to change also. You can think of enamel as a porous tissue.


Eventually the pores get filled up. Eventually you won’t be able to deposit more fluoride in terms of protecting the enamel because the pores have been all clogged up previously. And since I mentioned fluoride, this is a nice example of a condition known as fluorosis. As you look at this teeth you can see discolouration particularly in the central incisors. You’ll notice that most of the teeth have a similar effect, but you don’t notice that effect in the mandibular dentition. So fluoride, keep in mind, is a poison, you can actually die from excessive amounts of fluoride. And I had already mentioned that years ago there were deaths of children because the dental hygienist wasn’t paying attention when she should have, and this is nothing more than a dose relationship between size of tooth, age of patient, and dosage of fluoride. Now fluoride is in a gel like substances so they stick to tooth structure much easier than previously. But there is a discolouration, so small amounts of fluoride is good, too much fluoride is not good. You’re still maintaining the enamel to some extent, the effect of the fluoride may cause demineralization. And that’s what you’re seeing in these discoloured areas.

C 7.3 SINGLE CENTRAL INCISORInteresting, patient with one central incisor. So technically this should have been two tooth buds forming, two cap stages, two bell stages, etc. for some reason or another, only one developed or two fused together. And as you Look at b you’re seeing the erupted tooth and the tooth, the secondary tooth developing below.

C FIG 7.4 SUPERNUMERARYSeveral different scenarios here. This actually looks a little funny, we have this triangular tooth here, between the two central incisors, called the peg tooth. It’s an extra tooth that doesn’t belong here. It’s a supernumerary tooth, does anyone remember the name of the structure that gives rise to a supernumerary tooth [is it a tooth bud or extra tooth bud?] well that’s true, but there’s a special name to forerunner of this type of tooth. Begins with the letter V. Vestigial tooth bud. Don’t’ mix that up with vestibular lamina. Vestibular lamina gives rise to the vestibule. An extra tooth bud will form these supernumerary teeth. In this case it’s hard to see this x-ray but here’s that little peg tooth, the supernumerary tooth we see in picture A. Picture a looks like there’s perfect alignment. But in C it’s behind the central incisors. And this is not a particularly great x-ray but this looks like a large central incisor, but it’s not, it’s just an extra tooth that’s forming between these two incisors. And the x-ray doesn’t help as much for seeing it.

C FIG 7.5 18 SUPERNUMERARY TEETHNow this one if you have nothing to do, count the number of extra teeth. And believe it or not, There are 18 supernumerary teeth. So


there has to be a lot of extractions going on here. You can’t get the normal dentition into the dental arches comfortably. The 3rd molar presents a problem, can you imagine with 18 extra teeth?

NANCI TC FIG 7-63 ENAMEL: DEFECTS DUE TO ILLNESS (7TH ED)Here we have an illustration of some defects due to illness. This is a little bit light but there is something here, and here, they are like darker bands. At one point during development you could’ve had a strep infection. As a result the formation of the teeth were affected and you have a disturbance in the formation, etc. You got rid of strep infection and the enamel forms normally. But now notice, you can just about see something up there, there seems to be more or less a second line of brown bands. So the person could’ve come down with the strep infection later on in terms of development of the teeth. So when you have defects due to illness you’ll see a discolouration and you can have as many of these defects as the number of strep infections you can get. I’m using strep as an example.

C FIG 7.9 HYPOPLASIA; VITAMIN D DEFICIENCY; TERTRACYCLINESome more yummy situations. Hypoplasia, defect in organic matrix. This certainly is not a normal tooth, neither is this or that. These are all shorter teeth, call them runty looking, the enamel seems to be missing, and what you’re really seeing underneath is the dentin. So that’s hypoplasia. As we look at B we have these thick brown bands. They’re all located roughly in the same region. Somewhere along developmental process mom didn’t have enough vitamin D, the baby didn’t have enough vitamin D and so the calcification didn’t proceed as it should. Remember vitamin D and calcium go together. We discussed that in bone. If you have vitamin D deficiencies in children you get rickets and in adults a similar condition to rickets. Does anyone remember that name? Osteomalacia. In C in this particular case we see banding occurring in the dentition, also the colouration of teeth don’t seem to be that normal. What’s probably happening is a dual effect, you could’ve had some sort of deficiency growing giving the brown banding. You could’ve had deficiency in vitamin D. And this grain of teeth is sort of reminiscent of tetracycline staining. And of course D shows your tetracycline staining. It could be amber, light brown, dark brown, to literally black. In this particular case you can’t correct this condition. You have to replace crowns with a new set of crowns. The last thing I want to mention is acid etching. And acid etching is used to roughen up the dental tissue and if the defect extends pretty close to the dentin or literally on DEJ the acid etching is used not only on enamel but dentin, and as a result you want to create a scalloped region. So when you restore the tooth whether it’s with an amalgam or resin, that substances seeps in and adheres better. A rougher surface is always better for adhesion.


DOGThis is going to be our break picture. And have you noticed walking through the streets who the yappers are? Always the little dogs trying to prove itself. The big dogs are always quiet. 10 minute break.

27: enamel ii

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