Dental Health & Education P2

That’s where periodontal surgery really comes in but a lot of patients they are not going to go through periodontal surgery. They don’t want to have a full mouth of gingival surgery for a variety of reasons. And so they are left with, kind of, with the ravages of what the periodontal disease did to the architecture of the boning housing that houses the tooth and then…Essentially it’s a crater from inside to the outside and that negative crater…you can run a floss up and down all you want, you can’t clean the bottom of the crater. And in between roots when you get bone loss that bone as it goes down root exposes kind of [inaudible] of the root and you can’t get in there and clean. And in multi-rooted teeth we see periodontal disease advances much more rapidly than in single root teeth. So the upper back posterior teeth periodontal disease generally takes off faster than lower molars and then anteriors are generally spared of surgery. There’s two reactions to periodontal disease in its advanced stages. There is the gum’s gum recede and the pocket just gets really deep. Or in some patients, we don’t know why, the gums just recede and move up with the bone. Anyone may have seen that? They look… if somebody’s smiling and their teeth look like they’re real long. They’ve either gone through periodontal surgery or they have gingival biotype that remodels with the loss of the bone. As they lose bone so it goes the gum so they get the really…elongated tooth look. They have a pocketing but it doesn’t seem to get as deep but they just have the chronic disease. Kind of just keeps more [inaudible] the side of the tooth and eventually they’ll reach a point where from mechanical standpoint tooth does not have enough anchorage to withstand the forces of the chewing and it gets loose. Or what happens more commonly that you get an acute infection with severe inflammatory response, the facial swelling, the cellulitis, and a lot of bone destruction and that tooth is lost. Problem when that happens is it destroys a lot of bone and it takes teeth with it, adjacent teeth go as well. We’re getting much better as a profession at recognizing periodontal disease in its earlier stage and reprimanding it. About 15 years ago, I would say, there were attorneys that would advertise “Do you have periodontal disease? Did your dentist not tell you you have periodontal disease? Call me, well sue them.” It was…there were articles…my dad showed me an article, you know, dentists the nest source of money, the nest source for people to sue because we weren’t diagnosing periodontal disease or at least we weren’t informing patients of their periodontal disease and their options. I like to say I always did. When I worked at UCLA we were very big in periodontal department. I steered away a lot of patients wanting to go to Dr [?] practice and he was kind of old school and I was informing patients of everything they had going on and they were like “What are you telling me? I’m going somewhere else.” Young guy, just out of school, you know, and he’s telling me all this, you know, what does he know? Periodontal disease, we are looking at it completely different as a systemic infection. Because if you look at the palms of your hands, the surface area on the palms of your hands and the healthy gingival architecture there is that much gum under the gum line. So if you took the palms of your hand and put a suppurative infection on that tissue, Dr [?] would say we need to get you in a hospital, put you on antibiotics, we need to debris that and get you healing. When is under the gum, in the mouth it’s just a dental infection. It’s just a dental infection. And we now know that is not the case.

Student: When you do periodontal surgery to correct the deep pockets. What are you doing?

Some of it is resective. You actually take away. Some of it is you can actually do some bone grafting and fill in boning defects. So you can, not grow bone, but you can graft bone into the defect if it’s got enough walls to it. You can graft bone into that furcation area. In a lot of times when you lose tissue…there’s two types of gum tissue. There is attached tissue and there is loose mucosal tissue. Attached tissues is the tissue we all think of as our gum tissue. And there is a junction between mouth tissue and mucosal that becomes your cheek. In some people there is not a lot of that attached tissue. When they get gum disease and recession all of a sudden they don’t have any more of attached tissue. This attached tissue…because it is attached to the bone below, so it is firmly attached. Now when you lose all the attached tissue and you’re just left with mucosal, every time you smile or laugh the gum pulls away from the tooth. That’s not a good situation. so some periodontal procedures actually take ging…they have some synthetic wrap material now…but they take generally a slice of tissue from the roof of your mouth and graft it to that area to bring back that attachment, to reduce some of that severe recession and bring back the attached tissue because you can’t have a normal pocket when you just have the movable mucosa, the movable tissue around the tooth. Periodontal disease is resective and it’s regenerative. Some of the surgeries they do they use a membrane barrier technique in which they’ll put in a synthetic or sometimes bone from a bone [inaudible] and they’ll put a membrane over it that will not allow the gingival tissue to grow down. It heals much faster than bone so what happened in the past, you put the bone in, you stitch the tissue up and then the gum goes right down faster than the bone can fill in and regrow. So you really don’t get any…now they’re putting barrier membranes between the gingiva and the graft and they are getting a much more predictable result in grafting that…re-grafting those boney craters and defects back so that then they…it literally is a plastic surgery with gingiva, thinking the tissue so that when everything is stitched back u you’re left with pocket depths that you can maintain.

That’s it in a nutshell. If you can’t brush or floss and clean, it’s back. And it will just get worse again. And the worse it gets, the faster it gets worse and we are off to the races again. There is definitely a genetic component to it. Grandparents lost teeth due to periodontal disease, you’ll see kids that fight the periodontal disease, offsprings fight periodontal disease. So there’s a genetic component to it. It’s not really fully understood  we just know there is a genetic component to it. And I have some patients that come in once every five years and they have all this plaque and calculus and tartar but they have no gingival inflammation and no loss of attachment and no pocketing. I have patients that come in every 3 months and they are the most diligent flossers known to man, god or beast and they still are fighting the periodontal disease. We don’t understand everything that’s going on other than if you can eliminate the bacteria, you can eliminate the disease. But that’s the million dollar question because it’s an infectious disease. You go in and grab utensils at a restaurant, you got it back. We don’t live in an antibiotic environment. Kind of a side note, in Europe they treat decay differently. They treat it as a family infectious disease. So if one child or one adult has a lot of decay, they will actually give oral antibiotics to the whole family, and treat the whole family. They are trying to eliminate that virulent strain and strep mutants that’s causing the decay. You know, it’s a different way of looking at managing the disease. Whether they are managing decay better than we or not, I think there’re studies going on. They look at it a little differently than we do. We don’t necessarily treat the family as in infectious disease but decay really is an infectious disease. They’ve raised rabbits in antibiotic environment. You can feed them all the sugar and they won’t…they have no decay. They don’t have the bacteria to come and get the decay.  …new technologies in dentistry and one of them I’m very excited about…and that I love doing and got involved with is Cerec. Cerec is a technology in which…the crown made for a day. You can do a crown in one appointment essentially. Instead of a…people that have had crown or bridge before, when you had that crown…tooth, you had to do impressions and the temporaries made, the temporaries cemented, shades taken, off you go. Temporary stays on for 3 weeks because it’s cemented with temporary cement because when the patient comes back on we want to be able to take it off relatively easily without traumatizing the tooth…

Student: Has anybody had crowns?

Student: Lots of them. I have one that I need now too.

Student: I never had them. I just take amalgam.

No, we’ve done some ceramic outlines on you. But not a full crown. But the same process. You had to have a temporary. Now if I were to do what we did on you it would be done in one appointment. You wouldn’t had to have a temporary, come back and deliver the final result. So, traditionally you get the impressions, then those impressions go to a dental lab, the lab pours out he models and now they have a duplicate of you. And on those models they can fabricate the restoration. 2 or 3 weeks later you …sometimes I don’t. I take temporary crown off and deliver that crown and cement it in place. With the Cerec it’s a digital CAD cam technology. What that means is, for the patient when they come in I [inaudible], I prepare the tooth, I take a digital scan of the tooth preparation and the adjacent teeth. And I can scan the upper arch and then scan the [inaudible] of those 2 arches and then I have a virtual you with your prepared tooth in the computer software. And the biogeneric software will allow me to design a crown and I get to fool with all aspects of the crown and get it just the way I want it. My staff will tell you that’s why I like it so much because, you know, I have a total control over it. I get to play with all the contours, the emergence profile, the height of contour and where the cusps are located and how the bite comes together and then that information is sent to a milling machine, and I don’t know if you’ve ever seen on History Channel or Discovery Channel, they put a block of steel or aluminum in the machine and these burrs go whirling around and out pops a motorcycle.  Well I put a block of porcelain in the machine and on it goes and burrs spin around and move. It’s quite a process to watch and it cuts the tooth out that I’ve designed. Very, very, very accurately. If I give it good data it will make the restoration better than the lab can make. But it is that… it is garbage in, garbage out. You have to give it a good data, you have to get good scans. And when you get good scans it will give you a great restoration. And so, in 10 to 15 minutes that restoration is milled out of that block of porcelain. And that block of porcelain is a multi-shaded block of porcelain in the shade that meets your requirements, that meets your particular tooth. So we can match them very, very, well. And the advantage to the all ceramic, all ceramics don’t have a metal substructure. And the advantage of that is, when you have a porcelain fused to a metal crown, there’s a metal substructure under that crown. And so the light… the color that you see, that you perceive is reflected light, it’s all reflected. The light comes to the porcelain and bounces off the opaque layer that’s making out the metal color of the kind of sub crown underneath and then what you see…

Dental Health & Education

see the video:

I’ve been practicing in [inaudible] since 1986. The type of practice that I have…I am a general dentist and I do general dentistry. I can do fillings and crowns and bridges and cleanings. My practice has morphed into a little bit more complex restorative practices. That means…basically I do bigger cases. I tackle bigger and more complex cases. I don’t hold myself after being a specialist or a prosthodontist but in esthetic cases and implant cases and combination of various cases… I’ve just morphed into handling some of those cases and doing a lot with implants. What I want to talk about, what got Bill excited was that he saw brochures in the office when he came in about Cerec, Cerec technology and what that can do for patients. It was invisible aligners, invisible braces. That’s a new technology in dentistry. And then I wanted to mention a little about 3D imaging and how the cone beam scanning is being used in dentistry and how it relates to implant therapy. But probably the bulk we’ll talk about is periodontal disease and what does and how it relates to general health. When I first started practicing dentistry was its own little subspecialty of the mouth. It was…anything that happened in the mouth was dental. It was just either dental infection but it didn’t affect anything else in the body. It was just dental. That has changed dramatically over the 23 years I’ve been practicing. So now I get calls from physicians that I have to do and sign off on the patient’s oral health status prior to hip replacements, prior to going into therapy, how are they  doing because it affects their diabetic management. It’s “My gosh. The mouth really is connected to the body.” And what goes on in the mouth really affects the body. And in periodontal disease that’s been very significant in what’s been discovered and they are just now getting into…They’ve discovered associations and we’ve all kind of knew it but now we’re actually doing studies designed particularly to find out what’s going on there. So periodontal disease is an infection of the gums in your mouth. But it’s a unique infection. It’s a really unique infection in that the bacteria that are causing the infection are on your teeth or on your tooth, they’re on the gums, under the gum line, in your mouth but still anatomically outside your body. It’s anatomically outside your body. So your immune system detects that this bacteria and the bacterial byproducts are there and all the cellular mediators go out to elicit the immune system to come in and clear this infection. And in that initial stages, it brings in lots of blood vessels and the gums get swollen and red because of the proliferation of blood vessels. We call that gingivitis – swollen, red, puffy gums. In gingivitis stage the gum has not broken down yet. It’s just a puffy, red, bleeding gum. In the later stages, once you’ve had gingivitis for a period time, chronic immune response now becomes instead of acute. Immune response becomes a chronic immune response. And the cells become involved and the immune system’s reaction becomes different in the fact that it starts essentially attacking the attachment apparatus on the gum of the tooth. So that little crevice around your tooth [inaudible] of plaque and bacteria, now gets deeper, And when that crevice gets deeper, it gets harder to clean. The harder it is to clean, the more periodontal diseased you get, the more periodontal diseased you get…and in so it’s a feedback loop that is in the wrong direction.

The worse it gets, the faster it gets worse. Prolixity of the immune response triggers all these inflammatory…inflammation and all the inflammatory markers and that’s what is believed to be the mechanism that affects diabetic…diabetes patients their glycemic control. The chronic infection makes insulin resistance occur so that type 2 diabetic patients have more difficulties controlling their blood sugar if they have periodontal disease. Mechanism is believed to be these immune mediators, product of the immune response going around sensitizing the beta cells for insulin resistance so the insulin isn’t as effective as it should be and so blood sugar goes up. And the problem with diabetes is it promotes…it is…it makes the fighting infection more difficult. Periodontal disease worsens diabetes, diabetes worsens the periodontal disease. Once again it’s that feedback loop going the wrong way that can spiral out of control. The other thing that chronic periodontal disease is involved with is cardiovascular disease, myocardial infarction and stroke. At first they did the studies and just found associations. People with periodontal disease seem to be more prone to have myocardial infarction and ischemic and strokes. Now they’re doing studied to particularly discern the mechanism of action, why is that. It seems to be once again the cellular mediators that trigger the immune response and increase platelet aggregation. They have actually have found the bacteria in the periodontal pocket in the arthrosclerosis plaques in the myocardial infarcts. They don’t quite know how that’s happening other than the fact that advanced periodontal disease bacteria does eventually enter body. It does in fact enter into the tissues in the advanced periodontal disease. So that bacteria can flow around but how does it get into atherosclerotic plaque? And that is something being studied. From the studies that had been done and the associative studies are founding out that cardiovascular disease, stroke, COPD…Because the inhaling the bacteria from periodontal disease is causing low grade chronic infection in the lungs which worsens the COPD symptoms. So periodontal disease, COPD and the same with asthma.

I did kind of a quick publication search on periodontal disease and the relationship with diabetes, COPD and the others that we’ve talked about. I just want to read some of this because I find it interesting. This is periodontal outcomes in patients with diabetes. Studies to date have reported conflicting associations between oral infection, coronary heart disease, and incident coronary heart disease. However, there is evidence that dental infection is associated with coronary atherosclerosis and that bacterial DNA has been identified in atherosclerotic plaques, and other studies have related dental infection to the incidence of coronary events. That coronary events being myocardial infarctions. This one is the COPD and…I’m sorry, stroke. Two lines of evidence further support the hypothesis that active periodontal inflammation increases stroke risk. First, edentulousness. Endentulousness is missing all your teeth. In which periodontal inflammation is usually absent. Obviously there is no periodontal disease because there is no teeth but they had periodontal disease cause that’s why they lost their teeth.  First, edentulousness in which periodontal inflammation is usually absent was not an independent risk factor; in contrast, severe periodontitis was a more important risk factor in those with several teeth left. So the active infection was a bigger problem. Second, gingivitis, that early, early stages of periodontal disease which is bleeding, puffy gums but there has been no loss of attachment around the tooth. Gingivitis was strongly and independently associated with cerebral ischemia. Strokes. Cerebral ischemic strokes. When tested together with periodontitis, severe gingivitis even appeared as the more important risk factor. Gingivitis is an indicator for the actual status of periodontal inflammation. As shown recently, acute infection is a trigger for ischemic stroke. And when I first graduated from dental none of this, you know, this was… periodontal disease was a dental infection and managed the dental infection and you were good. Mouths connect to the body but what else does it have to do with it it’s turning out that it has quite a bit to do with it and it’s kind of scary because at times I wonder has the evidence come to the point that when I diagnose periodontal disease and review with the patient do I have to warn them that it increases the risk for cardiovascular disease, ischemic stroking, you know, has the evidence got to that point yet?

Student: Why would you not want to tell them?

Well because they’re still studying and if you scare someone to death, they’ll often leave your practice.

Student: Medicine now, they recognize that inflammation anywhere in your body, you increase your risk for…

Because cellular mediators, all those cytokines and [inaudible]

Student: When you get a gingivitis, does the flora in the mouth change? Most people have the same bacteria…

No. Gingivitis is [inaudible]. It’s the same flora. As periodontal disease worsens and becomes from gingivitis to periodontal disease the bacteria flora do change. The deeper the pocket gets, it becomes anaerobic environment so you get a shift to more virulent, aggressive strains of bacteria.

Student: So the gingivitis is primarily aerobic?

Yes. Aerobic flora. In advanced periodontitis it’s both. Cause of the depth of that pocket. And I think in millimeters, kind of a healthy pocket is an eighth of an inch or 2 to 3 millimeter and when you get periodontal disease we’re looking at your looking at 5 millimeter pockets and deeper. That 5 millimeters is the breakpoint in my mind. That’s not a set…there’s a whole diagnostic criteria hat basically boils down to can a patient clean to the depth of the pocket? Because if you can’t get a toothbrush bristle 5mm under the gum line, or even 4mm under the gum line in that area, I don’t care how many times per day you brush your teeth it’s like never brushing your teeth. And the flossing is the same way. If you can’t get the floss to the depth of the pocket it doesn’t matter how many times a day you floss. It’s anatomically impossible to clean that pocket. And that’s when periodontal surgery becomes involved. It corrects…it surgically…plastic surgery of the gums so that…to correct the pocketing so that the patient can maintain it. If we wave the magic wand and clean all the bacteria off the teeth, all the calculus off the teeth, in 24 hours, it’s back. It’s back. If the patient can’t brush it down at the bottom of that pocket it just…

Student: What about the rinse of some sort? Fluoride rinse?

Fluoride rinse works at the gum line but the periodontal disease is below the gum line. I don’t care what you put in your waterpik and turn it up as high as you want, it does not get under the gum line.

Student: [inaudible] That’s who you are right?

Student: Yes.

Student: I met her yesterday. You said he was…

Student: [inaudible]

Yes, so periodontal disease happens at the bottom of the pocket. You can’t clean the bottom of pocket with rinse. Now, that is a great segue into one of the other things that we do in our office and that is technology that’s been developed The gingivitis goes away. It clears out the teeth, the gingival health looks fantastic. Because we were using a peroxide and peroxide is very bactericidal and it kills he bacteria. So the gingivitis clears up. Dr Keller developed an idea that hey, what if we could get peroxide gel up under the gum line into those pockets? Regular tray won’t do it because saliva gets into the tray and dilutes the gel and it doesn’t stay in a significant amount of concentration to do any good. So he designed a tray with gaskets specifically made for each individual patient. And where are those gasket seals are dependent on the measurements that I give the lab, of the pocket around each tooth. So when you insert the tray, the peroxide gel will go up under the gum line into those pockets and the gasket seal keeps it from leaking out and it keeps the saliva from leaking in for that 10-15 minutes period so that the peroxide gel stays in concentrations to be effective. They’ve shown very conclusively that they can get that gel to go deeply up underneath the gum line and it’s very bactericidal and it’s a way of managing periodontal disease. It can be used as a standalone treatment. It doesn’t do a lot to correct the boning defects and gingival defects that can occur that make it difficult to clean.

Dental Anatomy P3

They have the same basic shape to the cusp, the lingual being a little bit more pointed, often times a little further from the cervical. We got the same number of pits and grooves in the occlusal and here we got very similar sizes to them. And really looking at it from the occlusal only it would be a little difficult but if we started to look towards the root structures I think we could tell very rapidly which was which because of the spreading and the divergence that occurs in the primary tooth and we get this much heavier roll at the cervical in the primary. And as I say within the same mouth primary tooth will be smaller in proportion. But just trying to emphasize the similarities, and terminology wise the terminology is exactly the same. Sometimes these are said not to have a root trunk where the permanent does but usually will have a very short root trunk on this. It’s not very much on the primary. Let’s take a closer look at these roots. This tooth has especially good roots. Actually complete roots in these primary teeth are hard to find because the roots start reabsorbing as the permanent teeth develop and erupt. These roots are very flat. They are broad from the mesial…pardon me, from the buccal to the lingual, and very narrow from the mesial to the distal. Got some other roots here. I’ll show you a set of four of them here. These are little unique in so much as they all come out of the same mouth and they all came out almost completely intact. We had some carries that was [inaudible] and cured in the same spot on both sides of the mouth. Here’s a marking from last year’s final exam I see. Identify the root on this tooth. Same basic principle except they are just wider spread on it. Lingual root being the longest and little bit on the round side. Broader flat on is the mesial buccal root. If you have a chance to have these in your hands you’ll be able to see them and tell the difference. This gives a good opportunity for a premolar crown to form right in the trifurcation here. Let’s look at some of the reabsorption patterns that do exist on these teeth. We indicated that on the eruption frequently that the anterior teeth come in little bit to the lingual.

So we’ll find that the…if these teeth are taken out in the process of their roots being reabsorbed, that frequently the reabsorption will be to the lingual on our anterior teeth. Of course sometimes our anterior teeth will end up like. This is way we’ll see most of them with absolutely no root on them at all. They come up by themselves. This also becomes a problem if you have to start restoring these teeth. These are small teeth. I had one here that had a carious lesion on it but if you were to have to start restoring carious lesions on there you’ll find that it’s rather difficult because of overall size. When we get to our molars they’ll reabsorb in many fashions. You can see right through this one it’s gotten so thin. This becomes a problem when these primary teeth abscess and you start removing them, you got these very, very thin spicules of tooth structure left and they’re hopefully capable of being removed without being fractured. If they are fractured they have to be retrieved and you got to know where they are and how they are and what to expect of them. These reabsorb from the inside of the trifurcation or bifurcation rea. They get very thin to the outer surfaces of it. Take a tooth like this. This reabsorbed so far that it even reabsorbed right up through the center of the crown of the tooth. This wasn’t anything left except for the enamel shell by the time this one got ready to come out. Just a real thin enamel shell. One of the main restorations that can be used on this. I shouldn’t say it’s a main one. It’s an occasional one. It’s one that tests your anatomy rather significantly when you have to start adapting these stainless steel crowns. I had a patient in the office that complained severely about the…her child had a crown that was falling off that I put on it. I wanted to see him so when we got a chance to see him we found that it was a stainless steel crown that had been put on 9 years previously and the tooth was just loose and ready to come out.

The root structure was almost completely dissolved off of it. But you’ll get involved in trying to adapt these crowns on when it becomes necessary and you’ve got to know the outlined form, you know the general size, were the deflecting ridge is the heaviest and most prominent and all your anatomy starts coming into place. We go back to a couple of slides. We may point out the mixed dentition. We get an opportunity in the mixed dentition to see differences in size here, two of them present within the same mouth, central incisors. Very significant size differentiation that exists but this is a period in which we have both teeth present and you got to be able to identify them. Very common question by parents is is this baby tooth or is it a permanent tooth. And often times students say well this is not, you know, that important. We can always tell which is which. And sometimes, you know, it becomes very important because some of these are good permanent teeth and some of them are decayed primary teeth and you got to know which ones are in need of coming out and which ones are in need of staying in. When they’re lined up in such a manner that x-rays can become confusing, your anatomy becomes very important. We’ve got primary teeth here. Another primary molar here. Which are due to be out and need some help getting out because these other teeth are being deflected to the buccal. And so we have to identify these teeth in the mouth, frequently they will be in combinations or have 2 or 3 of them. If we’re going to get our patients from a state of mixed dentition and from a state of disease to the permanent ones, we got to be able to know our anatomy. Why are the baby teeth important? You’ll have it asked you a million times and since you’re not all experts on this I’ll point it out to you two most important reasons. One is pain. You get abscess. You can get rather severe pain in these youngsters and this is not nice. Appearance is important and it may have significant psychological effects on it but I don’t list it as the number two most important.

Number two most important reason for taking care of these deciduous teeth is to help permanent teeth come in straight. If you start losing deciduous teeth before they are due to be lost, the chances of having crooked permanent teeth are much greater. Manmade crowding we call it and once you get crowding, the ability to keep it clean becomes a much bigger and the disease can just produce much more rapidly. So if we expect to guide our patients into a permanent dentition which is desirable, we got to know the anatomy of these deciduous teeth from many, many respects. Take a look at the pulpal morphology on these primary teeth. In the anterior we can remember that our root structure is basically the same as in our permanent teeth and our external morphology of our root determines rather significantly the internal morphology. When we come to our molars we got one major difference and that is our mesial distal width of these roots. They are very thin mesially distally and also very wide from the buccal to the lingual. And it’s this width that gives us a very flat ribbon shaped canal on the inside of these teeth. Very narrow width mesially distally. And very wide buccal lingually. Actually we’re not as concerned about the root canal structure on the inside of these teeth as we are in the permanent teeth because in the primary teeth we don’t get to treating these root canals with permanent restorations very often because of the reabsorption that occurs. We’re more concerned with the crown morphology of the pulp. And let’s go to some models and diagrams and some slides here. We’ll discuss a little bit of crown morphology of the pulp. This is the pulp chamber morphology. As we indicated this…these pulps are usually proportionally large. We’ll start with our mandibular, our largest tooth which is our mandibular second primary molar and here we have 3 canals,3 pulp horns rather I should say, to our buccal.

We got our mesial buccal pulp horn or just a buccal pulp horn and our distal which they got into this cutaway section. Actually if we were to look at the pulp itself, taking away the tooth, this is just a model of the pulp without any of the surrounding dentin or enamel over it. We find that the pulp structure itself, the pulp horns and the pulp chamber, follow very closely the external anatomy on these crowns. This is the first time we had a chance actually to view the pulp in this manner. We got 5 pulp horns on this tooth as we got 5 different cusps. And there of course in the central groove, central fossa area, where we get a rather significant depression in the tooth, we have a rather significant depression in the pulp. If we were to take this and superimpose it over a tooth we’ll find these pulp horns correspond rather significantly with the different cusps. One pulp horn being almost directly under each of the cusps. We look to our mandibular first molar. We’ll find that generally speaking we got a rectangular pulp chamber and this is just the pulp now again with the enamel and the dentin completely removed. The shape of it is rectangular as the crown of it is. And again we’ve got basically the pulp horns in this that we have crowns, the same shape, the same basic positions. We superimpose this into a tooth. Again we find that the pulp horns are directly underneath the various cusps. We look at a cutaway of a maxillary. We see a little bit of the proportion of the size, the thinner enamel and proportionally larger pulp. And again we can see that we got our low height of contour on the buccal, close to the cervical. Therefore we got our buccal pulp horn and a lingual pulp horn on the other side. If we superimpose this…well this is just a view here of the pulp itself. Again with the enamel and dentin gone. It gives you a little bit of a different view but if this was white you’d probably think this large pulp to be the actual tooth because the pulp chamber, pulp horns really are identical almost to the external morphology of the teeth. And if we transmit this to being inside of the tooth we’ll see that the relationships are very similar. This is a second molar here, second primary molar, and we can tell this by our small fifth cusp which is actually in the area of our cusp of Carabelli or the 5th cusp that occurs out on the mesial lingual area of the tooth. Actually I think in summarizing the thing that we really need to remember in relation to pulpal morphology of the primary dentition is that it follows very closely the external morphology of tooth, both in the crowns and in roots. But that the total pulp size is proportionally larger than what it is in a permanent teeth.


Dental Anatomy P2

Mesial incisor angle is a little sharper than the distal incisor angle. And you could go right down every difference of the…or every main characteristic of the permanent teeth and find them here but just not real prominent or characteristically different. Same exist on our maxillary lateral. One thing on the maxillary lateral that we never find…or I shouldn’t say never cause there’ll always be somebody that will find it, but I have never seen a lingual pit that has developed on the lingual of this tooth or actually the lingual of any of the primary incisors. Lingual pits in heavily rolled marginal ridges are very common in the permanent maxillary lateral incisors but the primary lateral incisors, the marginal ridges are not prominent and the lingual pit is absent. Same thing exist with all the rest of the anatomy on them. Maxillary cuspid, basically the same. You get a very wide, short crown on this. Remember this is one of the characteristics of the permanent cuspids just that crown was fairly wide in comparison to the mandibular cuspids, but here it’s even wider and proportioned yet. We have again just all basically the same characteristics on it. Same basic root form and shape and same basic cervical line.

The major difference is shortness of the crown, the heavy cervical ridge, the color and the difference and things that we’ve pointed out to as generalities to these teeth. We won’t go through the mandibular teeth all individually but again, same thing exist with all of them. Mandibular anterior is there, just miniature images of the permanent ones with the exceptions of the general differences that we’ve pointed out. When we get to our molars, our first molars, then we’re starting to come up with some rather major differences. We look at our maxillary first primary molar we find a tooth unlike any permanent tooth. Unlike any other tooth in the mouth and our maxillary first and mandibular first primary molars are the ones that we want to spend probably 50 percent of our time on. They are very commonly in need of restorative work and often times get into trouble very quickly and easily and this is 1 tooth that we have to know the anatomy on, especially cause it is not similar to the permanent teeth. Our maxillary one which we have here, both of these are maxillary, are called the most atypical tooth in the mouth.

They have a tremendous amount of variance. I would guess that you’d have to make the exception of the third molars which vary more. But as far as the primary teeth and all of permanent teeth with the exception of the wisdom teeth or third molars, this is the most atypical. It has many variations on it. Let’s consider some of the most commonly found anatomy. It has two very prominent cusps. Sometimes it is referred to as being similar to a bicuspid because of these two major cusps. But usually we have a smaller distal buccal cusps and sometimes even a distal lingual cusp. Although one is not seen in this tooth. Here we have two cusps on the buccal. And only one on the lingual. This change influences some of our terminology. We got a mesial buccal cusp which is the largest one by far, takes up 2/3, 3/4 of the buccal surface of this tooth, and then a very small distal buccal cusp. And then this leaves us with one lingual cusp on this tooth. We have a little different terminology in our occlusal on this tooth. We’re said to have a mesial pit, a central pit with a central groove which is often times somewhat egg shaped but then they term a ridge which runs from the distal buccal cusp over onto the lingual cusp and they call this an oblique ridge. This is not real prominent and not usually real important and not something that is found on all the teeth. This oen here for instance has absolutely no oblique ridge at all. But it is listed and termed in your textbook and you should recognize it. They are also changing the groove as it comes across this oblique ridge and calling it a distal groove. Now generally we have a central groove that follows all the way across the center of our teeth, the other teeth. This one changes and right in here it’s called a distal groove. Again, not a real prominent or important characteristic but it does end up in a small pit back here which frequently does become involved with carries and need restoration and other things which does increase its importance on it.

One of the things that’s very strong characteristic about this tooth is its shape, its overall shape. It’s said to be trapezoidal. Broader on the buccal than it is on a lingual. So it has a broad buccal and a narrower lingual and it tapers down as it comes to the lingual. But out on the buccal there’s this large prominence right here. Again this is a very important and very strong characteristics of the tooth here. This is the cervical deflecting ridge. It has many names, called the mesial buccal bulge or mesial buccal cervical bulge. In your handouts just calling it buccal ridge. Your text book calls it the buccal cervical ridge because it is at the cervical of the tooth. If we look at this from the side here, if I can get this, right here’s you’ll notice that this creates a very large roll at the cervical. This becomes very important when trying to restore these teeth and particularly if you’re trying to fit a stainless steel crown on it or something. Very important portion of the anatomy on this tooth. This is different than in any of the permanent teeth. We haven’t got this in any permanent teeth. Very strong here. If we look to our maxillary second deciduous molar we’ll find that really the anatomy on it is almost identical to the first permanent molar. Often times my hygienist will confuse these and take a quick look at them and she’ll call this the first permanent molar. The anatomy is almost exactly identical. The difference where you find the… is possibly in the depths of the pits and grooves on them, they are not quite as deep. And our overall crown length is not as great from the occlusal to the cervical. We have this heavy cervical ridge which is particularly prominent on the buccal, buccal ridge. And of course you got your root structure which is entirely different on it with a very short root trunk, if any at all, and these wide trifurcating roots on it which have the same names and same terms as our permanent teeth do. But from the strictly occlusal aspect very, very similar to our permanent first molar and the terminology on this tooth is almost 100 percent the same as your first permanent molar. So we’re not really picking up any new terms here.

The overall size is a little smaller than the first permanent molar in most mouth and as far as the dimensions mesially distally or buccal lingually as you look at extracted teeth and find the large primary that might be larger than the small permanent but within the same mouth they’re generally very similar. Here is a few teeth which show this cusp of Carabelli or this fifth cusp which develops out on the mesial lingual as it does on a permanent teeth. You can see restorations that have been placed in this. This has been the weakest part of these teeth which is broken down into carries quicker than any other area. These are very prominent ones but they have the same basic cusp of Carabelli as with our permanent teeth do also. We look to our mandibulars. Again the first mandibular primary molar is a very unique tooth in so much as it has no other tooth in the mouth which is similar to it. It is a 4 cusp tooth. It is rectangular in its basic orientation in outlined form. These are all basically the same, mandibular first molar, primary molar. On our 4 cusps we’re terming them by the corners in which they are located at: the mesial buccal, distal buccal, mesial lingual and distal lingual.  There’s differences in size, heights, shapes of these. Again our buccal as in our mandibular permanent are larger in proportion, fold closer into the center of the tooth and again we have a very large cervical ridge on these teeth and this is prominently in the mesial. Mesial cervical is much more prominent than the…I shouldn’t say mesial surface but the mesial buccal portion of the cervical ridge, is much more prominent towards the distal buccal here. Sometimes this is called a mesial buccal bulge, indicating it is more prominent in the mesial area of our buccal surface. Like most of our teeth where our mesial cusps are proportionally larger both on the buccal and the lingual. Our distal cusps become smaller and this is quite prominently so. Again the mesial buccal taking up a half to 2/3 of the bulk of the tooth in comparison to our distal buccal which becomes significantly smaller. Our distal lingual cusp frequently is a very small and sometimes it will be almost just a, what’s called, a tubercle or a protuberance on this distal lingual line angle area here. But nevertheless is generally present and is termed and specified as such.

Our central occlusal terminology within the occlusal aspect of our occlusal table is a mesial pit and a distal pit connected with a central groove. This is similar to our bicuspids, maxillary bicuspids. The mesial pit, the distal pit, the central groove. One thing that is different here and that…and it also is very important, that is it we have a transverse ridge. This transverse ridge runs from the mesial buccal to mesial lingual cusp. And it’s a very prominent ridge and it’s a ridge which causes a great deal of difficulty in restoring this tooth because, if we can look at the tooth in side, we’ll find that this mesial lingual cusp pulls well onto the tooth. Maybe I better get that white tooth. It might show a little better. Been bleached  little more here. Pulls well onto the tooth on the mesial lingual and also the mesial buccal is pulling well over to the center of the tooth which leaves a very short distance between our two mesial cusps and this ridge is quite prominent through there. And we’ll find as we study into our pulpal morphology more that our pulp horns or protuberances of our pulp are very prominent underneath our cusps and this is very prominent underneath these two cusps. And as you try to go between this with restorative procedures you very frequently can nick those cusps because if they’re so close together you nick he pulp horns under the cups and get into considerable amount of difficulty. If we look at our buccal surface on this, I think one of the things that’s characteristic on this, is that our buccal ridge is so prominent on the mesial that our enamel actually extends down onto the tooth considerably more at the buccal, mesial buccal, than it does towards the distal buccal. So we are quite prominent here and then it tapers up as it’s going towards occlusal as it goes towards the distal. And our cervical line which we hadn’t pointed out specifically was real important in relation to perio becomes not typical as it is found in the most of the other teeth.

It’s very prominent and down further onto the root in this mesial buccal area. If we look to our second primary molar. Again, we’ve got a very easy one because it is almost identical to the first permanent molar. We got the same general characteristics of the whiteness, the heavy ridge on the buccal and a cervical constriction or the cervical roll being very prominent. We got a color differentiation, usually a little whiter. We got our overall size differentiation from one tooth to another within the same mouth but I might let you look at these and find out which you think is a permanent and which is a deciduous tooth and it becomes fairly difficult. Each have the five cusps, 3 on the buccal, 2 on the lingual.

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