Transcribed by Chris Bedoya

April 16, 2014

Craniofacial Biology Lectures 23 CCP: Craniofacial Growth and Development by Dr. Teixeira Transcriber Note I had to transcribe this lecture off of a recording from my laptop which was not very high quality. I tried to decipher all that Dr. Teixeira mentioned, however I wasnt always successful. I apologize for that. In these places I have underlined the words I wasnt sure about. Also, some of the slides and their content may not completely sync up with the podcast once it gets posted. I tried to keep it matched up as best I could, however without having a posted lecture power point, it wasnt very easy. Sorry about that. Slide 1 Title Page, and several images of nature with gaps and bridges Hello everyone. I hope you know enjoyed Dr. Forseas lectures the last few days. Everything she talked about has an application in the clinic. Im here today to give you examples of how everything we do, all the learning now, through the first years of dental school, this is information youre going to use when youre in private practice treating your patients. Youll come back to these lectures. And Ill give you examples. I want to tell you a little bit before I give you some clinical cases, and some ideas about research still going on on how we grow, how the facial area grows. I want to tell you about CTOR. I dont know if many of you are familiar with CTOR. Who has heard of CTOR? Well, some of you. In orthodontics, and dentistry, and medicine, there is a huge gap between clinical activities and basic science. And you carry that on because you think that things you learn in your basic science courses will not have any clinical application, thats not true! There is a gap, and sometimes it feels like they even talk different languages, but sometimes we cross over a little bit, but most of the times there is a huge gap. I see that because we apply for grants.I see that because I speak both languages. My background is in basic science research, Im a trained developmental biologist and molecular biologist, and Im an orthodontist, a clinician. I love what I do in private practice. I have a private practice too, besides doing research at NYU. So I can talk the language, and I thought that there had to be people like me, and other members in the department that had the same background, we had people with both backgrounds that can talk to each side of this divide, that can seal the bridge. Youve got to have a bridge if youre going to advance practice and the way we treat our patients, and come up with more efficient therapies. So what are we doing? And thats why I want to tell you about CTOR. We created CTOR as a place where clinicians and scientists can talk, and they can pose questions, and find the answers. The department of orthodontics, many years ago, hired a second orthodontist with a research background, Dr. Mani Alikani, who is the director of CTOR, and in conversations with Dr. Alkani we came up with a conclusion. If no one is gonna do it, we gotta do it. We have to bridge this crucial.and bring this science to the clinic. And thats how CTOR was created. Slide 2 Mission

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Many of you working CTOR. Some of you participated in the clinical studies, the animal studies, some of the most basic project we have going on. And Im gonna tell you today. Im gonna start by showing you one of those projects. So we had different areas of research, they all had some clinical implications. Slide 3 CTOR Projects Were looking at craniofacial growth and development and were trying to find therapies for treating clefts in utero, before a cleft patient is born. But not by operating, but by making a correction in the developmental pathway. I have a project that Im going to tell you about today about engineering bone. And theres other projects going on about moving teeth, or bones in the jaws. Im gonna tell you about the tissue engineering project. Slide 4 Bone Tissue Regeneration You heard about this approach. If you Google or do a PubMed search, theres so much research on bone tissue engineering. Huge body of research. And they all take this approach, you pick a matrix that is gonna replace the extracellular matrix in the bone that you want to create, and you add cells and the signaling molecules that will tell those cells to make bone. And then, for some time you grow it in vitro in a lab, with the objective of injecting it back and restoring the function of a body part or body part that is missing. Thats the classical approach. Slide 5 Two Types of Skeletal Development Now these cells in all these approaches, guess what cells these are, theyre bone cells. Many years ago I had this PhD student from the University of Porto that had developed this great scaffold that looked just like cartilage or bone. Had the cells for the cells to grow. And he came to the lab and said, I want to make bone. So I thought, here we go another project of I want to make bone. So I asked, how you want to make bone? He said, I dont know, well grow some mesenchymal stem cells, bone marrow cells, some kind of cellsand put osteoblasts in my sponge (matrix) and voila, we have bone. Im a developmental biologist, so I had never looked at the tissue engineering. He told me to change (?) in the field. Ive been looking how bone forms, how cartilage forms, how born grows. So I said, why would you do that? Most of the bones in our body form via endochondral bone formation, why would you want to use mesenchymal cells to make bone (intramembranous bone formation), if all long bones form via endochondral bone formation. Only the flat bones go through intramembranous. So why is the whole tissue engineering field going this way (intramembranous)? The student said he had never heard about that. Student: I was going to say that its faster Is it? Then why the hell did nature decide to first make the cartilage template of the future bone, then take its time to convert that cartilage into a bone. To sort of have a base to build up on. Cartilage built fast, then bone gradually fills in the structure. I actually think there are a lot of advantages. Think about in the things you discussed, think about how bone grows. How does it grow? 2

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Slide 6 Hypothesis Once you have mineralized tissue does not have interstitial growth. It does not just go boom and now its _____ (?), you can add or remove inside/outside, right? Not endochondral bone. This is the endochondral pathway is the growing pathway. Because the long bones, the vertebra, all those bones that undergo major growth, theyre made out of cartilage first, then most of the cartilage converts to bone. But not all, theres a remaining cartilage that is not mineralized. You know what Im takin about, right? What is it? The growth plate! The growth plate is the remaining ___?___ cartilage between the epiphysis and diaphysis that allows for bone growth after birth. And then it disappears. Theres a time when it all mineralizes. When is that? After the growth spurt. And now you cannot growth anymore. You can remodel. In fact, its shrinking if you think about it. The following years as you lose bone mass with aging. So the idea was, I thought, (flips back to Two Types of Skeletal Development), going back to this question you asked me if endochondral bone formation is faster, more efficient maybe. Not really. You know why? You know why the whole bone tissue engineering field is growing and growing, because no one found a solution. Every time you graft, think about the cleft patients, you have a big gap involved, and you fill it up with bone. What happens? You always end up with less bone than you managed to insert because of remodeling and most of it resorbs. So there had to be a way where you put this much (a little bone) and end you end up with a lot. Because with a cleft palate and patient, you would want the bone not to shrink, but to grow with the patient, and it even grows in the direction you want it to go. Only this can do that, the other one will shrink and youll always end up with less bone then you put into the gap. So that was one of my advantages. The other one itsee these students really pulled me into the tissue-engineering field and I began to read the literature, and I thought hah! No wonder. You cannot grow big chunk of bone. Why? In vitro. Why cant you grow a whole tibia in vitro? Why? You know? You dont have the cartilage, the base. Now were talking bone. Youre talking about the people that want to make this kind of bone. They never succeeded in creating a big chunk of bone in vitro because you need irrigation. You need blood supply. Ok? Guess what, cartilage is an avascular tissue. You could grow a larger piece of cartilage before you start needing the nutrients and blood supply in it. So going this way, you could really create the tibia, and put it in the body, and let the body replace it with bone when its needed. Or you could mineralize it outside, well talk about that. So the hypothesis was that if you create the cartilage, a mature cartilage, like a growth plate cartilage, you could then after implanting in vivo, convert that cartilage to bone. Because that cartilage carries all the signals necessary. Slide 7 Sternal Chondrocyte Culture So thats the other thing. The whole field of tissue engineering is trying to figure out which molecules control this bone formation. I know from my studies in developmental biology, studying how growth plate cartilage converts to bone, that 3

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the cartilage has all the signals. Its avascular, but when it needs blood vessels, it releases VGF. Youve heard of VGF? Vasculature growth factor. So the tissue doesnt need blood, but when its ready, and the cartilage is ready to be mineralized and replaced by bone, the cartilage releases factors that bring the blood vessels. It releases factors that help themselves survive under hypoxia, low oxygen. It releases factors that activate osteoclasts and osteoblasts. So all the signals you need to convert a _____?___ of cartilage into bone, these cells carry. So my idea was like dont worry about the signals, just put the factory of the signals in there. Dont waste time, which would be more expensive also. So I went back to myI convinced (Serafin? - persons name) this is the way to make bone that will have the ability to grow with the patient and not shrink. And I went back to these developmental biology models that we use. So in the lab, you should know that you dont use humans in your research. You use chicken, rice, and mice, and its valid because all these biological principals are the same across species. So we use this chick embryo, and we use the sternum from the chick. We dissect it out from a 15 day embryo. This is big here (on slide), but you know how long it is? Its 34 mm. Its a tiny little thing. You have to dissect it under a microscope. And then you separate this top portion, throw away the middle one, and take the bottom part. And this very well described developmental model because the cells in the upper part of the sternum behave like growth place cells. Theyre temporary cartilage. They have the potential to convert to bone. The cells at the tip (bottom) behave like ___?___ cartilage. Theyre supposed to remain cartilage forever. So theyre called permanent cartilage phenotype. ___ permanent cartilage phenotype. So my hypothesis was that these cells (cephalic) could induce bone formation, these (caudal) cannot. This (caudal) is just reticular cartilage, and theres something in your joints that (?). This is a stain, so these are dishes in culture with the cells. Then we use this red stain to see which cells express alkaline phosphatase, which is a marker for mature cartilage, growth plate cartilage. The red is alkaline phosphatase. This is the dose (number in middle) of retinoic acid, thats vitamin A that Im throwing in the culture. So you can see that the more retinoic acid, the more vitamin A, the more mature the cartilage becomes. So that was my developmental ? , so I said Serafin (? persons name) we can even test this hypothesis because these cells can make bone (cephalic) and these will never make bone (caudal). Slide 8 In Vitro Studies So what I did was.I said alright show me your scaffolds. Its a very nice homogenous sponge that he created out of chitosan. So the first part of the project, we were gonna go chondrocytes in there, induce the maturation with vitamin A & C, and see what happens. See if the cells behave like growth place or reticular cells. Slide 9 Chitosan Then there was a second stage of this project that we were testing to see if we could make bone. So this was the scaffold we brought in. Its madechitosan is removed from exoskeletons of sea food, and flies. Its a polysaccharide. So its a natural polymer. Its biodegradable. Its FDA approved for human use, because some reason 4

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the properties of the material make it antibacterial and hemostatic. So every soldier in US Army has some chitosan in their backpack, so if they get wounded they stuff that in and it stops the bleeding and prevents microbial growth. So its ready for human application. Were ready to go to the humans to start using these things for the applications. Slide 10 SEM of Chitosan And they look like the sponges that Serafin brought in. They look just like the cartilage matrix without the cells, except these are really large, theyre like 100 microns, and cartilage cells are like 10 microns. So its a little large. And this is what we do, we put the cartilage cells on these sponges and the cells travel all the way to the inside, and it looks like cheese in a week or two. This is scanning electron microscopy. Now its very interesting because (a person) said, alright lets try to grow these cartilage cells in the sponges in a bioreactor. You know what a bioreactor is? Its a culture vessel to put the cells with rotating tubes. It creates a zero gravity environment. So when we put the cells in the tubes, and in the medium, you see them floating around because theres no gravity. So we put the cells in the sponges then the sponges in the bioreactor. We took the sponges out, and no cells. We were like, oh wow, where did they go? Then we decided, ok, throw the cells and sponges in the bioreactor together and let them find each other and see if they go to each other. So we took the sponges out and no cell. We looked at the sponges and no cell. Where did they go? They couldnt all die because thered be floating bodies and parts floating around. So we cut the sponges. You know what they were all? Inside. Hiding in the middle of the sponges like a ball. You know why? Because cartilage does not like oxygen. It doesnt need that environment with oxygen and nutrients floating around. First stage of cartilage differentiation is condensation, they hide into a ball with no vasculature. Then we went the more classic route and forget the fancy bioreactor that costs thousands of dollars, we just put the cells in culture, and the sponges in the culture disk. We put the cells on top of the sponges and just let them go. Gravity helps and they dont mind hiding all the way there. Look how far they travelled (4th SEM picture). So thats how we ended up with that spongy looking tissue. Slide 11 Hematoxylin & Eosin Alright so then as I told you we used both the upper sternal and lower sternal cells. When we looked at the histology of the cells.ok this is 5,10,15,20 days. They look the same. The cephalic and the caudal. They look exactly the same as chondrocytes. Just by H&E staining we couldnt tell a difference. Maybe there were a few larger cells here on the cephalic, here becoming mature hypertropic cells like the growth plate. Slide 12 Cephalic and Caudal blue/green stains Then we stained them and we saw a difference because only the cephalic could produce type 10 collagen, which is another marker for growth plate; alkaline phosphatase and type 10. And the stain hereso this is an immunostain, we use an 5

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April 16, 2014

antibody to find the protein in the tissue. And the caudal didnt have that much. So these are growth plate cells (cephalic), these are reticular cells (caudal). Slide 13 In Vivo Studies So then we took these sponges with the cells and we placed them in mice. So we went from chick to mice. And we placed them in immunocompromised mice because were crossing species and didnt want a reaction. We put it here, see? Under the skin. On one side we put one, the cephalic, and on the other we put the caudal. And then we looked to see what happens. Slide 14 Faxitron This is what happened over time...these are orthodontic wires because we were radiographing these things and seeing nothing. So we wondered if we even radiographed the right spot. So we marked it with orthodontic wires. What it shows is that cephalic zone, the ones that behave like growth plate, and caudal, the ones that behave like reticular cells. And this is x-rays showing mineralization. Mineralization only occurs in the cells that came from the top of the sternum, that had the ability to produce bone. The others, not much. Slide 15 Faxitron 5 months Look at this. 5 months. Not much going on there. But here, mineral. Mineral comparable to the vertebrae. There was a lot of mineral tissue being formed. Slide 16 Micro CT Now was it all bone? We were curious about. My guess was not because one of the steps in converting cartilage to bone is that the cartilage mineralizes. So some will be mineralized cartilage. This is micro CT showing those sponges from the cephalic. And not even showing those sponges from the caudal because there was no mineral. There was a little speck.and nothing outside. But here you see over time (talking about cephalic) it becomes more and more mineralized. Inside too, this is all mineral. Slide 17 SEM/EDAX So it helps to look by another SEM. EDAX its called because it looks at the minerals and can find out what molecules are there. And it was bits of calcium, phosphate, so this the hydroxyapatite being formed. Also, note the sponges are increasing in size, while the ones from the caudal portions keep the same exact shape..so this bone, or this cartilage is gonna grow (cephalic). Slide 18 Hematoxylin & Eosin These are histological sections showing from one side of the sponge, the other. We cut the body of the animal like that, axialand one of the sizes is shrinking because the one that had the cartilage from the bottom, that behaves like reticular cartilage was just creating a scar and being invaded by fibroblasts (?). We saw that here in these cells. Caudal, cephalic, and this is the vertebra because its _____ to keep control. Vertebra formed by endochondral ossification, so I wanted to see if these 6

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cells would do something like that. So with time they did, look in two months, first has a layer of bone, you see? .then they start to invade the cartilage. And it looks weird, the cartilage. Mineralized. Thats the mineral we saw in that micro CT. Slide 19 Hematoxylin & Eosin 3-4 months So here its 3 months. You see what I was saying that the fibroblasts were invading and converting that sponge to more like a scar. Well in this one there were blood vessels, lateral cavities forming just like in the first one. More disorganized. Its missing something else to be a true tissue engineered tissue. Slide 20 5 months after implantation Ok, question to you. Why did I put it under the skin when the whole tissue engineering field, you know where they put the scaffold when they want to test if they can make bone? Have you seen this project? Where do they put it? Near bone. Does that really test if they make bone? Because if you put it on the bone, the calvaria, the tibia, they make a special hole in the bone and plug it with something that is osteoconductive or osteoinductive. Its hard to find out because youre there, the bone cells will invade because youre providing a matrix. Good or bad its a support, right? We put it under the skin, and when I decided that wed put it in a pocket under the skin, we opened up the skin and made a pocket and put in the sponge. We were like, well what if it doesnt work? And I was saying well if it doesnt work itll get closer to the bone. This is the ultimate test if we want to find out does the cartilage carry all the signals to make bone, you have to put it in a valley, in the eye, or somewhere where you wouldnt expect bone, right? So it passed the test. So I started the most difficult experiment, and I was saying Ok well get it close, Ill put it in the calvaria and well have to tweak the results to present. But this proved our concept. You dont need to be close to the bone because these cartilage cells know how to make bone. And the bone was growing not only from outside in, but inside out. Again, they secrete the factors that stimulate the vascular invasion, so the blood vessels travelled through this cartilage ____. Slide 21 Engineering Growing Bone So this was the idea.went from the chicken to the mouse. We got cephalic cells to make bone, not those ones (caudal), as we were expecting. And the idea is that this bone can grow. And this just in 6 months we actually made the sponge into the shape of a femur, kind of, and we put it under the skin and look at this, in 6 months nothing here and there, a whole new bone under the skin of the mouse. Slide 22 Engineering Growing Bone MicroCT image I have microCT too. You see what I was saying. On this side its just a few specks, a few cells still tried to make bone but ___ contamination on that dissection. Right, so how far is this from the clinic? Not far. Chitosan is FDA approved. All we need is cartilage cells. Now where do we get these cartilage cells in a baby? Umbilical cord? So we could do that. I dont have to do that. I just proved the concept that cartilage can make bone, and its a bone that can grow with the patient. Theres a whole field 7

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of stem cell research thats trying to figure out how to make cartilage cells, bone cells, liver cells, out of ____. We can even scrape some noses and some ears because even though this is permanent cartilage, theres something thats holding that permanent phenotype. And in culture.alright so thats the other issue. Theres a whole field of bone tissue engineering, and theres an even larger field of cartilage tissue engineering to replace ____ cartilage. Why they not succeeding? Because when you get this cartilage in culture a long time, lets say replace the articular surface, it always becomes growth plate cartilage. Seems like with the whole pathway to cartilage, is to become growth plate. So they struggle with that. The cartilage doesnt remain permanent cartilage forever. So I have no problem with those.theres some kind of inhibitor in permanent cartilage of some kind that prevents them from becoming growth plate. But during arthritis, for example, articular cells behave like growth plate cells. They mineralize, they have type 10 collagen. So Im not worried because I think in some yearswe could make enough cartilage to grow something in the shape of a cleft, then go in as orthodontist to expand, advance, and shape the tissue. Because, I was telling you, the reason it was so disorganized tissue because it didnt have the environment to tell it to grow in this direction. There was no forces. It was under the skin. Now if you put it in an area with tension, pressure, then it will organize different. Its very interesting, one day I gave this lecture that included this research project at the Hospital for Special Surgery. And the guy who came to set up the computer had one arm this big, and the other this big (small). And I thought, thats an application. Why not create a growth plate and insert it in between a growing patient and thats it. Stimulate longitudinal growth. These are applications. When I get to this point Im happy. I proved a concept, and now other groups investigate the applications. We can move to the clinic practice if we had hands, if someone wants to carry on this research position. I give you these examples because you read in the books of the 2 ways to make bone, one is endochondral and one is intramembranous. And you think thats all you need to know about it. This project is contemporary and its like, alright you know that but apparently that is not enough because everyone is trying to engineer bone via intramembranous bone formation and disregard the developmental biology knowledge that we have.This information has to be applied to research, to advance to create new approaches to treating old problems, and to the _____. Slide 23 Early Treatment Ok, lets give you some cases. Same thing with the theories, you heard about the theories of growth, right? Do you know orthodontists still go to conferences and have big fights on how to treat cases? Some orthodontists will say, I tell all my patients to come back when all their permanent teeth come in. If they dont have enough space for all the teeth then well extract some teeth. They dont believe in functional matrix theory at all, because what theyre saying is that I cant do anything about the way your kid is growing. So let all the teeth come in, then Ill take a few teeth out and Ill straighten everything with braces. This is current. Im a developmental biologist. I think anything is possible. I could grow your face any way I want, I just need to figure out how to do that. So, 60-70% of my patients are younger than 8. Guess what? They dont have all their permanent teeth. They may 8

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have a few permanent teeth. They all have mixed dentition. I believe, Im going to show you, I can change the way theyre growing, I can change the ways the jaws articulate with each other, I can change function and push growth in another direction. Slide 24 Picture of blond girls profile and facing forward This is one of those younger patients. How old is she? What do you think just looking at the face? Skinny little girl. How old? 8? 7? 6? So the mom brought her in, and said the nurse told her I should take her to a growth specialist. She asked should I do that? I said Im your growth specialist. But why did the nurse say that? Slide 25 Same blond girl, now smiling Becauselook at the way she smiles. You could tell that maybe the mandible is a little back, we call it a class 2. A little retro-gnathic mandible. When she smiles you really see that.but she has a nice chin bottom that disguises how far back that jaw is. She has nice cheek bones. Slide 26 X-Ray of Hand Look at this hand/wrist. What are we looking at with the hand wrist. What is the space between epiphysis and diaphysis? The growth plate. It shows up dark because its not mineralized. So Im looking at the growth plate thats still there and doing their business. So chronological shes almost 9. Skeletal shes 7, almost 2 years behind. So thats why the nurse, when she plots her height and weight, she thought she was on the low side for her chronological age. Basically what the nurse found out is that these two dont agree. Without even looking at the hand/wrist, but instead just by looking at the height and weight she figured out this discrepancy. Slide 27 X-Ray of complete dentition Dentally was not bad. Dentally she was right on the chronological age. Sometimes these disagree. Slide 28 X-Ray Entire Skull Max-Max Now we take this, this is one of the x-rays we take in orthodontics for a diagnostic purpose. We measure the width of both jaws and find out if they match. Not so much of how big they are, but if they match, because in the end they have to match for normal occlusion. What the measurements told us is that these are her measurements according to norms. The mandible was right on. So she had a deficiency of about a centimeter, mostly on the maxilla. Thats a lot. Slide 29 Skull Profile Now we take this X-ray and we measure the position of the jaws to each other, to the rest of the face. And what this X-ray showed was what I was telling you that she is a class 2, meaning that this jaw is pushed back(?)..between the upper and lower jaw. The chin masked it a little bit, but its there. Slide 30 Lateral Cephalometric Analysis 9

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These are the numbers. Doesnt mean anything to you but this is between the upper and lower jaw, it should be 2 degrees when you measure the angulation, hers was 8. This makes her a class 2. (Max-Mand relationship ANB). Retro-gnathic mandible. Slide 31 Showing occluded mouth smiling, from anterior and 2 profiles The teeth look like that. Ok so cross bite a little bit, maybe an end to end relation (?), and a class 2 because this should be 1 step lower. Slide 32 Pictures of upper palate and lower jaw This doesnt mean much to you right? You havent seen many teeth, occlusion, or bite? The upper jaw is kind of narrower than the lower. You dont need to be an orthodontist to see that the mandible is kind of a U-shaped and the upper is really narrow. Slide 33 Problem List Objective List So we make this problem list. We take a systematic approach. We list the problems in the jaw, the profile, the teeth, and then we make an objective list and say I want to correct this. This is where orthodontists disagree (objective list). They more or less agree here (problem list), yes this is a class 2, the upper jaw is really narrow, but then how you want to correct is when you disagree. Depending on which philosophy you adopt. You believe in functional theory then Im gonna treat that jaw, Im gonna lower that jaw, Im gonna make this wider too. You dont believe in that? Youre gonna say, oh she looks small and cute, and just like mommy. Wait until all the teeth come in then were make sure she gets a nice straight smile. And theres nothing wrong with that. Its different treatment plans and different results. So, Im the one that believes, no, Im gonna change it. Im actually gonna correct it. Slide 34 Upper arch with a metallic expander inside ____ problem with the expander. Which is an appliance like that, that you plant on the teeth. Theres a screw here (middle) that you turn, its a little hole that you turn with a key, have you guys seen this? So what am I doing? There goes the other theories of growth, because Im changing the sutures. Sutural theory of growth, failed. Because as long as I apply a force on the two halves of maxilla, Im gonna get a larger maxilla. Theres no controlling that suture, its just reacting to the forces that Im applying. See you have to believe in that. If you think you can change sutures, you can. We do this all the time. It takes two weeks, and you go from here, to here Slide 35 Same arch and expander, just wider Sutural theory out the window. See, you can make the jaw really wide. Slide 36 Clear retainer-looking device picture Then because she has the incisal problem of having the jaw back because I think I can change that, we put an appliance like this. Do you know what it does? Slide 37 retainer device inside mouth

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It forces her, when she closes, the jaw to come forward to fit in that indentation. The way you take an impression, that jaw is like that right? I take an impression with the lower jaw coming here, then I create an appliance where that lower jaw fits and it goes back.Now in 6 months, I wanna show you something. Slide 38 End of Phase 1 Treatment This is at the end of phase 1. Now some more teeth came in, more permanent teeth. She doesnt have the overjet anymore. Shes class 1. Actually we expanded her again. Slide 39 Profile of Smile/Appliance Then we put the bionator, its called a functional appliance. Its actually called functional appliance ____. And 6 months later shes biting like that. But its not (broke?). Its just shes posturing. All the muscles have been stretched. Its comfortable bringing the jaw forward. But they can go like this, and go right backthe profile goes from here to here with the functional appliance. Slide 40 Picture of girl from front and profile Look at that. No braces at all. Look at that. There was a reasonable result to correct the skeletal discrepancy. In the process made room for all the teeth. Now its a question of perfecting. Slide 41, 42, 43, 44 Showing all the after pictures. #44 girl smiling The parents decided to go for braces, and now it looks very nice. She looks like that. All the teeth in. Wide upper jaw. Smile is nice. Slide 45, 46, 47 Profile shots progression And end. Phase 1, phase 2. All the way. Slide 48 Drawing of black/purple ink of profile So the question is, would this happen if you didnt disturb the system? If you didnt make it wider to allow this to come forward? If didnt stimulate the jaw to grow in the direction that you needed for the correction. And actually the research shows that if you dont do anything, that jaw, that mouth function is in equilibrium and it will continue to grow like that. Deficient growth between mandible and maxilla can only get worse. You know when it gets corrected? If the jaw now grows more, as a type 3 type of growth pattern. Slide 49 Lateral Cephalometric The numbers dont mean much to you, but some of them got corrected. Slide 50 Arch Development So, its possible. If you do it in the functional theory of growth, you can change using functional appliance, you can expand sutures, and do things like this. So Im gonna show you some examples of developing the arch. Alright, so from your lectures this week, you know that theres no growth here. This happens all the time to you in the clinic. Patients come looking like that, ok, crowding. You dont need an orthodontist 11

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to tell you theres crowding. Mom and dad can figure that out. But mom asks me, theyre growing right? Wont the growth correct that? Now well find out if they paid attention during lecture. What kind of growth do you have in the anterior area of the mandible. Do we have a suture here that.no. If anything we have absorption. And when those ___ come forward..So the answer to the parents is yes shes growing. But wheres shes gonna be growing is in the back of the mandible to make room for the second and third molars. This is it. So this will only get worse. Unless you do something about it. So let me show you what you can do. Slide 51 Arch Development with appliances Now look at this, so nice. See how nice you can really remodel the alveolar bone. You see this? You know what the difference is between this and that? There is an appliance that looks like that. Thats placed low in the vestibule to bring the cheeks up.So dump the cheeks outand let the tongue push those teeth out. So when the teeth erupt, they erupt more buccal. Now do the teeth just fall out the bone? No, because the bone follows the teeth. It all remodels. So you can do these things without the bracket. Thats a big deal. Parents take a while to understand that. Slide 52 Vertical correction What about this girl? Which was she growing? Very narrow. Very vertical grower. She does look like her dad, but can you do something about it because theres no space for her other teeth. You can see that the growth is more vertical than transverse, right? So look at this, this is just a year and a half Slide 53 After July 2008 With an appliance that expanded, but also had a bit plate that covered the teeth and kind of controlled the vertical growth a little bit. Look at that profile from here. Nice? Very high mandibular angle. This vertical growth taken care. See looks more balanced. This is the middle, this is not finished, just the beginning. Look at the smile, Took care of the narrow jaw, we expanded a little bit. Shes still vertical, see the gingival smile. Thats the way shes growing. But you could redirect it a little bit. Slide 54 Sagittal Correction Look at this class 2. And this I documented because she was not a good patient, but I was like, Im still gonna get it. See how the profile is changing. Isnt that nice? Its because the condyle is growing and there was all the growth in this area and I just needed to shift it in the direction that I wanted to correct the severe skeletal class 2. Slide 55 Severe Crowding Open Bite Now Im gonna show you other cases. Without braces, just taking advantage of ____ to change function with suture to stimulate condylar growth you can correct a lot of the skeletal and also dental, because they dont have space for all those teeth in the beginning. Slide 56, 57, 58 Progression shots: 2010, 2011, 2013

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2010. 2011. (flips through the shots). 2013. So you cannot do it in 6 months or anything like that. It takes a while because to modify growth you have to be there while theyre growing. I ask the kids sometimes, so when do you think youre growing. Because I have to explain this to the parents. The parents are like, what do you mean 3 years? Im like, were not fixing teeth. Were changing jaws and faces. If youre gonna do it while theyre growing, you have to be there while theyre growing. And theyre not growing in the next 6 months and then stop. I need to be there for a while. Now, what they have most of the time is a lip one, or a functional appliance that they sleep with, its almost like a retainer. Its slowly pushing things in the direction that we want. Slide 59 X-Ray 2010 I want to show you this x-ray that is a very crowded situation because you have to fit this teeth hereshe also had a kind of an open bite. Slide 60 X-Ray 2013 Slide 61, 62, 63 Palate/Smiles 2010, then 2011, then 2013 retention One expander. Two expander. So at the end of treatment, she really has only 2 rotated teeth. The parents decided they dont want to do braces to correct this, I can correct this with a removable appliance So in the west theres a push for fixed appliance. But in South America, in northern Europe, people with other less expensive appliance, removable appliance, or teen invisalign. Itll correct that rotation in no time and this kid never had braces or extractions. (flips through slides quick) I want to go fast because there are some cases I want to show you. Slide 64,65 Boy, 2009. Then in 2013 Good looking kid. He knows it, see the smile? Thats the face of someone who knows it. But look at the crowding. That canine completely blocked out. Theres no space for the lateral incisors. In fact, the reason hes even in my office is because the eruption is delayed. Then now the dental and the chronological dont agree. And the dentist, sometimes I hope you remember what Im telling you today, the dentist say, oh hes 9 years old and the incisors arent coming out. Lets take out the baby teeth. For what?? And then have the kids walk around with no permanent or baby teeth? The reason the permanent teeth arent coming in is not because of the baby teeth as an obstacle. This is a thing that annoys me a lot. Everyone thinks baby teeth are an obstacle. Teeth that melt (?) away are an obstacle to anything? No. There is no room. It cannot go in. You know when one of them go in? When they go like that. Then they come in. But as long as theyre straight like theyre supposed to and developing straight in those bones they cannot come in. Like you guys all trying to get out through that door. Unless you open that door well all be stuck. And thats the image I have. Theres no way those teeth will erupt. Slide 66 X-Ray 2013 13

Transcribed by Chris Bedoya Look at that. 09. 13. Im very proud of that. So look at this.

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Slide 67 Palate / Smiles 2009 but the most important problem is the severe crowding. This is the other interesting thing. The dentist will say, I see no crowding. Thats because hes not looking at permanent teeth. There will be crowding. The tooth is gonna be largerthe only permanent tooth that is smaller than the baby tooth is the second premolar, that replaces the 2nd molar. But that space is sometimes needed to correct the class 1and what good is that place there if I need it here? Braces they tell them. Thats why you get braces to get that extra space here.I dont know your experience but I never get 2 mm. (flips through slides, ending up on) Slide 68- 2013 So we got them here. No more crossbite. Look how nice they look. They even know where to stop. Its ok. Same thing, the parents decided not to do braces. Besides, why would we do braces on a moving target? Kid is pre-pubertal. How do you know the jaw, there wont be some surprises there. Right? So, the parents at this stage, the kid has not gone through puberty, but its in a nice normal occlusion, so with puberty it will just keep going. Then maybe if theres crowding he can treat them. He can get it treated as a young adult. And by the way hell pay the bill then, and not the parents, so they love that. But its true because a lot of my re-treatments are the young adults after college. Everyone loses those retainers in college. I dont know what happens in college, theres no college in my country, so I dont know exactly what you guys do, but all retainers gone. So they come back, theres crowdingwell do that then. Slide 69 X-Ray 2009 Look at the discrepancy here. Slide 70 X-Ray 2013 Nice, huh? Slide 71 Girl Smile and Profile 2007 Ok, this girl I asked if she liked her smile.people think its hard to treat kids. Kids are wonderful. Its harder to treat adultsShe told me, I dont know, I want like a big smile. She knew exactly what she wanted. She wanted a big smile, she got it. Slide 72 Progress 2 2009 And she wanted that big smile, and one day she tried to steal my safety goggles. She was funny. She thought they looked like Bono. Slide 73 After - 2012 Look at that. Now she has something very interesting that drove me nuts, because of this abnormal eruption pattern. The dentist couldnt care less about the fact that, look at this problem (bottom left of x-ray). That thing going on there, that was like a big issue. The dentist called me every 6 months to find out which teeth I wanted her to take out. Im like, dont touch baby teeth. Baby teeth are never an obstacle. If 14

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anything hang on to those baby teeth because theyll be a guide for the teeth. If you remove it, then bone heals, where is the tooth supposed to go? How does the tooth know where to go? You need a path of eruption. But this is what was very severe. Slide 73 X-Ray Progress 1 2009 And the dentist again calls, which tooth am I gonna take? I said no. Theyll grow and come in. The girl would ask if I was gonna take an x-ray, and I asked why. She said dont you want to know whats going on there? I was like, no I dont need an x-ray to find out whats going on there. Theyll find their way. Why wouldnt you want to take a tooth out? The dentist called, which one you want to take out? I dont want to take any out. I dont want to take that one because the only thing keeping that guy out of there is this and that baby tooth.I dont want to take any tooth out. Trust nature a little bit. Slide 74 X-Ray Progress 2 - 2010 Then finally, once permanent teeth were almost fully erupted, then I said they could take the baby teeth out. At the point where they practically had no more roots. Slide 75 X-Ray After 2012 So I knew that dentist was talking to mom because she would come in with those questions, ok what are you going to do today? I said, well Ill adjust your.She said, no about my teeth! Slide 76 Palate/Smiles Before - 2007 My gosh, she was pressing me. A 9 year old pressing me. This is how she looked like. Very severe crowding. The only reason they were coming in was because of that.So I dont understand this idea of waiting for eruption to deal with it.And like she said she wants the broad smile. Sometimes, its not that theres a discrepancy between the upper jaw and the lower jaw, its a discrepancy between the tooth size, and the jaw size. And you have potential to correct. Now, you want everyone to become Julia Roberts? No. Deal with it a little bit. Sometimes I correct the jaws and dont correct the crowding because its so severe no matter what you do youre gonna have to take some teeth out to reduce the tooth structure. Slides 77, 78, 79 Progress 1 (2008), 2 (2009), and after (2012) Now look at this. Isnt that surprising how nature took care of it? I didnt put the brackets on this case. I didnt put the teeth aligned to put them exactly where I want them. I did this without braces and wires. Ok, so how many times did I expand this kid with the expander? 1, 2, 3. Slide 80 MicroCT So she went from here to here. Thats what Im saying, I dont always do that because in some casesshe was so severe, she had no space for the lateral, we had to create space for the canine. Sometimes you can. But its better than stopping.

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Look at this, the change in the intermolar and intercanine distance. Its significant. You could move this jaw. Now she was my worst lip bumper patient. I tried everything. Slide 81 - MicroCT I said, you know what? I dont care about this minor crowding. Theres something that removable appliance corrects, like a (spring appliance?), theres some things that a removable appliance takes care of that. Thats all she needs now. Now, the patient that first came into my chair, she needed 4 premolar extrations, and long time with braces because if you add all those ____, you will be in trouble. Im gonna move quickly Slide 82 Girl Before - 2009 This is a class 2 case. Look at the change in the profile. Its an approach. Im just making my point. Im proving to you that you dont need braces to change skeletal development, eruption, or to make space for all the teeth. (flips through girls progress and x-rays) Slide 83 She was not very crowded, right? Compared to what I just showed you. She was a skeletal class 2. Deep bite, large overjet. Class 2 dental. Slide 84 Progress 2 First we create room in the jaws. Then she uses this biorator. Large overjet. You see the changes? I did a period of treatment where Im creating space for all the teeth. And then I correct this dimension. Slide 85 After - 2013 From here to here. Look how nice. Class 1. So with your kid, you want to do braces? You could, but you know for how long. 3-6 months, because its just finishing touches. Slide 86 X-Ray Look at the skeletal class 3. So the same is true for this case. Its just that you had a compensating maxillary. So if the lower jaw is growing too fast. In this case it was a maxillary deficient. Upper jaw deficient. Slide 87 Smiles/Profiles flips through a few slides Now the parents worry that the face and nose will change, do you see those changes? Look at the nose. Slide 88 X-Ray 2009 16

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This was crowded. Again the lack of.was there because of the late eruption. (flips through these) Slide 89 Palate/Smile 2009 Slide 90 After 2013 Slide 91 Skeletal profile X-Ray She went from this, angry looking, to normal looking guy. Alright, so I made my point. Youre going to have these patients in your practice. The mom that comes and says, too much crowding. And that the kid is 6. Shes going to grow till shes 16, thats 10 years of growth. Will this affect her teeth/bite? No. The growth is happening in other areas. Condylar growth, yes you can stimulateits not all about braces. Even without braces you can modify craniofacial growth.

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