Transcribed by Amit Amin [Basic Tissues] [19/20] [Bone IV] by [professor]

02/06/2014

[5] [Dr. Wishe] [speaker] Today Im going to finish up the bone and afterwards there will be a CCP by the Oral Surgeon. I asked him to post something, but sometimes you talk to the wall and the end results arent positive. So we were talking bone formation and we went over intramembranous bone formation and then we got into endochondral bone formation. Whether or not you have blood vessels is the difference. If you have blood vessels, intramembranous bone formation occurs. Bone requires a lot of oxygen. We went over the basic detail in previous time. [6] [Dr. Wishe] [speaker] This was the summary of endochondral bone formation. Via endochondral bone formation, no blood vessels, no oxygen, that means the first anatomic bone is made up of hyaline cartilage not bone tissue. And so youll have an area that represents the diaphysis and the epiphysis. IF you look at the diaphysis you can detect these various zone. The first one rest/reserve chondrocytes randomly arrange. Proliferation, Isogenous groups and btw this zone is the driving force for everything. Without mitosis youre not going to get more chondrocytes, and w/o more chondrocytes you wont get an increase in length of bone. Zone of maturation is something that I put in. Break up matrix synthesis into two zones. Not a big deal. AT the zone of maturation, you get break down of cartilage matrix. Then we go into zone of hypertrophy. Thats when lacunae and chondrocytes enlarge. The zone of provisional calcification, what happens in this point and time, periosteal buds invade the cartilage. They literally push in and the periosteal buds contain blood vessels and mesenchyme cells. With the blood vessels you are also bringing calcium. So what happens now to the cartilage is that it is going to calcify in this particular zone and it will begin to degenerate. You have cartilage reabsorption and you will have little remnants of cartilage that will look like this There wont be any cells left or anything and then what happens around this cartilage is the zone of bone formation so youre going to get woven bone forming around the cartilage pieces. Remember woven bone is the first type of bone formed wherever. [7] [Dr. Wishe] [speaker] We probably looked at this as well. Joint w/ 2 bones. Top bone has an articulating cartilage. Spongy bone in here, bone marrow etc. We see something different on the second bone. We see this area of secondary center of ossification that means that the cartilage is degenerating from within the epiphyseal end. This area was the primary center. What youre left w/ is a region right in here, which is the epiphyseal disc or plate, and that structure is responsible for growth in length of the bone. I can draw a simple picture to illustrate that. Lets say that this is the disc, the chondrocytes are going to undergo mitosis and give rise to Isogenous groups of chondrocytes and that area then gets longer. This is the additional layer is hyaline cartilage thats deposited. What happens to the first layer? This area will begin to degenerate and is following the guidelines of endochondral bone formation. One more step forward and again, more mitosis and then this layer begins to degenerate but if we started w/ the cartilage disc and now way back here what have we done? Weve increased the length of that particular part of the bone. Youre getting an 1

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increase in length of bone since more hyaline cartilage is formed. When it comes to width of the bone, thats brought about by this structure (periosteum). The width increases in this direction. The increase in width of bone is appositional growth and the increase in growth is interstitial growth of the hyaline cartilage. The bone is increasing in length not b/c the bone is increasing but b/c more hyaline cartilage, which then gives rise to bone. [8] [Dr. Wishe] [speaker] From textbook. Picture A is long bone or hyaline cartilage. You can see something going on in the middle, which is diaphysis. A periosteal bud is pushing in and bringing in blood vessels/ mesenchyme cells which leads to degeneration of the hyaline cartilage. As we look at the next diagram, you can see each end has a secondary center of ossification happening. As we go through from AD the bone is getting longer b/c of this area (disc) is going through interstitial growth where we have Isogenous chondrocyte groups. This is sort of clear looking, the top region still has cells so I think the diagram is trying to show you that the ephipsyeal disc is getting ready to disappear. Here we have a much more magnified view of the disc. The diaphysis is way down below. Heres an epiphyseal area and secondary center. Youll notice blood vessels coming in. I want to point out this structure, which is your bone collar. It s formed from the periostem which gave rise to osteoblasts and as a result the width or diameter of bone kept increasing. [9] [Dr. Wishe] [speaker] This is a picture looking at a long bone. A little hard to see, but way up here, the chondrocytes are not organized. They are scattered. When you come down to roughly this area, there seems to be some sort of organization to chondrocytes. They are lined up in longitudinal columns. These are the Isogenous groups. As a result of this activity, you get more cells produced, more matrix produced, and eventually the cartilage can be destroyed, eliminated, and replaced by bone. ZH= zone of hypertrophy w/ large lacunae and large chondrocytes. ZC= Zone of calcification. Not easy to see. If you look at the cartilage matrix, it looks little darker than the rest of the matrix. It is brought about by the calcification of the tissue. Whats being shown in this region is the zone of denegation where the cartilage is degenerating and then down here, you would have the zone of bone formation where youre getting woven bone formed around cartilage leftovers. The lighter stained tissue looks like the one up here. The lighter stained tissue is the remains of hyaline cartilage matrix. You will see an E stain tissue, which is the newly formed bone. The next few slides magnify this image. I just want to point out that this happens to be the bone collar and the bone collar extends up a certain distance around the shaft. You will never find a collar or periosteum over the articulating end. [10] [Dr. Wishe] [speaker] Here we have a higher power. Light stain= hyaline leftover, and Dark= newly formed bone. What we have happens to be cartilage pieces surrounded by woven bone. That doesnt make for strong supporting tissue. All that tissue has to be resorbed and eliminated. Fresh osteoblast are formed from mesenchyme cells that migrated in w/ periosteal bud and they form secondary/ mature spongy bone. This is the primary spongy bone or woven bone, etc. And all the tissue in b/w the light 2

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tissue sort of scattered about is your mesenchyme. From that youll get bone marrow, osteoblast forming, etc. If you look right here, youll see two arrow heads pointing to osteoclast cells. It not a matter of bone forming and then starting reabsorption. Bone can be growing in one location and be broken down in another location. [11] [Dr. Wishe] [speaker] This again is a much higher power and again the cartilage pieces, the woven bone, and all of this will eventually be eliminated. These cells look chubby like so they are the osteoblast, and you should have some sort of flattened cells, they might be bone lining cells. [12] [Dr. Wishe] [speaker] Again the same zones. We were looking at this from the view in the diaphysis. The same thing will happen in the epiphyseal disc. [13] [Dr. Wishe] [speaker] Additional pictures to show endochondral bone formation. Periosteal bud pushing into hyaline cartilage of the diaphysis. In diagram B, tremendous vascularity forming and all cartilage is gone to be replaced by bone. C is showing secondary center of bone formation. D shows articulating cartilage and secondary center and the chondrocytes all lined up before moving into diaphysis. You can see some tissue here and here, and thats where the periosteum is ending and the dark tissue and sides represent the bone collar. [14] [Dr. Wishe] [speaker] This elaborates a little further as to what happens with the hyaline cartilage. First lets just draw a simple diagram. Here we have two lacunae and hyaline cartilage and well put in two chondrocytes one in each lacunae. When the hyaline cartilage degenerates the part that degenerates are they horizontal septum. Some people refer to it as your room and his as your floor of your lacunae. Once that degenerates, the only thing youre left w/ is your vertical septum. Now as we look at the picture on the left, the dark stained tissue in here represents hyaline cartilage and you can see the dark staining tissue extending into each and every trabeculae. What you see around the dark staining tissue now, is woven bone that has formed around the hyaline cartilage leftovers. We are gradually degrading hyaline cartilage, and adding woven bone. The spongy bone is replaced w/ secondary bone. This occurs w/ the diaphysis as well as the epiphysis. [15] [Dr. Wishe] [speaker] Picture on the left is of someones hand. You can see the long bones and the shorter bones. Notice the short bone follows the contour of a long bone. Youre going to have the equivalent w/ an epiphysis and in the middle, a diaphysis. Picture on the right labels the different zone that ones find in the cartilage. Resting, proliferating, hypertrophic, calcified, zone of ossification. They did leave out the zone of degeneration. Cartilage needs to degenerate before you can get bone formation. [16] [Dr. Wishe] [speaker] In this picture, it is epiphyseal disc. You can see all the varying zones. Nice area of zone of hypertrophy, but then it gets confusing afterwards. [17] [Dr. Wishe] 3

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[speaker] This is a really high power. We have different change in the color of the tissues. Here we see purple and sort of a reddish color. Purple doesnt have cells in it so it must be bone or cartilage? Its the left over hyaline cartilage. The rest of the staining tissue has cells in the spaces in the lacunae (all of the woven bone forming around the leftovers). [18] [Dr. Wishe] [speaker] Before we get into that let me say a few words about osteogensis imperfeca. I know Dr. Craig mentioned it along w/ Dr. Lee in terms of collagen. Ostegoensis imp. Is a defect in collagen formation as are scurvy and there are something wrong in each of the cases in-terms of collagen formation. Scurvy is easy and can be fixed up based on the loss or lack of vitamin C. This particularly happened in the 1500s/1600s when the sailing trips took long periods and they ran out of vegetables gaining scurvy. Osteogenesis I. is just a simple change of one nucleotide in the genetic pattern. A lot of defects that do occur in the real world dont necessarily involve massive changes. Take something like sickle cell anemia. Only one amino acid substitute gives you the change. Bones become week and fracture easily. They are usually cardiac-insuficency associated w/ this disease. Sclera is blue and hearing problems are also there. Bone isnt as strong as a result and not be able to support the body very well. Leads to frequent falling of the individual and fracturing of individual bones. You never know when youll get a patient w/ it. Were not going to talk about bone remodeling. It happens w/ spongy and compact. Key in remodeling is there is no net gain or loss. Bone loss = bone gain. Reabsorption= formation. All occurs through ARF sequence but if you really list all the steps there should be a couple more letters than A, R, or F. In reality its ARRFR. Activation, Reabsorption, Reversal, Formation, and Rest. Bone formation is the longest stage w/ 13 weeks. Activation/ Reversal is about 1-2 weeks. Reabsorption is about 2 weeks. The big scenario is bone formation so whether youre having an implant or something in terms of alveolar bone, you have to expect healing to take a long time. In reality 10% of your bone is remodeled every year. In 10 years, all the bones in the body has been turned over. [19] [Dr. Wishe] [speaker] This came from the pathology book. It shows the ARF sequence and what were seeing on the top, heres some bone matrix, bone lining cells, and a sort of light pink area. Everything seems to be settled down. Then activation occurs and you being to see these folks. Those are the osteoclasts. We discussed last time about the interaction, b/w osteoblast and osteoclast. In reality, you are creating 2 depressions. Reabsorption based or Haversion canals and then we look at the next part so those two have joined up together and see a certain amount absorb by the clast. The bone knows when its been resorbed and there are various hormones that play a role. So now we go to this diagram, which is your reversal phase. You no longer see the clast, pulled in the ruffled border, unsealed them and move to another place to migrate. These sort of flattened cells are bone lining cells and could be osteoclast. They migrate to the area of the reabsorbtive bay. Then they start resorbing bone and thats what this pinkish area represents. We look at the last diagram and it is all woven bone, which has replaced bone that has been resorbed. All this resorbed bone will now be replaced by new bone that is equal in amount. No 4

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net gain or lost. Lets look at this resorbtion bay. Thats really a cement line. A reversal cement line. So we had bone resorbtion and now the process is being reversed and now you have bone formation. Thats why its called reversal cement line. This happens in both spongy and compact bone. [20] [Dr. Wishe] [speaker] This picture is from your dental textbook. Heres a big area where apparently our little friendly osteoclasts resorb bone and who made this picture put in part of the area as having newly formed osteoblasts. And the osteoblasts are laying down the bone. The orange color is referred to as the osteoid. Whats osteoid and how does it differ from mature bone? What does it have or doesnt have? Ok, next week is bone conference and next week is quiz on Dr. Craigs material. Thats your osteoid, uncalcified matrix so its missing mineralization. The white area is new bone that is formed and mineralized. The blue line is indicating reversal cement line. Heres your old bone. [21] [Dr. Wishe] [speaker] Here we have some pictures from an old version where you have compact bone that looks pretty dense and youre having bone reabsorbtion. It basically occurs from the inside (via the Haversion canal). Every osteoid has a Haversion canal. You have an endostium that gives rise to new osteoblasts. Coming in from blood vessels youll have monocyte type cells, which forms the clast (foreign body giant cell). Here we can see a number of osteoclasts eating away the bone and then we have new osteoblast coming in producing new bone. The difference b/w the two, is the osteoid and the calcified bone. The same thing happens in the bottom picture. The bottom shows you bone reabsorption going through the compact bone. [22] [Dr. Wishe] [speaker] This shows you the flaming color, essentially the same thing. Heres our nice osteoclast, Haversion canal and blood vessels and these folks down here represent freshly created osteoblast from mesenchyme cells. [23] [Dr. Wishe] [speaker] Some had asked a question about what Im showing you now. Obviously picture on the left is nothing more than a section through compact bone. Heres your osteon w/ your Haversion canal. You can see the Haversion lamella. As you look at the words underneath these 3 pictures, you should see in the first picture is a first generation. You see 3 osteons. The second picture doesnt show you how it happened but now you only have a certain remnant of the first generation. So osteoclast came in through Haversion canal and reabsorbed through the system. Thats what the little pieces that are left. A new osteon is then produced. Last picture shows your third generation. Something like this would be the remnant of the second generation. Something like these areas would be the remnant of the second generation. This is a generation by generation pattern. [24] [Dr. Wishe] [speaker] So we know that remodeling is no net gain or loss in bone but there is another word called modeling where you do have a net gain in bone. Youre creating a masterpiece. You take clay and mold it into a model. You have to have a gain in bone and there is a certain situation where this exists (called coupling). A couple is a osteoblast and osteoclasts. Its bone formation and reabsorption. They work 5

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together. Now lets say for argument this is how we start off w/ a parietal bone. You keep adding on material to it so by the time youre through thats what the parietal bone looks like. So this is your modeling process. Once this happens bone can be remodeled based on pressure that may be brought to bear on the bone itself. The items listed on the bone remodeling, 85% of phosphate in the body is in bone. PTH, produced by parathyroid gland, when released, will stimulate the osteoblast to produce osteoclast stimulating factor (RANKL) and has an effect on osteoblast. Osteoblast is supposed to interact w/ clast to stimulate it to reabsorb bone. Vitamin D is very important. The less you have, the less mineralization you have and the weaker it is. Calcitonin has receptors for it and then reabsorption is cut off. Growth/ thyroid hormones are important to all parts of the body. In terms of the body, they have a positive effect on the epiphyseal disc. There are a lot of other factors (bone morph genic proteins- BMP), which are osteo and dentin inductive. Bone is not only being effected. BMPs are used to promote healing of fractures and occurs much more quickly. [25] [Dr. Wishe] [speaker] Osteoporosis is either too much being absorbed or not enough being formed. Either case you have a loss in bone mass. Then you have problems and support. Two pictures (normal) osteoporosis, which has much less bone than the other sample. Much larger spaces seen. Osteoporosis which is the reverse where bone reabsorption doesnt really take place and thus you have a constant deposition of the bone and the bone thats formed is very dense and sometimes referred to as marble bone. [26] [Dr. Wishe] [speaker] We are looking at the oral cavity here. Right now Im not interested in the teeth per say but you can see part of the alveolar bone laterally being eaten away. [27] [Dr. Wishe] [speaker] The final part deals w/ fracture repair. 4 diagrams. This depicts a complete fracture, which has bleeding occurring throughout the fracture area, and the first thing that has to happen is a blood clot to form to seal off the fracture points. Once that happens, the periosteum regenerates and joins up w/ both sides of the fracture and forms what is known as a periosteal callus. In the mean time, the jagged edges is not really good so thats reabsorbed w/ all of the damaged tissue. Eventually a collateral circulation develops in the bone marrow and once you start getting fresh blood vessels, oxygen comes in and things will change. Before that happens you will get a hyaline cartilage callus. Once you get the blood vessels and oxygen youll get a bone callus. The first formed bone will be woven bone. Itll be remodeled and then become secondary spongy bone and then finally compact bone. These two are just higher powers so you can look at them carefully. [28] [Dr. Wishe] [speaker] I absolutely love this picture. Colorful, which illustrates a bone fracture and heres where all of your bleeding is occurring. Heres the blood clot sealing up the area .What happens is that youll get a periosteal callus and see fibroblast being formed which is part of the periosteum. These blue guys are supposed to be the hyaline cartilage callus thats filling in. The last picture is where youre getting the 6

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spongy bone. Theres one more picture but before I get to it, we mention Ricketts and osteomalatia. They are the same condition. Ricketts in children and the other in adults. Both from short of Vitamin D, which means short in calcium, which means bones, arent particularly strong. Pregnant women usually have this condition since the baby pulls out calcium from the mother. It can be quite severe but after pregnancy, the osteomalatia will disappear. Vitamin A deficiency will cause bone formation issues by suppressing it. Too much Vitamin A, which causes fracture of long bones by increasing fragility. We spoke about Vitamin D deficiency w/ collagen effecting bone formation. Arthritis is a bone disease involving your joints. Things happen to your articulating cartilage and since it doesnt do what it is supposed to, so it does more damage.