字幕列表 影片播放 列印英文字幕 >> This video is on bone and the tissues of the skeleton. The learning objectives that we'll cover are here. We'll cover a little bit about what bone's made of -- cells and matrix. We'll talk about bone growth and remodeling. And quite bit about calcium homeostasis which involves our bones. The functions of bones -- support and protection are probably pretty obvious and moving our muscles around. But also, don't forget that new blood cells are formed in our bone marrow. Also, the bones are going to play an important role in calcium homeostasis in maintaining our extracellular calcium -- serving as a calcium reservoir. In the first learning objective, we'll cover here is to describe the cells, matrix, and organization of bone and associated tissues. So we'll mention a little bit here about cartilage and ligaments. But mainly we'll focus on bone and bone marrow. So if we look at bone -- so we've learned so far as the osteocyte. The extracellular matrix around those cells is mainly collagen protein as well as the minerals calcium and phosphate. And so that's what gives bone its sort of hardened extracellular matrix is the calcium phosphate and mineral. If we look at tendons and ligaments, the cell we're interested in is the fibroblast which makes this dense connective tissue of collagen and elastin. These proteins make up these fibers, collagen and elastic fibers. A cell I don't think we've learned yet is the chondrocyte. Chondrocytes help maintain a special connective tissue called cartilage. Cartilage is mainly collagen and elastin proteins as well. So cartilage is kind of famous for making up things like your ears and nose and being on the ends of bones such as our ribs. So if you look at each of these, the sort of thing they share is that they're made of extracellular matrix of collagen built by certain cells. Okay, I just wanted to mention ligaments. Ligaments attach bone to bone. And they stabilize our skeleton. Tendons attach muscles to bone, and they allow movement of our bones. Okay, ligaments and tendons are basically just dense connective tissue. Cartilage, cartilage is well-known for being at the ends of our bones. So wherever we form a joint so that those bones don't clash against each other, it's protected by cartilage and also our ears and nose and things like that. So to summarize, keep in mind that when we talk about the skeleton, we're talking about the different types of cells that make up the different type of skeletal tissues. And each of them shares collagen as an important protein and then slightly different cells. If we look at this picture of bone here, and it's cut open to show you that inside the core, deep inside bone, are these marrow spaces and it includes red bone marrow and yellow bone marrow. There's usually an outer sort of shell of compact bone and then an inner core of trabecular bone for these marrow spaces. And what's interesting about bone marrow is in adults we have yellow bone marrow in certain places filling our bones with adipocytes -- kind of space filler, packaging so energy. The interesting stuff though is the red marrow found in certain parts of our skeleton which gives rise to all our new blood cells whether they're leucocytes for defense or erythrocytes carry oxygen around the body attached to hemoglobin the protein inside those erythrocytes. And also, the bone marrow also makes those little platelets which help in blood clotting. So red bone marrow gives rise using these hematopoietic stem cells to all the cells of our blood. If we look at real bone, what we see is this outer shell of compact dense bone covered by a fleshy periosteum which is sort of like a connective tissue cover of our bones. And then deep to the compact bone is this trabecular bone. Trabecular bone has these spaces or sort of grooves and little nooks and crannies where we have our bone marrow. And there's lots and lots of living cells in our bone, and so we need a rich blood supply that feeds our bone and helps keep it nourished. We also have a nervous supply as well so that's why if you've ever broken a bone you know it hurts so badly. So sometimes your blood supply can be interrupted to your bone. And in that case, we get a condition called osteonecrosis or avascular osteonecrosis which can cause death to your bone. Again, we have this fleshy outer cover of bone called the periosteum. It's mainly dense connective tissue of collagen built by fibroblast. But there's a couple of layers of fibroblast and osteogenic stem cells in there which will become important when we talk about fracture repair in that periosteum. Then there's compact bone just deep to that. The compact bone has mostly bone matrix with some osteocytes in there that maintain the bone matrix. And so again, that bone matrix is collagen protein with some calcium phosphate mineral. Then deeper to that is the trabecular bone. The trabecular bone you can see has little spaces that are filled with bone marrow, either red bone marrow or yellow bone marrow filling the trabecular bone. Trabecular bone is hardened. Some textbooks call it spongy bone, which I don't really like because that makes me think of it as soft. But it's really all hard. I think the reason they like spongy was because there were spaces in it. So we'll call it compact bone and trabecular bone. If we zoom in on compact bone, what we see is very little space, open space. It's instead these compact columns of bone matrix called an osteon. And you can see several osteons in this little picture here. The osteons have these little rings of osteocytes which help to build the osteon. And then they help maintain it. Each osteon has a little central canal, a little tunnel, that allows things -- soft things like blood vessels and nerves to run through the hardened bone. So again, the bone matrix is collagen and mineral. And so we see several osteons making up this compact bone section. If you look at trabecular bone, you don't see any osteons. Instead, you see marrow spaces. And then in the hardened bone matrix it's a little more irregularly shaped. It's still pretty much the same stuff, osteocytes embedded in a bone matrix of collagen and mineral. And then the other thing you'll notice is that you see these lining cells that cling to the edge of the bone in the marrow spaces. This is called endosteum. So endosteum is the cellular lining in the interior spaces of bone. It includes cells like the osteoclast, the osteoblast and osteogenic cells, which we'll learn more about. Again, if you look at the marrow spaces of trabecular bone, you see all these little cells clinging to the edge of the bone. And so we call those cells endosteum as a group. Okay, the fleshy outer cover of bone we call periosteum. And that's connective tissue, dense connective tissue somewhat similar to maybe the dermis of the skin. And it has cells in there as well. If we zoom in again to that same picture, you can pause it and check this out, but we can see the osteon. Compare that to trabecular bone where we see sort of this irregularly shaped bridges of hardened bone. What I wanted you to notice were the cells in there. You can see the osteoblast clinging to the edges of the bone. But the bones embedded in the matrix of the osteocytes. You even see some osteogenic stem cells clinging in there near the osteoblast and some really large osteoclast that eat away the bone. Stem cells called the osteogenic stem cells, create new osteoblasts in our bone. Those osteoblast build bone around themselves. And once they're surrounded, then they mature to become an osteocyte. Osteocytes maintain bone. And they sense any stress that's in the bone matrix. So they're going to be important for maintaining our healthy bones by sensing the stress. And they're sort of all big one family because each one gives rise to the other. Bone marrow stem cells, hematopoietic stem cells, give rise to these precursor cells that then fuse together to create this big giant large cell called an osteoclast. These large osteoclasts are multinucleated cells because they're created by the fusion of several precursor cells. The job of the osteoclast is to chew up bone. We call that bone reabsorption or bone break down. They're not related to the osteoblast and the osteocytes. They're derived from blood cells. They are related to these immune cells that eat up bacteria called macrophages. So I like to remember that they both like to eat stuff. The osteoclast eat the bone. And the macrophages eat bacteria and bad things in the body so maybe they're cousins. If we look at a skeleton, if we look at a child's skeleton, most of the bone is filled with red marrow because they're growing lots and need lots and lots of new blood cells. In the adult, we don't need as much red marrow so it's concentrated usually in our pelvis and in our skull. And some of the epiphysis, the proximal epiphysis of our long bones will have red bone marrow. So like at the near end of your femur or your humerus will have some of that red marrow. That red marrow is famous for bone marrow transplants. So you can take some of that bone marrow out and transplant it to another person. Why would you want to do that? Well, if you remember what's in the red bone marrow, it's those hematopoietic stem cells. Hematopoietic stem cells from the donor can then help a patient who receives them grow new erythrocytes and leucocytes. Obviously erythrocytes carry oxygen, and leucocytes will defend you. Okay, so that's the good reason for bone marrow transplants. What is bone made of? Again, the extracellular matrix we said hopefully is collagen and mineral. And so let's make sure we're clear on that. So the extracellular matrix is the material found outside the cells that the cells have built or that they maintain. Collagen is just a big, giant rope of protein, and specifically type one collagen is found in our bones. The calcium phosphate mineral is called hydroxyapatite. Hydroxyapatite is the mineralized form of calcium phosphate that makes our bones very, very hard. So I like to think of hydroxyapatite like rocks. So if we look at bone, it's about 30% protein, including collagen, and about 70% mineral which includes that hydroxyapatite calcium phosphate. A couple of the genes for collagen are collagen 1a1 and 1a2. And so if you have any problems in your collagen genes, then that can affect your bones. So again, the collagen makes your bones flexible and very strong. The calcium phosphate mineral hydroxyapatite makes your bones hard and resist compression. If you don't have collagen, your bones are brittle, and they break really easily. If you don't have calcium phosphate, the mineral, then you'll have bendy bones. Examples of diseases we'll talk about later. Osteogenesis imperfecta and rickets can affect your bones. Next, we're going to describe the mechanisms of bone growth both before you're born, when you're a child or teen. And then also when you're an adult. A vocabulary word we need to take note of is ossification. Ossification basically is bone formation. And it usually involves transformation of one tissue type into bone. And so we'll talk a little bit about different ways we can get ossification. If you look at a little embryo and early fetus, you can see that your bones will form very early. So I want to talk a little bit about how your bones form and development. One way is to use this collagen connective tissue made by mesenchymal stem cells or connective tissue stem cells. And they come in these sheets. And these sheets of connective tissue are then turned into bone by osteoblast. And remember turning something into bone we call that ossification. So this form of ossification because it involved sheets of connective tissue is called intramembranous ossification. So intramembranous ossification is how our skeleton forms when we have flat bones like your skull. And I believe, I'm not sure, part of the pelvis. So for sure the skull. How do we form the other bones in our skeleton? Well, in these cases, we start off with sort of a cartilage framework. Remember cartilage is just collagen and connective tissue too. In this case, we had chondroblast which might build some of that cartilage. And then we have osteoblast that are going to turn that collagen cartilage into bone. And again, if we turn another tissue into bone we just call that ossification. In this case, to remind us that it's coming from cartilage, we call it endochondral ossification. So endochondral ossification and intramembranous ossification is how we get our early skeleton. So again, if we look at a fetus, we'll see that some of the bones formed by intramembranous ossification, while others like the long bones will form from endochondral ossification. So much of our skeleton forms from this cartilage model which is then turned into bone. And then other bones like in our skull start from this sheet of connective tissue. And I believe some of the pelvis too. All right, so that's how we get our skeleton. We start with one tissue. And then it's ossified, ossification, into actual bone. Most of this involves collagen connective tissue being turned into bone. So we'll summarize a little bit here and make sure those steps are clear for you. So in endochondral ossification, we're starting with our product is cartilage which is mainly collagen. And then osteoblast turn that, which we call ossification, into bone. And we'll start with trabecular bone. And we could always remodel that into compact bone or back and forth, all right? So intrachondral ossification is one way if we start with cartilage that we can make bone. The other way we can make bone is if we start with connective tissue and stem cells. And if we take some connective tissue stem cells that make collagen and connective tissue and then sheets of that connective tissue are ossified into bone through osteoblast, we call that intramembranous ossification. Again, we can create trabecular bone or layers outside of our compact bone. All right, so two different ways that we make bone from other tissues. What about when you're a child or a teenager? How do you grow taller and how does your skeleton grow bigger? Well, it's similar methods that we just said. In the case of your long bones, it's endochondral ossification. You have have these little islands of cartilage that cause your bones to grow taller and taller or longer and longer. And this involves bones famous in the arms and legs and things like that. As far as the pelvis or skull, that's going to involve continuing that intramembranous ossification where those bones really become longer -- or excuse me -- larger rather than longer. So if we look at how do long bones grow, there's something called the epiphyseal growth plates which simply means these growth plates at the end of our bones. And so if we look at long bones in our fingers and hands and arms and legs, we see this little island of cartilage which continues to grow. And then osteoblast turn part of that island of cartilage into new bone. And your bones continue to grow and go. And hormones will regulate a lot of that. In the adult, your growth plates are no longer active. And so you don't keep growing taller. So if you look at an x-ray of a child or a teen, you'll actually see this epiphyseal growth plate. It looks almost like a fracture, but it's really just a cartilage not showing up on the x-ray because of these growth plates the cartilage looks similar and dark. It doesn't look actually like bone. And when you're actually an adolescent or child, you can actually sometimes get fractures if too much force is placed on these growth plates. And that's called an epiphyseal fracture. So some of the hormones that signal to your bones to grow taller or longer or bigger are growth hormone testosterone and estrogen. In all of these, you'd expect to go up during your various growth spurts. Until you get to an adult, then those little growth plates are turned into bone. And you're no longer growing taller. But your bones are still remodeling. The bones repair if they break. They can weaken if you don't exercise or you just get older. And so it's important to remember that bones are dynamic and always remodeling throughout our life. The next thing we're going to do is talk a little bit about bone repair looking at remodeling after a fracture and also when you exercise. So obviously, you know bones can repair after you break a bone. And they can actually change when you stress them. They can get stronger or weaker depending on what you're doing. So bones are in a continual state of change. So let's look at the steps in fracture repair or actually just as a summary. In an adults, we can either increase the diameter of our bones. That seems to be intramembranous ossification that happens right underneath that little periosteum where our bones slowly grow in diameter, and they can grow stronger. Again, it involves stem cells and connective tissue and so we call that intramembranous ossification. If you ever fracture a bone, that seems to be collagen -- cartilage excuse me -- cartilage collagen and connective tissue being turned into bone which seems a lot like endochondral ossification. And so we'll go through the specific steps of that next of fracture repair. So again, fractures heal on their own, hopefully, most of the time. This was a really bad break. That probably needs some help to fix that fracture. But what are the steps needed for the body to repair that bone. And again, we said it's very similar to endochondral ossification. So the first thing that happens is you break your bone which rips through the periosteum and crushes and destroys some of that compact and trabecular bone. And there's lots and lots of bleeding because we have the bone marrow spaces, and all the blood vessels get torn through our bone and so we have lots of bleeding. Maybe even some internal bleeding and swelling. One of the first things to happen is a blood clot forms. And the clot formation is important because part of that blood clot will involve the protein called fibrin. So we create this little fibrin protein meshwork which is going to help create a scaffold for healing. We're also going to have a lot of hematopoietic stem cells -- blood stem cells from both the blood and also the bone marrow and also osteogenic stem cells as well. And so that fibrin clot will be important to help those little stem cells grab on and start getting activated. The next step is going to be when those little stem cells help create a callus formation which is mainly cartilage. So it's probably going to involve chondroblast and fibroblast which start making a lot of, a lot of collagen. And some of this collagen is going to be in the form of cartilage. And so you make this big, giant knot of cartilage. We call that a callus. That collagen now is going to be our scaffold for bone formation. And so you remember when we turn one tissue into bone it's called ossification. Since we're turning mostly cartilage, connective tissue, into bone we call it endochondral ossification. So slowly over time now our osteoblast turn that cartilage into bone. And so now we have a bony callus. Eventually, we'll start remodeling that bony callus with things like osteoblast and osteoclast. And hopefully get that periosteum back covering the bone. And get the bone remodeled more like the bone that we had before the break. So now again, through ossification we have this bone remodeling that now the bone is repaired. And so again, I'm just drawing in some compact bone. That compact bone will be remodeled eventually to trabecular bone creating any marrow spaces that are needed that'll involve coordination of osteoblast and osteoclast. And you might be saying, hey, it looks good as new except it's a little crooked. Well, that's why often we need things like plates and screws and things like that to help it remodel perfectly. The other thing I wanted to remind you is that there's quite a rich blood supply to our bones that comes kind of through the periosteum through the compact bone. There's little tunnels, and there's also lots of nerves. So that's why there's so much bleeding and pain when you break a bone. There can even be bone death if the blood vessels are interrupted that supply your bones. And, of course, sometimes we need help in repairing our bones like hardware and casts. Bones remodel in response to forces like gravity and muscles pulling on them. So examples are sports which stress our bones or being lazy which causes your bones to not be stressed. And our bones are actually modeled to meet those demands. If you've had braces, your teeth had to move around. Inside, your bones were modeled around those little teeth so that they could move. So a classic study is to study unilateral athletes. So unilateral athletes use one arm versus the other. And so we can actually see does that arm -- does the bone in that exercised arm when it's stressed, does it actually change and does the bone adjust. So remember the dominant arm is the one stressed by throwing or pitching or tennis. And then the nondominant arm is not stressed as much. And the results of these studies seem to show mostly that the dominant arm will have a greater diameter, bone diameter. And a greater bone density, meaning it's more dense and more strong. So the bone is actually bigger than the nondominant arm in these pictures. And then, of course, in sedentary or normal students, there's no difference in the dominant versus nondominant arm. How does this take place? Well, stress on the bone is sensed by osteocytes which live in the bone matrix. The osteocytes then turn on osteoblast and turn off osteoclast so that the bones seems to grow thicker in diameter and higher in density. And that then makes the strength of the bone increased. So the osteocyte seems to be the main sensor of stress activating the other cells to either build bone or remove bone. In the case of exercise in the dominant arm, it'll actually slow down the osteoclast and turn on the osteoblast so your bones become bigger and stronger. We can actually see that. So again, the dominant arm increases in density, increases in strength to meet the demands of the stress. An interesting thing is if you look at the nondominant leg and the dominant leg, so comparing the leg, people push off their opposite leg which is called the nondominant leg. And in baseball pictures that's actually stronger with a higher bone density and bone diameter. So the remodeling is very specific. Probably more appropriate for all of us is whether you're exercising or not. So for example, if you're injured and in a hospital, your bone density will decrease because your bones aren't being stressed and same if you don't exercise. Your bone aren't stressed so the bones will actually sort of have less density, and they'll slowly break down. The reason is the osteocytes don't feel any stress. They signal to the osteoblast to turn off. And they turn on the osteoclast. So when you turn on the osteoclast, they start chewing up the bone. And the osteoblast stop building the bone. And so you start releasing the bone matrix of collagen and calcium and phosphate into the extracellular fluids. So basically, your bones start breaking down if they're not stressed. Explain the mechanism of calcium homeostasis. So hopefully you remember that homeostasis is stability in the body. In the case of calcium, we're talking about keeping calcium levels stable in the body's fluid or very bad things can happen like your brain and your heart and your skeletal muscles and other organs can stop working. So we want to keep our extracellular calcium stable. And you've probably seen ads before talking about how good milk is for you and for your bones. And so, of course, calcium's good for our bones. But we're going to talk more about calcium being good for the rest of our body. So calcium is for your cells. I want you to remember that. So since our cells live in extracellular fluid, that extracellular fluid has things like sodium and chloride and potassium, but also now calcium. Calcium floats around in that extracellular fluid. And calcium's going to be critical, important for all of our cells in our body, especially cells like our heart cells, our cardiac muscle cells, our skeletal muscle cells, and smooth muscle cells. So all the cells of the body actually need calcium in order to function. The most famous ones will be ones like our heart and muscles -- smooth muscle in your stomach and your intestines, neurons in your brain and in your spinal cord -- all of those. Every time they're active, they need calcium to rush in in a little burst. And so calcium's going to be important for all these cells to function. If you don't have the right levels of calcium, too high or too low, you can start messing with the function of your brain and messing with the function of your heart, which is never good. All right, so when we talk about homeostasis, we're talking about the extracellular fluid. And extracellular fluid calcium level's about the same as the plasma fluid calcium levels. So when doctors talk about plasma calcium, they're really just talking about the calcium levels in your extracellular fluid. Or if we just say blood calcium, again we're talking about extracellular fluid. Calcium levels inside your cells is usually pretty low. Of course, it's important, but what we can measure easily is the extracellular or plasma calcium levels. So what about calcium in our bones? Well, of course, calcium's important for our bones -- for our bones to be strong with the mineral being partially calcium and then the other part phosphate. So if you have enough calcium in your body, of course, you can store it in your bones which will give you strong healthy bones. But that calcium's also important to keep your cells alive. So if you ever don't have enough calcium floating around and your cells need more, you'll take that calcium from your bones to give it to the cells. So now I like to think of calcium's more important not for your bones but for your body's cells. So again, head and the heart, the brain, the heart require that calcium and will literally take it and steal it from your bones in order to give these cells enough calcium to keep you alive. In order to understand how the body regulates calcium levels in the fluid, we need to think about the endocrine system a little bit and hormones. Hopefully, you remember that hormones are chemical signals carried around the body in the bloodstream. So if you make a hormone, it'll circulate around your entire body in your blood vessels. And so the endocrine system's all about hormones and signaling to the body. We're going to just look at two hormones that are critical for extracellular calcium regulation. The first hormone is called parathyroid hormone, or PTH for short. It's made by these little teeny, tiny glands in your neck, right by your thyroid gland. The other hormone is called calcitriol or sometimes we'll just call it active vitamin D 3. Vitamin D 3 is made in places throughout your body, but mainly activated in your kidneys. So your kidneys are going to be important for making calcitriol. So these two hormones are going to be important in regulating our body calcium. Let's start with parathyroid hormone made by our parathyroid glands. You actually have cells in those parathyroid glands which literally are calcium sensors. Whenever calcium's too low, those little cells get concerned -- well, they don't really care -- but they notice it. And when calcium's low in your body or your plasma or your blood, those little parathyroid gland cells will release and secrete PTH, parathyroid hormone into your bloodstream. It'll circle all around your body and target specific organs. So again, parathyroid hormone is a hormone released to target body cells in order to regulate your calcium levels. Well, if the problem is reduced calcium and those little cells make PTH, we're going to signal to our bones in order to slow down our osteoblast and turn on our osteoclast so that would chew up the bone and release that stored calcium. So PTH signals to those little cells to release calcium into the fluid of the body. And that's going to help correct our problem with low calcium. It's going to tell the kidneys and the little cells in the kidney tubules, which you remember those little tubules cells. It's going to tell those little tubules cells to keep calcium in our body. Don't let the calcium go out in your pee, in your urine. And so again, that's PTH is signaling to your kidneys to help keep calcium in your body which is helping our problem which is low blood calcium. So we're going to reabsorb that calcium in our kidneys. The other thing that PTH does, it tells those little kidney cells to make the other hormone we talked about called calcitriol. So calcitriol gets activated in the kidneys there. And then the target for calcitriol is mainly the intestines. It also targets the bones, but in the intestines it tells those little intestinal cells to pick up the calcium from your food. So again, all of these responses in response to PTH by our cells is to help increase our calcium levels back up to normal. And so in that way PTH and calcitriol are regulating our calcium homeostasis because in this case we have hypocalcemia. We release lots of PTH, made come extra calcitriol. Those signaled to our body's cells to bring our calcium levels back up towards normal. Again, that's an example of negative feedback regulation and homeostasis trying to keep calcium stable in our body. Okay, so if you have low blood calcium, you're going to make lots of PHT and more calcitriol. So summary, parathyroid glands sense low calcium. We increase the amount of PTH circulating in our body. Tells your kidneys to keep the calcium. Tells your intestines absorb calcium. And tells your bones to release stored up calcium, okay? And so when you look at your urine, if you have lots of PTH, you'll have very little calcium in your urine. Funny, you actually have lots of phosphate. That's one of the signals of PTH is to get rid of that phosphate from your bones. So you want to keep the calcium and get rid of the phosphate. If you have too much calcium in your body, so if you have too much from your diet or maybe your bones are breaking apart for whatever reason, in that case your PTH will go down because your little parathyroid cells will be like, well, we have too much calcium. So we'll have low PTH secretion. The kidneys in that case will let the calcium go out in your pee. And you'll pee out lots of calcium. Your intestines will absorb less calcium, and it'll just stay in your food and go out in your poop. And, of course, the bones won't be chewing up and releasing as much stored calcium. Again, that will help reduce our calcium back down to normal. All of it involved just changes in PTH. All right, so that's how our body regulates calcium mainly with PTH. I just wanted to mention a little bit about where does calcitriol come from. Again, calcitriol has a couple of names active vitamin D 3. If you go to medical school 125 cholecalciferol. Where does vitamin D and calcitriol come from? Well, active vitamin D needs to be made in your body. But vitamin D can come from your milk and your pop-tarts and your food. And also vitamin D is made when sunlight hits your skin and converts cholesterol into vitamin D. Vitamin D though needs to be activated and chemically transformed into calcitriol, active vitamin D 3. And that occurs mostly in the kidney. So the kidney's job is to convert vitamin D to vitamin D 3. Again, we know calcitriol then goes and helps bring up our calcium levels by targeting our intestines. But it also targets your bones to make your bones healthy. So remember calcitriol and vitamin D are needed for healthy bones. We can see this because if you ever have low calcitriol, you'll have weak bones. And the bones won't be properly mineralized. An example of this is called rickets or osteomalacia in adults. And I think vitamin D is talked about a lot for health of other origins as well. Sometimes when your kidneys are sick, for reasons that aren't related to your bones, but your kidneys are sick, they won't make the right levels of calcitriol because remember they form the active form of vitamin D 3 calcitriol which then can affect your bones. So if you don't have enough calcitriol, you won't probably have enough calcium in your body. And you won't have correctly mineralized bones. Is calcium good for bones? You hear that a lot. And of course, we need to have some calcium coming in in our diet because we're peeing a little bit of calcium out in our kidneys and in our pee. So you have to have enough calcium coming in in your diet each day either from milk or dairy or certain green leaf vegetables and other sources in order to keep your bones healthy. An interesting example of calcium homeostasis is if you look at astronauts in zero gravity. In zero gravity, you remember that your bones don't have the correct stresses on them because you don't have gravity. In that case, the osteocytes tell your bones to break down by signaling to the osteoblast and the osteoclast. The osteoclast start chewing up your bone, releasing that calcium into your body's fluid and into the bloodstream. And suddenly now when you're in space, you have these really high calcium levels in your plasma and in your extracellular fluid. This then affects the little parathyroid cells to stop secreting PTH or lowering their PTH secretion. When you have low PTH, if you think about the body's response, the kidneys are then going to figure, well, I should just pee out the calcium because you don't need to keep it in your body because you've got too much calcium. So you start peeing out lots of your calcium that's basically coming from your bones. And if you're an astronaut, hopefully, you're peeing in a little bag. The other thing is calcitriol will go down, and so you won't be absorbing as much calcium from your diet as well. And those things will bring your calcium levels back down. And possibly even the low PTH would hopefully slow down that bone break down. But the whole case you had here was to regulate your body calcium back to normal. You'll still have weak bones though because your bones were being broken down by the lack of stress. There's lots of interesting bone health and bone disease issues. Hopefully, we'll cover some in class. But that's it. This is the end of the video so I'll see you guys in class. Bye.
B2 中高級 英國腔 BIO160 預覽視頻 第8講--骨骼與鈣質 (BIO160 Preview Video Lecture 8 - Bones and Calcium) 188 16 李佳憶 發佈於 2021 年 01 月 14 日 更多分享 分享 收藏 回報 影片單字