Welcome, I'm Dr. Samuel Ling from The Chinese University of Hong Kong. I am an orthopaedics surgeon at the Faculty of Medicine. Today we'll be talking about the introduction to the Neuromusculoskeletal System. Here are just some of my disclosures. I am actually the Assistant Program Director of the MSc in Sports Medicine and Health Science. What we will go through today? We will split this into four distinct sections and will be going into the basics of the bones, muscles, tendons and nerves. So to start off, we'll go to bones. What is the function of bones? The bone, aside from having its skeletal sort of structural functions, it also has its endocrine functions. The bone in your body is actually one of the biggest mineral reserves, especially for calcium. In addition, it also has blood-forming properties, the hematopoietic properties, especially within the bone marrow. Now, of course, aside from those, there are the structural things that we, as orthopaedics surgeons, are more interested in or we deal with a lot. Now, from a structural standpoint, the bone we can split it into two different or distinct regions. There is the outer, thicker cortical bone where I think it's basically if you can consider a pipe, it would be the lining of the pipe that's seen in this photo. And we have the so-called Inner Spongy Bone, that is the cancellous bone where there are multiple trabeculations which actually run through the entire shaft of the long bone. Let's look a little bit more in-depth. At the cortex, the thicker cortical bone, like trees in concentric rings, there are actually lamellae which are placed or are organized in concentric rings, and then these are lamellar form sort of two pillars osteons. This unit is called an osteon, each osteon has its own neurovascular channel called the Haversian Canal. The osteons, they basically run again in along the lines of force, so parallel to the bone axis. The osteons form the basic structure of the cortical bone. Now, aside from having these Haversian Canals that run up and down, we also have these Volkmann Canals running perpendicularly, and this connects the outside of the cortex to the inner of the cortical bone. The thing about cortical bone, and we'll talk a little bit more about this in the next slide, it’s that compared to cancellous bone, it has a relatively slower turnover rate. Now the cancellous bone, as we said is the so-called spongy bone, it's made up of many interconnecting trabeculations. Now, these trabeculae grow aligning with mechanical stress. It is less dense so we can see that in the photo above, these cancellous bones are less dense than the outer stronger cortex bone. But it has a much higher turnover, so around eight times the turnover rate of the cortical bone. You have to remember that bone or any tissue in your body essentially is always in a state of breaking down, rebuilding and remodeling. Okay, and it's the same for bone, the bone is not a static thing, it's a living structure. According to Wolff's Law, bone actually forms according to the different stresses you give it. So if you exercise a bit more, then your bone actually becomes stronger, and that's where the trabeculations actually come in. This is where osteoporosis actually comes in. What osteoporosis actually affects, you have fewer trabeculations, the cancellous bone especially is more affected and therefore the whole structure of your bone is weakened and you're more prone to fractures. Aside from the cortex and the cancellous bone, we actually have a periosteum that surrounds these bones. This is the thick covering tissue that surrounds the outside of the bone. Again, it's split into two different parts. You have the stronger, more fibrous outer part, and that is maybe a little bit more structural. And you have the inner which is more vascular, so it has a better blood supply. It's an osteogenic inner part, it actually is responsible for bone growth, especially in diameter. So you can imagine that for example in children, you're going to have a more prominent periosteum because children obviously would be growing faster. As you age, the osteogenic properties, osteogenic meaning bone-forming properties, of this periosteum actually the capacity or the capability actually decreases. In this diagram, we can see that this has its clinical applications or implications too. It’s that when you have a fracture, remember fractures are not just breaking the bone or the cortex, or the cancellous bone itself. It also will affect the surrounding soft tissues, and the periosteum is a very important thing because as we said, the periosteum gives it its blood supply and this is the thing that gives it a sort of an osteogenic or bone-building properties. If the periosteum is intact during a fracture, even if it's a complete fracture, then usually this fracture will heal quite well; if it's a really displaced fracture, then you'll be assuming that the periosteum is also injured. Therefore, you will have some periosteal stripping and poorer vascular supply and therefore probably poorer healing. If we look even closer at a more cellular level, in the bones, 90% of it is a matrix, and around 10% of this whole thing is really cells. There are three main types of cells that we talked about in the bones. You have the bone cells, the osteocytes, which make up 90% of the cellular components and these osteocytes are the ones that regulate the calcium and the phosphorus and the sort of mineralization thing. And then you get the builder cells, the osteoblasts. Let's go back to the osteocyte. Osteocytes are bone cells that respond to different stimuli. They respond to hormonal, mechanical and electrical stimuli. Now the osteoblasts, come from messenchymal stem cells, lay the surface of the bones. Basically, they are the ones that build it up and they have three different phases. Osteoblasts in the end, may become osteocytes or they become bone lining cells which are relatively inactive or they just undergo apoptosis and die. Osteoblasts, are three different phases. Then we go on to the destroyer cells, the osteoclasts. These are the ones that break down bones. Osteoclasts resorb bone in pits that we called Howship's lacunae. Basically, these are relatively larger cells, they have multiple nuclei. On one end you have osteoclasts, sort of eating away at the bones and on the other hand you have osteoblasts which are building up the bone. Therefore your bone is in a constant state of turnover and remodeling. Then we talk about bone metabolism. Bone, as we said before is the storage of minerals, the serum or the circulating concentration amount of minerals is actually controlled in a really complex mechanism feedback loop within the bone itself. All sorts of things such as PTH, which is parathyroid hormone, calcitonin, sex hormones such as oestrogen and Vitamin D. These are all things that will affect the mineralization and all the metabolism. Calcium, you've got to understand that it's not really just for bones, calcium is basically super essential for life. It's required in, for example, nerve conduction; it's required in muscle contraction. You can imagine one important muscle would be your heart. You're going to need calcium in order to have a normal heartbeat. It plays a role in multiple enzyme activities and even blood clotting. Calcium plays an important role in that. Similarly, phosphate plays a role in many, many of these enzymatic activities within your body. Vitamin D is something that we always hear about when we talk about bone health. What Vitamin D does? It enhances calcium and phosphate absorption within your gastrointestinal tract, within the GI tract. It basically increases osteoclastic activity, as we said before because osteoclasts start eating away into the bone, it actually releases the calcium and phosphate from the bone reservoirs into our serum, into our blood, into wherever we need it. Vitamin D can be absorbed by dietary means, so a lot of different fish oils, etc., or even through some tablets would be a common way that these are absorbed. The other source of Vitamin D would be via skin. When we are exposed to ultraviolet light, there's a process that actually goes on where the Vitamin D is actually absorbed or created by that. One interesting fact would be that it really doesn't ultraviolet, so sometimes we have patients or we have players who tell us, or we tell them to get a bit more sunlight so they get some more Vitamin D. They tell us “Doctor, I have a nice big office and the office has a nice big window, so sunbathing every time”. But that really doesn't produce Vitamin D because as you know, actually windows do block off the UV light. Okay, so getting that sunlight exposure is not really going to help you get Vitamin D, really got to be direct sunlight for you to get it. That's something that many, many patients are not really sure about. Let's get to some of the clinical implications, especially in terms of sports medicine regarding bone health. One thing that people always miss or and back in the days, there's an entity called the Female Athletic Triad. Some people would have this concept that sporting people should have good bone quality, but is that really the case? Sometimes not, and especially, for younger females that are in endurance sports or sports that promote leanness, such as gymnastics and dance. Although they have that really high training quality, these patients, if you see that they have menstrual disturbances, have low energy availability or have quite a low bone density, then always be aware of this disease or problem, called the Female Athletic Triad. Because these patients, depending on the severity, they will be at higher risk of musculoskeletal injuries being in the muscles and tendons or in the bones, so of course you can get fractures. You can get stress fractures and of course in their reproductive ability such as infertility. But regarding bones, we also have to know that there will obviously be a risk of fractures., If it's a single trauma, typically it's quite easily picked up. If we look at the X-ray on the right, this is an X-ray of the right foot of this patient and we can see that the second metatarsal and the third metatarsal actually have… there's a fracture over the mid-shaft of the second and the third metatarsal. And typically this will not really be missed because the players will come to you and there's going to be an acute injury. There's probably going to be some acute swelling, bruising… etc. over that area. Things that sometimes are missed are the so-called stress fracture. If we look at the X-ray on the left, we have the again a right foot X-ray and at the fourth metatarsal at the mid-shaft region, you can see that thickening of the cortex. This is quite a common site of repetitive or repetitive micro-trauma leading to a stress reaction or stress fracture. Stress fractures are common, especially if there is a sudden change in, for example, training loads. Typically, if your patient complains of persistent pain and then you ask them “Was there any change in your training regime before?” And then sometimes they tell you “Yes, maybe I've increased my training load because I am preparing for a competition”, or you know, just entered University from high school and the training loads are quite different. It's that really that inadequate adaptation that puts on these players or these sportsmen at risk of stress fractures. We do have this in mind, especially if they tell you that they have this repetitive pain or this chronic persistent pain over the same site. So anything that is persistent and it really always has the same site, you know, always think about it and try not to miss these stress fractures. Now, aside from stress fractures, of course, we really should be talking about normal fractures, I mean the regular fractures that we see all the time. In terms of treatment for fractures, there are basically two principles. It is for a proper reduction of the fracture and then some sort of fixation for the fracture. All the different treatment modalities would be based on these two goals. You want to achieve some sort of reduction. This reduction can be either open reduction, it could be surgically opening up this wound and placing the fragments together; or it can be a closed reduction, sometimes we see this quite often in patients with risk factors, distal radius fracture where a closed reduction maneuver is performed. If an adequate reduction is achieved, then we don't really need to open this patient up. Aside from reduction, you need to think about what type of fixation. In terms of surgery, it's going to be screws, plates and stuff like that where it is an internal fixation of the whole thing. But you can have external fixators. Some major trauma patients are sometimes you just put in a temporary external fixator or I would actually even classify casts and bracing as some sort of external device that helps give immobilization and provide so-called fixation to the fracture. For all fractures, always think about how this fracture or this patient or player’s needs. How should we reduce the factor and how should we actually fix it? Now in terms of fracture healing, again, there are two main types and it really depends on the type of fixation or the type of treatment that was administered. Now you get your primary type of healing where it's direct cortical healing, some even call it the Haversian healing, where we think about what we were just talking about our couple minutes ago, where you actually get really good bone contact, and it's a really stable construct. We can see that in this X-ray on the left side were over the fibula, there was a fibular fracture and then that fracture was actually fixed. It was an open reduction and internal fixation with plate and screw construct. You can see that the fracture gap has completely healed. You get that absolute stability because you've put in your hardware which is the plated screws. In these cases, you get primary healing where you don't see a callus formation. And what happens is, the osteoclasts form this cutting cone, which tunnels through the fracture sites. Then the osteoblasts actually followed the osteoclasts, they lay down the new bone formation directly there. This is called direct or primary bone healing. Now the second type of bone healing is where you actually see this callus formation. This can be seen on the X-ray on the right. So again, this is a right tibial fracture. It's a mid-shaft tibial fracture. What has happened here is, it has undergone some reductions where assuming this is a closed reduction, and then an intramedullary nail was placed through the middle. It's an internal fixation with this intramedullary nail device. This device does not have absolute stability. What happens is you actually get a hard periosteum, callus forming first, and then a hematoma surrounds this bone. You get a formation of cartilage which is subsequently replaced with bone, and we called this secondary factor healing. Most fractures heal in around 12 weeks, but sometimes complications do occur and for example in the forearm of this patient. There is evidence of non-union, there's no union or no healing of this fracture. When you see this, we always have to think about why. Why is there no union? Sometimes it could be an atrophic non-union, meaning that it could be a biological problem. A problem with the bone healing itself, this could be due to the patient's problem, or maybe, for example, the trauma was really severe and there was a lot of periosteal stripping as we said before, or maybe even there is an open wound that had some infection. It would give that biological problem or biology problem. You have the so-called hypertrophic non-union, this is what we probably see in this case. That is probably an inadequate fixation. Whoever fixed this fracture there probably didn't give it enough stability. Therefore it is a little bit too unstable, something that is too unstable, the bone will not heal. When we get non-unions, we have to think is this an atrophic type of non-union, or is this a hypertrophic type of non-union? Because you can imagine the treatment would be quite different. If it's a stability problem, then all you have to do is to revise the hardware, maybe put in more stable hardware, maybe a longer plate or stronger plate or something like that and that would probably solve that problem. If it's an atrophic thing, then you've got to increase the biology. Are there bone graphs that you need to put in? Or some sort of BMP or other types of stimulating substances that you can put there to augment the biology? Alright, so it's basically an overview, we didn't cover everything in-depth, of course, but that's an overview of the bone.
