All right, our next speaker is David Flanagan from Ohio State University. He's going to cover articular cartilage, osteoarthritis, OCDs, and synovial lesions. All right, David. Well, thank you everybody. I'm probably one of two people who've taken this test last year. Dr. Bishop tomorrow will be speaking as well. So I've redesigned this talk to be extremely high yield for you as far as what I saw on the test. I will make a lot of references to that as well. A couple of things I would say just from resources that were really, really good. I felt extremely overprepared. This course is phenomenal. Dr. Miller's talk on the statistics is really high yield. I would tell you to really review that right at the end. OKU5 Sports was very useful, kind of filled in a few gaps as well. And I would say there's probably six questions from OKU12, the Chapter 8 on polytrauma. They disguise it in a sports scenario, but it's really a trauma question. So anyways, a couple of things for you guys to review. Okay. All right. These are my disclosures. All right. So our objectives today are really to review the testable material on the following topics as Dr. Kading had already discussed. I really am not going to go through any controversial topics because they're not high yield. We're going to avoid a lot of these novel treatments and technical pearls and really kind of get into what's going to be on the test for you. So in each of these sections, I will kind of talk about some of the key points. It will be kind of my opening slide. So again, when you're reviewing, I would really kind of just, again, glance over these sections because they are going to be a little bit high yield for you. So for this section, zones of the cartilage, components of the cartilage, cartilage algorithm, which I think can be the most difficult thing when we're talking about cartilage. So we're going to spend a little bit of time just for your thought process of how to work through the questions. And then what is really key is these indications, contraindications, and complications for each of the procedures. So all of those are fair game for the test. So the zones of the cartilage, this is kind of going back towards residency for us and looking at the four main zones. So the superficial zone, it forms a gliding surface. It resists the tensile stress. It has very thin collagen fibrils, and these are parallel to the surface. The chondrocytes are also elongated and parallel to the surface. And then we'll see this again when we're talking about arthritis. Lubricant coats the articular surface. And so that has some properties, and you may see lubricant come up and where is it located and how it works. The proteoglycan content is the lowest, and the water content is the highest. Let's go to the middle zone. This is the transitional zone. This is where you have the largest diameter collagen fibers. It's more of a haphazard organization, and the chondrocytes are rounded in appearance. The deep zone, the proteoglycan content is the highest. The water content is the lowest. It has a larger diameter of collagen fibers, and these are oriented perpendicular to surface as with the cells, which are in columns. Where they may have a stem of a question that really is associated with this is if you look at the technique like ACI where you have to take a biopsy, you have to get to the deep layer of cartilage because this is where most of your chondrocytes are. So again, if you're looking at an application question of how it might be on the test, that's where you would see it. And then the last zone here is the zone of calcified cartilage. This is separated from the deep zone by the tide mark. Separates the hyaline cartilage from the subchondro bone. You have small rounded chondrocytes. The oxygen saturation is the lowest in this area. Tide mark, just so you know what it is, it's just this wavy blue line on H and E, and it's just that zone between the deep layer and the calcified cartilage. So we'll go through each of the components of cartilage. So chondrocytes, obviously these are the workhorse to synthesize and maintain the matrix. They rarely divide after skeletal maturity. The mitotic activity ceases with development of well-defined calcific zone or that tide mark. Chondrocyte undergoes or uses anaerobic metabolism and the rate slows with increasing age. Probably the most important part with chondrocytes is that they really have limited healing potential and there's no pluripotent cells within the mature cartilage. So let's go through the extracellular matrix components. Well obviously water, when we're looking at the weight, is the most highest component with 65-85% of the wet weight. It's hydrophilic nature to the proteoglycans. The permeability is quite low and the frictional resistance of flow and pressurization of the water enables the articular cartilage to support its high loads. Collagen, the big thing here is obviously type 2 collagen. If you look at the dry weight of cartilage, this is the most predominant component. Proteoglycans is the second, and that's anywhere from 10-20% of the cartilage. It has a high affinity for water and provides compressive strength for the cartilage. Collagen review, I'll just really want you to focus on type 2, type 9 and maybe type 10. I think the other ones really do not, are not seen much on the actual exam questions. Type 2 will come up in multiple different ways. Number one, realizing that that's the most, the collagen that is the most frequent within highland cartilage, and then type 9 and type 10 you may see occasionally in some questions. Proteoglycans, these are composed of glycosaminoglycans bound to a central protein core. It has an anionic charge. It's hydrophilic and is joined to hyaluronic acid by a link protein. Glycosaminoglycans are these long chain, unbranched, repeated disaccharide units. The key ones to know for any test question are chondroitin sulfate, keratin sulfate and the hyaluronate. Chondroitin sulfate is the most prevalent glycosaminoglycan in cartilage, but keratin sulfate will increase with age. Again, if you see this in bold, it's there for a reason because these are some things that you may see in questions. The hyaluronate, to realize that this is not a proteoglycan. It's truly a glycosaminoglycan because it's not bound to a protein core. Cartilage nutrition. It's avascular in adult life, so diffusion from the bone is really nonexistent and especially due to that calcified zone. So it gets all of its nutrition from diffusion from the synovial fluid, both the nutrients and the oxygen. Just as you saw from that lowest oxygen content or in the deep, the calcified cartilage layer, the oxygen concentration will go down as you get further into the deeper layers of the cartilage. It's also important, and this sometimes will come up in questions, that immobilization may contribute to chondrocyte hypoxia because you're not getting the normal motion of the synovial fluid, which can cause some lack of nutrition, and then the metabolism goes down and you can get some thinning of the articular cartilage. So we're going to kind of now go into chondral defects, and chondral defects are quite common. It's difficult to really know the true incidence or prevalence of articular cartilage lesions, but we know from good data from our arthroscopic patients that around 60% of them will have some sort of cartilage injury. We can see it in up to 36% of our athletes. The biggest thing that you'll see with articular cartilage lesions is that it's often associated with other injuries, and so similar to what Jonathan was talking about, the big thing where you're looking at concomitant diseases, if there is instability, if there is meniscus disease, if there's malalignment, all these type of things need to be considered when you're treating the articular cartilage. So patella dislocations, anywhere from 25% to 90% of the patients, ACL injuries, meniscal injuries, and again, natural history is poorly understood, so they won't really ask you a question on that. So when we look at articular cartilage lesions in their presentation, they're going to go through two different types of question stems. One is going to be an acute lesion, and the other one is going to be more of the chronic lesion. So from an acute standpoint, it will be a traumatic injury to the knee. You'll have a significant effusion. You may or may not have some mechanical symptoms or locking, and so if you think of locking, you always think of loose bodies, and so that's going to kind of put you down a decision tree because of an acute lesion and locking within the knee. From the other stem might be from this silent or this chronic type of presentation, and this is typically with recurrent effusions and pain with increasing activities. They may start getting some quad weakness, and so that's going to put you in that type of question tree. No history or exam finding is really sensitive or specific when we're talking about cartilage. So again, most will have effusions and may have some crepitus and often with focal pain. We're looking at imaging. Radiographs are usually negative unless there's bony involvement. MRI is the gold standard for imaging to determine if the cartilage defect is present, but beware it is not always accurate in determining the size of the defect. So they will be really clear if they want you to make a treatment decision on the MRI that it's large or it's small. At the time of arthroscopy, they'll tell you about a post-debridement size, and again, it will be either large or small, but MRI can underestimate the cartilage defect size by 70%, and that has been seen in some questions. You want to base your treatment off of arthroscopic sizing post-debridement, and if you're unable to get an MRI, sometimes a CT arthrogram can be useful. So when we're looking at treatment, again, if we think of these two different stems, if you have an acute traumatic injury, most acute chondral injuries with loose bodies will be treated acutely. So they're going to already kind of push you down that route to treat it. So very similar to what was talked about with patellofemoral instability, if you have a loose body, they're going to want you to treat that loose body. From a chronic standpoint, remember that cartilage really has no nerve fibers. So you have to rule out that that is the source of pain, and make sure that cartilage is the reason for the discomfort, and again, they will often want to make sure that you failed conservative measures, typically about six months of various measures that you can see listed here. When we look at operative management, you can look at all these different types of techniques. They can be non-restorative techniques, which can be just a debridement chondroplasty, which has limited role when we're looking at cartilage treatment. Different stem cell techniques, such as microfracture abrasion chondroplasty, chondrocyte cell-based techniques such as ACI and now MACI, and then structural techniques that can be OATS or osochondroallograft. So what are true-wrong answers at this point? Okay, so this is really key. They will potentially be in some of the answers. If you see it, you can pretty much cross it off. So de novo or juvenile mince cartilage, sometimes they will not put the trade name, will be a wrong answer. We really have limited data on that. Neocart or Novacart, if you see those, those are again some newer generation ACI, but they're in studies and trials. Myocartilage, if you guys have been using that, we have no good clinical evidence, and so the Academy is not going to question you on something that we don't have good clinical evidence. And cartiform very similarly. So we just don't have enough at this point for any of these to be the right answer on any question that you have, and especially if insurance companies deem that these be investigational or they have limited clinical evidence, then it's going to be the wrong answer. So just go ahead and eliminate those. So debridement. When can you use that? Well, it's commonly been used as a first-line procedure, especially if we look at ACI to remove loose bodies or unstable cartilage. But when we're looking at some of these cartilage stem questions, the indications are going to be a little bit limited. Okay? So they're going to be from a poor candidate for any other cartilage procedures. So they're older, they have a high BMI, they may have some advanced degenerative changes, they're unwilling to comply with rehab for the other procedures, or they might be an in-season athlete. And realistically, that may be the type of question that they ask you. So very similar to that chondral flap, you have an in-season athlete who's having continued pain and mechanical symptoms that's limiting their ability, and you may need to just go in there and do a chondroplasty and allow them to get back towards their sport. There's very limited short-term data that supports some symptom improvement in about a third of patients, but there's no long-term data for its efficacy. So when we go through the different classification systems, I know that most of you are aware of them. And so we have the OuterBridge, and then we have the ICRS grading system. The big thing here is they will typically name which one they're going to be using. When we're looking at articular cartilage treatment, we don't typically go down the pathway of treating a lesion unless it's a grade 3 or more. So if you see a grade 2 lesion, we call those non-treatable lesions, or they're not necessarily needed to be treated at that time. And a grade 2 lesion is not considered a kissing lesion when you're looking at contraindications. So a contraindication for a kissing lesion will be, again, a grade 3 or grade 4 on the opposing surface. So similarly, the ICRS, it's pretty much going to be the same. So the cutoff will be at that anything grade 3 or above will be something that you're considering treatment. So what are our tools of the trade? Well, if we look at what is predominantly within the literature, it's going to be these four things, and these are going to be the ones that they question you about. So it's going to be microfracture, OATs or osochondroautograph, osochondroallografts, and then ACI, which now has been replaced with MACI in the U.S. So either one of those can be fair questions. This is blown up for you at the end of my section. I have a couple of these algorithms that we've made bigger so that you can, when you're reviewing it, or even right now, can pull it out. I like to spend a minute or two just going through this algorithm because this is really key as far as how they're going to ask questions. There's lots of different algorithms out there, but they all have the same key concepts, okay? So when you're looking at treating articular cartilage lesions, first and foremost, you want to look at where is it. So is it in the femoral condyle, or are we talking the patellofemoral joint? So location is really kind of number one. The reason why location is important is in the patellofemoral joint, similar to what Jonathan was talking about earlier, if you have anything on the lateral trochlea or lateral patella, you are often thinking about an osteotomy. They're going to want you to go down that tree to think about a Fulkerson to offload that cartilage in that area. You can't offload the medial side, right? So that's where they're going to really use that location to be important. The next thing, again, is looking at that concomitant pathology. So again, what we just talked about with the patellofemoral joint, but on the femoral condyle, if you're talking about a medial femoral condylar lesion, they may ask about the meniscus status. Is that normal or abnormal? If they are post-meniscectomy, then you may need to, a total meniscectomy, you may need to think about a meniscus transplant. If they have a varus knee with a medial femoral condyle, again, you're going to want to think about an osteotomy. Then it's really lesion size. And I'll tell you, for most of these STEM questions, they're going to look at two square centimeters as your cutoff. Again, we don't like to have confusion, so most of the questions are going to be at that two square centimeter. Below that, they are considered small. And above that, you can consider large, okay? Once we get down to that small or large, then you're really looking at, again, demand of the patient. So if you have a very low demand patient, then you're really thinking of something that's not going to be as, I would say, significant to the patient. So a microfracture is typically a good option for them. The high demand are going to be really the ones where they're going to question you as to what may be the best option. And then you're really going to have the choice. And I'm going to try to make that choice pretty easy and pretty clear to you as we go through some of these questions and the rest of this talk. So again, some of the key thought processes for treatment. Fix any acute osseochondral fragment. That comes up again and again and again. So I can guarantee you, you will have a question about fixing an acute osseochondral fragment on your test. If the bone is involved and you can't fix it, so you have a bony structural lesion within the femoral condyle, think of a structural graft. So if it's small, under two square centimeters, you can consider an OATS procedure. If it's large, you're going to go to an osseochondral allograft, especially if the bone is involved. And again, the small and large ones, small again can be in the microfracture realm. The area where they may question you is that OATS for a small lesion is better for any active and athletes. So they may ask you which one may be better. And OATS has been shown in the literature to be more effective. You can get them back faster and higher return to play. If you have a large lesion, again, think ACI or osseochondral allograft. Some of the key things is ACI is contraindicated. If you have a kissing lesion in the patellofemoral joint, and again, look at your merchant view. If you have arthritic changes on your merchant view, that's a contraindication for ACI. Osteochondralograft requires a fresh graft transplantation before 28 days, and I'll kind of repeat that a few times because it's important, and it's definitely something that's been on test questions. So I like to repeat things because that's how we all remember them. So consideration, again, for all cartilage procedures. Mechanical alignment. So consider correction if the weight-bearing axis falls within the compartment. So again, if you're treating a lateral condyle lesion in a valgus knee, then you're going to be, that stem of the question is going to have you consider doing that distal femur osteotomy. Address any instability. So if they've had a previous ACL tear, now they have a cartilage lesion and re-torn their ACL, you have to address the ACL with a revision ACL reconstruction at the same time. Any significant meniscus deficiency. Again, meniscus deficiency is classified as greater than 50% of the meniscus excised or gone. So if you have that amount of the meniscus already excised, you think about treating it with a meniscal transplant. And then the big thing is whether you do a concomitant or stage, but they're not going to normally ask you that question. They're going to want you to make sure that you're addressing the concomitant pathology. So now we're going to go through each of those four slash five techniques and kind of talk about the indications, contraindications, and the complications that you can get with each of them. So microfracture forms fiber cartilage, which they will ask in one way or another on some sort of question. And remember, they'll either say it's fiber cartilage, or they'll ask you what type of collagen it is, and it's type 1 collagen. And this is inferior to hyaline cartilage, which has type 2 collagen. The indications are lesion size less than 2 square centimeters, age less than 30, poor candidate for other procedures, so then the age can be older, obviously, with that. Contraindications are any subchondral bone deficiency. So again, if you have a bony involvement, you're thinking of some sort of structural graft. Complications can be from an intralesional bony boss that can occur after microfracture. This is an osseous overgrowth. You have an increased risk if the patient is younger. You also have increased failure rate of ACI if this was needed later. So in other words, if microfracture failed, then ACI has an increased failure rate. And that may be something they can ask you as well, because that's been proven in a couple of different papers. One thing that can come up is, again, the success of microfracture. That is often dependent on the fill. So you can see here that about 54% of patients have a good fill. 17% have a poor fill. And the results of microfracture are really directly correlated with the percent of fill on MRI. Subchondral fracture can occur if you place the holes closer than three to four millimeters. So results are worse if it's over two square centimeters, and that's why they're gonna really make it clear if it's less than two square centimeters or over two square centimeters. Age over 40, higher BMI, symptoms over a year, or if they have a low activity level. The results typically decrease after two years. About 40 to 80% decline in function and activity after a microfracture. The deterioration of the repair tissue is seen on the MRI by 18 months with around a 40% failure rate, and has the lowest return to sport. Let's go to osseochondral autograft, or OAT, also called mosaicplasty. These are harvesting cylinders from a minimally weight-bearing area of the knee, so this can be around the notch, above the sulcus terminalis laterally, or medially at times, or the superior medial trochleum. And you transfer the plugs to the defect. Critical thing here is to remain perpendicular. So where they may have questions, or even an MRI or image, is if you have a non-congruent graft. And so they may ask a question, is what complication, or can this lead to failure? So any incongruities of the resulting cartilage can increase the contact pressures, and can lead to failure of that procedure. It's a press fit, obviously, with minimal impactions, so the more impaction you do, the higher chondrocyte death that you will get, and that can also be asked. The advantages, it provides hyaline cartilage, and addresses both the subchondral bone issues and loss. And that hyaline cartilage can be asked in a question that's comparing to microfracture, as to what type of cartilage you may see. Obviously, since you're just taking hyaline cartilage from a different area to this area, you're gonna see type two collagen, you're gonna see hyaline cartilage, compared to microfracture that has fibrocartilage. The indications for OATs is really for lesions under two square centimeters. Highest return to sport, so this is a great answer for athletes. Return to sport is also the fastest, can be anywhere from four to six months. The disadvantages of this, and these are gonna be things that can be questioned as well, is donor site issues. These can be from pain and bleeding. About 23% of people will have some telephermal pain, or some crepitus. Mosaicplasty will have some intervening fibrocartilage. Complications, as I already discussed, is the incongruity of the joint surface that can also cause damage to either the surrounding cartilage or to the plug. It's worse if you have a proud plug, or plugs that are greater than one millimeter recessed. The hematoma, hemarthrosis, are other complications that you can see. The donor site morbidity is worse if you have a plug over 10 millimeters. Graft fracture or chondral damage, again, beware of the tamp. If you tamp too much, you have a dose-response relationship. But again, one of the advantages is return to sport is the fastest. When we go to osseochondroallograft, these are really indications that you can take directly from our insurance companies. So this is what's gonna be what they consider what you need to know. It's a size of a defect over two square centimeters in total area, size of a defect over two square centimeters in total area in full thickness defect with no kissing lesions. Again, that's defined as greater than a grade two, so anything grade three, grade four. Lesion is largely contained or with near normal surrounding cartilage. The joint space has to be present, so it has to be equal or less than KL grade two, BMI less than 35, and they have to comply with, obviously, the restrictions. The contraindications, if they have more severe arthritis, it's been shown to have worse outcomes in poor survivorship. So if they do have any stem in a picture like this, that is not the right question. Obesity with a BMI of over 35, and then obviously some of the other issues that we normally think about. So what are some of the things that can influence success? More active patients have greater success. If you have a BMI greater than 35, you have a four-time greater risk of failure. If the graft is stored longer than 28 days, you have almost a three-fold greater risk of failure. And then, so at 28 days, the biggest thing to remember is a 70% cellular viability, and I'll show you a graph from the article because I'm a picture person. It helps me remember things. I think it's on the next slide. Osteotomy, obviously, if you have a varus or a valgus knee, to offload that area increases the success, and the return to sport is typically around nine months. So this is the slide I was telling you about. If you're a visual learner like I am, I think that this is very useful. The big thing is 28 days, 70% viability. Anything after that, it really precipitates, precipitately goes down, and the risk of failure goes way up. Complications are infection, loosening. Disease transmission is very low. Graft fragmentation can be seen, especially if you have unvascularized zones. Collapse is not uncommon. So you can get anywhere from one to three millimeters of collapse. About 30% of patients will have about a four to five millimeter of collapse. I did not bold this, but what may be coming up on questions now is this last one because 50% of people can develop these anti-HLA antibodies but at the current time, we really don't know what the significance of this is. But it's something that's been reported more and more. Let's go to ACI. It's a two-stage procedure. The first step, you harvest cells, and again, they may have a stem of a cell question like how deep do you need to go? Again, you wanna get to the deep layers of cartilage. Implantation of cells is the second stage. Just so you're aware of the different generations, the first generation was the periosteum. That's the classic ACI. It had the highest chance of complications and especially with hypertrophy. The second generation was a collagen cover which has shorter OR times, less morbidity. And the third generation which is in the US at this point and has replaced the two previous is a matrix with ACI. It creates highland-like cartilage. Indications are lesion size over two square centimeters. ACI originally was indicated only as a salvage procedure. You had to fail something else. Again, focal defects. You could not have any kissing lesions. Age under 50, BMI somewhere between 30 to 35. Contraindications are true kissing lesions. So if you see a picture like this where you're obviously down to bone on both sides, that's obviously not the right patient for any of these cartilage procedures. For patellofemoral lesions, what often can be asked as a question is if you see patellofemoral arthritis. So if you see a joint space narrowing that's significant on your merchant views, that's gonna be a contraindication for ACI. So what are the complications? Unplanned reoperation is not uncommon especially when you use the periosteal patch in 27% of patients. Main causes, and this is what you're gonna see for potential complication questions. Hypertrophy of the graft is something they like to ask a lot. It's most common for the patella or if you use periosteum. Graft delamination is really the next most common or inadequate incorporation, but they typically will ask you questions from the first two. Other complications can be arthrofibrosis. And again, insufficient regenerative cartilage similar to microfracture. If the fill of the defect is less than 50%, you have an increased risk of failure or poor outcomes. And that is something that can be seen on test questions. MACI is what is now currently in the US. So last year when I gave this talk, I did not think MACI would be a question that can be on the test, but now since it's been out, I do think it's fair game. It uses type one, type three collagen membrane, which is bovine. You use fiber and glue to glue it down through a mini arthrotomy. The advantages, it has shorter OR time, has an accelerated rehabilitation, and return to sports now can be anywhere from nine to 12 months. The success rate of MACI equals the same as ACI, and it has a decreased complication profile. And that might be the area where they really ask you a question. So as we kind of recap some of the articular cartilage treatment options, young patients less than 30 years old have less difficulty with rehabilitation and often have better outcomes. Remember size, size, size. So when you're looking through that algorithm, if they have small size, think OATS or microfracture. If they have a large, think ACI or allograft. And if they have something that's involving bone, use a structural graft like OATS or osteochondroallograft. Again, if they are an active athlete and they have a small lesion, they may really start pushing you towards that OATS treatment, because again, it has the highest return to sport in the fastest recovery, as you can see in this bar graph. Let's go through a couple of questions. So here's athletes with focal patellar trochlear condyle defects in the patellofemoral compartment can be successfully treated without ACI. Which situation is a contraindication? And again, if you have any advanced joint space narrowing on sunrise radiograph. Here's where I'm, again, you'll see a question like this where they want you to fix a piece. So you'll either see an MRI or you'll see arthroscopic pictures like this. So this is from a patellofemoral dislocation, an acute injury. You have a large osteochondral piece, as you can see from the x-ray. You can see the divot here. You can see the bony piece here. Here's how it looks like in arthroscopy. They want you to fix this, okay? Similarly, here's a 14-year-old. Again, a patellofemoral dislocation with a loose body that you can see here underneath the patella. It has a small sliver of bone. It came from the lateral femoral condyle. They want you to fix this. So acute injuries with a large, especially if it has bony fragment, fix. All right, we're gonna now go into osteoarthritis. And I know that some things have been covered by Dr. Borchers earlier this morning with injections. So I'm not gonna cover that. Key aspects for the tests are really looking at the changes in cartilage with aging and osteoarthritis. Those are favorite questions that they'd like to ask. Non-operative modalities, always remember, first time that anyone comes in with arthritis, they must fail previous non-operative modalities before thinking of surgery. And then what was on the test this last year, which I've added to this, is osteotomies. And so again, they're gonna want you to know the indication, contraindications, and the complications. So aging of normal joint, articular cartilage. Cell division is rare in the mature cartilage. Age-related downregulation of the proteoglycan synthesis. Overall, you get decreased strength and stiffness. You have loss of thickness and focal sites of degeneration. Key area on this slide is gonna be the decreased water concentration. Again, this is one of the things that they typically like to ask as far as with aging. How about the changes in cartilage proteoglycans as well? This is the other area they typically will ask questions on. So chondroitin sulfate, obviously, is the most prevalent proteoglycan within cartilage. As we age, the concentration of chondroitin full sulfate steadily decreases, while the chondroitin six sulfate increases, keratin sulfate concentration, again, rises with maturation. So again, remember, the C4 decreases, C6 increases, and the keratin sulfate, I should say, increases. So that's a typo, sorry. Articular cartilage changes with osteoarthritis. So again, they're gonna contrast osteoarthritis versus aging. So with osteoarthritis, you get increased water content. So you get the articular cartilage fibrillation, so you've got cracks in the cartilage, the water kind of starts seeping in. You get decreased proteoglycans, increased permeability, and decreased stiffness. And here's a chart that, for me, again, I like visual things, so this is a good thing, right at the end to review, right before you have a test. They typically will ask a question from here. Treatment for osteoarthritis, the mainstay is non-operative. So if they come in, first line, you see an X-ray with some medial joint space narrowing with some medial pain that's happened over the last couple weeks, they're gonna want you to go down that non-operative pathway for at least six months. So that can be activity modification, anti-inflammatories, bracing, therapy, and then again, injections, which was covered by Dr. Borchers earlier. This is from the Academy Clinical Practice Guidelines, and so this can be fair game, and I've seen this more on some, not on the test last year, but on other question banks. So any BMI over 25, they are recommending some weight loss, because obviously the forces of knee are magnified three to seven times by body weight, so the minimum goal that the Academy recommends is 5% of your current body weight. Also, exercise is the other thing that's currently recommended for the arthritic patient, and that's at least 150 minutes of moderate activity a week. Think of it as 30 minutes five times a week, and it has no risk of worsening progression. So this is definitely fair game, especially since our Academy is saying that this is good clinical practice guidelines. Bracing, they may have this as one of the options. I think it's gonna be a little bit hard now for some questions, because the evidence is a little bit weak in some areas, but it's historically, they've asked questions on who is the right person for bracing. So varus or valgus deformi of less than 10 degrees. It's best if you have pseudolaxity, so a little bit of play in your compartment and that ligament, and it has the best results with stair climbing, so up and down stairs, people typically feel better with the brace. It also has some evidence that it may predict a favorable outcome for realignment osteotomy. So again, arthroscopy for these arthritic patients, it is not recommended for arthritis. So it's typically the wrong answer. The only indication that you may see in that type of patient is if they have loose bodies, and you can see that in multiple different ways. So if they have synovial chondromatosis and they have loose bodies and they have arthritis and they're having locking, then they still want you to do a scope and remove those loose bodies. But for a plain arthritic patient, it is typically the wrong answer. And that comes from a lot of level one evidence, especially the Mosley and Kirkley article showing that it really has no improvement with the patient's symptoms. So osteotomy, this is an area that was definitely on the test last year, so it was something I added to the talk. It's useful for unit compartmental disease. You want to have an adequate workup to make sure there's no other concomitant pathology. Active patients less than 50 to 55 years old, BMI less than 35 to 40 with near normal range of motion. You need to get your long-leg films to assess their mechanical axis and their alignment and the degree of deformity. And again, you need to pay attention to all those associated injuries. Contraindications, tricompartmental osteoarthritis. If you have patellofemoral osteoarthritis when you're thinking about a medial or lateral compartment OA, those are going to be the wrong patients, and they're going to be a contraindication. So you may see that on the test. Inflammatory arthritis, obviously knee range of motion less than 120 degrees, so a good range of motion. Then they're typically contraindicated for an osteotomy. Flexion contracture is greater than 5 to 10 degrees. Again, in older age, you're usually thinking of a different procedure. For a various osteotomy, the goal is to shift to 62.5% of the width of the tibial plateau. For valgus, for cartilage treatment, we typically think of distal femur. There is some discussion in the literature as to a high tibial osteotomy or distal femur based on the degrees of deformity. So what are some of the high tibial osteotomy you're thinking of, closing wedge or opening wedge? And what are some of the drawbacks of each? So closing wedge drawbacks, you can have limb shortening. It's an extensive surgical dissection. You have to do a fibular osteotomy. Opening wedge drawbacks, you have to do bone grafting. Typically, longer weight-bearing restrictions and a higher risk of non-union. This is where they're really gonna ask you questions is more on the complications. So interarticular fracture can happen with an opening wedge osteotomy. If the pins are too close to the joint line, you have thick osteotomes going above the pins and opening the osteotomy before completed. This can cause a fracture into the interarticular surface. If you see that, the treatment is to place screws across, some raft screws across to reduce that area, usually from lateral to medial. You can also fracture through the lateral side as a complication, and if that is the case, then typically you're placing a staple or a small plate on the lateral aspect. For an opening wedge, the complications also can be undercorrection, which has been associated with poor survivorship and need for revision, overcorrection, malunion or non-union. Biggest risk factor there is smoking. Perineal nerve injury is a little bit more common with a closing wedge, and you can get irritation of plates, and typically anywhere from 30 to 50% of people want the plate removed. I'm just gonna touch just for completeness on uni-knee arthroplasty, but this has not been in any of the question stems at this point, or any of the question banks that are out there, so the contraindications are inflammatory arthritis. Again, if you have bi- or tricompartmental osteoarthritis, a large fixed deformity. If you have ACL deficiency or a previous meniscectomy in the other compartment. The classic indications are an age over 60 with a BMI of less than 35, a flexion contracture of less than 10 degrees, a varus deformity of less than 10 degrees, and a valgus deformity of less than 15. I think I'm gonna bypass a couple of these questions here just for the sake of getting through the rest of the material. But again, this is just an osteotomy question where they're considering a meniscal transplant. They have a varus knee. The first thing is obviously to recommend a high-telby osteotomy and evaluate for a meniscal transplant. For osteochondritis dissecans, key points for the test are the indications for conservative management. What are the findings of instability? Because you'll get a MRI and you'll need to be able to determine that this is an unstable lesion. And then the ways to treat. And again, very similar to the cartilage algorithm, always try to save the piece if you are able. So the definition is the focus of subchondral bone adjacent to articular cartilage or the progeny fragment that separates from the surrounding bone, which is known as the parent. Incidence is unclear, but it's relatively rare, most commonly between 12 and 19. And the etiology, though unknown, the most common thought process right now is repetitive microtrauma from sports. Knee is the most common site. The medial femoral condyle is the most common location, and they will ask that, they will ask that, they will ask that, that will be on the test. And they might ask where on the medial femoral condyle, if it's where on the medial femoral condyle, it's the lateral aspect of the medial femoral condyle. Bilateral, up to 30%. When you're looking at it as far as the history, typically they're gonna have pain, swelling, some catching or locking sensations. Physical exam, they'll have some loss of motion often, point tenderness, effusion, crepitus. Imaging, you'll see the radiographs. Always include the merchant in notch view because it'll increase your ability to diagnose it. Image both knees again because it can be bilateral and up to 25 to 30%, and MRI is often the most useful. The MRI classification is based on T2-weighted images. So stage one is thickening of the articular cartilage and a low signal change. Stage two, the articular cartilage is breached and low signal rim behind the fragment, including a fibrous attachment. Stage three, the articular cartilage is breached, high signal changes behind the fragment indicating synovial fluid between the fragment and underlying subchondral bone. So here's an unstable lesion. And then stage four is a loose body, so it's already floating around. Signs of instability. Again, if we look here, a radially-oriented hypo-intense signal at the margin of the OCD. So it's gonna be, you're gonna see a break in the articular cartilage on the sides here. Hyper-intense or the synovial fluid signal behind it. And then you're also gonna see some edema within the parent bone. Those are all signs that you can see with instability. So what are the best chances of non-operative management? And this is a question again and again and again and again. So they will ask this at some point on your test. If you have a skeletally immature patient with substantial growth remaining, so if they have wide-open growth plates, that's the best chances for non-operative treatment. Especially if they have no mechanical symptoms, they have no signs of instability. If they are smaller lesions, they have no cystic changes. The healing rates can be greater than 60% of the patients, especially if they're immature and it's up to six months of non-operative treatment. And that six months is key. So if you see that they've only done two months, and again, they have a stable lesion, wide-open growth plates, it's gonna be continued non-operative management for six months. So an example of some of the non-operative management. Initially, if you see them, you can do six weeks of weight-bearing immobilization in a cast or brace. And then you can slowly transition them back towards weight-bearing, especially if they have no pain. And then back to activities once you see radiographic signs of healing. This is, again, reproduced in the back of your, my talk here, so it's bigger. So you guys can kind of go through this and think through the logic. Again, if you look at this, if they have an open FICES, again, they want you to have about six months of conservative management, and they're either healed or not healed. And if they're still stable, and they've not healed, and they have open FICES, then you're thinking about drilling. If they have closed growth plates, they have a stable lesion, and they're symptomatic, again, they don't have that chance for healing like someone who has wide-open growth plates, so then you're going down that pathway for drilling right away. An unstable or displaced lesion. So if you see the fluid signal behind the piece, that's an unstable lesion. And if you're gonna see if it's salvageable or unsalvageable. If it's salvageable, you wanna fix it. And that may include bone grafting or microfracture beneath the base, and then fixing it. If it's unsalvageable, then you're really going down the same pathway as our cartilage treatment. So surgical treatment, again, for stable lesions, either transarticular or retroarticular, they both have excellent results, so they're not gonna really ask you one versus the other. Unstable lesion. The wrong answer is always remove the fragment alone. There is a lot of literature showing that just removement of the loose body with an osteochondral defect and leaving a hole there, they have good short-term results, but horrible long-term results. So that's always the wrong answer. They always want you to, if you have to remove the loose body, but then what is your next thing that you need to do to fill the pothole? If the fragment is salvageable, best if you fix it, again, with or without bone grafting, and then whether you use bioabsorbable metal implants. Both of them are good. They both have their issues. If it's not salvageable, again, you're thinking OATs or microfracture for small lesions. OATs can be better in the long-term. ACI or osteochondrolograph for larger lesions. For the adults, symptomatic lesions are always treated because they have a higher risk of developing arthritis if they're untreated, and that's proportional to the size of lesion. And this is just, again, another algorithm just to think through it, but more from an athlete standpoint, that if you have a stable lesion, you can continue to watch it to see if they can get through the season, but once they have significant symptoms, obviously you're going down that same OCD treatment algorithm. These questions are in there. I'm gonna kind of skip through. I think I can actually go through a couple of these. So here's a 13-year-old. Contact of a football game one month prior. He was able to return to play within a week of injury, but since he has persistent pain, denies any mechanical symptoms, has pain only with activities. His exam shows a stable knee, trace fusion, mild medial side of pain. What is the best predictor of good clinical outcome with non-operative treatment? As you can see on this X-ray, he has wide open growth plates. That is what they want you to remember. Similarly here, here's a 13-year-old male soccer player with atraumatic knee pain, no mechanical or locking symptoms. Physical exam is stable, no effusion. Radiographs again here. MRI here, you can see a stable lesion. You don't see any crack in the cartilage, no fluid behind it. That's gonna be non-operative treatment with activity restriction. Here's a good one to think of it differently, though. So here's a 17-year-old, one year old, one year history of pain, swelling, so we know it's been going on for a while. He was previously treated with non-operative treatment and protective weight-bearing and activity modification for six months. So they're already now pushing you down that stem to treat it. So what's the next appropriate treatment for this patient? And I think they had a very similar one to this on the test last year. Key things here, it's unstable. You see some fluid behind it, and it's fragmented. And he's failed conservatively. He's fragmented, and he's failed conservative measures. So this is a hard one to fix because you can't necessarily fix multiple pieces in an OCD with great success. So this is the best treated with an osochondrolograph, which is the right answer. All right, last part, synovial disease. Key points for the test is understanding aspirations like most of us do, and then pigmented villanogia, synovitis, synovial chondromatosis, and inflammatory conditions. The synovial, synovium has two distinct layers, the intimal layer and the sub-intimal supportive layer. Synovial sites are primarily in that intimal layer. You have type A and type B cells. The most predominant is type B, which actually makes the hyaluronate. Synovial fluid is composed of a dialysate of blood plasma, has no clotting factors, blood cells, or hemoglobin. It's made out of hyaluronate, which again is extended glycosaminoglycan, and lubricant. As I said, that was going to come up again, so here it is. The function is joint lubrication, joint nutrition. It has non-Newtonian flow characteristics, and the viscosity coefficient depends on the shear rate. Two types of lubrication you need to understand is the elasto-hydrodynamic lubrication and then the boundary lubrication, which will be on the next slide. This is the primary mechanism. Under condition of joint loading, the cartilage undergoes an elastic deformation, and so it spreads the joint load over a larger surface area, and it decreases the shear rate. The boundary lubrication is really the workhorse of the molecule lubricant, and this really works when the fluid film is depleted, and the lubricant is absorbed on each of the opposing articular surface, and it provides cushioning, and it protects against abrasion. Synovial fluid analysis, just remember anything you see over 50,000 white blood cells, you usually want to think of septic arthritis. Crystals will often also come up for gout and pseudogout, so we'll spend a little time going through each of those. I'm always, again, a visual person, so this chart is just for you for your review as far as what you want to look at for normal, non-inflammatory, inflammatory, septic, and hemorrhagic as far as some of what you can see for white cell counts, protein, and also glucose. So when we look at the synovial-based knee disorders, we're really looking at synovial chondromatosis, pigmented villanogia of synovitis, and the crystalline diseases. Synovial chondromatosis is a monotricular synovial proliferative disease characterized by conversion of cartilaginous tissue to ossified loose bodies, most often seen in middle-aged men. Symptoms are typically mechanical. Most common is in the knee. They have different phases from early transitional to late. The radiographs typically will show some loose bodies, especially as you get from transitional to late phases. And if the radiographs are negative, then MRI typically will show the cartilaginous bodies. Treatment is a complete synovectomy, and the recurrence rate is over 25%. PVNS is a slow-growing, benign, and locally invasive tumor of the synovium. It typically presents as a monoticular hemarthrosis, and patients may have mechanical symptoms or effusions. Most often involves the knee. There's two types, a nodular mass or diffuse. The key thing to recognize on MRI or in the question stem is that you have low signal intensity on all sequences. So if you see a T1 and a T2-weighted image, and it looks the same on both, so a low signal intensity, or they tell you about this in the stem, then you're thinking about PVNS. And this is really due to the hemocytorin deposits. It has hemorrhagic or dark brown synovial fluid, and a biopsy is typically diagnostic. The diffuse form or nodular form. Nodular form is less common and less destructive than the diffuse form. Histologic characteristics are similar to a giant cell tumor of the tenon sheath, and that may come up in a question. Thank goodness I did not see slides like the bottom right like I saw previously about 10 years ago. So they don't necessarily ask you to review the slide material anymore, thank goodness. PVNS treatment is with a thoracine vectomy. Arthroscopic is most effective for the nodular form, which can be curative, but you need to address the posterior compartment if you have more of that diffuse form. The recurrence rate is quite high, and obviously sometimes you may need to add low-dose radiation therapy or an open synovectomy to try to eradicate it. Gout is the deposition of monosodium urate crystals in the bursa and synovial membranes. It has other manifestations, such as TOFI. Again, they may always ask you that a male patient had great toe pain six months previously. It now has knee pain with an effusion. So they want you to think about the classic presentation of gout. And that now it's coming to the knee. Most common in men. There are some questions more recently about this next one with women. Because it's not as common in women. If you do see it in a woman, you need to think about some sort of enzyme deficiency, because that's the common cause for women to get gout. It has a lot of different associated diseases as well. Clinical presentation, it usually remits and recurs. And after the first two-thirds, we'll have the second attack within the year. And that's why they may, in that stem, talk about the great toe first. And then they have a knee effusion with significant pain. And again, they're taking you down this route. Laboratory studies with hyperuricemia, but that's not diagnostic. The synovial fluid really is diagnostic. The leukocyte counts can be high. With polarized light microscopy, you'll see negatively birefringent needle-shaped monosodium urate crystals. Acute treatment is with indomethacin or colchicine. It is contraindicated to use allopurinol or probenicid during an acute attack, as it can actually exacerbate it. Chronically, though, those are the treatment of choice and often are going to be treated by the prime care physicians. Pseudogout, calcium pyrophosphate dihydrate deposition can mimic gout during acute flare. It's often in patients over age 50. And you can see chondrocalcinosis of the meniscus. So they may show you an X-ray similar to this, where you see the chondrocalcinosis. It's associated with several metabolic disorders. And this may be within the stem of your question, that they may have hypothyroidism or they may have hyperparathyroidism. And again, they're taking you through this tree. With crystal analysis, you see weakly positive birefringent rhomboid-shaped crystals. The treatment is typically aspiration of the involved joint with a steroid injection. But you must rule out infection. Indomethacin can also be used in acute setting, but colchicine really does not have a role in this setting. And surgical lavage is really for refractory cases. Inflammatory arthritis, likely we don't have to do this too much because some of our medications have gotten so good for treatment of rheumatoid arthritis. But occasionally, you might do an arthroscopic synovectomy if they've been resistant to some pharmaceutical treatment. And for the sake of time, I won't go through the rest of these questions. Guidelines. All right, so my last little things. Focal problems need focal treatments, while regional problems like arthritis need regional treatments. Never change a winning game, so always change a losing game. If you look for clues, again, for that six months of physical therapy without any type of benefit, always try to save the native articular cartilage when possible. Fix the osteochondral fracture in salvageable OCD lesions. Good luck. You're going to do great. The best thing you've done is come to this course. You'll do awesome. Thank you.

video content summarization

articular cartilage

osteoarthritis

treatment options

microfracture

ACI

synovial chondromatosis

inflammatory conditions

Ohio State University