All right, well thank you and yes those course evaluations are key. In fact, I changed a couple of my slides this year based on some of those course evaluations. All right, so let's get into this. Similar to what Dr. Bishop said on their first day, I took this test two years ago. I found this course, as with OKU Sports 5, really the two key things that you needed to do to pass the test. This talk is really designed to give you every piece of information you need to pass the test when it comes to cartilage and the topics I've been assigned. I have one off-topic slide here. This was a whole stem of questions when I took the test. If you just remember this slide and you have common sense, you'll get that whole stem of questions correct. It was really looking at a trauma situation and how to take care of it. So if you're like me, I no longer take level one trauma call, but we take care of teams and so it's just kind of getting back towards that ATLS trauma type of mentality. So just remember that primary survey, work as a team. The big things that you're going to have as far as when it comes to trauma is protect the C-spine, right? So collar, inline immobilization. The next big thing here is with the circulation. If you have a major traumatic event and it may or may not be related to something that has to do with cars or something like that, two large bore IVs, get them fluids, pelvic binder if you have any concerns about that standpoint. And then the last part, the E is also the thing that they really want you to think about is the exposure environmental issues. So remove them from danger, address the hypo or hyperthermia, and then really look for any other signs of trauma. So here's the objectives for the topics that I'm going to be going through today. We have four areas somewhat related. My whole goal is to really get out of any type of controversial topics in no major novel treatments or technical pearls. There's a lot of that when it comes to cartilage and we're not going to really get into those areas. All right, articular cartilage. These are the key points and areas that you're going to see for the test. It's the zones of the articular cartilage, the components of cartilage. Have a working knowledge of the cartilage algorithm. You don't need to memorize a chart, but really kind of the key things I'll give you to take home points, just understand that algorithm. And then the other big thing is the indications, contraindications, and complications for each of the procedures. So that's the areas that they really want you to hone in on. So let's review the articular cartilage. There's four main zones here. The superficial zone forms the gliding surface and resists those tensile stress. It has thin collagen fibrils parallel to the surface. The chondrocytes are elongated and those are also parallel to the surface. And you have lubricant which coats the articular surface and we'll get into that again later on. The proteoglycan content is the lowest and the water content is the highest. Let's get into the middle or transitional zone. These are larger diameter collagen fibers. They're more kind of haphazard place and random and oblique. The chondrocytes are rounded in this area. When we get to the deep zone, the proteoglycan content is the highest and the water content is the lowest. It has larger diameter collagen fibers and these are perpendicular to the joint surface and the chondrocytes are also organized perpendicular to the joint surface and columns. The zone of the calcified cartilage is separated from the deep zone by the tide mark. It separates the hyaline cartilage from the subchondral bone. You have small round chondrocytes and the intratissue oxygen saturation is the lowest in this area. That tide mark is really this little wavy line that you see on the H&E stains and again that separates the deep zone from the calcified cartilage. Well how about the chondrocytes? Chondrocytes obviously synthesize and maintain the matrix. They rarely divide after skeletal maturity and their mitotic activity really ceases with the development of that tide mark that we just talked about. It's anaerobic metabolism and the metabolic rate also slows with increasing age. There's no pluripotent cells within mature cartilage so the healing potential is really minimized. And there's limited ability for any type of repair tissue once you're more mature. The extracellular components, the main one, and so this will come up on test at times, is water. Water is 65 to 85% of the wet weight. It's hydrophilic nature with the proteoglycans. It has low permeability and this frictional resistance of flow and pressurization of the water enables the articular cartilage to support these high loads that we typically see. The main collagen is type 2 collagen. That will come up again and again and again on tests. So they really want you to remember that and really contrast that to type 1 collagen which we will see in fiber cartilage. The proteoglycans are anywhere from 10 to 20% of the cartilage with a high affinity for water. This is really our collagen review and I highlighted again the two things that have come up on tests. I would see on some in training about 10 years ago they had type 10. I've not seen that in the last decade come up at all. So they really want you to again remember type 2 collagen and there was one esoteric question many years ago on the type 9 collagen as far as stabilizing the collagen network by linking to the type 2 collagen. So proteoglycans, proteoglycans are the definition is a glycosaminoglycan that's bound to a central protein core. It's anionic charge, it's hydrophilic, and it's linked to hyaluronic acid by a linked protein. The main ones that you're going to need to know here are the chondroitin sulfate, the keratin sulfate, and the hyaluronate. So chondroitin sulfate is the most prevalent glycosaminoglycan. It's anywhere from 55 to 90%. Keratin sulfate is really number 2 in this composition, the degree of sulfonation will vary versus age. It increases with age. And so if you're going to get some questions, it's typically going to be with some of these components with aging. Hyaluronate is not a proteoglycan because it's not covalently bound to a protein core. And again it's commonly found within our cartilage. Nutrition, our cartilage is avascular in adult life so it gets most of its nutrition through diffusion from that synovial fluid, both the nutrients and the oxygen. This is part of the reason why if you have immobilization it can contribute to the chondrocytes getting hypoxia, decrease proteoglycan metabolism, and thinning of the cartilage. And these were through a lot of early dog studies from a basic science standpoint. So we know chondral defects are common. It's difficult to really know the true incidence or prevalence of this. It's around 60% of people as they go through arthroscopy that goes from early stages of cartilage defects all the way to arthritis. We know that in athletes it's a little bit more common due to the repetitive microtrauma and traumatic events and it can be in 36% of the athletes. It's often associated to other injuries, especially patella dislocations. So if you get a question with patella dislocations you have to be thinking about a chondral or osteochondral defect, ACL injuries, and meniscal injuries. But the natural history is pretty poorly understood. So how do they present? And I think this is kind of the key thing to think about when they go through STEM questions. So you're going to have either a scenario of an acute injury or more of a chronic injury. So if it's an acute injury they're going to have a traumatic injury to the knee, they'll have some sort of significant effusion, and typically they're going to give you something like they have mechanical symptoms or they have locking and you want to be thinking of the loose body. The other one is more the silent or chronic issue where you have recurrent effusions, pain with increasing activities, and potentially weakness. And they'll kind of again bring you down that route that they've tried six months of this or whatever and they're still having pain. There's no history or exam findings that are sensitive or specific when it comes to cartilage. So unlike all the other talks where we have different type of exam findings and what are the sensitivities, we really don't have that with cartilage. So again they'll kind of lead you down this pathway with some of the STEM questions. Imaging radiographs are usually negative unless there is bony involvement. So really pay attention when you look at some of the x-rays. If you do see any type of bone defect then you really know where they're taking you with this. MRI imaging is really the gold standard to determine if a cartilage defect is present. But beware, it's not always accurate in determining the size of the defect. It's been shown that about 70% of the defects are under-essayed by the size on MR. So you want to base your treatment off the arthroscopic sizing post-debridement. A CT arthrogram can also be useful in cases where you can't get an MRI. So here's some key things to think about when they go through these STEM questions. Most acute chondral injuries with loose bodies will need to be treated acutely. So if you have an acute trauma, you have a loose body, you're going to be going down this pathway to treat it acutely. Chronic, again remember that cartilage is aneural. So you really need to rule out all other sources of pain in making sure that cartilage is truly the reason for discomfort. And so there's always going to be this initial trial of conservative treatment prior to jumping in towards any surgical management for a chronic issue. So operative management, as we know, there's multiple different things that we can do to treat the cartilage defects. These can be non-restorative techniques like debridement chondroplasty, any type of mesenchymal stem cell techniques. This can be the microfracture, abrasion chondroplasty, drilling, chondrocyte cell-based therapies like ACI, now MACI that we have within the U.S., structural techniques which can be OATs or an osteochondro-allograft. These are the wrong answers, okay. So if you see this on there, you can eliminate that as a choice. So anything with juvenile cartilage, otherwise known as de novo, anything that is being investigated such as hyalofas, Novacart, biocartilage, decellulized cartilage, Cardiform, microfracture plus techniques, if this is an answer on that, you're going to cross it off. It's not the right answer. So anything that's being investigated and anything that insurance companies consider as investigational or not having good evidence for it is the wrong answer. Debridement. So it's commonly used as a first-line procedure. You can remove loose bodies and any unstable cartilage. The indications are really for those who are poor candidates for other procedures, age of over 55, high BMI, advanced degenerative changes. So they're not going to be candidates for some of these other type of techniques. Or if they're unwilling to comply to rehab for the other procedures. And sometimes it's a good choice for that in-season athlete. The short-term data supports some symptom improvement, but no long-term data on its efficacy. I want to go through just briefly the classification as far as when we see cartilage defects arthroscopically. Many of us know the Outerbridge classification. It's a four-point scale, zero being normal, softening the cartilage being one, two you have some fragmentation, three it's a larger area, typically in greater depth of over 50%, and four down to bone. This unfortunately did not get transferred when I sent my talk in. I'm sorry about that. It will be updated for the online version, but this is the ICRS classification. This is truly the classification that's being used more in the literature as with when you're grading defects. It's very similar to Outerbridge, it just gives you some other ABCs. So again, zero is normal, 1A is soft indentation, 1B is with cracks, three is up to 50%. So again, it's kind of a more shallow lesion. And then once you get into three, now you're going above 50% thickness. And it's either going to be to the calcified cartilage layer, to the subchondral bone, delamination or bulging of the cartilage. So if you see a blister of the cartilage, that is also a 3D lesion because that's a full thickness cartilage defect. And then four again is down to bone. These are the main tools of trade, and honestly these are going to be the things that are going to be tested. We're not going to ask you questions on all these other investigational or not well-established products. You do not need to memorize this. I will give you the take-home points so that you understand how to work through this algorithm. But this is probably the best diagram that I use for a thought process and it's from Cole's article in 2009. But where is it located is on the femoral condyle or the patellofemoral joint. You always have to remember with cartilage defects, you need to address all concomitant pathology. So if they have ligament instability, you need to address it. If they have a meniscal deficiency, you need to address it. If they have malalignment, you need to address that. Lesion size. When it comes to this test, I know this one says 2 to 3, it's going to be very clear of under 2 square centimeters or over 2 square centimeters. They're not going to give you this gray zone. And so they're going to really say if it's big or small. And then you want to think of the demand. There are some options that are going to be better for athletes and we will highlight that. So key thought process for treatment. First and foremost, fix any acute osteochondral fragment that is appropriate. So if it's a big piece and it looks good, fix it. If the bone is involved, think of some sort of structural graft. So that's going to be an osteochondral allograft or an osteochondral autograft and it's going to depend on size. If it's a small lesion, you're going to be thinking of microfracture or that osteochondral autograft. If it's a large lesion, you're going to be thinking of ACI, which is now MACI or an osteochondral allograft. ACI is contraindicated if a kissing lesion, especially patella femoral area. An osteochondral allograft requires a fresh graft transplantation before 28 days due to cell survivorship. Those two key points will come up again and again as far as questionings. So as I already alluded to, you always have to think of the other concomitant pathology with the stem questions. What is the mechanical alignment, address any instability, and address any significant meniscal deficiency. And then they're not going to really ask you do you do this all at once or stage, but they can potentially say what would you do first and what would you potentially do second. And it really doesn't matter if you do it all at once or in stage. It's really up to each surgeon. So I want to go through each of the techniques again as we talked about what are the key things about the technique, the indications, contraindications, and complications. So microfracture, marrow stimulation, it forms fiber cartilage. This will come up on the test again and again and again. It is type 1 collagen. This is inferior to hyaline cartilage. The indications are for lesions less than 2 square centimeters. Typically does better for age that is younger and poor candidates for other procedures. Contraindications are if you have any subchondral bone deficiency. What are the complications? Well, it can form an intralesional bone boss or an osseous overgrowth and this is increased risk if you're younger. We know from a few papers that if you have that and if you ever need to revise it to something else, there's increased failure rate for ACI if you have a bony boss. There's also as far as complications is poor defect fill. You can see it's just over 50%. You get good fill. The results of microfracture are very dependent on how much it's filled. So a lot of these defects are poorly filled with and poor tissue quality. You can also get a subchondral fracture if your microfracture punctures are too close together. The results, you have worse outcomes if it's over 2 square centimeters. So again, they're going to really kind of give you this pretty clearly. If your age is over 40, if you have a higher BMI, if you have symptoms over a year, and if you have low activity. Results typically decrease after 2 years. There's a 40 to 80% decline in function and activity and there's deterioration of repair tissue on an MRI by 18 months. There's around a 40% failure rate and it has the lowest return to sport. So oats, also called mosaicplasty. This is when we're harvesting cylinders from minimally weight-bearing areas of the knee. It could be around the notch, above the sulcus terminalis laterally, superior medial trochlea. The lowest joint forces for a graft is actually in the inferior medial trochlea. So those are your areas that you can get your plugs and you transfer the plugs to the defect. It's critical to remain perpendicular so any incongruities can result in the cartilage surface increasing contact pressures. And it's a press fit with minimal impaction. So the more that you impact the plug, the higher amounts of chondrocyte death you can occur within your plug. The advantages is it provides hyaline cartilage. So if they give you a question saying what type of collagen is seen in the cartilage surface after an oats procedure, it would be type 2 collagen. Because again, it's cartilage. It also can address the subgondral bone issues and loss. It's indicated best for less than 2 square centimeters size and it's the highest return to sport. So it's a great answer for athletes. If you have a choice when it comes to microfracture or oats for an athlete, especially a high caliber athlete, oats is your answer. Fastest return to sport as well. The disadvantages are that there is donor site pain. You can get pain in the patellofemoral joint, crepitus. We have limited sources for how big of a defect we can make. Our complications can be incongruity of the joint surface or damage to the plug. So a lot worse outcomes if you have proud plugs or if the plugs are recessed greater than 1 millimeter. Again, you can have donor site morbidity, especially for larger plugs. And again, you have to be careful of how much you tamp the plug as far as the chondrocyte death on the chondral surface. Fastest return to sport, again, is the fastest. I put that there because that can come up on the test. When it comes to osteochondroallograft, this is for a cartilage defect that is greater than 2 square centimeters. So allograft will be for greater than 2 square centimeters. Contraindicate, it's for discrete, singular, unipolar. So again, kissing lesions are an exclusion. BMI has to be less than or equal to 35. Main reasons for that, we'll go on in just a second. The contraindications are significant osteoarthritic changes, so KL grade of 3 or greater. It typically has worse outcomes, poor graft survivorship, higher BMI is usually a contraindication as with the normal things we would think about, infection, inflammatory arthropathies. And again, you have to correct all the other issues that are going on within the knee. So here's the factors that influence the success of osteochondroallograft. So this can pop up on the test. Obviously, younger people always do better for any cartilage things, but it's the negative influence that may really come up on the test. So a higher BMI, if you have a BMI greater than 35, 4 times greater risk of failure. Also for standard graft storage, anything over 28 days, you can have nearly a 3 times greater risk of failure and this is all due to the cellular viability. Cellular viability return to sport is around 9 months. This slide is from Dr. Bugbee's work. It's really the classic article that talks about cell viability and I'm a picture person, so I like to look at it visually. So you can see here that the chondrocyte viability is great. You have 70% at that 4-week mark and after that it plummets. So we know that the results of your osteochondroallograft are good within this 4-week mark, but after that when the cell viability dips below 70%, it's much more unpredictable. What are the complications? Well, that can be infection, loosening, disease transmission can come up. It's again very rare, 1 in 1 million chance of HIV, 1 in 300,000 to 450,000 for hepatitis C. You can get graft fragmentation. The most common thing is to be more of a collapse. It typically happens with larger grafts. It usually will subside anywhere to 1 to 3 millimeters and there is a percentage of them that can be up to 4 to 5 millimeters. It is interesting and this has come up on some in-training questions as more of this immune response. 50% of people will develop an anti-HLA antibody. ACI is a two-stage procedure where you harvest the cells at stage 1, you implant the cells at stage 2. It's gone through various reiterations. The initial one as we remember here in the U.S. is the periosteum. It has the highest chance of complications with the periosteum, especially with hypertrophy. Second generation had a collagen cover that had less morbidity, but what we have in the U.S. at the current time is MACI or matrix autologous constipation implantation. This creates a highland-like cartilage. I am going to cover both ACI, especially do the complications because that will come up as with some things on MACI. ACI, the typical indications, and this is similar to MACI, is a lesion size of over 2 square centimeters, typically in age less than 50 years old, and BMI, again, less than 30 to 35. The contraindications are any kissing lesions. If that is in any of the stem question, then this is a contraindication for this procedure. If you have a total meniscectomy, unless you are dealing with a meniscus at the same time, if you're older, over 50 years old, and high BMI, and the key thing here is this bottom one is for patellofemoral lesions. If you have patellofemoral arthritis on x-rays, so if they give you a merchant view, skyline view, a Lauren view, and you see that there's arthritic changes, then this is a contraindication. What are the complications? Unplanned reoperation is common when it comes to ACI. It can be in over 25% of people, especially with the periosteum, but with the newer techniques, it's much less common. The main causes, and this will come up on the questions, is either hypertrophy of the graft, and they give you a picture similar to the one here, where you can see that it's bubbled up, it looks bigger. This is the most common, and then graft delamination is the next most common. Other complications can be arthrofibrosis, and again, if you have insufficient fill, less than 50% fill is correlated to worse or poorer outcomes. MACI is what has really replaced ACI at this point, so I think you probably next year you'll start seeing questions on MACI more than ACI as far as the lag with some of the questions coming on the test. There is one typo on here. This uses type 1, type 3 collagen membrane. It's porcine. I don't think they would ask you if it's porcine, but they would ask you if it's potentially type 1, type 3 collagen. The advantage of this is accelerated rehabilitation, and the difference now is you can get people back to return to sport between 9 to 12 months. The success rate of MACI is equal to ACI, but the biggest difference is it has a decreased complication profile. So what are, again, just to rehash some of these treatment options, younger patients have less difficulty with rehabilitation and overall have better outcomes regardless of what we do, but size, size, size is going to be what matters here. If you have small defects, you're going to be thinking of an OATS or a microfracture technique. Large defects is an ACI or an oligraft. Patients with higher activity levels, if you're an athlete, if you're a college athlete, if they have that in the stem and it's a small lesion, again, OATS. Return to sport, I put this up here just because this is something that's critical, especially since we're sports surgeons here. Return to sport is the best with OATS, as we've already highlighted, and it's worst with microfracture. Similarly for a return to sport to pre-injury level, it's worse with microfracture. Average time to sport, this was before we have some of our data on MACI, but you can see that historically the ACI would take the longest, but OATS is the fastest. So let's go through a couple of questions. An athlete with a focal patella or trochlear chondral defect in the patella thermal compartment can be successfully treated with ACI. Which situation is strongest contraindication for surgical management? Workers' compensation, well that really should not matter. A young, highly active patient, again, that would not make a difference. Advanced joint space loss on sunrise radiograph, we've already talked about this. This is what they want you to remember, and that is the right answer as far as this question. Fourteen-year-old female basketball player sustains an acute patella thermal dislocation radiographs and arthroscopy identifying osseochondral fracture. So they're already kind of giving you some of the key components here on the medial patella facet. If you look at the x-ray, you can see a chunk of bone is missing. You can see it in the gutter, and now if you look at the arthroscopic finding, you see this very large, nice, big piece of bone and cartilage in a 14-year-old. They want you to say, fix this, okay? So if you look at all these other things, you do not want to excise. You're not going, when you have something so pretty, to say I'm going to excise and go to an ACI. They didn't give you the size aspects of that either. You're not thinking of microfracture. It's really fixation, fixation, fixation. Fourteen-year-old girl experiences awkward landing after making a layup during a basketball game. She develops pain and swelling next day. Later that week, she has a locking episode. Radiographs are read as negative, and the MRI is obtained and shown below. So again, you have an acute traumatic injury, all right, symptomatic, locking, so you're thinking loose body. You look at your images, and you can see underneath the kneecap, you have a loose body on both the T1 and T2 aspects. If you look at it carefully, you can see the subchondral bone, so that darker layer of bone that's involved, and on your coronal, you're seeing far off to the lateral there that there's a piece missing, and that's what they're really wanting you to identify on this, that again, it's an acute injury, loose body, there's associated bone. And so when we're thinking of the best course of action, microfracture, again, you have a piece that looks good that you can potentially fix. You don't want to necessarily debride it. You just don't want to remove the loose body. So if you always want to think about treatment, especially in someone young, if they have an acute injury, if there's an option of just removing the loose body and doing nothing, that's usually the wrong answer. So here, again, is open reduction internal fixation because of the parts that we talked about. All right, let's move to osteoarthritis. These are the three key things they're going to test you on for the exam. So they're going to ask you the changes in cartilage with aging and osteoarthritis. They're going to hit home in one or two or three questions, non-operative modalities for osteoarthritis. And then the third thing that came up on the test when I took it was they want you to have some working knowledge of osteotomies when it comes to arthritis. So those are the three key areas that you really need to know for the test. So aging of the normal joint as far as the articular cartilage. Again, cell division is rare in mature cartilage. There's an age down regulation of the proteoglycan synthesis. Overall, there's decreased strength and stiffness, and you have these macroscopic changes of loss of thickness in focal sites of degeneration. The size of the proteoglycan aggregates decreases. The aggregant molecules become shorter as do their chondroitin sulfate chains. The mean number of aggregants in each aggregate decreases. There's increasing collagen cross-linking. And then the big thing here is decreased water concentration. That's the big thing they want you to know with aging. Aging also causes changes in the proteoglycans that we've also alluded to earlier. Chondroitin sulfate is the most common proteoglycan, but that chondroitin 4 sulfate will decrease steadily with aging, while chondroitin 6 sulfate will increase with aging. And keratin sulfate concentration rises with maturation. There was a typo on my slides I caught last night, so remember the C4 decreases, C6 increases, and the chondroitin sulfate also increases. I think it had decreases there, so just put increases there. This will be contrasted to what we see with arthritis. So with arthritis, we see that there's cartilage fibrillation. So once you have cracks in the cartilage, we're getting access to the lower portions of the cartilage area. You're gonna have increased water content. So aging decreased, arthritis increased. Again, you'll still have decreased proteoglycans. You'll have increased permeability because the water's coming in, and you still have decreased stiffness. So when it comes to the test taking, the one I've seen again and again is the top portion here, the water content. So with aging, it decreases. With arthritis, it increases. This is really key. Our academy wants you to always remember when it comes to arthritis that non-operative treatment is your go-to as first-line management again and again and again. I'm doing the longitudinal assessment right now, and this is the paper that came up as far as what our academy wants us to know. The top five have good evidence. Activity modification, self-management programs, that's mostly weight loss. Anti-inflammatories, Tylenol, and physical therapy. So those are your five key ones. You can see nowhere in here is opioids. Never give opioids. Bracing, again, has some mild indications as with injections, but the five main ones are those top. So weight loss and exercise, what do we know about it? Again, this is recommended by our academy as far as best clinical practice guidelines. For anyone whose BMI is over 25, you can have three to seven times your body weight as far as force that kind of goes across that. So their goal is weight reduction. The minimum goal is to lose 5% of the current body weight. Exercise, the recommendation is at least 150 minutes of moderate activity per week, and this has been shown not to have any risk of worsening progression of arthritis. Bracing, again, on loader bracing, just for working knowledge, is for varicose and valgus deformity of less than 10 degrees. It's best if you have some pseudo-laxity. The best results are with stairs. The evidence to support it is actually pretty weak, and it may predict a favorable outcome of a realignment osteotomy. So if you have a choice for arthroscopy and arthritic patient, it is the wrong choice. It is not recommended for arthritis. There's numerous studies against it, and it is typically the wrong answer. The only indications you can ever think about is truly with a loose body or a mechanical block that you need to go in there, but they aren't really gonna ask you for that. They want you to eliminate the choice. This has been borne out with a lot of level one evidence that shows that arthroscopic lavage or debridement were no better than the placebo procedure, so it's really not our treatment for arthritis. So when it comes to osteotomies, it's useful for unicompartmental disease. You need to have an adequate workup to make sure they are candidates, so that will include are they an active patient? Is their age typically less than 50 to 55? BMI less than 35 to 40? Near normal range of motion? You need to get long leg films to assess their alignment and their degree of deformity. You always wanna assess the associated injuries like meniscus, cartilage, and ligament like we've talked about. The contraindications are tricompartmental osteoarthritis, or if you have patellofemoral arthritis when you're thinking about unloading the medial or lateral compartment, that would be a contraindication. Inflammatory arthritis, if your range of motion is less than 120. If you have a flexion contracture of greater than five to 10 degrees, usually the number is 10 degrees, or if you have an age that is over 50 or 55. When it comes to osteotomies for a varus osteotomy, we're typically thinking of a high tibial osteotomy that can be either an opening or a closed wedge. Our goal is to shift to the 62.5% width of the tibial plateau, and that's really the big thing they wanna know for the test. For valgus, you can do either on the tibial base or the femoral base. Either one is applicable. I would say for most of us, we're doing distal femur osteotomies. So what are some of the drawbacks for some high tibial osteotomies for closing wedge versus opening wedge? So this can be on the test as far as they're questioning. Closing wedge drawbacks, you get limb shortening, you have more of an extensive surgical dissection, and you often have to do a fibular osteotomy. The opening wedge, the drawbacks are you have to bone graft, you have longer weight-bearing restrictions, and there is a higher risk of nonunion. The main complications that you can see with an opening wedge are an intra-articular fracture. Some of the reasons that can cause this are the pin is too close to the joint line. When you're templating out your bone cut, you use thick osteotomes, you go above the pin so you have a higher chance of cracking through the articular surface. If you're opening the osteotomy before the osteotomy is nearly complete, if you do have this, you want to place screws across and reduce that joint fracture. You can also get fracture through the lateral side. This is more easily dealt with by just placing a staple or a small plate on the outside part of the knee. Other complications that can happen with both open and closing wedge is an undercorrection. This is probably the worst. It's associated with poor survivorship of the knee and a need for revision. You can overcorrect and cause issues on the opposite side. Malunion, nonunion, this is especially for early weight-bearing or if you're a smoker. You can get peroneal nerve injuries or irritation because of the plate. I will briefly go on a couple aspects of UKAs, but this has not been on the test, but just to be complete. Contraindications are inflammatory arthritis, bi- or tri-compartmental osteoarthritis, a large fixed deformity, ligamentous laxity, unless that's being dealt with at the same time, previous meniscectomy in the other compartment. The indications are age over 60, BMI less than 35, and again, that you don't have a significant flexion contracture or varus or valgus deformity. Let's go through a couple of questions here. A 23-year-old former handball player presents to your office for evaluation of right medial knee pain. Surgical history reveals he underwent meniscal surgery four years prior, in which the surgeon reported he removed most of the meniscus. Initially, patient says he had improvement of his pain and catching symptoms, but reports progressive pain, swelling, and activity limitations due to medial pain. He's attempted anti-inflammatories and no longer runs, but reports pain with walking and prolonged standing. Already, we know this is a chronic issue. He's already tried some conserved measures with anti-inflammatories, activity modifications, and this patient now has pain, even with activities of daily living. On the medial side, has had most of the meniscus removed. This is a post-meniscectomy syndrome patient, so you're already kind of thinking through that through the STEM question. We're gonna see the radiographs and the MR scan. You can see that his BMI is ideal. His examination shows good strength, normal ligaments, and full range of motion in the knees. So any of those other contraindications are all gone. There's a trace effusion, medial joint line pain. He wants to be active, and he's asked about a meniscal transplantation. So after we look at his imaging studies, what is the best thing for the patient? So what we see on his imaging is that he has avarice knees, so the line does not go through the middle or onto the outside part of the knee, so it goes in the compartment on the medial side. His next x-ray shows that you have normal, in essence, normal joint space. We don't see significant arthritic changes. The MRI, I doubt that this is the same patient between the x-ray and the MRI, but anyways, on the MRI, what they're trying to show you is there's no meniscus, right? So if you look at all this stuff, here's avarice knee with no meniscus, so what is gonna be our treatment options? And so they say recommend unicompartmental knee arthroplasty. Well, this is a young patient. That's not gonna be our treatment of choice. Recommend an isolated meniscal allograft transplantation. Well, we know he's invarice, so that would increase the risk of failure, so we need to address the malalignment as well. Recommend a high-tibial osteotomy, but a meniscal transplant is contraindicated. Well, we won't really say it's contraindicated by his x-rays. There's no contraindication on what we saw there. Recommend a high-tibial osteotomy in consideration for a meniscal transplant. That would be really the treatment of choice. All right, let's go to osteochondritis dissecans. The key point for the test is, again, indications for conservative treatment. That's gonna come up again and again. Findings of instability, especially on the MRI, so you need to know how to determine that there is an unstable fragment, and then the ways to treat. You always wanna try to save the piece of fable. That's kind of you're just working a thought process with this. So what's the definition of an OCD? It's a focus of subchondral bone-adjacent cartilage called the progeny fragment that separates the surrounding bone, which is called the parent. Its incidence is unclear but rare, most common between 12 and 19. Its etiology is unknown, but probably the best working thought process is repetitive microtrauma with sports, and that's what we're looking at right there. So the knee is the most common site. The medial femoral condyle is the most common location, but typically they're gonna ask you this in this way. It's the lateral aspect of the medial femoral condyle, and they are gonna try to switch medial and lateral in different ways to kind of screw you up, but it's the lateral aspect of the medial femoral condyle is the most common site. Bilateral, up to 30%. It's more common in males and African Americans. Evaluation, you wanna look for their history, pain, swelling, catching, or locking sensations. Their exam, they may have lost motion, effusion, point tenderness, crepitus, but the x-rays are gonna be really kind of your key, and then your MRI. So you need to include a merchant and notch view to help increase the percentage of diagnosis, because you can see some of them in the patella femoral joint, and again, with the notch view, sometimes you'll see more of those posterior ones a little bit easier. You need to image both knees, as it can be bilateral in 25 to 30%. The MRI classification is based on the T2 images. So stage one is thickening of the articular cartilage and low signal changes. Stage two is articular cartilage is breached, low signal rim behind the fragment indicates fibrous attachment. Stage three, this is when it really becomes unstable. The articular cartilage is breached, there's a high signal change behind the fragment indicating synovial fluid between the fragment and the subcaudal bone, and stage four is a loose body. So again, the signs of instability, or you're gonna see this radially oriented hypo-intense signal at the margin of the OCD on the cartilage. That means that you have a fracture line in the cartilage. The big thing is if you see fluid, like same as the synovial fluid behind the piece, that means that that's within that interface between the parent and the progeny. And then if you have edema within the parent bone, that means it's moving and it's causing some irritation. Best chances for non-operative management, this comes up again and again and again. They want you to know which ones you can treat non-operatively. If you have a skeletally immature patient with substantial growth remaining, so if you have open growth plates, and again, it's a stable piece with no mechanical symptoms, no MRI signs of instability, smaller lesions, no cystic changes, then you can consider the non-operative treatment for these patients with good success, about 60% healing rate. And it's typically six months of non-operative treatment. So the other stem portion is if they've tried this and they still have pain and discomfort, then you know that they've done this and you're thinking more surgically at this point. Non-operative treatment, this is just kind of what it can look like, but it's really activity modification, whether you use or don't use immobilization. But it's really taking them out of the activities, making sure they're pain-free, and then as you see some healing, slowly increasing some of their activities. Again, you don't need to memorize this, just kind of working diagnosis. We'll just walk through this. When you think of OCD lesions, first thing, is it stable or unstable? If it's stable, you want to think about, are their growth plates open or closed? If it's stable and they're open, you can try conservative management. If it fails, you're thinking about drilling. If it's stable and they have closed feces and they're symptomatic, that's the big thing, they're symptomatic, then you're gonna go down the pathway of drilling. If it's unstable, then you really need to think about, can I save the piece or can I not save the piece? If you can save the piece, you fix it. If you can't save the piece, then it really goes down that same cartilage algorithm, is it big or small, how much bone is involved? So surgical treatment against stable lesions, you can drill, whether you go transarticular or retrograde, it doesn't matter, they both have excellent results, so you're not gonna ask you the difference between the two. For unstable lesions, the wrong answer is always just to remove the fragment only. There's lots of literature showing that that is the worst result for anyone, is just remove the loose body without doing any treatment to the actual defect. So if you just have that as an answer, you can eliminate right off the bat. Short-term results are good, but again, long-term results are very poor. If the fragment is salvageable, best is to fix it, you can use drilling, you can use bone grafting, again, healing is anywhere from 70 to 100%, and they're not gonna really ask you bioabsorbable versus metal implants, both of them work, both of them have some drawbacks. The main drawbacks for bioabsorbable is you can get some implant failures or cyst formation. With metal ones, you can get artifact and you may need to remove the screws, especially if it subsides. If the fragment is not salvageable, then you're thinking OATs or microfracture for small lesions, OATs may be better in the long-term, especially if there's more bone involvement. ACI and osteochondralografts for large lesions. So in adult OCD, symptomatic lesions are always treated. Higher risk for developing arthritis if they're left untreated, and this is proportional to the size of the lesion. This is just kind of thought process for adult athletes, but the big thing here is you may incidentally find an OCD lesion and they have no symptoms, well, we're not treating that if they don't have symptoms. And those are someone that you're gonna observe. But again, if you find out that they are having symptoms and it's a stable lesion, then sometimes you can get them through that season. If it's an unstable lesion, then you're going towards surgery on a more acute basis. Let's go through a couple of questions here. Here's a 13-year-old male who presents with knee pain that was first noted following a contact injury sustained during a football game one month prior. He was able to return to play within a week of injury, but has since had persistent pain, denies any locking, catching station, and he has only pain with activities. His exam has a trace effusion, medial joint-sided pain. His radiograph is here. What is the best predictor of a good outcome of non-operative treatment? So we're already wanting what is the best treatment, what is the best outcome for non-operative treatment? Is open growth plates. So we see that this person is skeletally mature. They have open growth plates. That is gonna be really the key things that we wanna see here. Next, we have a 13-year-old male soccer player who presents atraumatic knee pain, no mechanical or locking symptoms. Physical exam reveals a stable knee with an effusion. Radiographs and MRI scans are shown here. What is the most appropriate treatment? Pretty much looks like the same x-rays. So we see an OCD lesion on the lateral aspect of the medial femoral condyle. This is a skeletally mature patient. He has no mechanical symptoms or locking, so we assume that this is not an unstable fragment. This is what it looks like on MRI, and our assumption is correct. So we don't see that really white fluid underneath the piece. We see the cartilage layers intact. So this is an ideal person, again, for non-operative treatment because of the open growth plates. So that's what we really want you to go through here. So non-operative treatment, including activity restriction. 17-year-old male high school basketball player presents one year history of pain, swelling, so already know it's chronic. It was previously treated with non-operative and protective weight bearings, so they've already tried that over a six-month period. So they failed what we would have potentially thought. What is the next appropriate treatment for the patient? We see that they're skeletally mature, so we know that we're already thinking about that. They failed conservative measures, and you can also see a fragmented piece. So what they really want you to kind of pick up here, it's a fragmented piece that's failed conservative measures, so we're already thinking of surgical management, and then we're looking at what are the answers. Open reduction intervixation, likely not the best treatment choice because of the fragmentation. ACI can be an option, but they would have had to put something like bone grafting at the same time because of the thickness and how deep it is. Juvenile cartilage, allograft transplantation. As we talked, that is always the wrong answer because it's not proven yet. Placement of ossochondroallograft, definitely a good thought process because we're addressing both bone and cartilage, and it's a big defect. Orthoscopic-assisted retrograde drilling. Again, this is an unstable fragment at this point, so you know that that would not be the right treatment choice, especially if it's not fixed at the same time. So they really want you to go towards that ossochondroallograft in this type of situation. All right, last one. How am I doing on time? Good? Great. All right, so synovial disease. So here's the key points for the test is understanding the aspiration, as we all know, just from treating our patients. Pigmented villanodular synovitis, synovial chondromatosis, and inflammatory conditions. So normal synovium has two distinct layers. The intimal layer, which are synovial sites which produce our synovial fluid content, and the sub-intimal supportive layer, which is the fibrous adipose tissue with a rich capillary network. Synovial sites in the intimal layers are of two types. The type A, which is about 25% of them, are tissue macrophages. So these are really kind of clean up everything. The type B secrete are hyaluronate, and they really are rich in all these Golgi complex and the enzymes to produce that. Synovial fluid is a dialysate of blood plasma, has no clotting factors, no red blood cells. It's primarily hyaluronate and lubricant. The function is joint lubrication, and it's under two different forms, which we'll go in the next two slides. It has non-Newtonian flow characteristics, and the viscosity coefficient depends on the shear rate. So the two different types of lubrications are the elasto-hydrodynamic. This is the primary mechanism. So under condition of loading, the cartilage undergoes elastic deformation, and it spreads the joint load over a larger surface area, and this really decreases the shear rate. The boundary lubricant works best when the fluid film is depleted, and this is really due to the lubricant. So there's a monolayer of the glycoprotein, and that's absorbed on the opposing articular surface, and this provides cushioning and protects against the abrasion. We're looking at synovial fluid analysis. We're thinking of gram staining and culturing for bacteria. Obviously, with septic arthritis, anything over 50,000 white blood cells, we're thinking about a potentially septic joint. Gout and pseudogout, the white cells can be high, but it's usually less turbine. Crystals, so if we get crystal analysis, they're gonna want you to know about gout and pseudogout, so negatively birefringent needles and polarized microscopy is gonna be gout. Rod-shaped or rhomboid shape with weak positive birefringence is pseudogout. Here's the characteristics of synovial fluid. If anything comes up on the test, it's typically just that septic arthritis. That's gonna be the one that commonly comes up on the test as far as what you need to know. Again, over 50% WBCs, or 50,000 WBCs, over 75% PMNs. What are some of the synovial-based knee disorders? Synovial chondromatosis, pigmented villanotary synovitis, again, gout and pseudogout, we'll go through all those. Synovial chondromatosis is a monoticular, synovial, proliferative disease characterized by conversion of the cartilaginous tissue to ossified loose bodies. It's most often in middle-aged men. You can get pain, limitation of motion, mechanical catching, clicking. Most common is a knee followed by the elbow. There's different stages of this, in classification, early, where you won't see any loose bodies, transitional, where it's a very active synovial disease and loose bodies are seen, and late, where there's loose bodies but no synovial disease. You typically can see these on x-rays, and if the x-rays are negative, you may see them on MRI. The treatment is complete synovectomy. The recurrence rate is about 25%. PVNS, this is the one they, if they show you the other one for synovial chondromatosis, again, they just want you to clean up the loose bodies. For pigmented villanodular synovitis, they do want you to know a few other things. This is a slow-growing, benign, locally invasive tumor. It usually presents as a monoarticular hemarthrosis. Patients may have mechanical symptoms of effusion. Most often involves a knee. It can be nodular or diffuse. It's typically low signal intensity on all sequences, both T1 and T2. They may have a hemorrhagic, dark brown synovial fluid, and the biopsy is typically diagnostic. The diffused form or nodular form is less common and is less destructive than the diffuse form. The histology, the big thing here, it's similar to giant cell tumors. You're gonna see multinucleated giant cells. Treatment is a thorough synovectomy. Arthroscopy is most effective for those nodular forms, and it can often be curative or the inactive form of the diffuse disease. You must address the posterior compartment if you're gonna do it arthroscopically. Low-dose radiation therapy has been used as an adjunct. Open synovectomy can be considered for those with diffuse disease. The diffuse form has a high recurrence rate, and total knee arthroplasty can be indicated, especially if destructive changes in the joint. I put this up here because, again, on the longitudinal assessment, this is one of the articles that they had that you can choose from. So what they want you to know is really the recurrence rate from PVNS and looking at both the arthroscopic or adjunct type of treatment. So this is for more of the diffuse type of ones, that lower portion there. If you did an arthroscopy only, you had the highest risk of recurrence rate. If you did arthroscopy with adjunct of radiotherapy, then you actually reduced that rate significantly to about 12%. Also, similarly, if you had an open, I'm sorry, an arthroscopy with an open procedure, that also had better results. So the big thing here with the diffuse form, if it comes up on a question, they're gonna want you to either say you're doing an arthroscopy with an open procedure or arthroscopy with radiotherapy. Gout is deposition of monosodium urate crystals in the bursa and synovial membranes. Often, it's first attack is the first MTP joint. It's more common in men age 30 to 50. If you see gout in women, you really need to be thinking about a detailed workup of the enzyme deficiency. So that would be really the key thing if it comes up as a woman. Clinical presentation, it typically remits and recurs. After the first episode, two thirds of patient will have a second attack within the first year. There's a high rate of recurrency, especially postoperatively. Synovial fluid analysis, you'll have negatively birefringent eel-shaped monosodium urate crystals. That's really the key thing they want you to know about. Acute treatment is with indomethacin or colchicine. Chronic treatment can be with allipurinol or probenicin. Pseudogout, it really mimics a lot of what gout can do. This is a calcium pyrophosphate dehydrate deposition. It's typically for age over 50. You can see chondrocalcinosis of the meniscus. It occurs, again, in older age groups. It is associated with other metabolic disorders, and that's just something, again, they may not ask you all the different ones, but they may ask you if it's associated with other metabolic disorders. You'll see weak, positive birefringency of rhomboid shape. Treatment is typically aspiration of the involved joint and a steroid injection. You need to rule out any type of infection. Again, indomethacin can be used. Colchicine is not as useful in this type of condition, and surgical lavage can be beneficial if you have refactored cases. Briefly, we'll talk about inflammatory arthritis, as this typically is not as much of an issue that we have to deal with anymore with some of the newer drugs. So rheumatoid arthritis, lupus, inflammatory bowel disease, arthroscopic synovectomy may be used in conjunction with the medical management, and the results of the treatment related to the degree of cartilage degeneration. So we'll go through a couple of questions, and we're all done here. A 36-year-old female runner presents to your office with a history of worsening right knee pain over the previous five months. In addition to pain and swelling of the knee, she has multiple episodes of catching and locking of the knee. No history of trauma is noted. On physical exam, she has an effusion of the knee with a range of motion from zero to 85 degrees of flexion. She has crepitus throughout range of motion. The rest of the exam is otherwise normal. Radiographs are shown here. What's the most appropriate next step? So what they want you to see here, again, loss of motion, locking, and you see all these kind of pieces, loose pieces in the back part of the knee. So this is synovial chondromatosis. Again, by x-ray. So what they really want you to be thinking about, again, is removing the loose pieces, restoring their motion. And so that's gonna be the answer here. Here's a 25-year-old female comes to your office in 12-month history of medial knee pain. Pain is intermittent and associated with increasing running. Pain improves with rest and worsens with increased activities. On physical exam, she has medial pain is medial and has a mild click when going from flexion extension. After failing, conserve treatment. So again, that's your stem. So they failed that. So you're already thinking about, okay, what are we thinking about surgically? Wants to undergo arthroscopy. The image is seen here. What is the best treatment option for this patient? So we really didn't cover this, and this has really been on some of the self-assessment questions. I've not seen it, and it wasn't on my test. But this is a medial plica. She's kind of have that classic plica syndrome. And so you're gonna be talking about debreeding that plica. All right, so guidelines. Remember focal problems need focal treatments, while regional problems like arthritis need regional treatments. Never change a winning game. Always change a losing game. So always look for that six month of failing of physical therapy or conserved measures. Try to save native articular cartilage whenever possible. Fix acute osteochondral fractures and salvageable OCD lesions. I think if you keep some of these key points, you will get every one of these questions correct. I wanna say a big thank you to my fellow. I flagged, when I studied for this two years ago, all the questions related to my topic. So you have every question from self-assessments over the last, I think, six to seven years concerning this topic for your own study, okay? All right, good luck. Thank you.

synovial disease

pigmented villanodular synovitis

synovial chondromatosis

inflammatory conditions

complete synovectomy

gout

pseudogout

inflammatory arthritis

arthroscopic synovectomy