I'd like to thank everyone who has joined in to hear me talk about patella-femoral meniscus for the AOSSM board review course. My name is Latul Farrow. I am director of sports medicine clinical operations at the Cleveland Clinic. I'm also program director for the orthopedic sports medicine fellowship program. These are my disclosures and they can be found on the AOSSM website. This is a brief outline of what we will be covering anatomy, biomechanics, history, physical examination, conservative management, operative management, and conclusions and presenting the evidence-based literature related to both patella-femoral pathology as well as the meniscus. We'll start with patella-femoral. So, as we all know, the patella is the largest sesamoid bone within the human body. Its shape is that of an inverted teardrop. Medially and laterally, it is bound by a soft tissue retinaculum, which helps provide stability for the patella and the medial and lateral facets articulate with the femoral trochlea. We can see the osseous anatomy of the patella where the inferior portion is actually non-articular and essentially encompassed by the quadriceps, sorry, the patellar tendon. The posterior surface, the superior three-quarters, is really the articular surface, and in most patella you can find a medial facet, a lateral facet, and a central ridge. The odd facet is not as common, but certainly present in some individuals. We should all be familiar with the Weyberg classification, and it essentially looks at the shape of the patella. In type 1, we can see to the far left, the facets are equal. In type 2, the medial facet is smaller than the lateral. In type 3, there's a very small medial facet. And in type 4, there's no central ridge or medial facet. And we know form follows function, so it's highly likely that these patella shapes are highly associated with dysplasia of the trochlea. The more dysplastic, the less presence that you have with the medial facet. Speaking of the femoral trochlea, it has a central sulcus, and then it also has medial and lateral facets that are highly congruent with the patella. In normal knees, the lateral facet is much more prominent than the medial, and these are highly congruent with the patella itself. Passive and active restraints are important for the patella. The patellar tendon is one of the main passive restraints distally, and where that attaches to the tibia is very important for instability. The lateral retinaculum that we can see here actually imparts some stability to the patella also, and we'll go over that later. And then a deeper layer to that, the IT band, the epicondylar band of the lateral retinaculum, or what some people call the lateral patellofemoral ligament, and then there are also some ligaments that travel from the patella down to the meniscus as well as the tibia, and these are all important stabilizers of the patellofemoral joint. With respect to the medial side of the knee, the NPFL is really the workhorse, and it attaches to the upper two-thirds of the patella. This is important anatomically as well as surgically, and we'll go over that later. It has two distinct portions, the medial patellofemoral ligament, which provides 50 to 60 percent of the restraint to lateral displacement of the patella, and also there are medial patello-tibial ligaments, which provide 24 percent of the restraint to lateral displacement of the patella. And we can see here some of the cadaveric anatomy here, so this is the medial patellar meniscal ligament here, this is the NPFL, which lies near the medial epicondyle as well as the adductor tubercle. Approximately the quadriceps tendon comes in to attach to the superior pole of the patella, and this is the common tendon that is the common tendon for both the vastus lateralis, the vastus medialis oblique, the rectus femoris, and the vastus intermedius. And importantly, the VMO attaches at about a 55 to 70 degree angle to the patella, and this also helps with dynamic stability. So patellofemoral question one, a 24-year-old female presents to the emergency room with increased pain and swelling following an arthroscopic patellar chondroplasty lateral release for lateral patellar overload syndrome the day before. On exam, she has significantly swollen knee. What is the most common cause of her pain and swelling? The medial geniculate injury, swelling from tourniquet use, arthroscopic fluid extravasation, blood contusion, or the superior lateral geniculate injury. So the superior geniculate artery, superior lateral geniculate artery, is very important, and an overzealous release of the lateral retinaculum can result in hemorrhage and complications related to that. So question two, a 17-year-old soccer player has a first-time lateral patellar dislocation last year. He was initially treated conservatively but developed recurrent patellar instability. What is the primary stabilizer of the patella beyond 30 degrees of flexion? The lateral retinaculum, the NPFL, the lateral facet of the trochlea, the lateral patellofemoral ligament, or the medial retinaculum. So the lateral facet of the trochlea, so the NPFL is really shown to be the primary stabilizer at more lesser degrees of motion from 0 to 30 degrees, but typically around 30 degrees of flexion, the patella, the osseous anatomy becomes the primary stabilizer once it engages the trochlea. The patellofemoral biomechanics. So as we know, the patellofemoral, sorry, the patella actually acts to increase the movement arm of the quadriceps mechanism, patelectomy, which has largely fallen out of favor because it decreases the quad torque quite substantially, and this is most pronounced between 10 and 30 degrees of motion, but this can decrease at least 40%. The stability of the extension mechanism under load is also assisted with the patella trochlear articulation, and then this helps to centralize the quad force from these four muscles that come in into the quadriceps tendon, and then carries that down to the tibia, and so a very important function from that. It also helps to shield the femoral articular surface. So as mentioned, the patella increases the movement arm of the patella, and this is only 10 degrees at full flexion, so that's when the patella is actually not in the trochlea, it's actually distal to the trochlea, and this is maximum at about 45 degrees of knee flexion, and this increases the movement arm by 30%, and this diminishes from 45 degrees to full extension. So the quad force to achieve full extension against gravity after patelectomy is increased 15 to 30%, and that's largely why this procedure has fallen out of favor. So we look at contact area as the patella travels distally, so as the patella goes into flexion, the contact area travels from distal to proximal with flexion, and we can see that in the diagram to the right, and the medial facet only articulates at higher flexion angles, and we can see that there from our schematic, and as mentioned before, at 90 degrees, the quad tendon articulates with the femur. So we look at patella femoral joint reaction forces, and we can see that near 40 to 50 degrees of knee flexion, the force really takes off, and so when we talk to patients about patella femoral loading activities, typically if they stay within a fairly low range from zero to about 45 degrees or so, they can actually still strengthen the quads without providing too much stress to the quadriceps mechanism, and that can be really helpful for our patients with patella femoral pain, and we know that contact pressures are increased by things like increased Q angle, and it's again most pronounced between 35 and 70 degrees of knee motion. So joint stability depends somewhat on the Q angle, also depends on lateral trochlear steepness, tone and strength of the vastus medialis oblique, and also the patellar tendon length. Patella typically engages the trochlea somewhere between 20 and 30 degrees. When you have patella alta, that engagement doesn't happen until much later, and that can put a lot of stress onto the patella femoral joint and also the ligaments which are associated which are primary stabilizers. So we know the quad angle is the angle between the anterior superior iliac spine carried down through the patella, and then the angle made by the line drawn through the patella and down through the tibial tubercle. So we can see as the pelvis gets wider, this angle can increase. Certainly with lateralization of the tibia, the tibial tubercle, we can also see how this can increase, and we know that the Q angle is normally much elevated in women compared to men, normally somewhere between 10 and 15 degrees. Women it's somewhat higher. And abnormally high Q angles can lead to increased patella femoral contact pressures and unpredictable loading patterns and also increased risk of instability. So we look at joint compressive forces across the patella femoral joint. Normal walking, zero to five times body weight, and that's a lot of times why your runners may not actually have a whole lot of issues with patella femoral arthrosis, but when you go upstairs or running up hills or going up and down stairs, you get two to three times your body weight, and with deep knee bends, seven to eight times your body weight can go through the patella femoral joint alone. So question number three, a 44-year-old man presents to your office with increasing anterior knee pain after returning to his weekly basketball game. His pain is activity related and is most painful at the end of activity, but it persists for several days thereafter. Physical examination demonstrates no effusion, full range of motion of the knee, and a stable ligamentous examination. There is discrete tenderness at the inferior pole of the patella. Radiographic examination demonstrates only mild narrowing of the medial compartment joint space, but otherwise normal appearance. As you are instructing the patient, you advise him to begin physical therapy and to consider avoiding certain repetitive motions. Which of the following is most likely to aggravate his pain? Deep press machine between 20 and 40 degrees, an elliptical machine, squats past 90 degrees of flexion, hamstring curls, or running on a treadmill. So squats past 90 degrees of flexion, so you go from full extension, you go past that very painful zone between 45 and 60 degrees, and then down into deflection, so that helps to explain exactly why this question is answer C. So what about the patella femoral history, which is probably the most important part of the patella femoral workup? So with our patients with pain, pain is most likely, most commonly occurs at the anterior medial knee. Some patients will tell you it's behind the patella. It can be at the medial joint line, so it's the great masquerader, and then very rarely patients can actually feel pain in their popliteal fossa, so that's referred pain. And typically this is activity related, so squatting, typically patients will tell you it hurts worse going downstairs as opposed to going upstairs. Things like skiing, and then biking uphill. And what I call the movie theater sign or the airplane sign, so patients sit with their knee bent for a long period of time, that can actually increase their pain. So most commonly, again, we see the pain with squatting, but again, joint line pain is not uncommon with these patients. So just because it's patella femoral does not necessarily rule out joint line pain. Most commonly, again, we see a lot of medial parapatellar pain with respect to the location. So what about instability? So patients can say my knee dislocated, and obviously that's much different than what we think about with traumatic knee dislocations, and they can say their knee popped out. So a lot of patients won't say that their kneecap popped out laterally, they actually say medially, because that's a kneecap goes laterally, they actually see the prominent femoral condyle on the medial side due to the displacement of the patella, and that's what they sort of relate to what's sort of popped out. This can happen with a pivoting or twisting mechanism, they feel that the knee buckles, collapses, knee bent forward, and this may be followed by pain and swelling if it's a true dislocation. So lateral dislocation or subluxation is most common, this can be indirect versus direct. The indirect mechanism is most common, so planted, twisted, patella dislocated, happens with strong quad contraction, typically happens in somewhat of a flexed knee, it's an internal rotation of the femur, and external rotation of the tibia as the foot stays planted. So our direct mechanism, so this is something that we see commonly in football, so direct blow to the medial patella, patella pops out. This can resolve spontaneously, so it goes back on its own, or it can go back with a closed reduction. So after going up for a layup, a 15-year-old male lands awkwardly on his left leg, he remains on the court in tremendous pain and is unable to extend his knee. Initial assessment shows intact motor and sensory function to the foot and palpable pedal pulses symmetric to the contralateral side. So there are two figures, what is the next step in management of this injury? These are our figures here, so we see this forward-facing view and then sort of this equilateral view. So urgent transfer to the nearest trauma center for a CT angio and possible vascular procedure. Urgent transfer to the nearest trauma center, planning for open reduction in internal fixation and intramedullary nailing, closed reduction by gently extending the knee and applying slight lateral pressure to the lateral aspect of the knee, ice and immobilize the knee followed by outpatient orthopedic follow-up, take the player to the bench and reassess at halftime. So what we see is a lateral patellar dislocation and the closed reduction maneuver with this is gently extending the knee and applying slight lateral pressure and the knee should go back into place and the patient will feel much better about that. So what about patellar subluxation versus dislocation? So subluxation is alteration in normal tracking, but the patella remains in the sulcus and in dislocation, the patella completely dislocates out of the sulcus. Physical examination. So predisposing anatomic factors, femoral anaversion, genu-valgum, patellar dysplasia, femoral dysplasia, patella alta, VMO atrophy, high Q angle and then pes planus and generalized hyperlaxity. We see in this patient very valgus knees. So standing exam is very important, this can assess for either genu-verum or genu-valgum. We can see in the picture to the far right, the upper picture and the lower picture show rotatory malalignment. So this is a patient with tremendous femoral anaversion and we can see with her feet pointing forward, her patella should also be pointing forward, but what we can see here is that her patellas are actually pointing towards the midline when her feet are pointing forward. In order to get her patella pointing forward, she has to externally rotate her lower extremities and her feet are now pointing outwards. And so this is malalignment. And when I remind people of children with miserable malalignment, so increased femoral anaversion and external tibial torsion, they turn into adults or teenagers with miserable malalignment. So that can certainly be a part of the exam that we see here. She may have decreased quad tone. And then in this patient on the picture to the left, she has significant pes planus and a valgus hind foot. So we can see here her alignment, so leg and then her heel. So a lot of valgus, pes planus. This is not a good situation. So the seated exam. So we want patients to actively extend and we can evaluate patellar tracking. We can see when the patella engages or not, whether it's dislocating an extension or whether it dislocates inflection. We can also evaluate the J sign, so the rapid displacement of the patella. And this is what I call the poor man's Q angle here. So this is a poor person's Q angle. This here is a marker on the patella, another marker on the tibial tuberosity. So when you draw a line between the medial and lateral epicondyles, so the trans epicondylar line, and then you drop this plumb line from the patella down to the tibial tuberosity, this is much less than 90 degrees, and that's abnormal for these patients. So that certainly is an easier way of doing a quick and dirty Q angle if you don't have a goniometer in clinic to do a formal Q angle. So the supine examination. We want to test the apprehension test, and again, we see this person providing a medial pressure on the patella to dislocate or glide the patella laterally. We want to press down the patella and compress that into the trochlea to assess for patella femoral pain. And normally, when we look at the amount of glides, the bottom right picture should have about two quadrants of glide, both medially and laterally. That's pretty normal for the most part. We can also assess patella tilt to assess whether they have tightness of the lateral retinaculum. So what about imaging? So plain film images are key for these patients. Standard series may include an AP, a lateral, and then axial views or merchant views or sunrise, and then advanced imaging if necessary. So weight-bearing plain film AP, not a whole lot of value with this. It can show you patella magna or parva. It can look at bipartite patellas. Also important for fractures and marked subluxation, but really low yield for evaluating the patient patella femoral pain or instability. The lateral view has the most information, even more than your merchant or sunrise view. This should be done at least 30 degrees of flexion, avoid malrotation, so get the condyles lined up, and then you can determine patellar height through a lot of different methods. So the InStyle Salvadi method, this looks at patellar tendon length and then dividing that by the cross length of the patella here. Lengthing over 1.2, so obviously this is the numerator. So the longer this is, so this patella obviously doesn't change, but the longer this is, then the higher that number becomes. And likewise, the shorter the numerator is, then the lower this number comes. So patella infero, which is previously known as Baja, and these are the normative values. The Blackburn and Pill Ratio is another one. Some people prefer not to use this because this can be altered by tibial slope. But again, looking at this distance between A divided by the articular surface B and again norm was 0.8, so probably one of the less popular methods. And then the Ketan Deschamps index, this is my workhorse and a lot of people within the patella femoral world also utilize this. And in this, you draw a line from the inferior articular surface to the tibial plateau. So this is better than Blackburn and Pill because the tibial plateau angulation does not come into play or slope does not come into play. And then that's divided by the articular surface. So the higher up the patella gets, the higher this number becomes. And so any value over 1.2 to 1.3 is considered alta, anything lower than 0.8 to 0.6 is considered infra. And again, this is, I think, has more reproducibility and it's really a very popular method to Ketan Deschamps. So more on the lateral side. So again, with the lateral x-ray, a lot of information seen here. So we can see the sulcus of the patella of the trochlea. So when you measure from the trochlea to the sulcus to this here, that tells you how much trochlear depth that you have. You can evaluate for crossover sign approximately. You can see the patella ridge. You can see the facets. And again, just gives you a lot of information. So you can say our patient is plastic. Are they alta or not? Is there OA in the knee? A lot of different things that you can see from a good lateral x-ray. This is an example. We can see the crossover sign, which then represents the base of the trochlea. So when the base of the trochlea crosses over the condyle, that's considered a crossover sign. So that's consistent with the dysplastic trochlea. We see in a normal setting that the trochlear depth never crosses over the condyle. So this is a nice deep groove on the picture up top, normal. So merchant view should be done about 45 degrees of flexion. Still gives you some good information. Certainly, we can see the sulcus angle here, which should be less than 150 degrees. So as you can see, the more dysplasia that you get, the wider that angle will be. And then when you look at the congruence angle, you basically bisect this angle here. And then you draw a line to the apex of the patella. If that line is medial, that's a negative value. If that line is lateral, that's a positive value. So negative is good. So we want negative. So in terms of community tomography, I will measure my TTTG distance most commonly on MRI. But I used to get CT, CT, dynamic CTs all the time. Really fall out of favor in my practice because I found it was not necessarily changing my management unless we have really complex instability or pain patterns. And this is typically measured in extension. And sometimes you can also remeasure this inflection. Greater than two centimeters is typically abnormal for the TTTG distance. And if you are going to do this by MRI. Just remember MRI underestimates by about five millimeters. So if you have a TTTG on MRI, which is 19, the reality is if you got a CT, that may be as high as 24. So just kind of keep that in mind. So the CT can evaluate all these things. So the trochlear dysplasia, patellar tilt at a much higher level. So certainly for some complex pathology, it can still be utilized. So what about treatment of patellar instability? This is our algorithm. I'll leave that up for just a second here. But essentially, in our patients with subluxation, you really want to trial rehabilitation for these patients first. And if they fail that, then consider reconstructive options. When they have a lateral dislocation, no osteochondral fracture, young patient, no predisposing factors, or older patient, no predisposing factors. That's somebody you can rehabilitate and then fix or reconstruct if they fail conservative management. If there's an osteochondral fragment, then that leads patients to arthroscopy and stabilization for any recurring dislocator. And that's really affecting their lifestyle. Really consider MPFL reconstruction. So conservative treatment, close reduction. So extend the knee, gentle pressure on the medial lateral side, direct it medially. And then mobilize an extension for some authors, three weeks in a hinge brace. And then weight bearing is tolerated and immediate quad strengthening. More of a accelerated program. You can get a patient into a knee immobilizer acutely just for a few days, maybe a week or so. And then get them over to a patellar stabilizing brace right after that and start full motion right away. And that you can get patients back to activity a little bit quicker than sort of this more conservative approach with respect to rehabilitation. So what do we know about the numbers? So about 50% of patients will re-dislocate or subluxate again after a first dislocation. But only 33% of people will ultimately fail conservative management. So that means about 17 to 20% of people will be copers, meaning that they dislocate or they subluxate. It only happens once a year, once every few years. They can live with it, does not necessarily bother their day-to-day functioning. So pay attention to this article. This is important. So this is looking at systematic review and meta-analysis of all the available literature out there. So 17 studies, a lot of patients, and they found a re-dislocation rate somewhere around 34%. And they kind of looked at what are the factors most responsible for dislocation in the young, sorry, in the first time dislocator. So young is important. Open physis is important, which again is young. Trochlear dysplasia gives the highest odds ratio at 4.15. So elevated TTTG, so rotatory abnormalities, and then patella alta, but really the biggest effect with trochlear dysplasia. So these authors came up with a system of risk stratifying. So if a patient has no risk factors, so they're male, they're older, no dysplasia, no rotatory issues, they have a low risk of ever dislocating again. Likewise, if they're young, the growth plates are open, they have a high TTTG, they're alta, and they have trochlear dysplasia, that's a patient that they probably have well over 80% chance of re-dislocating. So you may want to move towards surgery sooner than later in those patients. So question five, patella femoral. A 15-year-old female presents to your office complaining that her knee is loose and that it buckles. She denies any trauma and reports that she has had her knee come out of place with abrupt turns. On physical examination, she has signs of hyperlaxity. She has increased lateral patella glide and a J-sign. Which of the following imaging findings is most likely? A TTTG distance greater than 20, Sulkin's angle less than 145 degrees, blackburn and pill ratio less than 0.8, Weiberg A patella intact MPFL. Oh, essentially all the other answers were normal and TTTG distance of 20 millimeters is the correct answer. So question number six, a 13-year-old female presents to the office after twisting her twisting injury to her knee five weeks ago in which her patella dislocated and was manually reduced. This was the patient's first instability event. She is asking about her risk of recurrence and whether she should have surgery to prevent another event. Compared to asymptomatic individuals, what radiographic finding is the most likely to be present in this young athlete? So trochlear depth less than three millimeters, elevated TTTG distance, patella alta greater than 1.2, patellar tilt or elevated tibial tubercle to PCL distance. Trochlear dysplasia depth less than three millimeters. And again, when you look at morphological characteristics between normal and people with lateral instability, this was probably the most common finding was trochlear dysplasia less than three millimeters. Very strong effect. So what about the surgical anatomy? So MPFL attaches somewhere between the adductor tubercle and the medial pacondyle. It's a very thin kind of wimpy ligament. Some of the new literature that has come out looking at not just the MPFL, but really probably more commonly, and we should more appropriately call this the medial patellofemoral complex, because this is not only made up of the MPFL, but also the MQTFL. So the medial quadriceps tendon tendofemoral ligament. And so this is the portion of these medial stabilizers that attaches to the quadriceps tendon and goes down to a common attachment site on the femur. And this is done by Miho Tanaka as well as Jorge Chalaf. And we can see here some of that very elegant dissection in both pictures. Proximal was above us, distal was beneath us, and we can see that this whole complex actually attaches right along the quadriceps tendon, as well as the patella. And actually found that the midpoint of this whole complex was actually above the patella. So that's kind of food for thought and very important when looking at anatomy and reconstruction of the MPFL. So this is an important paper also looking at the anatomic sites for placement of your anchors. So on the patella, you really want to be up towards this upper, at least upper half, upper third, but the upper portion of the patella with your anatomy here. And we can see when you lift up the VMO, MPFL actually runs underneath the VMO on its way to the quadriceps tendon. So this we can see here. And if you are going to place anchors, patella is important, but the femur is much more important. Or if you're going to drill a tunnel, sorry, but fixation on the femur is also very important. So if you place your fixation proximal, that's bad because that can lead to a tighter graph going into flexion. So you want your graph, if anything, to loosen up as you move into flexion. So if you're going to air, so air distal, but really want to be right at this point, which correlates to what we refer to now as Schottel's point. So these are isometric or loosening flexion, so that's a better place to be. So avoid proximal placement on the femur. So Schottel's point is the anatomic attachment side of the femur and is made by drawing a line along the poster cortex of the femur. And then another line perpendicular to that at the level of the poster aspect of the condyle. Another line can be drawn with this also at the poster extent of Blumenstadt's line, but really these two lines are what's most important. And it approximates the area of anatomy of the MPFL femoral attachment. And in kids, this is beneath the growth plate. So on the lateral, it looks like it's at the growth plate. But on the AP, we can actually see that it's actually well beneath the growth plate, anywhere from six to nine millimeters, essentially. And what we're seeing on the lateral is actually the undulating portion of the growth plates here that makes it look like we're right at the growth plate. So acute operative management. So acute arthroscopy for large osteochondral fragments. And a lot of these are not seen on x-rays, so you can make an argument for doing an MRI for all these patients with dislocations. Not necessarily required, but certainly food for thought. Most of these fragments are not repairable, but yes, acute arthroscopy and fixation for large repairable osteochondral fragments. Do not throw those in the trash. You can fix most of these, even if they're mostly chondral. So question number seven, a 17-year-old football player twists his right knee and sustains an acute patellar dislocation. The patella is reduced in the emergency room and he presents two days later in the office. He has a large effusion and radiographs show an osteochondral fragment. You plan to operatively fix the fracture fragment. What is the most likely origin of the osteochondral fragment? Medial trochlea, lateral trochlea, medial patellar facet, lateral femoral condyle, or the lateral patellar facet? So the medial patellar facet. So when the patella dislocates, it's actually this inferior aspect of the medial patellar facet where these osteochondral fragments are almost always from. They can be big, and so sometimes it can encroach upon the other facet, but in general, that's the common location for these. And usually these things are able to be fixed, and they can be either fixed with screws if the bony fragment is large enough. If it's just a common location for these, if it's just a condyle, these can be fixed with trans-osteosutures, and it actually works pretty well. But certainly medial patellar facet and actually the inferior aspect of medial patellar facet. So acute operative management, acute NPFL repair, indications for that. So young athletes with indirect mechanisms, no pathologic anatomy, avulsions off the femur are common. You can repair these directly with suture anchors, but less than 10% re-dislocation rate, depending on what studies you look at. Largely, I think NPFL repair is kind of falling out of favor because certainly Marie Askenberger and others have shown re-dislocation rates upwards of 30% after repair. And so these patients can have persistent pain. So a common question that pops up, does it matter where the ligament injury occurs? It does. So Dr. Salonpa from Finland looked at location of NPFL injury and found that re-dislocation rate was highest when the NPFL was injured at the femur. So reality is good luck looking at an MRI and trying to figure out exactly where this injury occurred. Sometimes we're not very good at doing that, but certainly if you can see a femoral avulsion, those patients are much more likely to dislocate than patients with patellar side of injuries or with mid-substance injuries. So this is also very interesting. So what's our reconstruction technique and indications? So instability with normal osseous alignment for patients who continue to have recurring dislocation and have felt previous distal realignment. So we see a fair amount of patients in our practice who have had TTOs for instability and they continue to be unstable. Surprise. And those patients, you have to address the soft tissues. So 22-year-old woman presents to orthopedic clinic with chief complaint of patellar instability. Her history began several years prior with a traumatic patellar dislocation while playing soccer. She was treated unoperatively and did well until the second dislocation three months ago while playing Frisbee. Since that time, she has experienced significant apprehension and feeling as though her patella would dislocate laterally with any pivoting activity. She has completed six weeks of physical therapy and brace wear without resolution of her symptoms. On examination, she has positive patellar apprehension tests, radiograph demonstrate no abnormalities, and MRI reveals an isolated medial patellofemoral ligament tear. She undergoes medial patellofemoral ligament reconstruction with semi-tendinosis autograft, which of the following is the most common complication of this procedure? Painful hardware, stiffness, patella fracture, infection, or patella persistent apprehension without instability. This is a very good surgery. And of all the things I've mentioned, these patients can continue to have apprehension and that's in exam finding, right? So these are patients and it's almost like PTSD when they've had recurrent dislocations and you fix them. A lot of times you bring them to the office and you move the patella around. They're still very apprehensive about you moving it, even though the patella is rock solid and stable. So that's the most common instability, which is pretty good for surgery, right? So when we look at surgical outcomes, the risk of re-dislocation is extremely low following NPFL reconstruction. When done well, this is a highly successful surgery. So what about other treatments? So isolated lateral release. I don't think it has an indication for patellofemoral instability. Probably should not be ever done in isolation. The results are all over the board. And more importantly, this can lead to iatrogenic medial instability. So we see that commonly probably do somewhere between eight and ten patients a year who had overzealous lateral releases and now have medial instability. So really just stay away from that in the patella instability patient. So one biomechanics study from Ostermeyer et al that we like to mention is that with lateral release, lateral tracking of the patella actually was increased. So beware. And then when we look at this study from Bob Burks and company over at Utah, they looked at, you know, classic literature. You know, this is where that number comes from, from the NPFL. Sixty percent of the restraining force lateral dislocation was from the NPFL. Medial patella meniscal ligaments was 13 percent. And lateral retinaculum, even though it's lateral, imparts about 10 percent of stability to the patella femoral joint. So the lateral retinaculum actually helps to hold the patella down in the trochlea. And remember, when a patella dislocates, it has to come up and out of the groove. So the lateral retinaculum, as the patella tries to come up and out of the groove, it actually helps to tension that and keep it down in there. So that's important. So different treatment options. So what we call proximal realignment. So rearranged muscle pull. So that's where the VMO advancement comes into play. And again, these are patients with failed conservative management, maltracking. And this is not a surgery just for strictly malalignment. And you want to do this in conjunction with NPFL reconstruction. You don't do a VMO realignment or VMO advancement, so forth and so on, as an isolated, standalone procedure. So in conclusion, patella stability is not common, not uncommon, rather. Accurate assessment and diagnosis is key. All patients will succeed with conservative, most patients will succeed with conservative treatment. Approximately one third may require surgical treatment. Appropriate surgical management is indicated by or dictated by anatomic findings if present. So when you see something that's able to be corrected, in my opinion, I think that's the highest rate of success for these patients. Surgical treatment results in low re-dislocation rates. And some of these patients may continue to have pain at long term, but it's a successful surgery, probably one of the most successful things that I do. So question number nine, patella femoral. An 18-year-old female volleyball player had symptomatic recurrent lateral patellar instability in her right knee for greater than 12 months. She has failed extensive non-operative treatment. Her radiograph demonstrates skeletal maturity, mild lateral patellar translation, de jure A trochlear dysplasia with a sulcus angle of 146 degrees and a Catan-Deschamps angle of 1.2. On a CT scan, there's a tibial tubercle trochlear groove distance of 24 millimeters. Given her recurrent instability and failure of non-surgical treatment, she undergoes arthroscopy, debridement of a one square centimeter grade three articular cartilage defect in the lateral patella, and NPFL reconstruction using a double bundle semiteninosis allograft. Upon returning to volleyball six months following surgery, she has multiple episodes of patellar instability. So what is the most likely reason for failure for NPFL reconstruction and recurrent postoperative lateral patellar dislocation? So is it her trochlear dysplasia or patellar alta, her rotational malalignment of the tibial tubercle relative to the trochlea, patellar articular cartilage defect, or placement of the thermotunnel at shuttle's point? So we're going to say this is rotational malalignment of the tibial tubercle relative to the femur, relative to the trochlea. And there's a lot of studies looking at this, that when you have such high TTTG, her dysplasia is actually not bad. Her sulcus angle is 146 degrees. Her CDI, Catan-Deschamps angle is 1.2, so she's not really severely alta, but that TTTG and CT of 24 millimeters is, that gets my attention for sure. So what about bony realignment? Speaking of, so distal realignment indications, so malalignment still in mature patients can't do this with an open apotheosis at the tibial tubercle, lateral tracking, and then recurrent subluxation or dislocation. And there's different ways to do this, sort of medial, medial and anterior, and then distalization. Or straight anterior for that matter. So really the workhorses in our instability patients are medialization, which we know as the Elmsley-Triat procedure, and then anterior medialization, also known as the Fulkerson osteotomy. So when do I add bony procedures? Trochlear, dysplasia, which is severe, revision surgery, significant rotational malalignment, and we also want to offload chondro abnormalities with this. And then if you're ever doing any chondral procedures where the rotational malalignment is present, helps protect your cartilage. So again, TTTG greater than 20 millimeters. If you have lateral facet chondrosis, this can be certainly helpful. Distal chondrosis, so as you do like a anterior medialization or Fulkerson, you offload the distal patella and shift your weight bearing to the medial and lateral, sorry, medial superior patella. And then patients who have revision instability, that's important. So looking at anterior medialization of the tibial tubercle with NPFL versus NPFL alone, it's a great step. What they found for patients with high TTTG, they actually did better with NPFL reconstruction with TTO compared to NPFL alone, even though the NPFL group alone did not have recurrent instability, they found that better function in kinematics with the combined procedure. So don't ignore the rotatory malalignment, and this was not even tremendously high, just 17 to 20 millimeters. So that we can look at their outcome. So Kujala scores with our patella-formal outcome score and then our Lysholm and then IKDC. So question number 10. So 35-year-old recreational volleyball player comes to your office to discuss her chronic patellar instability. On exam, her patella translates greater than two quadrants. She has a moderate crevice from extension to flexion. Her CT of the knee demonstrates the tibial tubercle to trochlear groove distance of 25 millimeters. Her MRI shows significant patellar chondrosarthrosis. You're considering a antiremedialization osteotomy slash Fulkerson to correct the problem. An antiremedialization osteotomy is best indicated in the treatment of which pattern of patellar cartilage where proximal and lateral lesions, central lesions, proximal and medial lesions, distal and medial lesions, or distal and lateral lesions. So distal and lateral is the answer here. And then question number 11 patella-formal. So 20-year-old college of female tennis player presents with four months of atraumatic anterior knee pain. Her season ended one week prior and she has played tennis every day for the past six months. She denies any mechanical symptoms or swelling. On physical examination, she has core and hip weakness. There's tenderness over the lateral patellar facet and Hoffa's fat pad. She has stable ligament exam and no joint line tenderness. Her MRI is shown in figure one. So we see what appears to be some subcontrabal merodema and a fissure in her articular cartilage. So what is the recommended treatment at this time? So four months of atraumatic anterior knee pain. So knee arthroscopy and debridement of the fat pad, anterior medial tibial tubercle osteotomy, activity modification and physical therapy, clinical steroid injection, and a knee arthroscopy and patellar chondroplasty. So again, that's her MRI. So activity modification and physical therapy. So patella-formal pain is likely due to overuse and proximal weakness. There are some findings of fissuring and subchondroedema, but again, this could be an incidental finding. And even if symptomatic, I think warrants first time conservative management because patella-formal stuff can be very difficult to treat, but so certainly should definitely try to get this patient better with non-operative treatment. So what about trochleoplasty? So indication, so severe trochlear dysplasia, de jure B or D, what is the de jure classification all about? This is here an example of that in our de jure A, which is the most common type. So just a flat trochlea, positive crossing sign, but no spur. So in type B, they have a flat trochlea, and they have a crossing sign, and they have a super patellar spur. In type C, they have a very flat groove. They have this sort of medial hypoplasia. They have a double contour sign on x-ray, and they also have a crossover sign and super patellar spur. And in de jure D, which is the worst, so they have everything basically, they're flat, they have a cliff sign, they have super trochlear spur, and they also have a crossing sign. So, sorry, I misspoke. So de jure C does not really have a tremendous super patellar spur. So the Bs and Ds have spurs and are flat, and the As and Cs are flat without a spur. The Cs and Ds have a double contour sign. And again, that just goes along with the medial hypoplasia that we see in both. So these are examples of what we just talked about, but in the actual anatomic specimen, this is a normal trochlea. This is just flat, so like a de jure A, and this is kind of a de jure either C or D, where they have that medial hypoplasia here. So flat with medial hypoplasia. So takeaways, isolated TTO is often not indicated for patellar femoral instability. TTO in cases with TTTG greater than 20 millimeters, so that's our kind of buzz term, 20 millimeters, and the trochleoplasty for high-grade trochlear dysplasia. But reality is, I'm not sure we're at a point now where trochleoplasty is gonna be part of a test question. I think it's still very controversial, so I wouldn't expect that you're gonna see it on the test. But again, if you do see it, revision situations, buzz terms are de jure B and D with a large super trochlear spur. In the type C trochleas and the type A trochleas, the trochlea is already flat and in line with the anterior cortex of the femur. So there's no spur, there's nowhere really to drop the groove because it's already flat. So trochleoplasty is not the option for that. So, extensive mechanism trauma. So different entities. So contusions, I think we're missing a picture here, but there we go. So this happens typically as a direct blow, it can have some potential for significant disability if not treated correctly. Myositis ossificans can form if you don't treat it appropriately. And compartment syndrome can happen. I've been in and around orthopedics for 20 years, and I think I've seen two compartment syndromes in a quad following a quad contusion, very rare. So how do we treat these? Our cadets at West Point and our medical professionals showed us how to do this many years ago before they were put in immobilizers and they were treated and it took forever for them to get back. With this protocol, so essentially, so you see even on the field, they get the athletes put into hyperflexion and what they found initially with the ACEPRAP and hyperflexion, it actually probably helps to tampon out the blood a bit. And then that then in turn decreases the disability from this. And then you get them in this immediately, you treat them like that for over 24 hours. So you put them in this hinged knee brace once you're able to get them out of their uniform and everything. And they found that this actually decreased time for return to play. So it was something like three to four weeks with knee immobilizer treatment. And that got it down to like seven to 10 days when treated with this method. So question whether you should avoid NSAIDs. One of the cases that I saw a quad contusion was on NSAIDs that then developed a compartment syndrome, which is true, true, unrelated, who knows. But you do want to work on passive stretching to the point of pain, but not overstretching. And then begin some isometrics to tolerate it but your typical, you know, rice mechanism, but the hyperflexion is really the key. And outcome wise, this reduces return to play and decreases the incidence of myositis ossificans. So what about apophysitis of the patella tendon? What we also know is Osch-Gutsch-Schlatter. So rest activity modification, when a stretch, the patella tendon straps can help. And this typically will resolve with age as kids get older and the growth plates close and surgery is rarely ever needed for these. So nine-year-old complains of anterior knee pain when running and jumping. It hurts along the patella tendon and there is insertion on the tibia. There's no specific source of injury. He plays in a travel basketball league, frequently playing three to four games per weekend. Examination demonstrates palpable tibial tubercles bilaterally. The patella shows no apprehension and ligaments are stable to examination. Straight leg raises increases the pain. What can be said about the long-term prognosis of this individual disease process? Activity modification is frequently curative and the disease self-limited. Surgery is frequently offered for cases in adults, but not usually in children. Cases arising in early adulthood are usually more severe. Subsequent bony abnormalities rarely occur, even in neglected cases. A predisposition to other injuries such as patellar tendon eruptions are often reported. Activity modification is frequently curative and the disease self-limited. So patella formula 13, question 13. A 12-year-old boy presents to your clinic with three months history of increasing right knee pain. He knows that the pain began at the start of his basketball season and has progressed since then. The pain is worse when he is playing or when he has issues with periods of rest. Clinical examination demonstrates a bony prominence and tenderness to palpation at his tibial tubercle. Radiographs are shown in figure one. So corticosteroid injection, activity modification, ice stretching and strengthening exercises, immobilization with a locked knee brace, surgical fixation of the bony fragment or surgical excision of the bony fragment. And there we go. So activity modification, ice stretching and strengthening exercises. So question number 14. A 12-year-old boy who started playing basketball last season has been complaining of right knee pain. He was seen and evaluated by an orthopedist and diagnosed with Osgood-Schlatter disease. His mother questions whether he will have the same issue on the left side if he continues playing basketball. What is the approximate incidence of bilateral Osgood-Schlatter disease? 35%. Oh, what about tendinopathy? So quadriceps tendinitis is much less common. Superior strength, better mechanical advantage, vascularity might be better, a lot of muscles in that area. And then no impingement that we'll talk about with the patellar tendon. But typically patients have pain at the proximal pole. It's gonna be more insidious and onset and really correlates with a recent activity increase. So superior pole, tendinous palpation, pain with resisted range of motion and extension, hamstring flexibility. So if they're tight, they can have, this predisposes to quadriceps tendinitis. Imaging is largely not helpful, but you can see some calcifications on playing films. And then MRI sometimes can show changes in the tendon, but indications for that for patients with defects or weakness. So non-operative and operative treatment mirrors patellar tendinopathy, which we'll go over. So patellar tendinitis or tendinopathy, very common entity. It's also known as jumper's knee or runner's knee. Any activity with repetitive knee extension. So mucoid degeneration is typically what we see. We don't like calling this tendinitis because generally there's a lack of inflammatory cells, especially later in disease. Although it does not mean they're completely devoid early in the process, they may actually be present. So angiofibroblastic hyperplasia, buzz term, neovascularization, buzz term, increased cellularity, buzz term. So when does this happen? Second to fourth decades. So basketball, soccer, volleyball are common. Greater and taller athletes, maybe because they're playing more basketball and also greater with increased BMI. And this can be associated with RA, gout, or Sending Larson Johansson syndrome. So what's the mechanism of injury? Chronic overuse, probably most commonly. This can happen as an acute episode, but usually it's repetitive phenomenon. The question of whether you're getting some impingement of the patella on the inferior pole and that decreases vascularity and can then lead to tendinopathy. A two-year-old basketball player presents to your office and is worse with activity and at night. It has been worsening over the past two months of the basketball season without any antecedent trauma. Examination reveals tendinous palpation at the inferior pole of the patella that is worse in extension than inflection. Which of the following pathologic findings is associated with this diagnosis? Increased pathophagocytosis by macrophages, increased activated platelets, decreased transforming growth factor beta-1 in cyclooxygenase-2, increased neutrophils, increased cellularity, and angiofibroblastic dysplasia. A lot of big words. Increased cellularity and angiofibroblastic dysplasia. And then some of the other things that we see when we talk about TGF-beta-1 and then cyclooxygenase-2 and then inflammatory cells kind of contradict what was said in the answer choices. So etiology, intrinsic factors and extrinsic factors. So intrinsic, so hamstring tightness, we talked a little bit about that. So always test the hamstrings and address that in these patients with quad or patellar tendinitis or tendinopathy. High forces and rate of loading, deep knee flexion. So assess what your athletes are doing from a practice play standpoint because certainly you can alter these things and improve this. So what about extrinsic? Maybe these are most important. So hard playing surfaces and then length of the training sessions, which obviously is probably very important. So risk factors, again, as we mentioned, hamstring tightness, quad tightness, bad jumping mechanics, landing mechanics that are bad, and then low hamstring to quad ratio. So these are quad dominant people. And then genu recurvital. So presentation can be acute onset anterior knee pain. It can also be insidious. In stage one disease, they only get pain after activity. In stage two, they get pain at the onset of activity. In stage three, it's constant. In stage four, it's bad because that's rupture. So this is all a continuum, right? And then on exam, tendon can be boggy. You can get some crepitants with range of motion, kind of like popping and crackling almost. Pain with palpation at the anterior pole of the patella. And then the pain is present with patient in extension. But when you flex your knee up and then palpate the same area, the pain goes away. So that's a positive Bassett sign. So plane radiography. So decreased bone mineral density. We can see that, but it's usually not common to see changes on plane films. So MRI is really a workhorse. So chronic cases, we get MRI. So this can help with surgical planning. We typically see this sort of abnormal signal, which is caused like partial thickness tearing. The reality is the tendon is all here. That's all sort of mucoid degeneration, which is showing up. So it's not like, even though it's frequently called partial thickness tearing of the patellar tendon, there's substance there. So it's not true partial tearing, in my opinion. It's more just a mucoid degeneration that shows up on MRI that looks like partial tearing. But those of us who have been in there to debrief this stuff, you're scooping out stuff that's the mucoid degeneration and tendon tissue, but not necessarily a true tear. So non-operative treatment, relative rest. So avoid stuff that hurts. Iontophoresis, phonophoresis can be an adjunct. We'll talk about the efficacy of those. And then PT is huge. So what to do, what not to do. Iontophoresis has been shown to be benefit. So that's medicated cream. You put these pads on, you jack up the voltage, and, well, not jack up the voltage, but you turn on the voltage, and the voltage helps to drive that, the ions of the medication into the area of interest. Phonophoresis, which kind of has the same idea, but it's done with ultrasound, has not been shown to have any benefit. So what are the buzz terms? So stretching and then eccentric exercises. So these are on a slant board. So eccentric knee exercises on a slant board is kind of the buzz term for improvement with patellar tendonitis. And isometric exercise still works. Ultrasound and massage can work, but very important. So three principles of eccentric exercise. So length, you want to increase the resting length of the myotendinous unit. So that tightness is important. So you want to reverse that. And then you want to progressively increase the load and then increase the speed of contraction. So an eccentric contraction is important. So it generates 20 to 30% higher forces than iso or concentric contraction. So some people believe you actually place the tendon into an anabolic state. So building up by first inducing some injuries. So by increasing the forces within the tendon actually causes some internal injury, the theory, and then that induces the body to then heal this. And so those are important things. And the goal is really to strengthen the tendon. So non-operative treatment. So other options that we sort of mentioned here. So shockwave has some efficacy, but in some other articles I haven't shown not to be beneficial. Corticosteroid, just say no. So don't inject tendons with corticosteroid no matter where you are in the body because that will cause them to rupture. So they can feel good early and then poor long-term results when they rupture, that's bad. Platelet-rich plasma has had some efficacy, but the results of that are all over the place. So 40-year-old recreational basketball player presents to your clinic. Complained of chronic anterior knee pain localized to the inferior pole of the patella. He denies any specific injury. He has no knee swelling or mechanical symptoms and MRI is obtained in figure one. Oh, patellar tendon. So what is the histologic examination of the pathologic tissue causing this patient's symptoms most likely to reveal? So chondrocyte apoptosis, well-organized collagen bundles, hypocellularity, multiple inflammatory cells or mucoid degeneration. Here we go again. So mucoid degeneration is the answer what we just sort of mentioned. So question number 17, a 25-year-old professional basketball player presents to your office with chronic anterior knee pain. Radiographs and MRI demonstrate patellar tendinopathy. Which treatment option is associated with a higher risk of patellar tendon rupture? Corticosteroid injection, platelet-rich plasma injection, shockwave therapy, ionophoresis or dry needling. Corticosteroid injections, just say no. So surgical indications or persistent symptoms despite conservative management or obviously stage four injuries once they rupture, those are the easy ones. So you could do longitudinal tenotomy, ossicle excision. You can excise these arthroscopically. You can debride the tendon open or you could do a wide excision and reattachment of the patellar tendon. A little drastic, but certainly are options. So what about rupture? So looking at this, one of the sort of seminal articles on extensive mechanism injury. So 34 patients with quad tendon ruptures, average age was over 40. 33 patients with patellar tendon, they were 80% were less than 40. So older patients tear quad, younger patients tear their patellar tendon. So 38% initially are misdiagnosed. So history, eccentric mechanism, they feel a pop, pain, sometimes prodromal pain. So preceding pain can be important, so always ask about that. In an exam, pain of palpation, defect, extensive mechanism, lag, ecchymosis, and then a large effusion. So surgical treatment is indicated for complete ruptures. Rarely repair through trans-osseous drill holes. So early repair through trans-osseous drill holes and increased complications with delayed repair. Heavy non-adjustable stitches for the tendon and pull these through longitudinal drill holes. In terms of literature revisions, outcome has been shown to be better with suture anchor repair. But suture anchors are becoming more and more common even for primary ruptures. So question 18, patella femoral. An active 51-year-old runner presents to your office with acute onset distal thigh pain after slipping on snow and ice covering his front stairs. Prior to this incident, he had had some distal thigh pain that would occur after his normal workouts, but it would not stop him from training. On physical examination, he has a swollen distal thigh and a palpable defect in his extensor mechanism superior to his patella. He is unable to do a straight leg raise and MRI of the knee is shown in figure one and two. On further questioning, he reports that he recently had an upper respiratory infection that had finished a course of oral antibiotics. Guess we're missing figure one and two. Sorry about that. So which class antibiotics are associated with this injury? Sulfonamides, aminoglycosides, macrolides, penicillins, or fluoroquinolones. Everyone should know this. So fluoroquinolones. So on to the meniscus. Oh, I'm gonna start outline. So once thought to be a vestigial structure, picture on the upper right is a proud surgeon who had seen small meniscus tears probably back in the 70s, early 80s. And so they very elegantly whacked out the whole meniscus and kind of patted themselves on the back. And the picture on the bottom right is what typically happened to these patients. So they would get what we call Fairbanks changes. So squaring of the condyle, joint space narrowing, spur formation, which we now know as the hallmarks of osteoarthritis. So don't whack out the meniscus. So, cause we know this is what would happen. So in the Fairbanks changes were actually described for the patient who had post-meniscectomy knee. So acute meniscal tear 61 per 100,000 people. So 850,000 procedures a year. And that's probably even more now. Sports related about a third of patients. Medium meniscus is greater than the lateral meniscus except for wrestlers. So be aware of the wrestler who felt the pop and they're having pain. That's lateral meniscus until proven otherwise. So male female ratio is 2.5 to one. Peak age or 40 years old for males and 20 years old for females, or sorry, second decade for females. And then the third, sorry, I guess fourth decade for men. So less than 30 tend to be traumatic and peripheral. Greater than 30 tend to be degenerative and complex. So with acute ACLs, lateral meniscus is much more common than medial. For chronic ACL, the medial meniscus becomes more common because that's a secondary stabilizer. Tibial plateau fracture up to 47% of knees with tibial plateau fracture can have a meniscus tear. Most of these are repairable. So your trauma people are probably just whacking or ignoring these things, but certainly get the sports people involved if you have concerns. And then degenerative tears anywhere from the fourth to sixth decades and beyond. So development. So in eighth week, the meniscus is clearly defined. By the 14th week, it has normal adult relationships and is entirely vascularized. So after, so enter third is avascular by nine months after birth. Adult vascularity by 10 years old. Densely cellular at birth, and then less cellular with age. So meniscus anatomy. So medial meniscus, semicircular cartilage. So roots are very far apart. 3.5 centimeters long, firmly attached to the deep MCL. And then coronary ligament is responsible for helping to hold the medial meniscus to the tibia. And this is important because between this and also the fact that it sits on the concave tibia has much less motion than the lateral meniscus. So the lateral meniscus is more circular. The roots are very close together, which helps with the increased mobility of the lateral meniscus. and it's loosely attached to the joint capsule, and it has a point back at the palpiteal hiatus where it's not attached at all. So this is more mobile than a medial meniscus, sits on a convex tibia, and because of that the lateral meniscus is a little bit more mobile and probably less prone to tearing in general. So the coverage of the plateau is greater on the lateral side. So we see in this picture in the middle, or bottom I guess, medial side, this is the lateral side. So lateral meniscus tears tend to be a lot less forgiving. So we look at other anatomies of discoid meniscus, first described by Young in 1887. This is a lateral predominance, it does happen medially, but it's very rare. Very high in Japan, less so in the United States. Is this a congenital anomaly? It can certainly be a part of Staphy knee syndrome. What we see in this bottom right picture, this is a complete discoid for one of our patients. So that meniscus covers the entire plateau. So this is the Watanabe classification. So type one is complete, what we just showed you. Type two is an incomplete one, so it doesn't cover the whole plateau, but covers a lot of it. And then type three, what we call the Ritzberg type, it has no attachment posteriorly, and it only has an attachment to the Ritzberg ligament. So you can go in there and start trimming this away, but you end up with a lateral meniscus which is still unstable over the posterolateral horn, and this is a problem. So that you want to identify. So question one for the meniscus, a 10-year-old soccer player presents with a six-month history of snapping and pain at the lateral joint line of the knee. Physical examination shows a 10-degree loss of extension. An MRI was ordered, figures one and two. So this is a sagittal MRI on the left, and on the right there is a coronal view. Let's look at that for a second. So what is the best surgical indication for this patient? Relatively low fibular head, symptoms of the involved structure, bilateral involvement, medial compartment involvement, history of contralateral knee surgery. That's what we're seeing here. So symptoms of the involved structure. So this is a disc-weight meniscus. And again, don't necessarily need to address them if they're not symptomatic, but if they are, they may need to be addressed. So what about the histology of the meniscus? It is fibro cartilage. So type one cartilage, network of interlacing collagen fibers, intersposed fibrochondrocytes, superficial oval spindle cells, and deep polygonal cells. So the fibrochondrocytes maintain the extracellular matrix. And again, type one collagen is huge for the meniscus. And peripheral cells respond to growth factors. Central cells are a lot less responsive. So these may have implications with respect to healing. So this is a biphasic structure, so made of both solid as well as fluid portions. So 90% of this is type one collagen, and this increases until age 30. So three structural layers, superficial layer, a surface layer, and a middle layer. And the whole goal of the meniscus is to convert axial load to circumferential stress. And this is done by the circumferential fibers that are connected by the radial type fibers. That kind of helps turn these stresses, axial stresses, into hoop stresses. So vascular supply, so gestation, nearly all the meniscus is vascularized. And this comes from medial and lateral geniculates. Synovial plexus is also very important. And really the outer 10 to 25% is vascular. Very little vascularity at the palpital hiatus. And the roots are more vascular. So this is some of the classic stuff from Dr. Arnosy, who showed, you know, certainly way out here in this part of the meniscus, that's all sort of the white zone. As we get more towards this vascular diet stuff here, this is peripheral aspect. So that's the vascularized portion of the meniscus. So there's nutrient canals and compression for the meniscus is key because it helps to nourish, kind of like a sponge, kind of helps to nourish the meniscus. So what about the neuroanatomy? The medial and posterior articular nerves help to innervate the meniscus. The vast majority of the innervation is at the horns. Really no nervous supply at the central third. And the perimeniscal tissue is highly, highly innervated. So tears that go out to the meniscal capsular junction, they hurt. And there's mechanoreceptors in there, which are also important. So what's the meniscus do? So low sharing, shock absorption, helps decrease joint contact stresses, provides some passive stability for the knee, increase congruity, contact area, and limit extreme flexion extension. And then also helps with proprioception. It's important, very important. So low transmission in the extension, 50 to 70 percent in the flexion even more. So the medial side. So as you decrease the contact area, 50 to 70 percent, the contact stress goes up 100 percent. But again, as we mentioned, the lateral meniscus is very unforgiving. So as you decrease the contact area, 40 to 50 percent, the contact stress goes up 200 to 300 percent. So this is huge. So when you look at hoop stresses again, training that axial load for this sort of helps to distribute the load coming down, actually. So the axial load converts hoop stresses. These stresses are resisted by the meniscus. So that's what we're looking at with those hoop stresses. So the meniscus function, when you look at this, lateral is more important than the medial with respect to motion. And you see as we go into knee flexion, the lateral posterior horn moves a lot more than the medial side. It's important stuff. So tibial femoral contact mechanics after serial medial meniscectomies. So upper left-hand corner, so normal state. And then you look at a 50 percent partial meniscectomy, so a little bit more greens and yellows. When you have a 75 percent partial meniscectomy, you start to get some of these reds. Reds are bad, so some more point loading. And then, sorry, let's see. So a segmental reconstruction. So even though there's 50 percent of the meniscus remaining, you get high point loading and segmental resection essentially is as bad as a total resection. So if you have to go all the way to the meniscal capsule junction, if you remove the entire posterior horn, it's like there's no meniscus there at all. So joint stability is a secondary stabilizer, so in the ACL-deficient knee. So with chronic ACL deficiency, more meniscus tears happen. So typical mechanism, twisting, hyperflexion. A lot of patients may not recall actually injuring their knee. So what do these present with? So pain, they can feel a pop, swelling, locking, catching, decreased motion, and this can be acute versus indolent. So joint line palpation is the most sensitive finding for meniscus tears. McMurray's is not very sensitive at all. You have to have a large, unstable meniscus flap or bucket handle or something like that for the McMurray's to be positive. And likewise, there's only positive in about 30 percent of meniscus tears. Apley's we'll talk about and Thessaly's. So McMurray's, I'm sorry, so other things that we consider, so capsule irritation, so I bounce the knee and if you have pericapsular tearing, you know, they'll feel that. So pain with forced hyperextension, that's another good meniscal irritation sign. Apley's, so right now is the joint relief portion of Apley's. So he's putting this knee on the back of the thigh and then he's distracting. So distracting the tibia and then you twist it around and then you press down and then you twist again and press down and twist and again should cause symptoms. So that's a positive Apley's. And then Thessaly's, which I love this test, but if patients have a lot of patella from away or they're older, it can be difficult to interpret or do. Sorry, and then Thessaly's is again squat down and then you twist, you do the twist and they will complain of joint line pain. So plain films, this is our series, you get AP, PA flexed to better look at the articular surface under weight bearing and a lateral and a merchant. They should always be weight bearing views. So MRI, not always necessary, but can be used to evaluate for other pathology. Very high sensitivity for the medial over the lateral and then the cruise classification. We see this here, type 0, no signal. In type 1, you have some signal in the meniscus. It's kind of more mucoid degeneration. In type 2, you don't have a signal, but does not reach the articular surface. This is a linear signal, so that's not consistent with tear. So in order for it to be read as a tear on MRI, that linear signal needs to reach one or both articular surfaces. And this is what we can see here in their classic paper. Grade 1 and 2, no tear with scope. Grade 3, 94% had a tear with a scope. So when we look at meniscus classification for decision making, what's the size of it? Location is stable. Does it have vascularity? What's the tissue look like? And does this appear to be chronic? So classic types, location, so vascular or not, and then orientation and then chronicity. So this is looking at kind of a degenerative type of tear, so kind of complex. So tear is going in multiple directions. There's a flap, there's probably a little bit of horizontal cleavage, there's some undersurface tearing. And then there's root tear, so this patient has a degenerative root tear, also has a lot of OA in the knee, so the horse is probably out of the barn. That's a root tear. And then this is a root tear in a young person, so these are the ones that you really like to see. So normal cartilage, but this root is just detached from the back of the knee. You can see that on the actual images on the MRI. And then, yeah, treatment, you know, again, MRI can kind of help us with this. You know, this is very subtle, but that looks like a radial tear. So what's your options? Remove, repair, or leave it alone? So current teaching is mechanical symptoms, pain, recurrent effusions. Reality is people live and die with meniscus tears. Mechanical symptoms can come from the meniscus, so bottom image. But guess what? This is chondral. This can be mechanical also. So not every mechanical symptom means meniscus tears, and there's actually a lot of literature that shows that patients with a lot of mechanical symptoms when they're older, that's actually a poor prognostic indicator of improvement with surgery. Because typically, if they had a lot of mechanical symptoms, it typically meant that there was something going on with respect to arthritis inside those knees. So what's the culprit? Again, is it this bad chondral injury here, or chondral wear, or is this the meniscus tear? Mechanical symptoms are more reliable in young patients with no OA. But once patients get OA, that kind of goes out the window, because it's hard to know what the mechanical symptoms are coming from. So when you look at the prevalence of asymptomatic meniscus tears and asymptomatic controls with OA, so high prevalence, so 76% of patients with OA may have meniscus tears they didn't know about. If they're symptomatic, that's even higher. So what do we remove? So tears in the avascular zone, complex ones with little flap radial cleavage tears, so don't have a chance of really healing. Severe damage to the body and or root. And then degenerative meniscal cyst, and then arthritis. So we can see this meniscectomy, clean that up, and then take a shaver in there and get that smoothed out, only remove the torn part of the meniscus. And then what about resecting methods? So we can see on the bottom left, you really want to try to create a smooth contour for the meniscus. So we see the flap, we trim, and then that's kind of what we end up with here. So I want to reserve tissue or refrain or keep as much tissue as possible. So what about repair? So young, so stable knees, so ACL intact, so you don't want to repair something when the ligaments are unstable. Traumatic injuries, so longitudinal tears that are larger than, you know, one to one and a half centimeters in size. If they're smaller than that, you can treat those non-operatively. Extend into the avascular zone with ACL reconstruction, so we can sometimes stretch the limits with ACL reconstruction. And then patients who are able to adhere to the rehabilitation. And we see the meniscal repair sutures going in here. So question two, 49-year-old Caucasian female presents with a two-month history of medial knee pain after feeling a pop when stepping off a curb. On physical examination, she has medial joint line tenderness. On weight-bearing radiograph, the joint spaces are preserved, and alignment is neutral, and MRI is obtained. Figures one and two. So figure one and then figure two. Let's dwell on that for a little bit. So what is the next most, so what's the appropriate next step in management of this patient's condition? Meniscus root repair, inside out meniscus repair, all inside meniscus repair, meniscectomy, or meniscus transplant. So again, images. So meniscus root repair. This is a degenerative root tear, but her knee is not arthritic, kind of acute phenomenon. You can try non-operative treatment for these patients, but certainly, you know, she's already through two months of knee pain, maybe time to fix it now. So what's the technique for repairs in general? Use as many sutures as you need to to get it back in the right place. So vertical mattress is better biomechanically, buzz term, but you get what you get. So if all you can get is a horizontal mattress, that's fine. Doesn't mean that they're crap, just means that the vertical is better, but does not mean that the medial, that the horizontal should not be done. So be aggressive in younger patients. So try to fix them and, you know, get them to heal. So long question. So 15-year-old male high school wrestler accompanied by his father, seen in the clinic, and I just had this very same scenario today, actually, but with a, not a wrestler, so a female athlete. He sustained a twisting injury four days ago in practice and was not been able to fully extend his knee since having injured it. Physical examination identified a 10-degree flexion contracture and moderate effusion. The ligament exam is stable. Radiographs are normal and the physis are closed. An MRI was performed and demonstrates a displaced bucket handle medial meniscus tear. You review all the surgical and non-surgical options as well as the associated risks and benefits of each. Surgical options of partial meniscectomy and meniscus repair are reviewed in detail, including the rehabilitation involved and the short and long-term consequences of both choices. You feel that the athlete and his father having an excellent understanding of the information provided and that they both have had adequate opportunity to ask questions. So the athlete and his father decided to have a partial meniscectomy performed. His coach has told them that no wrestler he knows has successfully returned to play after repair at the meniscus usually re-tears. The athlete also reports that he needs to get back to wrestling as soon as possible as a college scholarship is at stake and due to his family's financial situation, he likely won't be able to attend college if he doesn't get an athletic scholarship. He is therefore opting for quicker recovery. In this situation, what treatment do you provide for the athlete? So you continue to discuss the detriment outcomes of meniscectomy in the young athlete in hopes of persuading the young athlete and his father that meniscus repair is the better long-term option. You agree to perform surgery on the athlete, but during the surgery the extent of the tear leads you to perform a meniscus repair as you consider that treatment to be in the best long-term interest of the patient. Having given what you consider an unbiased presentation of the facts surrounding the treatment options, you agree to perform a partial meniscectomy in line with the athlete's wishes. Given the decision of the athlete and his father, you question their competency and decide appropriately. You send them away to think about the decision and tell them to come back when they agree to have a meniscus repair. Refer the patient to another physician and discharge from your practice as they are unwilling to listen to your advice about what is best for the athlete's need. This is a very tough one. So, answer C, having given them consider an unbiased presentation of the facts surrounding the treatment options, you agree to perform a partial meniscectomy in line with the athlete's wishes. So, this is an ethical dilemma, obviously, and certainly the key thing is that you've explained the facts and you weighed everything and they're educated consumers, but the reality is the wrong answer is to ever you don't want to abandon the patient and you actually don't want to push them towards a certain decision. This is the right answer. I can't say I fully agree with it, but this is what we know. So, meniscus treatment, all-in-sight repair, posterior horn, not as amenable to anterior horn tears, although there are some newer devices that kind of help you get there with an all-in-sight repair. Inside-out is the gold standard, inexpensive, nitinol needles, anatomic cannulas to help with the repair, requires slow advancement of the needles, can access all parts of the meniscus. So, a 16-year-old soccer player presents to your office after sustaining a twisting injury, inflection, and lateral knee pain. Sorry, a knee injury, inflection with lateral knee pain, and persistent mechanical symptoms. He has a small effusion, full motion, a symmetric ligamentous exam, and a positive McMurray test. An MRI reveals an isolated peripheral longitudinal tear of the posterior horn of his lateral meniscus. Which of the following meniscal repair techniques can place a suture perpendicular to the tear with the lowest risk of injury to the popliteal artery and perineal nerve? All-in-sight repair with the knee fully extended. All-in-sight repair with the knee flexed to 45 degrees. All-in-sight repair with the knee flexed to 90 degrees. Outside-in repair with the knee flexed to 90 degrees. Outside-in repair with the knee fully extended. All-in-sight repair with the knee flexed to 90 degrees. Sorry. This helps to get that vascular, neurovascular structures away from the knee. So, leave alone stable tear in the avascular zone, sorry, the vascular zone. Stable tear with an ACL reconstruction because you're going to get a lot of hematoma, PRP and marrow elements and all that good stuff. And then the stable degenerative components of the tears and clinically insignificant degenerative frame. So, don't just shave the frame and try to bill for it. So, post-op management for meniscectomy, immediate weight bearing or weight bearing is tolerated. Progressive range of motion strengthening and then return to play somewhere between four and six weeks for the medial side. Left lateral meniscus is again less forgiving, so it can be six to eight weeks or sometimes longer. So, with repair, I brace my patients, get them into a brace for six weeks. Their weight bearing is tolerated with the brace locked and extension for uncomplicated repairs. You can wean them off crutches as they're able to walk with the stiff brace locked out straight. Limit flexion for four weeks because deep flexion can cause stress in that posterior horn. Running at three to four months and return to play approximately five to six months. So, meniscus outcomes inside out repair anywhere from 62 to 96% healing rates. This is improved with ACL reconstruction again because of all the marrow elements and stuff that spilled into the knee. And then only 17 to 62% in ACL deficiency. So, don't fix the meniscus if you never plan on doing the ACL. So, all inside repair, no difference between devices. In conclusion, meniscal tears are very common. The inner portion of this is avascular. Meniscus is important for load transmission, has an important role as a secondary stabilizer. Successful management requires a thorough knowledge of the meniscal anatomy and function. Thank you very much. Hopefully, you enjoyed the presentation. Sorry about my voice. I've been at a track meet all day today and was yelling at my son. But, you know, certainly, hopefully, got everything you needed to get out of the presentation and good.

patellofemoral pathology

meniscus injuries

anatomy

biomechanics

physical examination

conservative management

operative management

evidence-based literature

diagnosis

surgical treatment options

non-surgical treatment options

rehabilitation process

repair techniques