Thanks so much, and thanks, Mark, for spearheading our educational initiatives for the Oskendorf-Susskind group. And so my disclosures are on the Academy website, nothing related to this talk, and all of our work with the OCD group is volunteer work as well, as are all the things listed below AJSM. At the conclusion of this activity, we'd like to be able to discuss imaging findings, non-operative management, and we'll briefly touch base on surgical options based on the imaging findings, and we'll discuss OCD genetics in the discussion portion of today's talks. In terms of an outline, we'll address pathophysiology, imaging assistant, and we'll go over briefly three cases. OCD is described historically by Dr. Sir James Padgett and Dr. Koenig in the 1800s. In terms of physiologic standpoint, it's a breakdown of the normal pathway of endochondral ossification, certainly aware of the primary physis, and we'll touch base on the secondary ossification center. And this is the secondary growth plate shown in illustration form, and the relationship of the secondary ossification center to the articular cartilage. When we look at radiographs, we'd like to see if there are acute or chronic findings. When we look at MR, we'd like to see if there are signs of stability or instability, if you will, and we note that CT and ultrasound are not routinely used. For radiographs, for plain radiographs of the knee, we like to see AP, lateral notch, and merchant, I like the merchant as opposed to sunrise views. OCD, however, can be subtle, and so they can just be simply an effusion with or without interarticular loose bodies, or sometimes palpable as a joint mouse. Eric Wall led our OCD group in a reliability study, 45 knees. We had seven of us at different institutions and did inter-reader reliability on radiographic characteristics, as shown on the right, and we'll go over those individually. Radiographic assessment, we looked at fragmentation, and so the progeny fragment, and so the progeny is the OCD fragment. So the progeny is like the kids, that's a small area of the OCD, and the parent is the bone above, which is the metaphysis and the remainder of the epiphysis. So fragmentation would be two or more pieces. Fragmentation can be non-displaced, partially displaced, or fully displaced. Contour can be convex, linear, or concave. Boundary, which is the density of the boundary that separates the progeny from the parent bone, can be indistinct or distinct. In terms of the parent bone, the density of the progeny to the unaffected bone. So in this case, the progeny is less dense than the parent or unaffected bone. In this case, it's the same. In this case, it's more dense than the parent adjacent bone. MRI characterization, you can see the advantages of MRI above and the disadvantages below. I like to have, certainly we like to have three planes, axial, coronal, and sagittal. At least three millimeter or less slices, and shown is a proton density fat suppressed as well as proton density images, and your T2 on the left. De Smet looked at signs of lesion stability based on MR, and noted high signal deep to the OCD, articular fracture, cysts, or osteocondal defect. O'Connor looked at 33 knees and a comparison of MR and arthroscopic findings, and MRI prediction with arthroscopic findings accuracy improved if there was a T2 weighted high rim plus T1 weighted cartilage breach. De Smet looked at 33 knees and similar findings. Key was T2 weighted high rim again, just like his prior author, as well as multi-center circumferential cysts and single cysts, and we'll show those in a minute. Our rock group, this is as yet unpublished data, but looked at that negative effect of the secondary physis, and you can see the illustration and the pathologically thick cartilage as shown in orange, and the yellow is the secondary physis, and then we've located the lesion lateral central intercondylar, and you see the size of the lesion on the sagittal and coronal images. Looking at the width and depth and a number of other features that we'll describe above, and I will point out to you on the lower right what we call an omen sign, which is a black line through the white articular cartilage that can be a bad sign for impending doom for that cartilage stability, and again, these we'll touch base on shortly. I'm looking at four established criteria for lesion stability, direct and indirect signs. We will show examples of those. A 10-year-old male with an empty crater, as shown by the arrow. Cartilage injury, 14-year-old female, loss and disruption of that normal signal, as shown on the above and below images. Indirect signs of fluid on the interface, and then cysts, which can be circumferential or single large cysts. We like to distinguish that from physiologic variance. Normal developing endocrinal ossification front, which can occur in significantly younger patients, posterior third, no intracondylar extension, and no marrow edema. So a variation of normal. We've all seen the algorithms of conservative management. If they've healed at three to six months, and if they haven't healed, we'll encourage that healing surgically. Let's go over cases. Case number one, 11-year-old female swimmer, bilateral anterior knee pain with running and swimming for one year, no acute injury. Physical exam, no effusion, negative Wilson's, but pain with single leg hopping on the left. Radiographs and MR showed OCD, which was with intact cartilage. And this was the radiographs, AP, notch, and lateral. Sometimes these are tough to see, so I'll outline those for you. And we'll zoom in on your AP here, and then show the area of involvement, that classic lateral aspect, medial femoral condyle, that's 70% of the time, that's the location. And these are the features that are favorable. No fragmentation, no displacement, normal contour, no defined boundary, and the parent bone has higher density. Radiograph at presentation of the notch view, and again, we zoomed in on that for you and outlined it. And then again, a sagittal lateral film, the same. Looking at the MRI, do we see signs of lesion instability? Is there an empty crater? No cartilage injuries, interface, and cysts, so no significant cysts, okay, so no signs of instability on that. So therefore, patient was treated conservative management, in this case, six weeks of a knee immobilizer, then six weeks of physical therapy, but no high impact running or jumping sports at three months, she was pain free, but OCD was not fully resolved. So therefore, she's advanced back to swimming, but not high impact running or jumping, remained pain free, six months, radiographs were improved, she was fully cleared. She did return two years later, seen for different injury, and remained pain free. Case number two, 12-year-old multi-sport athlete wrestling and football, bilateral anterior knee pain, occasional popping, sensation of right knee locking for one year, limp at times when running, however, the physical exam was full range of motion, just pain, tenderness over the medial femoral condyle, but negative Wilson's, and single leg hopping, some pain on the left. Radiographs from an outside hospital, as well as MRI, you can see the plain films here, AP and lateral views, area of involvement. Do we see signs of lesion instability, okay, so we'll run through these rather quickly, so the answer is no to that. Same for the proton density, coronal images. And so therefore, six weeks neomobilizer, then six weeks of PT. At three months, no pain, mild tenderness over the medial femoral condyle, radiographs, no significant substantial improvements, so they went to six months. Radiograph was improved, restricted to one sport per season for three months. At 11 months, radiograph shows some persistent OCD with possible sclerosis, so repeat MRI to see if there's a surgical issue, and do we see signs of instability? And the answer is no to that. Lesion was a little larger on the T2 fat-suppressed image. Looking at the coronal, again, no signs of instability. So therefore, the patient did return to football, parents requested he continue to play. Two weeks later, they had new onset of knee pain. So therefore, 14 months after the initial diagnosis, patient was treated because of persistent symptoms with intact cartilage drilling, so transarticular drilling, and then shown at one month, and then four months later, radiograph, a near-complete resolution of the OCD, and cleared to return to activities. Case number three, anterior knee pain of six months duration while playing capture the flag. No mechanical symptoms or knee swelling at the time of presentation, and physical exam was rather unremarkable. Radiographs, however, shown AP, notch, and lateral film. Again, we'll outline those areas for you. Do we see signs of instability? There was cartilage injury as shown on the T2 fat-suppressed image, as well as proton density image, and your axial image as well. Also, T2 relaxation color mapping showed signal change, which was significant. The patient then, after that, had knee buckling for a period of one month. So it wasn't just radiographic reasons, but also mechanical reasons. So they went arthroscopy, there was friable, fibrillated, non-viable cartilage, so therefore they had a chondroplasty, as well as abrasion arthroplasty to stimulate scar cartilage to fill a defect, so a rather small lesion. Hopefully we've addressed our pathophysiology imaging assessment and addressed three cases. And so we've reviewed imaging findings, non-operative, and touched base on some surgical findings. I'd like to thank you for your time, and I'm happy to answer any questions. I'd like to thank those who are directly involved in support of this, as well as the entire ROC group. And again, Mark, thank you for setting up this question, and look forward to the discussion portion of this talk today. Thank you.

osteochondritis dissecans

radiographic assessment

MRI characterization

evaluation

treatment options