Wonderful group of people to share slides with, and there'll be a little over wrap, and I think a lot of complimentary things that we say today. So I'm just gonna talk about some of the new things we've been learning about, the causes, etiology of OCD, no relevant disclosures, everything I have is update on AOSSM, the academy's website. And we're gonna talk a little bit about, basically there's still a lot more questions, a lot more questions than answers, but some of the things that have been raised as possible etiology include pharmacological, mechanical overloading, vascularity, and Utah Ellermann here, Dr. Ellermann's here, is gonna talk a lot about that later. A little bit about genetics, and maybe some future questions on why this vascularity issue may matter. This term, as Ted said, was first described quite some time ago by Koenig, and really that osteochondral sequestrum, that separation, that fragmentation within the joint is sort of the hallmark feature of more advanced cases and what we're all trying to prevent reaching that stage. Despite what we've learned clinically, I think we're still making slow, but not as much progress we'd like to really understand the pathogenesis of this condition. The OCD group has a couple definitions over the last 11, 12 years. A recent definition as of this last year is a focal idiopathic alteration of subchondral bone and or its precursors, and Dr. Ellermann's gonna talk a little bit more about that precursor, but with risk for instability and disruption of adjacent articular cartilage that may result in premature osteoarthritis. And once again, these precursors, these avascular regions that may start in the cartilage rather than bone is something that's changed the way we think about this over the last few years. We know that if you look at most biopsies of OCD specimens, necrosis is a common finding, but the cartilage itself, actually in many cases, is very normal and quite healthy, except in maybe more advanced cases of bone failure. The cartilage can degenerate with time. There's a case report of fluoroquinolone. For those of you who don't know much about it, but fluoroquinolone is usually contraindicated in children because of its impact on cartilage. We know it has problems with tendons in adults, but there's also concerns about cartilage problems. This is actually a case report of a non-athletic 10-year-old girl who developed bilateral mutiformal columnar OCDs, and she had a chronic UTI reflux problem, and it was multi-drug resistant. The only antibiotic that worked effectively was fluoroquinolone, so she had well over a year of prophylactic treatment and developed bilateral OCDs. Was it related to fluoroquinolone? We don't know, but we know there is some evidence of cartilage toxicity in animal studies. Lots of things suggest mechanical factors, including malalignment, repetitive loads, microtrauma, abnormal meniscus pathology. Acute bone contusions have actually been described. There are case reports of several acute bone contusions, later on turning into OCD. So a bone bruise, in some cases, may turn into OCD, but probably not the most common. We know discoid meniscus, there's multiple studies showing an association between discoid meniscus and lateral formal condyle OCDs. That's a common combination we all see in the ROT group. And this may represent a chronic overload. You've got a stuffed meniscus that puts more load on that lateral condyle. Maybe that's part of what predisposes it to developing in that location. We know that running sports, loading sports, running, we typically see this in the knee and the tail, this in running athlete, running sports, throwing athletes involve the elbow, and gymnasts also involve the elbow. So these are probably overload phenomenons. Malalignment, there are some reports looking at varus and valgus. You know, a varus knee may be more medial. Here's an example of a valgus knee that's got a lateral condyle OCD. So there may be some loading alignment issues here as well. Now there's a nice epidemiological study by Jeff Kessler and Jen Weiss showing higher rates of OCD in obese children, which also suggests that, once again, mechanical loading may aggravate or contribute to the development of OCD. Elbow throwers, you know, when you throw, you're loaded more in a flexed position. So the high loads, high peak loads are in flexed elbow, and guess what? We see the OCDs in the elbow in the anter aspect of throwers. You contrast that to gymnasts. Gymnasts, by and large, bear weight on their fully extended elbows. They're walking on their hands during their routines, and guess what? We see OCD in the poster aspect of gymnasts typically. So that suggests, once again, that mechanical loading is part of the ideology or maybe the worsening of a preexisting condition. Running sports, central weight-bearing area. Minh Coker published this a few years ago looking at baseball players. It's actually a baseball athlete that I took care of, but baseball catchers who sit in a hyper-flexed knee position while they're catching are more likely to get OCD in the well poster aspect of the condyle. Once again, suggestion that loading does have some contributing effect on OCD. Once again, I just talk about this definition again about these avascular regions that can lead to cartilage necrosis, and Dr. Elliman's gonna go into that a little more, but I'm gonna talk about something that Dr. Elliman has worked with, this group up in Minnesota with Mark Tompkins and others, is can we learn about the causes of OCD by looking at other mammals? What other animals get this? We know that vertebrates, the axial skeleton, it starts out as a cartilage model and slowly undergoes endoconal ossification. Judith's gonna talk more about this, the AEC, the articular epiphyseal cartilage complex. This is the structure at the end of the bone with our growth plates, and the end of the bone that hasn't ossified yet. These contribute to full adult development, and eventually our adult shape is defined by the cartilage endocondyl ossification of the entire skeleton. We know that the epiphyseal cartilage relies on this rich, dense vascular network to provide cells. These grow in and penetrate, subsequently the ossification, the secondary ossification centers. These complex arteries, veins, capillaries are critical for this development, and these development of these cartilage canals to nourish these developing tissue. And once again, these come from the periphery. These vessels come in from the periphery, this very strong, dense peripheral network. And as we get older, we lose this. This is part of defining skeletal maturity. We lose that invasive peripheral vascular network in the structures. Well, we know that in the veterinary world, they use the term OC, osteochondrosis, more so than osteochondritis dissecans. But focal failure of endocardial ossification is one of the things that's associated with development of OC or osteochondrosis in veterinarians. Once again, if you look at the literature, those terms overlap. We might need to switch our term, but right now, humans talk about OCD and veterinarians talk about OC. Avascular necrosis is a unique and defining characteristics about OC and OCD. And there are predilection sites. There are humans and mammals that have OCDs in similar locations. And so that was the foundation of some of this research work. Looking at the distal femoral articular complex, we know there's predilection sites for OCD and OC that's similar in humans and pigs, the lateral aspect of the medial condyle. This study looked at imaging, high-resolution imaging of pigs, goats, and humans, and we wanted to compare the vascular development of this region of the joint for those who are predisposed to OC and OCD. And the hypothesis was that we could use these high-quality MRI, high-field-strength MRI to very carefully and with fine resolution characterize the vascular development of the femoral condyle. And also, we know that humans and pigs have similar locations, the lateral aspect of medial femoral condyle, and goats, as far as we know, correct me if I'm wrong, but I don't think we've ever seen OCD in goats. And we want to know, is there something different about the vascular architecture of humans, pigs, and goats that might explain this? And so this study took pediatric cadavers of various different ages, but mainly young cadavers, and did a 9.4 test MRI with something called SWI, susceptibility-weighted imaging. And this allows for very complex, fine-detailed vascular reconstructions of the anatomy and the vascular anatomy of these joints. And this has allowed us to clearly see these vessels, both in the humans, the pigs, and the goats. And it really was very helpful as we started thinking about what might be the cause. And what we found is that the vessel architecture was quite similar between humans and pigs. I've said for many years, humans and pigs have a lot more in common than we probably want to admit. But that area that develops necrosis and OCD has a vascular compromise area. And goats have a much richer vascular network and do not develop OCD. And maybe it's because they have this rich overlapping network that does not lead to a watershed area or a vascular failure zone. And these are, once again, some of these images of the goats, the pigs, and the humans at one day, or newborn, and then a few weeks of development or a few months of development. So we found, once again, nearly identical predilection vascular sites on humans and pigs, but didn't see it in goats. And maybe that suggests that this vascular etiology really is, at least in some cases, an aggravating or contributing factor to the development of the OCD. And SWI and other approaches might be something we use more in the future as we try to really fully understand this disease. Genetics, Ted talked about briefly. There's some familial case reports. Some people think it's somewhere from five to 10% maybe familial. This patient right here, this is a child, this father, who had two daughters and a son who all developed lateral fromal condyle OCD before the age of 12, all serious injuries. And so there clearly is a familial database. We're currently looking at the Utah Population Database, which allows us to look at ICD-9 codes and CPT codes and classify them through a very large population. And we're trying to see if there is a familial association with OCD. More work to come on that. And Ted has done some very nice GWAS work at CHOP, looking at genomic-wide association studies and how that may relate to OCD. I think etiology really matters, especially if there's genetic markers, because these could help with predictions both for who's going to develop OCD and perhaps who may have a good prognosis for healing with non-operative versus operative treatment. And I think the vascular thing is of particular interest to us because we focus a lot on mechanical stability with how we treat things. But we may have to focus even more on the biological approach to getting the vascular signals to change and improve vascularity in those necrotic areas. So we may need more of a vascular biological approach than simply a mechanical stabilization approach. I think we're gonna need more evidence and hopefully the Brock Prospective Cohort Registry will give us more information. Thank you, we'll take questions at the end.

OCD

etiology

vascularity

genetics

treatment