When the Dallas Stars announced that Mattias Janmark was going to miss the next 5-6 months with a knee injury suffered in practice, my first thought was he'd torn his ACL. That's the most common hockey knee injury that takes that time frame for recovery, and it's notorious for occurring in low-or-no contact scenarios.
But, for better or worse, that wasn't the case with Janmark. He has an injury/underlying condition called osteochondritis dissecans, a name that made me go "huh?" the first time it was reported by Jim Nill. So as is in my nature, I went digging on the internet for more information.
What I found isn't entirely negative, but it's definitely a reason for some concern. This particular injury is a little more involved than the simple tearing of a ligament or breaking of a bone and deserves our attention in terms of what it means for Janmark's immediate and long-term future.
A couple general roots to make things seem a little less foreign: osteo- is a root word that indicates bone and chondro- is used for cartilage. The root dissec-, which you have come across in the word dissection, means to separate. Fittingly, then, osteochondritis dissecans is a condition where a problem in the underlying bone leads to damage to the layer of cartilage that covers bony surfaces (called articular cartilage, which is different from the more-often-discussed meniscus in a knee) and can cause it to separate from its usual surface.
(For the record, -itis usually indicates a condition caused inflammation, but in this case it's a relic of the person who initially named the condition back in the late 1800s. He thought inflammation would be a part of the mechanism, but this hasn't turned out to be the case.)
Bone, contrary to its popular reputation, is a very vascularized, dynamic system. There are a few big blood vessels and lots of tiny ones that run in and out to nourish the cells that build and break down bone, to bring calcium ions to and from the area and to take blood cells made in the marrow of the long bones to the rest of the body.
The "compact bone," or hard part of bone, is constantly in a state of flux, being built up at certain times and broken down in others in response to things like mechanical stresses and calcium levels. A complex system regulates this, but all those things depend on an intact set of vessels to bring the supplies.
In OCD, a small section of bone loses that blood supply. Reasons for loss include repetitive major or micro traumas and potentially genetic factors. When the blood supply is lost, the bone cells in that area die and can no longer repair wear and tear. This process, called avascular necrosis, results in a weakening of the bone in the area. The articular cartilage no longer has a strong place to attach and can turn into a "lesion" with fluid or, in more severe cases, have partial or complete detachment of the cartilage and some of the weakened subchondral (below the cartilage) bone into the joint cavity.
For what it's worth, the most common place for this to occur in adults is the knee, and the most common part of the knee to be affected is one of the surfaces of the femur. So how do they fix that? There's usually a two-part answer. The cartilage/bone flap must be reattached to its original location so the joint can move smoothly. That's done via things like nails and screws designed for use in joints. The second part is to address the underlying problem of the dead bone itself, which is stimulated via a few techniques, including the introduction of stem cells.
Jim Nill mentioned the use of stem cells for Janmark, which has been a part of the treatment for this condition in some form or another as far back as the 1950s. These are specific immature cells that can mature into healthy tissue and give the reattached section of cartilage and bone a healthy place to hook on to.
Like all biological processes, particularly ones that involve the maturation of immature cells, the process takes time and patience. Nill mentioned that there will be a scan after three months to see how those stem cells have matured and changed the affected problematic area.
Nill also mentioned that this injury was much more common in children and teenagers, and he's right. Unfortunately, that's not necessarily good news for Janmark, as younger age and immature bones lead to better prognoses for healing, even with non-surgical treatment. This makes sense - since kids' bones are still growing, it's easier for healthy tissue to displace diseased tissue.
As far as prognosis goes, that's hard to say. There's certainly a degree of measured caution - much more so than for things like ligament or tendon injuries. Most sources I came across had "good recovery" numbers of 70-85 percent in surgically treated adult patients and only a small percentage of patients needing follow-up repair to the initial lesion. Things that influence this prognosis are size and location of the lesion. Bigger is obviously worse, but a one in a critical weight-bearing area may be worse than a bigger one elsewhere. Nill didn't mention location, but he did give a size that was a the upper end of what is considered a "small" lesion according to some literature.
Assuming relatively average other risk factors, Janmark should have the underlying factors to be at the high end of those numbers, including outstanding overall health and mobility as well as access to top-end medical care and rehabilitation. To some extent, though, it will just be a wait and see process at this point.
(A big stick tap to actual orthopedic surgeon @bonebrokemefix on Twitter for looking this over and making sure it was accurate. While I don't even play a doctor on television yet, he's been through the whole process and actually knows what he's talking about.)