Treating Medial Side Knee Pain in a 43-Year-Old Rock Climber

At the 2019 Orthopaedic Summit: Evolving Techniques (OSET) held in Las Vegas this past December, two well-respected orthopedic surgeons debated the issue of whether bone edema is a bone or a joint issue. Peter F. Sharkey, M.S., M.D., Professor of Orthopaedic Surgery, Rothman Orthopaedic Institute, Sidney Kimmel Medical College and Adam B. Yanke, M.D., Ph.D., of the Cartilage Restoration Center at Midwest Orthopaedics at Rush—debated the treatment of a 43-Year-Old Rock Climber With Pain On Medial Side Of Her Knee, MRI Confirms Bone Edema & A Narrow Medial Joint Line But Not Bone On Bone – What To Do?

Subchondral Bone: Importance in OA Pathogenesis, Focused Intervention and Results of Subchondroplasty

Dr. Sharkey: Thank you very much. Today we are debating the role of bone versus cartilage in the pathogenesis of osteoarthritis (OA)…and I’ve been tasked with the bone portion of this equation, i.e., the culprit. Adam is young and wrong! Let me say it again, this is a bone issue!

After 35 years of orthopedic experience, I can tell you that there are only a handful of principles that are absolutely true. We know that radiographs, at least when it concerns osteoarthritis, are not very good predictors of patient symptoms. I think we’d all agree on that, Adam.

Conversely, an MRI provides data that is very relevant to OA pathogenesis. Not only does an MRI show soft tissue and inflammation but—critically—it shows subchondral bone damage. And that damage is the most important finding related to the pathogenesis of osteoarthritis.

Here is why.

Reason number one. An abundance of literature demonstrates that OA-associated BMLs (bone marrow lesions) are a much better predictor of symptoms than cartilage loss. While we know that from X-rays, in addition, multiple studies have shown that BMLs are the strongest predictor of symptoms in patients with OA.

Reason number two. We know the histopathology and the effect on subchondral bone mechanical properties associated with these lesions because we have an enormous amount of retrieval data from total knees and total hips. This bone represents stress and fatigue fractures. And the bone is structurally compromised—irreversibly so. It does not resemble normal subchondral bone.

Reason number three. The weakened subchondral bone can no longer support the subchondral bone plate, which leads to collapse and progressive deformity, referred to by radiologists as subchondral bone attrition and accelerated cartilage loss. In a recent study, there was an incredible correlation between BML grade and the risk of developing subchondral bone attrition.

Reason number four. The progression of pathology leads to the need for a partial or total knee replacement, a fact that has been demonstrated in multiple studies. Many total joint surgeons are of the opinion that an untreated BML will lead to a total knee arthroplasty.

If you consider this finding in terms of function, take a look at the 25-year track record of the brilliant Scott Dye. He realized that as we get older, we lose cartilage. It may be age-related. It may be trauma-related; all sorts of reasons exist. Perhaps our menisci start to fail. If we start to exercise in the zone of structural failure, then we get supraphysiological overload. We develop stress fractures in the subchondral bone. There is subchondral bone attrition, deforming bone, progressive deformity, and accelerated cartilage loss which leads to knee pain and ultimately, arthroplasty.

So, what are the options for this 43-year-old rock climber after non-surgical care fails? (Of course, it’s always non-surgical care first.)

A high tibial osteotomy would unload the bone…or we could do a partial or total knee to put a metal plate over the bone and relieve the focal stresses. Or perhaps we could magically thicken her thinning cartilage to realign her joint and reduce pressure on the subchondral bone.

Or better yet, we could repair and strengthen her histologically altered and mechanically compromised subchondral bone, i.e., subchondroplasty. This is a very simple procedure with only three steps.

First, you get a preoperative MRI and then you use it to develop a plan to localize the lesion.

Then, using fluoroscopy, you take a three 3D MRI, convert it to two dimensions and localize this by fluoroscopy. Target the legion, place a cannula, and then inject a flowable bone substitute material to repair the damage. This is really easy, Adam. Just don’t deal with the joint.

To date, 29 manuscripts have been published on the benefits of subchondroplasty. The most recent one—a multicenter study involving surgeons who do not have significant financial interest in the product—found that at 24 months, Knee Injury and Osteoarthritis Outcome Scores (KOOS) were significantly improved. Also note that these improvements were statistically significant at all time points except for two weeks.

When you consider the subscales—activities of daily living, symptoms, sports and recreation, quality of life—it is clear that each one substantially improved from pre-op to 24 months. Additionally, Visual Analogue Scores (VAS) significantly improved: 31.6 mm on an 11-point scale. Finally, both VAS and KOOS showed significant improvement at 24 months.

So based on extensive data, I advocate for subchondroplasty for this rock climber. Thank you. I rest my case!

“Leave the Subchondral Bone Alone: It Is the Cartilage Stupid!”

Dr. Yanke: Thank you. First of all, Peter, you and I have a similar amount of clinical experience. You have 35 years, while I have three to five years…but I have been very busy. This is a joint issue, Peter.

If this patient had significant varus-associated pain, then I certainly would take the high tibial osteotomy (HTO) approach. However, I’m going in a different direction here: bone marrow lesions can play a role but they’re just not the only thing that matters.

When you have large cartilage loss and a Kellgren-Lawrence grade 3 or greater, then I would not advocate for a cartilage procedure in this patient—nor would I recommend a subchondroplasty. I would try to mitigate her symptoms as much as possible in order to obtain a functionally asymptomatic X-ray or MRI.

While you can’t make a clinical decision based solely on X-rays, we must also take care not to make such judgements on an MRI alone. So, this could be an example of what this patient could look like where she has some joint space left. An HTO would work just fine—forget injecting something into the bone marrow edema.

Just remember, Peter, that the bone marrow lesions on a tibia will have a degenerative meniscus tear as well as early cartilage damage. It is imperative that both of these issues are addressed.

This young and active patient—a 43-year-old rock climber—is similar to the asymptomatic NBA players I treat in Chicago. We find that on their MRIs, 7% have a focal cartilage defect, 25% have a subchondral bone marrow lesion, and almost half of them have some cartilage abnormality. Overall, only 18% of people have asymptomatic normal MRIs.

There are two unseemly possibilities here. First, as physicians we don’t want BARF (Brainless Application of Radiologic Findings). And for patients, we don’t want a VOMIT situation (Victim of Modern Imaging Technology).

So, we have to definitively determine if this is clinically relevant for the patient or if it’s just something we see on the scan, but don’t have to worry about.

We know that there are many more contributors to pain than just the cartilage surface or the subchondral bone. And as we delve into these, we see that they actually play a much bigger role than some of the other structural aspects that we have focused on in the past.

I’ll also reference Scott Dye—who scoped his own knee—I believe with the help of his brother. Upon touching different parts of the knee with minimal anesthesia, he found that the soft tissues surrounding the knee were some of the most painful areas. Granted, he did not have an exposed cartilage defect that exposes bone but I’m sure that would be painful as well. However, this does highlight the importance of that soft tissue envelope.

Work by Eric Strauss and others looked at cytokine levels and correlation with functional and pain scales after arthroscopy. He found that IL-6, an inflammatory cytokine, was significantly correlated with pain, with patients in greater pain having higher concentrations of IL-6 within the joint.

I think that if we’re not addressing the synovium and the synovial lining then we are potentially missing part of the picture in these patients.

When we look at the presence of a subchondral bone marrow signal with a cartilage procedure, even though I wouldn’t recommend it for this patient, it’s essentially equivocal.

My argument, Peter, is that there are studies showing that bone marrow lesions correlate with OA-associated pain. While this is certainly part of the story, those studies don’t control for these other factors. They look at the amount of arthritis that’s present, as well as the MR findings, but it may be that those cytokine levels may preempt and actually cause more symptoms for the patients.

We have at least three or four pain generators. In this case, Peter, it is not the bone. It could be the cartilage, it could be the meniscus, and it could be also the synovium or the lining of the joint. I think we have to be careful not to hyper focus on this as the pain generator and not rush to squirt something into the “bone marrow edema.”

Where does the pain start and where does it end? In order to thoughtfully address these questions, we must take into consideration each of the things I have mentioned today. We don’t need to treat just the bone marrow edema. You need to do an HTO. We need to treat the source and I do think that for most of these patients, it starts within the joint and expands outwards. Peter, you’re just wrong.

Thank you very much.

Please visit https://orthosummit.com/ for more information on this year’s upcoming 10th Anniversary Orthopedic Summit 2020 event on December 8-12, 2020 at the Bellagio in Las Vegas, Nevada.