Since there are not yet any PT CPGs for knee OA, we pull together information from textbooks, articles, and two physician CPGs to cover what does and doesn't work for knee OA. We also review physiology, diagnosis, and an easy little CPR at the end.
Use code FIELDGUIDE for 40% off a MedBridge subscription.
Find more resources and subscribe to practice questions at PhysioFieldGuide.com.
Use code FIELDGUIDE for 40% off a MedBridge subscription.
Support the podcast and get study guides and bonus episodes at Patreon.com/physiofieldguide.
Find more resources and subscribe to practice questions at PhysioFieldGuide.com.
Since there are not yet any PT CPGs for knee OA, we pull together information from textbooks, articles, and two physician CPGs to cover what does and doesn't work for knee OA. We also review physiology, diagnosis, and an easy little CPR at the end.
Use code FIELDGUIDE for 40% off a MedBridge subscription.
Find more resources and subscribe to practice questions at PhysioFieldGuide.com.
Use code FIELDGUIDE for 40% off a MedBridge subscription.
Support the podcast and get study guides and bonus episodes at Patreon.com/physiofieldguide.
Find more resources and subscribe to practice questions at PhysioFieldGuide.com.
Hello everyone. Today we’re planning to finish the last episode on the knee for a while with a discussion of knee osteoarthritis. As you might have noticed, we do not yet have a physical therapy clinical practice guideline for knee OA as of September 2021. Yet this is a very common condition, and we see it all the time in the clinic, so we suspect it is bound to show up in some fashion on the exam. So what we’ve done for this episode is we pulled together information from textbooks, articles, Current Concepts, and two physician clinical practice guidelines to try to summarize and provide you the best information on knee OA as efficiently as possible. Let’s jump in.
First, let’s talk about the physiology of the condition itself. For a long time, knee OA was described as a “wear and tear” condition—that over time the articular cartilage in the knee starts to break down and osteophytes start to form, and it’s that breakdown and loss of cartilage that causes knee pain. However, a few facts have challenged that perspective. First, remember that hyaline cartilage is avascular and aneural, so the cartilage itself is not a pain generator. Second, studies that try to link the amount of joint degeneration seen on imaging to patient pain level offer inconsistent results, with some patients demonstrating severe degenerative changes and little to no pain, while other patients have less degeneration and high amounts of pain. At the very least, I think it’s safe to say that there is not a perfect, clear, linear association between amount of degeneration and pain.
So in recent decades, inflammation—not just degenerative changes—has been recognized more and more as a source of pain in knee OA. And increased attention has been given to considering osteoarthritis as a condition that affects the whole joint—not just cartilage and bone. Since 10% of the exam is pathophysiology and pain science, I think it’s valuable to dig a little deeper into knee OA pathology.
We’ve already briefly mentioned cartilage changes, because they’re often the most apparent. In OA, the cartilage gradually erodes. The collagen matrix in the cartilage becomes less organized due to uncontrolled production of matrix-degrading enzymes. The cartilage becomes increasingly filled with water and decreasingly filled with proteoglycans, which makes the it less capable of absorbing forces. At the same time, chondrocytes proliferate and hypertrophy, which increases the metabolic activity of the chondrocytes and accelerates degenerative changes.
Just beneath the cartilage, in the subchondral bone, we find calcification, hardening, and subchondral cysts forming. Deeper into the bone, some individuals with OA also have bone marrow lesions, which are a possible source of pain in those with knee OA. And at the edges of the joint, abnormal bone growth creates osteophytes, or bone spurs.
But perhaps the overlooked tissue in all of this is the synovium. OA is not just a disease of the cartilage and bone, but of the entire joint, including the synovium. In OA, the synovium begins to acquire more inflammatory markers and inflammatory cells. Fragments of bone or cartilage may become embedded in the synovium. This can exacerbate inflammation of the synovium and lead to synovitis. Over time, we also see thickening and possible fibrosis of the synovium. So the synovium—especially if inflamed—is another possible source of pain in those with OA.
And finally, it’s thought that the nerves that innervate the joint may also be affected by these structural and chemical changes and become more sensitive, so some have suggested a possible neuropathic source of pain.
When you add all of that up, and when you consider that degeneration on radiograph is only weakly associated with pain, I hope you’ll agree that describing OA as “bone on bone” is a very poor way of explaining this condition. The loss of cartilage itself is not so much the source of pain in knee OA as bone marrow lesions, synovitis and inflammation, and possible peripheral nerve sensitization—with increasing evidence that central sensitization plays a very large role here as well.
I don’t know exactly how much of this could show up on the exam. I do think it’s helpful to recognize the different tissues that are affected and the different possible sources of pain. I also think it’s important to know this so that when my patient says, “The doc says it’s bone on bone—worst he’s ever seen! And there’s nothing you can do about it!” we can at least explain that there is more to the story. But let’s move on.
Let’s talk diagnosis. We already covered how to distinguish OA from other forms of arthritis in our arthritis episode, so I encourage you to review that material to aid in your differential diagnosis.
I do want to briefly mention that when we’re talking about knee OA, we’re typically talking about tibiofemoral OA. And we know that while this often affects both condyles, it may affect one more than the other—and that might affect our treatment options, which we will talk about in a minute. The other form of OA in the knee is patellofemoral OA. It’s less common, but may be associated with abnormal trochlear morphology and patella alta. One significant predictor of development of patellofemoral OA is history of patellar dislocation or a history of adolescent knee pain. In one study, adolescents who experienced anterior knee pain before the age of 18 are 7.5 times more likely to develop severe, symptomatic patellofemoral OA as they age. That’s an interesting risk factor that I might want to store away for the exam.
Patellofemoral arthritis is often going to present like patellofemoral pain syndrome with patients reporting pain negotiating stairs or sitting for a long time and presenting with associated quadriceps and hip weaknesses. To distinguish patellofemoral arthritis from patellofemoral pain syndrome, consider the age of the patient and the presence of any knee or patellar deformities.
That’s about all we’re going to cover on patellofemoral OA. The rest of the episode, we will generally be discussing tibiofemoral OA.
The American College of Rheumatology has a few different methods for diagnosing knee OA: it can be done through history and physical exam alone, or it can be done through history, physical exam, and radiographs, or it can be done through history, physical exam, and lab test. You might hear these called the “ACR criteria” (after American College of Rhematology) or the “Altman criteria” after the principal investigator on the study that developed the criteria. Of the three, I wouldn’t spend much time on anything but the physical exam and history criteria. It’s such a simple diagnosis, and we’re so rarely going to bother with radiographs and lab tests, that this is the criteria you’re most likely to see and use. The criteria requires that the patient have pain in the knee and any three of the following: age over 50, less than 30 minutes of morning stiffness, crepitus on active motion, bony tenderness, bony enlargement, and no palpable warmth of synovium. Remember that you only need three of these to make a diagnosis. So even if you get a question where the morning stiffness lasts, say, 45 minutes, but everything else looks like knee OA and doesn’t look like a different type of arthritis, then it’s probably knee OA. So once more, the criteria are pain in the knee plus any three of the following: age over 50, less than 30 minutes of morning stiffness, crepitus, bony tenderness, bony enlargement, and no palpable warmth of the synovium.
Once radiographs are ordered and interpreted, knee OA can be graded using the Kellgren-Lawrence Classification system. This system applies to OA at any joint, so it could also pop up on a question about hand or cervical or lumbar OA. There have also been modifications suggested in the literature, so you might see some variations, but I’m going to cover the original scale.The grading system runs from 0 to 4 as follows:
Now honestly, I’m not sure it’s worth your time to memorize every little detail of this scale. I think if you can remember a few key facts about the scale, you’ll be able to fill in the gaps. So here are a few things that make the Kellgren-Lawrence system tricky, and how I would recommend remembering it.
The first tricky part is that the scale is from 0 to 4—not 1 to 5. So remember that 0 is the lowest on this scale, and 4 is the highest. The second tricky part is that 0 means no OA, but 1 means “doubtful”—or probably no OA. So there aren’t actually clear signs of OA until you get to grade 2. Grades 2 through 4 are where you can actually make a diagnosis of osteoarthritis. So since there are three grades of clear arthritis (2, 3, and 4), it should be easy to remember that those represent minimal, moderate, and severe. So if you remember that the top of the scale is grade 4, and that represents “severe,” you should be able to work backwards from there. Or if you remember that grade 2 is where there are the first clear signs of OA, you can work forwards from that point . At that point, just remember that in OA, osteophytes are usually the first thing seen on radiographs, and joint space narrowing comes later. So grade 2 is minimal with clear osteophytes but only possible joint space narrowing, grade 3 is moderate with multiple osteophytes and definite joint space narrowing, and grade 4 is severe where everything just looks awful. Or, as seemingly every single patient with knee OA says, “It’s all bone-on-bone—worst the doc has ever seen!”
Well that’s probably more time spent on the Kellgren-Lawrence scale than I spent on it when I was prepping for the exam, so let’s move into treatment.
It's difficult to find good practice guidelines for treatment of knee OA, because there is no PT guideline, and the MD guidelines conflict or can show bias depending on which group created them. I am going to summarize information primarily from the American Academy of Orthopedic Surgeons (or AAOS) guideline, which seems to me to be a little less biased than the American College of Rheumatology (or ACR) guideline. The orthopedic surgeons’ guideline was also just published August 31, 2021, so it’s hot off the press and just slightly more current than ACR guideline. However, I will pull in some information from the ACR guideline and from other sources where necessary.
First, I want to cover three interventions that are unique in that the recommendations really only apply to unicompartmental knee OA: bracing, lateral heel wedges, and tibial osteotomy.
Personally, I have never met a knee brace that I liked—either due to fit or due to function. But there’s relatively good evidence for valgus offloading braces for medial compartment OA. The idea is that, by applying a valgus force at the knee, the brace can make the lateral compartment bear a little more weight and relieve the medial compartment. So the guideline makes a moderately strong recommendation in favor of bracing—but this mostly applies to valgus offloading bracing for medial compartment OA.
Another conservative treatment that is sometimes used to treat medial compartment OA is a lateral heel wedge. The AAOS guideline cites a ton of recent research to make a strong recommendation against lateral wedge insoles. They don't work, many subjects had worse pain, and compliance was poor due to discomfort and adverse events.
The guideline gives a “limited” recommendation for high tibial osteotomy in those with medial compartment OA. In order to relieve pressure on the medial condyle, a surgeon will fracture one side of the the superior portion of the tibia and then do an ORIF to reshape the tibial plateau in an attempt to change the joint space shape and redistribute the load of weight bearing. For most patients, a unilateral knee arthroplasty is going to be a better option here, but tibial osteotomy might be recommended for those desiring to function at a higher level than is typically recommended after a UKA. So what you should remember here is that tibial osteotomy is only weakly recommended and only for medial compartment OA.
So for medial compartment OA: yes to valgus offload bracing, no to lateral heel wedges, and maybe for tibial osteotomy in just the right circumstance.
Okay, let’s move on and talk about conservative treatments commonly performed by physical therapists for more general knee OA.
Exercise gets resounding, strong recommendations from everyone. And just about any form of exercise that is studied yields good results: supervised, unsupervised, land-based, water-based, weightbearing, non-weightbearing, aerobic, anaerobic, low resistance, high resistance, with hip strengthening, without hip strengthening—every group that exercises in a study on OA makes significant improvements, and no single form has been shown to be consistently better than another. Of course, a treatment plan based on an individualized examination and patient preferences is probably going to yield the best results, but if you can get your patient to buy into any exercise program they like, they will likely make improvements.
In contrast, neuromuscular training only receives a moderate level recommendation due to a study showing that traditional exercise plus neuromuscular training was not superior to traditional exercise alone. Again, this is where your individualized assessment is important: neuromuscular reeducation is most likely to help those with neuromuscular deficits, not a randomly selected group of people with knee OA. So the important thing here is that if you get an OCS question that makes you choose between therapeutic exercise and neuromuscular reeducation in an individual with knee OA, it seems that therapeutic exercise is the best option.
Next let’s consider another of our most-billed services: manual therapy. The AAOS only gives a limited recommendation for manual therapy, and the American College of Rheumatology actually recommends against it. I think this is one spot where some of the bias of these groups comes through. The AAOS guideline cites a couple studies—Deyle in 2000 and Fitzgerald in 2016—that compared exercise plus manual therapy to exercise alone. Both studies showed significant improvements with manual therapy, with the Fitzgerald study finding superiority of the manual therapy plus exercise intervention on the WOMAC. The complaint of the AAOS is that in both studies, there was no difference between the groups at a 1-year follow-up. If you're a physical therapist, this is no surprise: manual therapy is not a long-term cure. You stop doing it, you stop reaping the benefits. What we should be focusing on is the manual therapy plus exercise group that performed better during the period of the intervention, because that time period is still valuable for our patients. And because we know the effects don’t last forever, there have been some trials recently recommending a decreased frequency of PT with sessions spread over a longer period of time, or even periodic “booster” PT sessions.
We really do have a large amount of evidence that favors manual therapy in the treatment of knee OA. If you really want to dig into it, I think Gail Deyle does a great summary in his MedBridge course. For the OCS, I think you should just know that manual therapy is effective, but it is not a long-term solution. The long-term solution is exercise.
Similarly, the AAOS also evaluated the usefulness of massage—which, of course, we don’t do unless you’re a PT who is also a licensed massage therapist, but it makes sense to cover it here. They cite a study where subjects got ongoing massages for a full year. The massage group improved at 8 weeks, but they failed to maintain that improvement for the rest of the year. So in this case—unlike the manual therapy studies—the intervention was ongoing and still failed to produce significant results. So the AAOS gives it a “limited” recommendation and the ACR recommends against it.
Let’s move on to modalities. Evidence for high-level laser therapy showed significant improvement compared to placebos and no treatment, and a study comparing high-level to low-level found no difference between the two. So lasers so seem to work, but they get a “limited” recommendation due to cost, feasibility, and unclear ideal dosing parameters.
Research on TENS has produced unclear results, sometimes finding significant improvement and sometimes finding no difference compared to controls. So the AAOS allows it a “limited” recommendation, but the ACR, always a bit more cruel and harsh, gives a strong recommendation against TENS. My opinion probably lies a bit closer to the ACR on this one.
Similarly, extracorporeal shockwave therapy and dry needling have found mixed results and receive a “limited recommendation” and a “no recommendation,” respectively.
Let’s move on and talk about educational or lifestyle interventions.
The AAOS makes a strong recommendation in favor of self-management programs and patient education (which they break into two separate interventions, but there’s so much overlap that I’m treating it as one). The self-management programs focused on training patients in medication compliance, pain management and pain coping strategies, joint protection strategies during physical activity, exercise advice, problem solving approaches and stress management techniques. This training helped. Similarly, a variety of educational techniques and modalities, including motivational interviewing, also helped.
Speaking of joint protection strategies, we also have a moderate strength recommendation in favor of canes in the AAOS guideline and a strong recommendation for them in the ACR guideline.
Next is weight loss. The AAOS makes a moderate recommendation and the ACR makes a strong recommendation in favor of weight loss for those who are overweight or obese. In general, it takes at least a 5-10% decrease in weight for improvement in symptoms. And the studies that compare diet to exercise or to diet plus exercise favor the groups that get exercise.
Let’s turn our attention to supplements and pharmaceutical interventions.
The short version of the supplement recommendation is that there is inconsistent evidence for turmeric, ginger extract, glucosamine, chondroitin, or vitamin D. Because of this, the AAOS says, hey, if it seems to help the patient, great, and the ACR—brutally—gives a strong recommendation against.
Moving on to topical treatments: both guidelines make strong recommendations for topical NSAIDs. The most popular that I see is diclofenac gel, or brand name Voltaren.
For oral medications, we have a strong recommendation in favor of oral NSAIDs with the caveat that they can cause increased risk of serious cardiovascular thrombotic events and serious GI events. (Remember how, at the beginning of the episode, we suggested inflammation may play a bigger role than degeneration in OA? If that’s the case, it makes sense that NSAIDs would be so effective.)
We also have a strong recommendation in favor of acetominophen, but it isn’t as good as NSAIDs when they’re compared directly, and remember that there is a risk of hepatotoxicity.
Oral narcotics are strongly recommended against. They don’t work. They cause adverse events. Don’t let your patients self-prescribe oral narcotics, or call the MD and recommend against them if the MD prescribed them for your patient.
There are just a couple reasons why you might want to review these pharmaceutical recommendations for knee OA. One is for an advanced practice setting where PTs might have some prescription rights. Although it’s unlikely, it is possible that the OCS writers might want to test your knowledge and ability to practice in that kind of setting. The more likely scenario is a patient case where you might have to recognize an adverse event from medications—like a GI bleed from an NSAID or liver toxicity from acetaminophen—and correctly identify the medication at fault.
Finally, I want to cover medical procedures. Either on the OCS or in the clinic, a patient is likely to ask you about some of these, and it would be good to be able to point to the evidence.
First is hyaluronic acid injections, which is sometimes called viscosupplementation. The most common viscosupplementation that I hear about is the Supartz injection. Both guidelines recommend against these injections. The research on hyaluronic acid injections does sometimes show a statistically significant difference between groups that favors the injection group, but the effect in these studies failed to exceed the minimally clinically important difference, or MCID. So both guidelines recommend against hyaluronic acid injections.
Next is corticosteroid injections. The research indicates that corticosteroid injections do improve pain and function for up to 3 months, but no longer. So we have recommendations in favor of corticosteroid injections for short-term relief only.
Next is platelet-rich plasma, or PRP injections. Right now, the research on single PRP injections or a series of two injections have yielded inconsistent results. Research looking at a series of three PRP injections demonstrated more consistently positive results in favor of PRP. However, one 2018 study examining adverse events from PRP injections have raised some safety questions, so the AAOS only gives a limited recommendation for PRP, and ever the wet blanket, the ACR gives a strong recommendation against.
The ACR also recommends against several other injections not mentioned by the AAOS, including botulinum toxin, prolotherapy, stem cells, and tumor necrosis factor inhibitors and interleukin-1 receptor antagonists. It's starting to sound like they’ll inject just about anything into a knee joint these days.
Last, we will quickly cover surgical interventions.
There is some evidence for denervation therapy—yes, we’re talking about nerve ablations at the knee—but the AAOS only gives it a limited recommendation due to inconsistency and bias in the studies.
The AAOS also gives a moderate recommendation against lavage and debridement, noting that some studies show it is no better than placebo. However, they note that patients who had meniscus tears or loose bodies were excluded from most of these studies, so they give themselves a little wiggle room there.
The academy of surgeons also gives a moderate recommendation in favor of partial meniscectomy in patients with OA after they have failed physical therapy or other nonsurgical options. Now, we spoke in our meniscus episode about how large studies in the British Medical Journal and the British Journal of Sports Medicine have pretty convincingly shown that partial meniscectomies in patients with knee OA should not be recommended over exercise and physical therapy. But again, this is the American Academy of Orthopedic Surgeons, so they cite several of the same studies showing that the surgery is no more effective than conservative treatments, and then make a moderate recommendation in favor of it. I guess it’s pretty hard to recommend against one of the most popular orthopedic surgeries when you’re an orthopedic surgeon.
There are no recommendations made about knee replacements here. However, given the overall very positive outcomes following TKAs, it’s probably safe to assume they would receive a glowing recommendation.
That was a lot, so I’m going to repeat the most important recommendations very briefly.
Before we sign off, I want to mention one more nugget that could pop up on the exam. A clinical prediction rule was derived in 2007 that attempted to determine which individuals with knee OA would benefit from hip mobilizations. If an individual has knee OA plus at least one or two of the following, they are likely to benefit from hip mobilization: hip or groin pain or paresthesia, anterior thigh pain, passive knee flexion less than 122 degrees, passive hip internal rotation less than 17 degrees, or pain with hip distraction. In the derivation study, having one of these factors led to a 92% probability of success, but having 2 of these factors led to a 97% probability of success. And these factors make since, right? We’re talking about different ends of the same bone, and if there is pain or hypo mobility at one joint, then improving the mobility of the other joint might help make up the difference. So again we’re looking for at least one—but ideally two—of the following: hip or groin pain or paresthesia, anterior thigh pain, passive knee flexion less than 122 degrees, passive hip internal rotation less than 17 degrees, or pain with hip distraction.
Although we don’t usually recommend devoting a lot of effort to clinical prediction rules that haven’t been validated yet, this one is so straightforward and makes such good clinical sense that I would still recommend it.
We’re going to wrap up there for today, and we look forward to introducing a new body region next time.