Receding Hair Lines and Joint Lines
... A Process of Life
Osteoarthritis (OA) is the most common joint disorder in the United States. Symptomatic knee OA occurs in 10% men and 13% in women aged 60 years or older (1). An estimated 4 million adults in the US are trotting on bionic knees, and the rate of TKAs has doubled in the last decade and continues to be on the rise (2). In reality, knee arthritis is a process of aging, its inevitable, and will happen just like a receding hair-line. Even if you are this guy:
Impeding hair line
Of course, there are always options:
But is a receding joint necessarily in doom? In Paul Dieppe's article (3) he demonstrates the disconnect between pain and radiographic findings, and the problem that the "radiographic finding" can give us the disease and is pushing us toward a much overzealous surgical fix.
"We should be looking for low tech, inexpensive, simple ways of reducing the burden of illness with respect to pain, limitation of activities, and participation in life by older people. If we're going to progress in this field, I believe we must make these paradigm shifts."
–Paul Dieppe
What Matters: Pain?
What seems to matter most is the amount of pain, and the age of the person (perhaps the older population has been to the doc for an image they feel due for a TKA?) as McAlindon et al demonstrated that knee pain and age are more important determinants of functional impairments in elderly subjects than the severity of knee OA as assessed by radiographic features (4).
To put it simply, it seems pain is to be implemented, not the radiographic features, in the diagnostic category of knee OA. Jordan et al. also concluded that knee pain severity was more important than radiographic knee OA severity in determining disability (5).
One study of over 2000 persons shows about 44% of people have radiographic OA, and about 20% have symptoms. The same study shows quad weakness associated with pain, but not radiographic knee OA (6). Other authors point to the need to look toward quad strength and motor control as opposed to a massive operation, in light of the pandemic arthroplastic surge. Brandt reminds us that OA is not a cartilage disease alone, but involves the whole joint. OA is about bone, synovium, and capsule as much as if not more than cartilage (7). I think this is an important way to view things, and can be used in explanation to patients: there is more to the picture than just the picture (x-ray).
Receding Cartilage
Studies have indicated that prior to cartilage deterioration, the knee shows signs of inflammation and medial meniscus damage early on, inflammation (Hoffa synovitis and effusion synovitis), along with meniscal "extrusion." Furthering Brant et al's findings (8). This should give us reason to suggest frequent movement/cycling/etc to our patients, as a prevention measure, to minimize inflammation.
When comparing prevalence among differing sex, women seem to be more OA-prone, both in pain reports as well as radiographic findings. One study shows that out of a group over 600, women showed slightly higher radiographic OA than men (35 % vs 31 %) but twice as many women reported knee pain than men. Over 60% of persons over 60 had radiographic knee OA (9).
The consensus is clear that as age and OA findings have a linear relationship, which does not come as a surprise. But remember, OA does not equal pain. The Framingham Osteoarthritis Study found that 10% of people aged 63 years and over had symptomatic knee OA (pain) in the presence of radiographic changes (10). In people with severe OA, it seems about half report pain (11). Although some studies find the link of reported pain and OA severity less clear, large scale studies (4000 subjects) finds a clear relations between the roughly 40% of persons with radiographic OA and pain (12). Even in these studies, 60% of the persons with radiographic OA did not have pain. Further, can the 40% improve? If so, their "radiographic" OA isn't changing….
Factors in Joint Stress
When considering factors with joints and stress, obesity is a topic often broached. Some really interesting things are brought up the "lower extremity review" regarding obesity and knee OA. In looking at WOMAC scores (questionnaire on ADLs and pain), obese people had higher risk for reporting bilateral knee pain, EVEN in persons with little to no "radiographic OA" changes(13). This indicates that the pain felt can be variable and not dependent on changes in the knee, even in knees you may think must be over-stressed.
Dr Weiss of LE review found that though her extensive research, knee pain does correspond to physical joint changes, but individuals with higher BMIs experience more pain, regardless of the amount of radiographic OA (14). Again this information begs the psychosocial implications of knee pain, however reasons might be explained by physiological change as well: one suggestion was that obese people have more pain in their joints due to an increase in "leptin" which modulates inflammation, as chronic low levels of inflammation are correlated with Obesity (15).
It may be proper to educate not only on weight loss, but also anti-inflammatory diet.
Further, there may be a lot of knee-related benefits that come from weight loss, not only decreased joint loading (think increased mobility, increased mood, positive outlook, increased activity, slimmer jeans and so on).
Loading & Biomechanics
When considering specific loading, we look no further than upon the medial condyle to enlighten us, as the medial condyle takes the majority of loading in the knee. Kumar et al. showed that knee OA subjects have high medial contact loads in early stance, and greater knee adduction moment (KAM). They also demonstrate greater static and dynamic varus of the knee.
In the biomechanics world, KAM (knee adduction moment) has been a topic of discussion, and thus effort to change it dynamically has been suggested. KAM is the torsion force which adducts the tibia on the femur. The magnitude of KAM during walking has been related to tibial bone changes, as well as OA severity (17,18).
Some suggest altering gait to reduce KAM: one being the "toe out" angle of the foot: apparently toe out stance during initial contact and the first 50% loading doesn't really affect KAM, though in the last 50% of stance, toe-out position can reduce KAM (19, 20). Other biomechanical factors include lateral trunk lean (which in magnitude has shown to be related to disease severity as well as reported pain) (21, 22). Though because lateral trunk lean actually orients the ground reaction force closer to knee joint center and lessens the medial compartment loading and KAM, we are thinking this is a compensation…this always brings up the notion that when we analyze a patient's gait, we are only seeing how they move in pain (ie the pain itself is influencing what we are seeing, not necessarily the other way around). These strategies may be adaptive or maladaptive.
Other strategies to reduce KAM include increasing hip internal rotation and adduction, and slight knee flexion, to get the knee physically closer to the GRF (23). Subjects instructed to walk with their knees as close together as possible (to reduce dynamic varus) showed major decrease in KAM magnitude (24, 25). Other research recommends treadmill walking and an incline greater than 5% to significantly decrease frontal knee loading (26).
Even delving into the patient's personal fashion sense can provoke load changing solutions: what shoes we wear also affect dynamic knee stress, as Ho KY et al points out in noting an increase in patella-femoral joint stress in women wearing heels due to higher knee extension moments and knee flexion angles (27).
One clinical trial states "Gait retraining reduced the first peak KAM by 20% (p < 0.01) post-training as a result of a 7° decrease in foot progression angle (i.e., increased internal foot rotation), compared to baseline (p < 0.01)." though the N is only 7, and it is not clear what instruction/method helped the patients gait chance (what they did differently) or if they retained this long term (28).
It seems the logic of all this KAM research is this: we see a lot of medial joint deterioration on images, this is probably the cause of pain, joint deterioration must be associated with high loads on the medial joint, so we should reduce loads at the medial joint and disperse them through out the joint with by changing GRF. So we will tell people to walk in ways that have the least load at the medial knee, so we don't cause more damage here. It seems logical, but to me more a tactic to take a break from the consistent loading that become associated with pain. It is important to note there are many factors beyond mechanical loading that can affect pain: Central sensitization has also been though to contribute to the more painful cases of knee OA, as the radiographic evidence can also be disproportionate (29).
From what I can gather from the knee OA research is that there is a high prevalence of radiographic knee OA with a linear relationship to our age. Joint space and cartilage health can be factors in whether the person has pain, but are not alone indicative of pain. People with more "bone on bone" tend to have more pain, but not overwhelmingly. Obese people tend to have more pain, regardless of their "bone on bone". Changing loading can affect how much pain a person has, despite the "BOB" extent. It makes sense to me to lessen the load on any sensitive tissue temporarily, change loading in a way that is functional and appropriate for the patient, and allow the "painful area" to become more resilient, and less sensitive. To me, the mechanisms of this outcome are part mechanical via altering the load, while allowing exercise and movement and life to resume, part mechanical in the sense that having stronger more resilient structure surrounding the painful and "threatened" knee allow for reductions in true joint stresses, as well as the patients psychological benefit from being able to resume some sort of strengthening to the area despite their belief that their joint is "no good", and in part due to the patient having a plan to return their knee to a more useful state. Graded exposure can be huge here: if a patient has severe pain after 5 minutes of walking, get them timing themselves for 2 minutes, 5 times per day. If going up a step seems a nightmare, have the patient unload themselves somehow: elbows on a table practicing a 2" step, or just pushing 50% into the step up motion. Allow progressions as the patient stays sub-threshold of a "flare up" and make them aware of their progressions.
As the patient sees some sort of progress (even if that is open-chain quad strength improving) they are gaining potential to fall into the demographic of "asymptomatic radiographic knee OA". The fact that there exists such a category should be bookmarked in your patients thought process. Your pre-TKA patients will undoubtedly have a neighbor, Sally or Bill, that can't stop talking on the greatness of their new knee. Even with the patients that undergo surgery and are smiling, it still doesn't prove that their intervention was implemented in their result: interestingly placebo surgery was no different than actual arthroscopic debridement in 180 patients with pain: in both, the majority of people got better (30)! Furthermore, some research comparing non-op and operative patients (regarding PFPS) show persons (N=56) undergoing knee arthroscopy and exercise is no better than exercise alone for people with PFPS (31)! I am not suggesting that the TKA be removed from the menu, but that there be some hope in persons who have been told they have radiographic knee OA, have pain and decreased function, to significantly improve their condition and resume a life, without removing a small portion of their lower extremity.
While the massive amount of research can be daunting, and somewhat conflicting and confusing, I think the take home point is to decrease the concept that cartilage deterioration itself is a disease that once present is detrimental to life and function, that we can temporarily change loading, both mechanically and in terms of dosage to make tissue more accepting and less painful (regardless of the Kellgren and Lawrence system findings) as well as change the way a person perceives their knee (although this can be difficult after the "nocebo" effect from white jackets pointing to thin joint lines).
You can use visual feedback cues to change loading strategy, and modify or promote ROM.
Some applications include:
Obtaining terminal knee extension in those lacking, for improved mechanical quad functioning during gait
Promoting loading awareness, by improving joint positional sense during closed chain exercises (if a person can only load one way, and the current route is paved in sensitive tissues, then they need to find alternatives at least temporarily)
Adding a visual component to simple exercise: balance reaches, hip stability, squatting, and any component I feel the patient has potential to gain more control of.
More importantly, they can see this change in motor control and positional awareness!
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