18. Knee Pain - And Why You've Been Thinking of it Wrongly

PFPS or Patellofemoral Pain Syndrome,

aka. PFS (Patellofemoral syndrome), Patellar pain, AKP(Anterior Knee Pain Syndrome), Runners Knee, IAKP (idiopathic anterior knee pain), etc. (or Non-Specific Anterior Knee Pain as I like to call it ‘in my own ignorant ways’)

*Imagine having something called ‘Runner’s knee’ and wondering when did you ever run?*

These are simply fancy ways of saying anterior knee(front of the knee) pain, that pertains majorly to the PFJ (patellofemoral joint), a joint that exists between our thigh bone and knee cap.

1. ≈ 25% of people with AKP (anterior knee pain) have PFPS or associated issues

2. It predominantly affects young females,

3. Usually atraumatic in origin,

4. Gradually progressive pain that starts with difficulty in recreational activities – daily living activities – sitting pain (funnily called the ‘movie theatre sign’).

How is it diagnosed?

While there are many supposed ‘causes’ of PFPS most(almost all) of the internal derangement, cartilage softening(chondromalacia), Q-angle, and other pathoanatomical claims have been poorly associated with the symptoms. A cluster of functional PFJ loading tasks and pain provocation are the best diagnostic tests at hand:

1. The presence of retropatellar or peripatellar pain.

2. Reproduction of retropatellar or peripatellar pain with squatting, stair climbing, prolonged sitting, or other functional activities loading the PFJ in a flexed position

3. Exclusion of all other conditions that may cause AKP, including tibiofemoral(knee joint) pathologies.

4. Some clinicians often use/apply McConnel taping (reduction of pain/symptoms after which is considered a differentiating factor) to differentiate between PFPS and Patellar tendinopathy. *(use with caution! There isn’t enough evidence to use this technique or of its diagnostic accuracy)

Thus, PFPS remains a diagnosis of exclusion, wherein special tests aren’t too special.

What is the ‘CAUSE’? Do structural abnormalities make a difference?

To explain in more ‘sciency’ words, the presently acceptable model of pathophysiology of PFPS:

‘The Tissue Homeostasis Model’ states that; Despite seeming like a deceptively simple musculoskeletal system disorder, the pathophysiological processes in PFPS range beyond the supreme importance of certain structural characteristics like Chondromalacia or Q-angle, To more inflammation, intra-articular pressure, (increased) tissue metabolism-based pathways, or simply a disruption of the normal tissue homeostasis.

Scott F. Dye in his paper ‘The Pathophysiology of Patellofemoral Pain: A Tissue Homeostasis Perspective’ states:

“A single loading event of sufficient magnitude or a series of repetitive loading events of a lesser magnitude can cause an injury-inducing cascade of reparative biochemical

processes which reflect a loss, at least temporarily, of normal tissue homeostasis”

So, to simplify the whole ‘cause’ argument. Most of the structural irregularities don’t correlate well with PFPS and the occurrence is probably due to a varied and rapid increase/change in physical activities that your body couldn’t cope with; at a particular time.

(here, here, here, here)

What to do about it?

Compared to a control or placebo, current evidence indicates exercise prescription is clearly effective in pain reduction and improved functional outcomes.

How to go about it?

1. Step 1– get in touch with a Rehabilitation professional)

2. Step 2– know that there is no bad exercise, you just have to introduce provocative movements and activities gradually.

3. Step 3– Challenge the structures optimally for a good recovery. (don’t let stress physical, social or mental pile up)

4. Step 4– Become a champ at self-management! (figure out when, how and at what intensities your knee is happy and keep at it)

What about the MVP? VMO?

What is this VMO? VMO or Vastus Medialis Oblique is the ‘oblique’ distal portion of the Vastus Medialis muscle which is one of the 4 muscles that the Quadriceps is made of.

It’s named so because the fibers of this specific portion of muscle are ‘too slanted’ to be called the same.

Fixation on biomechanical variables like Patella maltracking, VMO firing lag, and muscle activation as a cause of PFPS has led to a lot of aggressive “VMO strengthening” exercises that claim to activate/recruit and strengthen VMO in isolation.

Looking at the evidence, it seems likely that,

1. VMO can’t be isolated.

2. Isolated VMO exercises are not superior to generalized Quads strengthening.

3. VMO atrophy isn’t a cause of PFPS.

4. VMO firing lag (which is already a few milliseconds) has no significant effect on patellar tracking(unlikely to be significant enough for concern).

5. Altering the leg position doesn’t change much for muscle isolation.

(here, here, here, here)

Thus, a global Quadriceps resistance exercise-based approach is enough to be less fancy, more adherable, and equally effective(probably more effective when considered contextually).

Quadriceps Resistance training you say?

Yep, Good ol’ knee extensions! Although there is always a skeptical side that questions; How (potentially) increasing PFJ stress and compression by exposing the PFJ to high reaction forces(of quadriceps strengthening exercises) which are thought to exacerbate PFP can be helpful for the condition?

(here, here)

A fancy way of saying that the joint touches more & better, leading to a better load tolerance even with increased cumulative loads. Thus, quadriceps resistance training like knee extensions (preferably using a machine with a cable and weight stack system) seems to be safe and even beneficial for joint load tolerance, improving the surface area in contact and strengthening the muscle. Especially in the early stages of rehab.

Additional considerations for rehabilitation:

• Besides Quadriceps strengthening, focused Hip abductors and Gluteal muscle-strengthening programs seem to be beneficial for pain and function.

• Closed kinetic (on your feet) exercises (like squatting) can be re-introduced once load tolerance is better, or as early as the patient seems confident.

• Running and landing mechanics modifications must be looked into for better load tolerance, for example; “Cueing a modest increase in step rate (cadence) during running has been shown to reduce PFJ contact forces and stress in individuals with and without PFP.”

• A medially directed McConnel style taping has shown to be effective in pain reduction superior to sham (fake taping) *Thus, it can be looked into with caution and clarity that the tape can only symptomatically modify the situation, no structural modifications/improvements are seen due to taping.

• Foot orthoses and bracing can be used acutely for pain reduction and activity modifications but they don’t seem to change much in terms of outcome.

• Passive modalities (like K-tape, Dry needling, Cupping, Electrotherapy, etc.) for pain and functional outcomes must be skeptically analyzed and weighed against active mobility exercises.

(here, here)

What else to look out for in someone with anterior knee pain?

The knee is a complex structure, some of which can be a cause/contributor to pain in certain circumstances.

It is also layered (much to our convenience) like all other similar structures in the human body. Thus it’s smart to be on the lookout for a structural cause/pathology with a layered mental checklist.

Begining superficially with the :

1. Soft tissues (including the skin, subcutaneous fat, bursae, and fascia.): Prepatellar, Infrapatellar, Pes anserine, MCL, and Semimembranosus Bursitis.

2. The extensor mechanism (comprising the quadriceps tendon, patella, patellar tendon, and tibial tuberosity.): Patellar tendinopathy, Quadriceps tendinopathy.

3. Capsular+Synovial: Fat Pad Impingement Syndromes, Synovial impingement syndromes, Hoffa’s syndrome, Ligamentous tear.

4. Intra-articular/Bony: Plica Syndromes, Meniscus tear, Articular cartilage injury, Bipartite patella, Bone tumors, Loose bodies, Osteochondritis dissecans, Patellofemoral instability, Patellar stress fracture, Trauma, Infection

5. Apophyseal(adolescents): Osteosynchondroses, Osgood–Schlatter’s disease, Sinding–Larsen–Johansson’s disease

6. Nerve: CRPS, Neuroma, Saphenous neuritis

7. Referred pain: Lumbar spine, Hip joint pathology (such as SCFE or Legg–Calve–Perthes’ disease)

A lot right ?!!!

To conclude

Even though it’s a lot to consider, clinical presentations are usually clear enough to point to an obvious structural cause (if it’s the case), often even with an obvious structural abnormality people are asymptomatic (meaning that pain doesn’t really depend on structure alone) and almost all of these conditions can be effectively managed.

In the case of PFPS, structural deviations don’t matter much, in terms of pathophysiology. We should be aware and cautious of this while labeling/identifying a singular ’cause’ of PFPS with surety as it might affect the outcomes in long term.

So, if you are someone who treats people with knee pain or has knee pain yourself, just help yourself understand how complex the human body is and be assured that it can manage within a very wide band of ‘normalcy’.

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Cover Photo by cottonbro from Pexels

Disclaimer: This blog is for educational purposes only.