60 year old female with PFJ OA

60 year old female executice with Patellofemoral Osteoarthritis

 PC. Vague distributed antero-medially located right knee pain. Ache with occasional sharp pain. No giving-way but feels less confident in knee. No locking, aware of some swelling.

Thoughts: This sounds like PFJ  but must also remember it could be tibiofemoral, fat pad, hip joint or L spine referral.

Aggravated. Stairs, heels.

24 hour. Very stiff knee on waking. Much better at weekends.

Thoughts. The stiffness on waking tells us there is an inflammatory component here.What is she doing differently at the weekends?-that needs to be established.

Eased. Doesn’t hurt when much on holiday and re-iterates better at weekend.

Thoughts. This indicates there is something around lifestyle. It may be physical, or it be cognitive-affective.

HPC. Insidious onset 10 months ago, and steadily getting worse in terms of intensity of pain.

Thoughts. No trauma so more likely at age 60 to be a degenerative problem.

SH. Works in London and uses escalator steps as her exercise during commute at both ends of the day. Loves to look smart and wear thin, high heels. Commutes in heels.

Thoughts. Although stairs to offer some fitness benefit, in this case because stairs load the PFJ x3-4 the downsides probably outweigh the positives. Furthermore the commute in thin heels that shift the centre of mass forwards towards the PFJ, and create more instability through the limb through being a thin heel challenge the PFJ more. Need to explore alternative footwear and exercise options. This helps to explain the difference between weekday and weekend pain.

PMH. Nothing.

DH Nil

On Examination-Main Findings.

Observation. Very small effusion but very large oedematous right fat pad. Poor muscle definition.

Thoughts. Effusion may be causing some quads inhibition and the fat pad swelling may be a cause of pain and also promoting the pro-inflammatory cycle, and possibly encouraging pro-fibrotic, chondrocytic catabolic activity which is highly undesirable.

Muscle Length: Modified Thomas test reveals really tight hip flexors bilaterally.

Thoughts. The tight hip flexor means a greater percentage of the gait cycle will be spend in knee flexion. This has been evidenced to increase the likelihood of bone marrow lesions in the PFJ. BML are a potential source of pain, but are also reversible.

Quads. Poor bulk with VM wasting.

Thoughts. The effusion may be inhibiting the VM. The loss of VM means the fibres are more vertical and hence poorer at medializing the patella. The loss of quads function may be contributing to the loss of confidence in her knee, ie decreased dynamic stability.

Proprioception. Poor control of single stance. Touching down with the other leg and needing a hand hold. No pain, but very unstable. Lots of uncontrolled limb rotation and excess movement around the fat pad.

Thoughts. The poor limb control will increase the patients risk of falling. She is also going to enhance this instability in her high thin heels. The excess limb rotation is causing micro trauma to the fat pad which in turn causes a macro problem.

MRI- Severe degeneration of the PFJ with associated effusion and fat pad oedema. Presence of multiple bone marrow lesions in the PFJ.

Overall Impression:

Pain due to:

            Inflamed fat pad and PFJ with bone marrow lesions.



Long discussion re shoes! Compromised on wedged heels at work and commute in trainers.

Stop doing escalator stairs.

Start doing walks at weekend as long as no significant downhill. Ideally progress her exercise as her knee permits and she wants to.

Hip flexor stretches.

Ice massage to fat pad and fat pad offloading tape taught to patient.

Isometric quads at 20 degrees to avoid aggravating either PFJ or fat pad. Little and often initially to be progressed to alternate days with longer holds.

65 year old male runner with left anteriorly located knee pain.

PC. Deep ache antero-lateral PFJ. Occasional sharp pain. ‘Loss of confidence’ in knee.

Thoughts. The age of this patient increases the likelihood of OA but must not presume this is the source of the pain. Loss of confidence may be from pain, and or instability and instability may be from the joint or from reduced dynamic control.


Aggravating Factors:

Pain increases for 2 days after running.

Twisting on a fixed foot to the right can create sharp pain.


Stair descent creates pain during the movement.

Thoughts: Pain lasting this long after running indicates either an inflammatory reaction and/or increase in bone marrow oedema.

Twisting to the right could indicate tibiofemoral pathology or lateral PFJ as the femur medialises.

Kneeling compresses the PFJ but also stresses many other structures eg tibiofemoral jt, fat pad, and streteches quads and patella tendons.

Stair descent increases load on PFJ.




Thoughts: Fits with decrease in either inflammation or bone marrow oedema, (also referred to as bone marrow lesion).


24 hour pattern.

Pain at night. No extra stiffness in the am in the knee.

Thoughts: Night pain suggests one/combination of:

            Red Flag, (on questioning, no weight loss or history of Ca. No feeling of malaise).

            Inflammation-but I would expect increased stiffness in joint on waking.

            Bone marrow oedema. This characteristically can increase pain at night.



Gradual onset over last 3 months. No fall or trauma. He has been doing sprint intervals as part of his running training for variety over the last 6 months.

Thoughts. No trauma makes ligament injury very unlikely. Distance runner and therefore cannot exclude insufficiency fracture. Degenerate meniscal tear unlikely given location of pain. PFJ/lateral tibiofemoral joint OA most likely with this age and history.

Running faster means using greater hip adduction and increases load on the PFJ. It also requires more strength in both the quads and gluts.



Nil. V healthy. Low but healthy BMI.


Retired. Wife died last year.

Runs 3×10 km per week. Describes his running as, ‘sanity time’.


Running incredibly important to this patient and contributes significantly to his mental well-being.



Grade IV lateral PFJ chondral damage with associated bone marrow lesion, (BML) Otherwise healthy.

Thoughts. BML likely source of pain, not the cartilage-remember cartilage is aneural.




Good muscle bulk with symmetry right to left.

Standing with left knee in 10 degrees of flexion. Unable to correct when asked.

Highly visible ITB

No effusion

Thoughts. Good muscle definition fits with running levels, but doesn’t mean there is sufficient phasic activity to cope with sprint intervals. Phasic activity also declines rapidly with age.

Lack of effusion reassuring.

Really need to look at fixed flexion deformity and its cause. PFJ never gets a rest from loading in a knee that won’t go straight. Highly visible ITB suggests high tone/ overactivity in proximal contractile origins. Need to explore further.



10 to full flexion passively, 0 to full flexion actively. Extension tight.

Thoughts. Not a complete block to extension and therefore should respond to stretching/ mobilizing.


Muscle length Assessment.

Modified Thomas test=20 degrees hip flexion.

TFL via ITB tight in 10 degrees hip adduction.

Thoughts: Loss of hip flexion will increase amount of time spent in knee flexion, and correlates with increasing BML, (see Teng et al., 2015).

Tight TFL means in smaller degrees of hip adduction the patella will tilt and or lateralize, (more of a problem with fast running).


Gluteal Assessment.

Static Gluteus medius good on plinth but functionally pelvis drops with landing from a hop.

Thoughts: Insufficient phasic capacity to counteract sudden increased force on pelvis. Once again more of an issue running at greater speeds.


Single Leg Squat.

Very painful in lateral PFJ, with pseudo giving-way. Complete abolition with medial glide manually performed.

Thoughts: Off loading lateral PFJ with Q brace will help off load BML and allow it to settle. (see Callaghan’s work, 2015). This pseudo gving-way is pain driven and on questioning is the element that has led to a loss of confidence in the knee.



Source of pain, BML lateral PFJ.

Cause: increased load on lateral PFJ from;

            Intrinsically, tight TFL, tight hip flexors and insufficient gluteal phasic activity.

            Extrinsically, running especially sprint intervals.



Q brace to be worn all day every day as a treatment for 6 weeks.

Mobilise terminal extension and teach pt how to stretch at home.

Hip flexor stretches.

Once pain settling, start some small hops to work on stable pelvis, for better neuromuscular use of GMed in weight bearing. Progress this to ensure adequate phasic performance in gluteus medius in frontal plane.

Aquarunning for 6 weeks whilst joint is de-loaded to give BML chance to settle. Really important to keep this man active. If aquarunning not available, then cross-trainer wearing Q brace, not on consecutive days.

Long-term exploration of need for sprint intervals. Look at better ways to have variety with lower PFJ stress.

Teach pt to self-tape to off-load lateral PFJ for running.





13 year old county netballer with Patellofemoral Pain


 PC. Vague distributed anteriorly located left knee pain. Ache with occasional sharp pain. No giving-way but feels a sense of ‘slipping’. No locking, no swelling.

Thoughts: This sounds like PFP but must also remember it could be patella tendon, fat pad, Sinding-Larsen-Johansson(SLJ) and/or Osgood-Schlatters.

Aggravated. Landing from a jump in netball. Stair descent after netball for the rest of the day but not into the next day. Kneeling fine.

24 hour. No pain/stiffness on waking. Fine until pays netball. Pain on stairs for 1-2 hours post netball.

Thoughts. The fact that the pain does not extend into the next day suggests very little inflammation. No stiffness on waking makes it less likely to be tendon, and also that kneeling is fine makes it less likely to be fat pad, (SLJ) or Osgood-Schlatters.

Eased. Doesn’t hurt when on holiday ad not playing netball.

Thoughts. This indicates there is something around the netball. Need To explore volume of load more.

HPC. Insidious onset 9 months ago, and steadily getting worse in terms of intensity of pain. On questioning, she has grown 10 cm in the last 18 months, and also got into the county netball squad 9 months ago which added in x2 more training sessions a week. She has not had any treatment so far but has had an MRI.

Thoughts. Growth of this volume will alter the relative length of soft tissues, alter proprioception, and the trochlea shape can alter in this final growth spurt.

Need to ask about total training across a week.

MRI. Normal chondral surfaces but shallow inclination of lateral side of trochlea. Normal patella tendon length and tibial tuberosity position, (TTTG). Tendon, fat pad, and growth plates all normal.

Thoughts. Great news re growth plates/ joint surfaces, tendon and fat pad. The shallow slope subtly compromises the lateral stability of the PFJ However, the TTTG and tendon length being normal suggest that it should be possible to have a stable PFJ.

PMH. Nothing.

DH Nil

SH On a sports scholarship to her school. Anxious re ability to keep playing as feels her scholarship is at risk. Plays Centre for school team and WA for county. X2 training and x1 match per week for school, x2 training and x1 match per week for county. Also enjoys running so runs for a cross-country club at weekend.

Thoughts. Accumulatively this is a lot! X6 netball plus her cross country means no days off. Her position for the school involves more movement than her position for the county. Cross country aerobic so not particularly giving her very useful fitness for her netball. The scholarship is heightening her anxiety about the situation which may be altering pain processing.

On Examination-Main Findings.

Observation. No effusion, no fat pad oedema. Good muscle definition. Very prominent ITB’s bilaterally. Medialising femurs.

Thoughts. Is this an anteverted femoral neck, lengthened hip external rotators, lazy posture, or the foot driving the limb into medial collapse?

Craig’s Test. Neutral hip, i.e. not anteverted.

Gluts Assessment. Good static resisted hip abduction and external rotation at 20 and 90 degrees of hip flexion.

Hop test. Poor landing technique. Dropping into adduction and medial rotation, with inadequate hip and knee flexion. Able to correct with instruction.

Thoughts. Proximally her femoral neck appears in a good position and her strength appears good. However, she is not using this strength and is dropping into a large valgus moment, which overloads the lateral PFJ. This combined with her poor lateral trcochlea means two risk factors are coming together.

Muscle Length. All normal except 1.TFL/ Gmax, which are very tight. No passive adduction available on modified Thomas test. N2. Soleus tight so in knee flexion there is little dorsiflexion.

Thoughts. This may be due to the growth spurt. The TFL/GMax tightness is pulling on the ITB which given the poor lateral trochlea will lateralize the patella. The tight soleus encourages excessive pronation on landing and encourages whole limb medial collapse.


Overall Impression:

PFP due to:

            Growth revealing poor lateral trcochlea shape.

            Growth and? habit leading to poor landing technique.

            Sluggish control of femoral adduction and medial rotation.

            Proximal tightness leading to lateralizing of patella via ITB.

            Tight calf encouraging excessive pronation.



Temporarily stop cross country to have a day off per week.

Liaise with school about her changing to WA temporarily.

Soleus, TFL and GMax stretches to be performed x3 a week, x3 sets of 30 secs.

Proprioceptive training with bias on landing technique.

GUEST BLOG by Dr Lee Herrington-Patellofemoral joint pain post ACL reconstruction, a change of thinking in early rehab required?

Patellofemoral joint pain (PFP) and its sequelae Patellofemoral joint osteoarthritis have been reported to occur in significant numbers of patients following ACL reconstruction (ACLR) and have a substantial impact on function and quality of life1. Researchers have for a long time now theorized that a diminished capacity of the quadriceps to control loads and provide joint stability may place abnormal stresses on articular structures of the knee, predisposing the knee to degeneration2,3. The first part of this blog will present some of the growing body of evidence showing that ACLR patients have deficits in performance which can be linked to deficiencies in their quadriceps function, both of which can then be associated with abnormal patellofemoral joint loading. The second part of the blog will discuss how ACLR rehab might have to be modified to reduce the ACLR patient’s susceptibility to developing PFP.


ACLR patients have abnormal movement patterns such as decreased knee flexion angles (and excursion), knee extensor moments and higher initial peak loading rates compared to controls, when descending stairs, landing, walking and running, which are present from three months post op and can persist beyond two years post op4,5,6,7. These behaviours are indicative of “quads avoidance” a phenomena described by Powers et al8 as occurring in PFP patients. Alongside the abnormal movement patterns ACLR patients also present with significant deficits in quadriceps strength, force development and activation levels (degree of inhibition)6,9,10,11. These strength changes and movement patterns would appear to pre date the onset of osteoarthritis certainly and possibly PFP reported by Culvenor1. So the question might be why could these changes predispose the individual to PFP?


Why ACLR patients develop PFP could be due to a number of factors, but principle amongst them is likely to be the development and maintenance of bony oedema and the alteration in the loading environment within the patellofemoral joint. The presence and extent of subchondral bone marrow lesion (bony oedema) is significantly related to subchondral bone attrition and damage12, with up to 80% of ACLR patients having significant bony oedema on MRI scanning, so provides an overt link to osteoarthritis. Elevated levels of water content in the patella have been shown to be related to increased pain levels in PFP patients13, linking this to PFP. The presence of pain and bony oedema is likely to have a significant impact on levels of quadriceps inhibition and so strength3, this in turn limits the ability to absorb impact, through eccentric contraction and is borne out by the reduced knee flexion angles and increased early peak loading found during functional tasks, which is associated with increased patellofemoral joint loading14. So the local tissue homeostasis is significantly disrupted by both the presence of oedema and the altered loading environment.


The question then becomes how to reverse this downward spiral of quadriceps dysfunction, aberrant movement and perpetuation of the bony oedema. The most obvious place to break into this circle would appear to be at the beginning! Patients with greater quadriceps strength pre-op have superior function and at a variety of stages post op15, this also fits with what is known in PFP were those patients even with PFP who have stronger quadriceps have less pain and greater function(17). So first thing would be have the patients engage in a pre-operative strengthening programme (we’ll get onto defining what that means shortly) and very early post op starting strengthening and improving quadriceps function. Wang et al16 reported greater than 80% recovery of quads strength after ACLR is associated with less severe patellar cartilage damage, so it all appears to make sense. So why isn’t it happening already? The improvement in quadriceps function and reduction patellofemoral joint vulnerability are almost certainly impacted upon by two factors, first is a poor understanding of what strengthening exercises are and the second is the open kinetic chain exercise issue.


Though it might appear obvious, in order to strengthen muscles a suitable amount of external load needs to be lifted. The majority of patients undertake (body) weight bearing exercises (closed chain exercises such as squatting and step ups) which involve just moving their own body weight or small (relative to their body weight) additional external loads; they then do multiple repetitions of this. Plainly lifting a load for a large number of repetitions will not develop strength, this requires high loads which only can be lifted for a small number of repetitions. The best way to do this for quadriceps would be to do loaded open chain knee extension exercises; this takes us to the second problem the open chain exercise issue.


The open kinetic chain quadriceps exercise issue comes from the belief that quadriceps contraction creates anterior tibial translation and so could stress the ACL graft, there is no doubt that quadriceps contraction can create translation, but is it sufficient to actually create damage? If a maximal isometric quadriceps contraction is carried out at 20 degrees knee flexion (point of greatest potential translation), the level of translation load recorded is significantly less than that found undertaking a maximal lachmans test at the same angle(18). The amount of potential for anterior translation is angle specific with no translation occurring on quadriceps contraction at angles greater than 60 degrees knee flexion(19). In studies were open chain quadriceps exercises have been added to a rehabilitation programme, there was no significant differences in laxity across groups(20).


So to conclude, there is a strong likelihood that quadriceps dysfunction is related to PFP in the ACLR patient. In order to mitigate the risk, the patient needs to engage in a: preoperative training programme; early in the post op phase start to activate (overcome inhibition) and then strengthen the quadriceps. As part of this restricted range open chain knee extension exercises are likely to be a good option, alongside more traditional neuromuscular control exercises aimed at improving limb alignment and general whole limb work capacity.



  1. Culvenor et al 2016 Arthritis Care and Research. 68,6,784-792
  2. Hurley 1999 Rheumatological Disorder Clinics of North America 25,2,283-298
  3. Palmieri-Smith et al 2009 Exercise and Sport Science Reviews 37,3,147-153
  4. Thomas et al 2015 Journal of Orthopaedic and Sports Physical Therapy 45,12,1042-1050
  5. Di Stasi et al 2015 Journal of Orthopaedic and Sports Physical Therapy 45,3,207-214
  6. Lepley & Palmieri-Smith 2015 Journal of Orthopaedic and Sports Physical Therapy 45,12,1017-1025
  7. Noehren et al 2013 Medicine and Science in Sport and Exercise 45,7,1340-1347
  8. Powers et al 2004 Clinical Journal of Sports Medicine 14,4,277-284
  9. Laudner et al 2015 International Journal of Sports Physical Therapy 10,3,272-280
  10. Kline et al 2015 American Journal of Sports Medicine 43,10,2553-2558
  11. Harput et al 2015 Journal of Sports Rehabilitation 24,4,398-404
  12. Roemer et al 2010 Osteoarthritis & Cartilage 18,1,47-53
  13. Ho et al 2014 European Journal of Sport Science 14,6,628-634
  14. Silva et al 2015 Clinical Biomechanics 30,971-975
  15. Logerstedt et al 2013 The Knee 20,3,208-212
  16. Wang et al 2015 American Journal of Sports Medicine 43,9,2286-2292
  17. Culvenor et al 2016 Arthritis Care & Research DOI 10.1002/acr.23005
  18. Yack et al 1994 Journal of Sports Physical Therapy 20,5,247-253
  19. Beynnon et al 1997 American Journal of Sports Medicine 25,823-829
  20.  Glass et al 2010 North American Journal of Sports Physical Therapy 5,2,74-84

Dr Lee Herrington is the programme lead for the MSc in Sports Injury Rehabilitation at Salford Click here