Patellofemoral pain: is it time for a rethink?

This blog is an amended version of an essay first published in the McKenzie Institute Mechanical Diagnosis and Therapy Practitioners (MIMDTP) UK Newsletter.  It also represents some of my early work leading to the start of my PhD in 2016. So I would like to acknowledge and thank my supervisors Pip Logan and Paul Hendrick, and collaborators Marcus BatemanChris LittlewoodFiona Moffatt, Michael Rathleff, James Selfe and Toby Smith.


Leslie is 19 years old and presents at the clinic with an insidious onset of anterior knee pain. She doesn’t quite remember when it started but states that it started 2 or 3 years ago. Leslie has diffuse anterior knee pain during stair walking, bicycling to university, and when she tries to run. Consequently, she now no longer does any regular exercise. She was later diagnosed with patellofemoral pain (PFP) by the physiotherapist.

person riding bicycle wearing backpack

Patellofemoral pain (PFP) is a common musculoskeletal (MSK) disorder and one of the most common reasons why adolescents and young adults seek medical help with 1 in 6 suffering at any one time [1,2]. The main symptoms include retropatella pain, or diffuse peripatellar pain, aggravated by activities that load the patellofemoral joint such as climbing and descending stairs, squatting and sitting with prolonged knee flexion [3–5]. Other symptoms include patella crepitus and giving way sensations [6–8].

Despite the implementation of evidence-based treatment, including exercise therapy, the long-term prognosis for PFP is still poor, with only one third being pain-free, one year after the initial diagnosis [9]. Patients who complain of high base levels and pain and a longer duration of symptoms typically have the most unfavourable recovery [9].

The Chartered Society of Physiotherapy, UK (CSP) has ranked PFP the 3rd most important topic out of 185 in their Musculoskeletal Research Priority Project [10].

Recent findings have led us to evolve the thinking of patellofemoral pain. Once we thought it was only about the knee itself. Then we started to discover the importance of the foot, hip and trunk. This led to ‘sub-grouping’, which has been highlighted as a research priority to investigate the effectiveness of targeted treatments based upon a classification system [11]. To date, no large randomised controlled trial has been published, but currently, this approach is being investigated [12]. However, now it appears that we should perhaps broaden our perspective even more and re-examine relevant current evidence surrounding different models of pain mechanisms and the development of PFP. This blog will look at this and some of the underpinning theoretical effects of exercise intervention and put forward a rationale for a different approach.

Tissue Pathology Models of Pain:

There is no consensus on the mechanisms that cause PFP [13] but it seems likely that the cause is multifactorial and includes loading of the patellofemoral joint [14]. Tissue-based pathology models have suggested various risk factors such as general muscle weakness [15], soft tissue tightness [16], lower limb structural abnormalities [17], movement dysfunction [18] and quadriceps mal-timing [19]. These MSK abnormalities are often assumed to affect the patella alignment or kinematics, resulting in greater stress between the patella and femur and the development of pain and dysfunction [14,20–22]. Despite positive results with exercise therapy, patients kinematics and assumed ‘alignment dysfunction’ at the knee or patella typically remain unchanged [23], questioning the role of such anatomical structures in patients with PFP.person putting bandages on another person s knee

Usual physiotherapy typically involves exercises and treatments aimed at reducing pain and restoring the assumed patella malalignment [20,21]. These include strengthening and stretching exercises, taping, and foot orthoses [24].

Reviews of taping and foot orthoses conclude that there is limited evidence for their long term effectiveness in pain when combined with exercises, compared to exercise alone [21,25,26]. Taping has shown some benefit in terms of short term pain reduction, and it is it thought current best practice to tailor the application to control specific patella movement, i.e. lateral tilt, glide and spin [24]. There does however remain some debate over the inter-rater reliability of assessing patella position and Q-angle[27,28], and the effect taping has on patella alignment and position [29], which suggests that any taping application cannot truly be specific. It is thought by the current authors that potential mechanisms behind short term taping efficacy could be attributed to central pain processes via an enhancement of proprioceptive feedback [30].

side view photo of woman doing squats against black background

A recent review of exercise therapy reported strong evidence existed for exercise therapy over no treatment, particularly with strengthening exercises [14]. Although there remains some debate over whether hip or knee strength exercises are superior Peters and Tyson (2013) reported hip strengthening is superior, while Papadopoulos et al. (2015) reported knee extension exercises were superior. These findings are supported by a systematic review in 2012 looking into the risk factors associated with PFP; they included seven studies with a total of 135 variables which only found evidence for having weak knee extension and being female as a risk factor for developing PFP [33]. Another review reported that reduced hip strength is likely a result of PFP but not part of the risk factors associated with the development of PFP [23]. Both further questioning the role of anatomical structures with the development of PFP.

There remains some debate over the role of anatomical variations/dysfunction in the development of PFP with a lack of association between structural changes and pain [34]. Structural changes do not fully explain the positive response to therapeutic exercise, and structural pathology resulting in nocioceptive input with a pain response seem inadequate for PFP.


Traditional pain models that describe tissue pathology as a source of nocioceptive input and a pain response have been insufficient in the assessment and treatment of PFP. Other models reconceptualise pain and put forward concepts that are based upon the premise that pain does not provide a measure of the state of tissue, that it is modulated by many factors, and the relationship between pain and tissue becomes less predictable the longer pain persists [35]. Known as central sensitisation, nocioceptive inputs are modulated centrally and can lead to an enhancement of pain output in the absence of tissue pathology [36,37].

Altered central processing of pain may be present in patients presenting with long-standing PFP [38–40]. Patients have also been shown to often have excessively negative thoughts towards pain and function. They believe the pain will not get better, and that movement will cause further tissue damage and worsening of the pain [41,42]. Pain catastrophising is thought to influence the shaping and physiological responses to pain, and as such, contributes to the development and maintenance of central sensitisation [43].

Local tissue pathology models of pain do not fully recognise the role and importance of the central nervous system in the development of pain and disability. It is understood that nocioception is neither sufficient nor necessary for pain [35], and therefore, a new approach may be needed for patients suffering from long term PFP.

Rationale for a different approach:

orange and and brown chess pieces

High levels of central sensitisation may be present in a subgroup of patients with long-standing PFP [38–40]. Other MSK conditions also present with signs of central sensitisation [44], for example, low back pain [45] and shoulder pain [46]. Exercise therapy based upon painful movements has been shown to be beneficial for both low back pain [47,48] and shoulder pain in patients presenting with central sensitisation [49–51]. Littlewood et al. (2013) hypothesised that the response to the painful loaded exercise programme for shoulder pain could be attributed to the therapeutic impact upon the central nervous system. Specifically, the exercise prescribed is aimed at addressing fear avoidance and catastrophising beliefs within a framework of ‘hurt not equalling harm’, and pain described as ‘de-conditioned’ tissue. This having a positive impact on the central nervous system with a modified pain output.

Within the field of PFP, only one study has looked specifically at the effect of high-dose, high-repetition exercise therapy versus low-dose, low-repetition exercise therapy for PFP [3]. Forty-two patients with PFP were randomly assigned into two groups of exercise intervention. Both groups received the same exercise regime 3 x a week for 12 weeks (stationary bike, step-ups, knee extension, squats and step-downs), but one group had high dosage, high repetition; and the other low dosage and low repetition. The high dose group exercised for 1 hour and the low dose for 20 minutes. Pain was allowed during the high dose exercise, but increases in pain were not. The results showed a significant benefit of the high dose exercises versus low dose in terms of pain and function at 12 weeks. The between-group difference was even greater at one year post-intervention, as the high dose group continued to improve in terms of pain and function, while the low dose group had relapsed [52]. This finding is confirmed by a more recent study looking at pain-free exercises and education versus education alone [53]. Compliance diaries completed by the patients indicated that those who performed the exercises with a greater dose had the greater benefit, thus indicating that there exists a similar dose-response to exercise intervention for PFP patients as for other MSK conditions.


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