Clinical synthesis based on the Myerson 2020 international consensus (Progressive Collapsing Foot Deformity), the Kulig 2009 randomised trial and the Alvarez 2006 prospective protocol.

How is this condition defined, who is affected and what are the risk factors?

The tibialis posterior is the principal dynamic stabiliser of the medial arch. Its main insertion on the navicular tuberosity, its plantar expansions and its retromalleolar course make it a vulnerable biomechanical system.³ When its function degrades, load shifts onto the static stabilisers (spring ligament, plantar ligaments, deep deltoid ligament), whose secondary failure marks the transition to a visible deformity.⁴

• Anatomical anomalies : pre-existing congenital flatfoot, accessory navicular bone (type II especially), a shallow medial retromalleolar groove or hypoplasia of the sustentaculum tali.¹
• Systemic inflammatory diseases : rheumatoid arthritis, spondyloarthropathies, lupus, all of which can directly involve the synovial sheath of the tendon.⁹
• Trauma : ankle fractures, severe sprains with injury to the medial stabilisers, repeated microtrauma linked to physical activity on uneven ground.⁹
• Iatrogenic : local corticosteroid injections into the tendon sheath (to be avoided), prolonged systemic corticosteroid therapy.⁹

What happens in the body and how does PTTD progress naturally?

The tendon is particularly vulnerable in its medial retromalleolar zone of hypovascularity, located about 14 mm distal to the medial malleolus.¹¹ Repeated microtrauma at this level, on an unfavourable metabolic background, leads to collagen disorganisation, to progressive elongation and then to partial or complete rupture.

When the tendon loses its dynamic stabilising function, the load transfers to the static stabilisers. The spring ligament complex (plantar calcaneonavicular), comprising three bands (superomedial, medioplantar oblique and inferoplantar longitudinal), is the first to give way.¹² Its failure is a major tipping point: it marks the transition from the “isolated tendinopathy” stage to the “visible and progressive deformity” stage.¹³ The deep deltoid ligament (talotibial) follows in the advanced stages, then allowing the talus to tilt into valgus within the mortise.

• Stage I : tenosynovitis or tendinosis with no visible deformity. Single heel rise possible but often painful, with reduced strength compared with the healthy side.
• Stage II : deformity that is supple and reducible (calcaneal valgus + forefoot abduction + arch collapse). Single heel rise impossible or without calcaneal inversion. Often subdivided into IIA (moderate, < 30 % radiographic abduction) and IIB (severe, ≥ 30 %).
• Stage III : deformity that is rigid and non-reducible with arthritic changes (subtalar, talonavicular, calcaneocuboid). Pain is often lateral (sinus tarsi impingement).
• Stage IV : added by Myerson, tilt of the talus within the tibiofibular mortise (deep deltoid ligament involvement), with secondary tibiotalar osteoarthritis.¹⁵

Which questions should you ask to understand the patient and their history?

• Location and nature of the pain : classically posteromedial (along the tendon, from the medial malleolus to the navicular insertion). Often described as a dull, burning pain, made worse by prolonged standing and walking. Migration towards the lateral aspect of the foot suggests an advanced stage with sinus tarsi impingement.³
• Timeline and triggering factors : typically a gradual onset. An abrupt post-traumatic onset suggests an acute rupture (Holmes-Mann 1992 found a history of trauma in 36 % of cases).⁴ Worsening when walking on uneven ground, climbing stairs, or wearing poorly supportive shoes.
• Functional and morphological impact : does the patient notice a collapse of the arch, a “spreading” of the foot, asymmetrical shoe wear? The impact on activities of daily living (walking, driving, stairs) and on work is crucial in stratifying severity.⁵
• Past history and risk factors : age, sex, BMI, hypertension, diabetes, medication (corticosteroids), systemic inflammatory diseases, old trauma, previous ankle surgery.⁴˒⁶
• Red flags : non-mechanical night pain, unexplained weight loss, fever, distal neurological deficit (tibial nerve territory), a history of cancer. The presence of a red flag requires medical referral before any physiotherapy treatment.⁷

Which clinical tests should you carry out and which other conditions must be ruled out?

Weight-bearing inspection (standing, posterior view) :

• Too many toes sign : more than two toes visible on the outer side of the affected foot, reflecting calcaneal valgus and forefoot abduction. Sensitive for stages II and above.³
• Collapse of the medial longitudinal arch : visible on weight-bearing, to be compared with the non-weight-bearing appearance (reducible vs rigid).
• Calcaneal valgus : measurable clinically (goniometry) or radiographically.

Functional tests :

• Single-leg heel rise test (SHR) : the reference test. The patient is asked to rise onto the toes of one foot. Normal test : full rise with visible calcaneal inversion (a sign of effective tibialis posterior contraction). Abnormal : rise impossible, incomplete, or without calcaneal inversion. A healthy subject can usually perform 8 to 10 repetitions without fatigue; the criterion “10-25 pain-free repetitions” is used as a return-to-activity target (see Houck 2009 on the kinematic analysis of the heel rise).⁹
• Manual muscle testing of inversion : the patient resists an eversion force applied by the clinician to the medial border of the foot. Weakness compared with the healthy side is typical of stages I and II.¹⁰
• Hip & ankle assessment : Kulig 2011 showed that women with PTTD present a bilateral reduction in the performance of the hip abductors and external rotators and of the ankle invertors, which justifies a strengthening programme across the wider kinetic chain.¹¹

Essential differential diagnoses to know ⚠️:

• Tarsal tunnel syndrome : compression of the tibial nerve in the retromalleolar canal. It gives burning, medial plantar paraesthesia and a positive Tinel sign. It can coexist with PTTD (tenosynovitis pressing on the adjacent nerve) or be mimicked by it.¹²
• Navicular stress fracture : dorsomedial pain at the N-spot, gradual onset in a runner, focal tenderness on palpation. Imaging is essential (MRI or bone scan).¹³
• Primary talonavicular or subtalar osteoarthritis : stiffness dominates, diffuse pain, a history of trauma or overload.¹
• Isolated spring ligament injury : acquired deformity with no obvious clinical tendinopathy of the tibialis posterior. The diagnosis is often made on MRI, raising the question of targeted surgical repair.¹⁴
• Gastrocnemius-soleus tightness (functional equinus) : biomechanically worsens PCFD and must be looked for systematically (Silfverskiöld test).¹
• Tendinopathy of the tibialis anterior : the two names resemble each other closely enough to be swapped in reports, yet everything differs. The tibialis anterior is a dorsiflexor of the foot: its pain sits in front of the ankle and over the instep, the arch is not collapsed, and the single heel rise remains normal. Its failure gives a foot that slaps the ground, never a flat foot. See tibialis anterior tendinopathy.

Should patients with PTTD / PCFD be classified, and what does it gain them?

1. The Johnson & Strom 1989 classification, modified by Myerson : 4 stages of increasing severity (see chapter 1). Advantage: simplicity, long standing, wide use. Limitation: it focuses on the hindfoot and the midfoot, and neglects the forefoot, gastrocnemius tightness, lateral instability and ligament involvement.¹⁵
2. The Myerson 2020 PCFD classification : an international consensus system that rates 5 independent anatomical classes, modulated by flexibility (A = supple, B = rigid). It allows a three-dimensional and personalised description, aligned with modern surgical choices (Sangeorzan 2020 operative consensus).²˒¹⁶

Critique and controversies

Moreover, the classic clinical tests have heterogeneous reliability. Ross 2021 showed that tendon palpation, the single heel rise and morphological observation are the most reliable, while other manoeuvres (tibialis posterior edge test, foot posture index, navicular drop) have more variable reliability.⁸ The clinician should favour the highly reliable tests and combine them to optimise diagnostic value.

Where do you start? What is the recommended hierarchy of interventions?

1. Activity modification and load management : temporary reduction of high-impact activities (running, jumping), adjustment of walking distances, alternation with off-loading activities (cycling, swimming). Progression follows tolerance.⁴
2. Foot orthoses supporting the medial arch : the Gomez-Jurado 2021 SR (Clin Rehabil) confirms that orthoses are effective for pain reduction at stages I-II.⁵ The debate concerns custom versus prefabricated orthoses: Houck 2009 showed that patients preferred custom orthoses but with no clear clinical superiority; good-quality prefabricated devices are a cost-effective alternative for many patients.⁶ For advanced stage II, an articulated ankle-foot orthosis (articulated AFO) or a custom UCBL insert may be indicated.⁷
3. Structured exercise programme : started as soon as the initial pain is controlled. It is the most validated and most durable intervention (see the next section).¹˒²
4. Stable footwear : rigid heel counter, supported medial sole, moderate drop. Avoid flat unsupportive shoes during the symptomatic phase.⁷

The Kulig RCT (Phys Ther 2009, n = 36) showed that the combination of “orthosis + progressive resistance exercise” brings greater gains in pain and function than orthosis + stretching alone, over 12 weeks.⁸ This study remains the evidence-based pivot of modern rehabilitation. Houck 2015 rounded out this result in a later RCT (n = 36) comparing orthosis + stretching versus orthosis + stretching + strengthening: functional gains were greater in the strengthening group.⁹

The Alvarez prospective protocol (Foot Ankle Int 2006) is a practical benchmark: of 47 stage I-II patients followed with a structured programme (orthosis + exercise + education), 83 % (39/47) achieved a satisfactory subjective and functional outcome over a median of 10 sessions spread across 4 months.¹⁰ This success rate is confirmed by later SRs and remains the realistic clinical target to present to the patient.

What is the place of exercise, and is any one approach superior?

• Progressive strengthening of the tibialis posterior : resisted inversion exercises (elastic band, machine), with progression of load and of the number of repetitions. Kulig 2009 (Foot Ankle Int) showed that a 10-week eccentric programme (twice daily, progressive load) significantly improves pain, function and the SHR in early-stage patients.¹¹
• Heavy-slow resistance (HSR) : a protocol inspired by Achilles (Beyer 2015) and patellar tendinopathies. High load (70-85 % 1RM), slow speed (6 sec per repetition), 3 sets × 15-6 repetitions, progression over 12 weeks.¹² Extrapolation to PTTD is biomechanically plausible but the specific evidence remains limited (extrapolated from analogous tendinopathies).
• Strengthening across the wider kinetic chain : hip (abductors, external rotators), knee (quadriceps, hamstrings), ankle (gastrocnemius-soleus) and the intrinsic foot muscles. Justified by Kulig 2011, which showed bilateral weakness of the chain in affected women.¹³
• Gastrocnemius-soleus mobility : tightness is a biomechanical aggravating factor. Silfverskiöld test, progressive stretching, tibiotalar mobility exercises.⁴
• Motor control and proprioception : single-leg stability exercises, unstable surfaces, integration of correct propulsion strategies (foot core training).¹

Manual therapy, shockwave therapy: how effective are they really?

• Manual therapy : joint mobilisations (subtalar, talonavicular, tibiotalar), soft-tissue massage, peritendinous neural desensitisation techniques. Widely used in everyday practice, but no specific high-quality RCT quantifies its isolated effect on PTTD. It is generally regarded as an adjunct therapy.²
• Extracorporeal shockwave therapy (ESWT) : a solid level of evidence for Achilles and plantar tendinopathies, but no specific quality SR/MA has confirmed its effectiveness for PTTD (the reviews supposedly available on the subject are extrapolations from other tendinopathies). To be considered with caution, making the context clear to the patient.¹⁴
• Tape, strapping, K-taping : a short-term effect on pain and posture, but with no demonstrated lasting benefit. They can serve as transitional help in the acute phase.²
• Ultrasound, laser, electrotherapy : very weak or absent evidence specifically for PTTD; not to be favoured as a main intervention.²
• Injections : local corticosteroids into the tendon sheath are contraindicated (rupture risk, see Holmes-Mann 1992). PRP, ozone or prolotherapy injections have no solid level of evidence for PTTD specifically.²

Beyond the physical: how do you educate the patient and address psychological factors?

• Understanding the nature of the condition : degenerative tendinosis, not simple inflammation. The concept of “tendon capacity”, which must exceed the demands of activity, is central to explaining why exercise progression matters.
• Load management : a pragmatic rule inspired by Silbernagel 2007, in which pain during and after effort must stay ≤ 4-5/10, settle within 24h, and not increase from session to session. This framework lets the patient dose activity without fear and without overload.¹⁶
• Adherence to the exercise programme : the Mallows 2017 SR (BJSM) stresses that psychological factors (kinesiophobia, self-efficacy, catastrophising) influence prognosis. High self-efficacy is a positive predictor of recovery.¹⁷
• Role of orthoses : presented as a transitional tool that facilitates rehabilitation, and not as a permanent passive solution. Gradual weaning after stabilisation can be discussed depending on the profile.
• Choice of footwear : a simple intervention with a strong impact (rigid heel counter, supported medial sole, moderate drop).⁷
• Comorbidities to take into account : smoking, excess weight, glycaemic control, sedentary behaviour. Collaborative discussion and referral where needed (dietitian, GP).

Critique and controversies

Next, the custom versus prefabricated orthoses debate is not settled. Cost and accessibility argue for good-quality prefabricated devices in many patients, but severe or atypical cases, or those with marked deformity, benefit from custom orthoses. The decision is often guided by availability, reimbursement and patient preference as much as by pure science.⁶

Finally, the timing of the transition to surgery remains poorly codified. There is no universal criterion for identifying the patient who “will fail” conservative treatment. The empirical rule of 3-6 months of well-conducted management before surgical referral is consensual, but patients with severe stage IIB may benefit from earlier surgery to avoid arthritic progression.¹⁸ The decision must be shared between physiotherapist, referring doctor, surgeon and patient.

How do you make the patient an active partner in their own recovery through self-management?

• Understanding the condition : degenerative tendinosis, and the importance of “tendon capacity”, which must exceed the demands of the target activities. Explaining the continuum of activity, symptom and adaptation.²
• Load management : a pragmatic rule inspired by Silbernagel 2007 (an RCT on the Achilles tendon): pain during and after exercise must stay ≤ 4-5/10 on the VAS, settle within 24h, and not increase from session to session.³ A simple monitoring diary (morning pain, activity intensity, satisfaction) can be offered. Pain within this zone is considered a positive stimulus for adaptation and not a warning signal.
• Adherence to the home exercise programme : the Mallows 2017 SR showed that self-efficacy and perceived control predict adherence. A simple programme, built into the daily routine, with visual reminders or mobile apps where relevant.⁴ The minimum effective duration appears to be 12 weeks, but long-term maintenance is often necessary in at-risk patients (postmenopausal women with comorbidities).
• The role of orthoses and footwear : presented as a transitional enabling tool, not as a permanent crutch. Gradual weaning can be discussed after 3-6 months of symptomatic and functional stabilisation, under supervision.⁵
• Lifestyle : weight management (reducing mechanical load), glycaemic control, smoking. Collaborative discussion and referral where needed (nutritionist, general practitioner).
• Recognising warning signs : a flare persisting > 1 week, a new visible deformity, new night pain, motor deficit → medical consultation.

When and how should a safe return to sport and activity be planned?

A staged approach is consensual:

1. Baseline criteria before resuming :
   • Minimal or absent pain during activities of daily living (walking > 30 min, stairs, prolonged standing)
   • Single-leg heel rise : ≥ 15-25 repetitions depending on the target demands, with visible calcaneal inversion and no significant pain
   • Plantar flexor and invertor strength: symmetry ≥ 90 % compared with the uninvolved side (manual testing or dynamometer)
   • No swelling or tenderness on palpation of the tendon at the end of a session
2. Gradual introduction of activity load :
   • Sustained brisk walking → Nordic walking → cycling / swimming → graded running (very short intervals, flat ground, supportive shoes)
   • For runners: a typical restart of “1 min running + 4 min walking” over 20-30 min, progressing by no more than 10 % of volume per week (the 10 % rule)
   • Gradual introduction of gradients, hopping and changes of direction according to the target sport
3. Sport-specific functional tests : single-leg hops (vertical, horizontal, hop test), change-of-direction tests, asymmetry < 10 % compared with the uninvolved side. Criteria inspired by return-to-sport consensus statements for lower-limb tendinopathies.⁶
4. Continuous monitoring using the zone model : using pain monitoring (see the chart above). Persistent morning pain, or worsening from session to session, are early warning signals.
5. Maintaining a prevention programme : key exercises (single-leg heel rise, hip strengthening, gastrocnemius mobility) to be kept up 2-3 times a week over the long term, especially in at-risk patients (women > 50 with cardiometabolic comorbidities).

Critique and controversies

First, the optimal long-term exercise dosage remains unclear. While the principle of progressive strengthening is universally accepted, precise quantification and the best progression (isometric, concentric, eccentric, HSR) are not the subject of any numerical consensus for PTTD specifically. Many protocols are extrapolated from other tendinopathies (Achilles, patellar).¹˒⁷

Second, the timing and criteria for weaning off the orthosis are poorly codified. Some patients (notably stage IIA with a moderate deformity) can hope for gradual weaning after 6 months of stabilisation; others (severe stage IIB, heavy comorbidity) need an orthosis over the long term. Direct comparative data are lacking.⁵

Third, psychosocial factors (kinesiophobia, beliefs, expectations) are little studied specifically in PTTD, although they are recognised as major predictors in other tendinopathies (Mallows 2017).⁴ Taking them into account systematically in everyday practice remains imperfect.

Fourth, validated PROM tools that are sensitive to change for PTTD/PCFD specifically are few. The FAOS and the FFI are the most used, but their MCID in this population is not precisely established.⁸ The Core Outcome Sets for tendinopathy (ICON 2023 for the Achilles) have not yet been transposed to the tibialis posterior.⁹

Analysis of a "classic" case: from assessment to resolution at an early stage

This case, although of low evidential value (n=1), illustrates several consensual principles:

• Early-stage PTTD responds well to structured multimodal management, consistent with the Alvarez 2006 prospective protocol (83 % success, median 10 sessions) and the Kulig 2009 RCT.²˒³
• The orthosis + progressive exercise combination is central.
• Assessment and rehabilitation must reach beyond the tendon: kinetic chain strengthening (hip, gastrocnemius, intrinsic foot muscles), in line with Kulig 2011, which demonstrated bilateral weakness in affected women.⁴
• Patient education and self-management are necessary to prevent long-term recurrence.

The clinical outcome expected in this profile is a significant reduction in pain, progressive restoration of function (notably the single heel rise) and a return to meaningful activities. Prospective data from the Alvarez 2006 study indicate that this outcome is reached in about 83 % of stage I-II patients over a median of 10 sessions, with subjective satisfaction in 89 % (42/47).²

The diagnostic challenge: PTTD, tarsal tunnel and associated conditions

The recent review on posterior tarsal tunnel syndrome (Ahmad, Faisal, Khan - Orthop Rev 2022, PMC9235437) states that TTS is a compressive neuropathy of the tibial nerve or of its branches within the tarsal tunnel.⁶ Aetiologies include trauma, vascular anomalies, soft-tissue inflammation (including tibialis posterior tenosynovitis), compressive bone disease or tumour masses. Clinically, TTS produces:

• Burning, tingling and mid-plantar paraesthesia
• A positive Tinel sign over the tarsal tunnel
• Worsening with prolonged walking, sometimes at night
• Possible distal sensory and motor deficits (intrinsic musculature)

A cohort study (Foster et al. J Knee Surg 2022 - PMID 35944572) quantified the co-occurrence after ankle sprain : PTTD and TTS can occur sequentially after trauma, underlining the need for cross-screening.⁷

The classic pitfall is that severe tibialis posterior tenosynovitis can displace the adjacent tibial nerve and cause neurological symptoms (burning, paraesthesia) that suggest a primary TTS. Treating the PTTD may then resolve the neurological symptoms without nerve surgery. Conversely, a primary TTS can be mistaken for painful PTTD.⁵˒⁶

Clinical implications:

• A full biomechanical examination as a matter of course, even when the picture looks purely neurological
• Tinel sign, mid-plantar sensory testing and tendon palpation are complementary
• MRI can distinguish tendon tenosynovitis from true compressive neuropathy
• EMG/nerve conduction studies if clinical doubt persists
• The conservative treatment of PTTD (orthosis, exercise, load management) must be tried first even when the neurological symptoms dominate: whether or not it improves them then guides the diagnosis

Study of a complex case at an advanced stage

A recent illustrative case (Wang et al. Int J Surg Case Rep 2024) concerns an elderly patient with a fixed rigid valgus flatfoot deformity following an old, neglected rupture of the tibialis posterior, together with painful hindfoot osteoarthritis.⁸ The patient could no longer wear ordinary shoes and had disabling pain.

Faced with such rigidity, conservative approaches and targeted surgery (tendon repair, realignment osteotomies) are no longer sufficient. The surgical solution was a triple arthrodesis : fusion of the subtalar, talonavicular and calcaneocuboid joints. The aim is no longer to restore tendon function, but to create a stable, pain-free and well-aligned bony structure, by sacrificing hindfoot mobility in favour of stability and pain relief.⁸

The Sangeorzan 2020 international consensus on the operative goals of PCFD supports this approach for rigid arthritic stages: the priority is realignment, balancing and maximal preservation of mobility where possible, but selective fusion remains necessary in fixed, arthritic deformities.⁹

In younger patients at stage IIB-III with a still flexible deformity, less radical procedures can be considered:

• Subtalar arthroereisis : inserting an implant into the sinus tarsi to limit excessive pronation and stabilise the hindfoot. A minimally invasive procedure, often combined with other steps (Achilles lengthening, Cotton osteotomy, tendon transfer).¹⁰
• FDL (flexor digitorum longus) tendon transfers onto the navicular, combined with realignment osteotomies (calcaneal medial slide, Evans lateral column lengthening).⁹

Post-surgical physiotherapy follow-up is essential: initial protection, progressive rehabilitation, reconditioning, and return to activity over 6-12 months depending on the procedure. The physiotherapist-surgeon collaboration is decisive in optimising the functional outcome.

Critique and controversies

First, the Johnson-Strom classification as modified by Myerson, although universally used, suggests a linear progression (from stage I to IV) that is not always seen in practice. A patient may have a tendon rupture with a still flexible deformity, or the reverse. The new Myerson 2020 PCFD classification (5 independent classes × A/B) captures this complexity better.⁹

Second, the “best” conservative treatment remains debated in its fine composition (eccentric dose, type of orthosis, duration). High-quality data directly comparing these variables are lacking.²

Third, the optimal timing of surgery is one of the greatest challenges. There is no universal criterion for deciding on surgical referral. The decision combines clinical signs (progression of the deformity), imaging (spring ligament and deltoid involvement, osteoarthritis), and the functional impact reported by the patient.⁹

Fourth, the initial causality remains a subject of biomechanical debate: is tendon failure the primary cause of the collapse, or does a progressive flattening (constitutional ligamentous laxity) overload and eventually damage the tendon? The new “PCFD” nomenclature implicitly acknowledges this ambiguity by moving away from an exclusive focus on one tendon.⁹

When and to which other health professionals should you refer?

The international framework (Finucane 2020 JOSPT) on red flags in spinal pathology laid the modern methodological foundations: most individual red flags have low specificity, but their combination and contextual analysis remain essential.¹ Specifically for the foot and ankle:

• Acute post-traumatic rupture of the tibialis posterior with sudden loss of function → prompt surgical referral
• Distal neurological deficit (altered mid-plantar sensation, weakness of the intrinsic muscles) → suspected severe tarsal tunnel or underlying neurological disease → doctor / neurologist
• Charcot foot in a patient with diabetes, with swelling, erythema and rapid deformity → diabetes and orthopaedic emergency (immobilisation, complete offloading)
• Suspected infection (septic tenosynovitis, osteomyelitis) with fever, heat, erythema → medical emergency
• Suspected malignancy : palpable mass, progressive night pain, weight loss → prompt referral for work-up
• Failure of conservative treatment well conducted, after 3-6 months with progression of the deformity → orthopaedic surgical referral

Beyond emergencies, referral should be considered when psychosocial factors (yellow flags) become the main obstacle. Kinesiophobia, catastrophising beliefs, anxiety or depressive symptoms are documented predictors of poor prognosis in tendinopathy (Mallows 2017).² Collaboration with a pain psychologist, a specialist doctor or a general practitioner is then indicated.

The structured interprofessional collaboration is a mark of quality 🤝:

• General practitioner / sports physician : overall coordination, management of cardiometabolic comorbidities (hypertension, diabetes, obesity: major factors documented by Holmes-Mann 1992)³
• Podiatrist / orthotist : design, fitting and maintenance of foot and ankle orthoses
• Foot and ankle orthopaedic surgeon : assessment for refractory advanced stage II and for stages III-IV (Sangeorzan 2020 operative consensus)⁴
• Diabetologist : glycaemic control and diabetic foot surveillance
• Rheumatologist : if an underlying systemic inflammatory disease is suspected
• Nutritionist : support for weight loss where there is significant excess weight (a major mechanical risk factor)

How do you measure outcomes and overcome the barriers to implementation?

For PTTD / PCFD, two foot-specific PROMs are validated in French:

• FAOS (Foot and Ankle Outcome Score) : 5 subscales (pain, symptoms, ADL, sport, QoL), 0-100. Validated in its French translation.
• FFI (Foot Functional Index) : 23 items across 3 subscales (pain, disability, activity limitation). Shorter, validated across several conditions.

The ICON 2019 international consensus (Vicenzino BJSM 2020) on the core domains of tendinopathy identifies 9 domains to measure systematically : patient rating, participation, pain on activity, function, psychological factors, physical function capacity, disability, quality of life, and pain over a defined period.⁶ Although this consensus is not specific to PTTD, its methodological principles apply and point towards an assessment more complete than a simple pain score.

The barriers to implementing evidence-based practice in physiotherapy are well documented: lack of time, difficulty interpreting research, lack of organisational support, variable access to resources.² The Mallows 2017 SR underlines that patients’ psychological factors are little addressed in everyday practice although they are major predictors.²

Several facilitators have been identified 🎯:

• Easy access to syntheses : reviews, guidelines, practice sheets (the aim of this kind of article!)
• Building PROMs into the patient record : digitisation, short forms, automatic scoring
• Mentoring and continuing education : taking part in learned societies (SFRE, GETM), specialist foot and ankle courses
• Shared decision-making : actively involving the patient in the choice of strategies, based on evidence + personal values
• Structured interprofessional collaboration : clear referral protocols, multidisciplinary communication
• Audit and feedback cycles : comparing current practice with the recommendations in order to adjust

Critique and controversies: the grey areas of implementation

First, the predictive validity of red flags is increasingly questioned: most have low specificity and low positive predictive value taken in isolation.¹ Over-vigilance can lead to costly, anxiety-provoking and unnecessary imaging. The challenge is to interpret red flags within the whole clinical context, avoiding both under-diagnosis and over-diagnosis.

Second, the gap between knowing and doing (the knowing-doing gap) remains substantial. Systemic barriers (economic pressure, reimbursement models, cultural expectations) are far more powerful than individual reluctance. The effort must be collective.²

Third, the tension between standardisation and personalisation deserves thought. PROMs, COS and guidelines are essential for quality and research, but capture only a fraction of the patient’s experience. True expertise navigates between science and individual nuance, using standardised tools to enrich the dialogue rather than as an end in themselves.⁶

Fourth, in the specific field of PTTD / PCFD, the French and European guidelines are out of date. The new PCFD 2020 nomenclature and the evidence-based principles (the Kulig RCT, the Alvarez protocol, the ICON principles) are insufficiently integrated into French-language professional recommendations, creating a gap with international best practice.