Clinical synthesis based on the most recent narrative review (Aicale 2024), the 2025 systematic review of the knee bursae (Hasan 2025) and the 2023-2024 RCTs (Babaei-Ghazani, a multicentre trial, and Gouda), for an evidence-based approach to medial knee pain.

“Pes anserine pain syndrome” (in French: syndrome douloureux de la patte d'oie, PAPS) denotes pain on the anteromedial aspect of the knee centred on the conjoined insertion area of the sartorius, gracilis and semitendinosus tendons on the superomedial part of the tibia.¹ The name “pes anserinus” (goose's foot) comes from the three-pronged arrangement of these tendons, which recalls a bird's webbed foot.² A serous bursa, the anserine bursa, lies between this tendon complex and the deep plane formed by the tibial metaphysis and the medial collateral ligament (MCL).¹

How is this condition defined, and why do we now speak of a “syndrome” rather than a “bursitis”?

The historical terminology of “anserine bursitis” is reductive and often inaccurate. 🧐 Modern imaging studies (high-frequency ultrasound and MRI) consistently show that most patients clinically labelled with “bursitis” in fact have insertional tendon thickening (enthesopathy), a hypoechoic tendinopathy or infiltration of the periarticular soft tissues, without significant fluid distension of the bursa.¹,² This is why the scientific community has gradually adopted the generic term “pes anserine pain syndrome” (PAPS), covering both true bursitis (rare) and insertional tendinopathy (by far the majority).¹,³

The exact incidence of PAPS in the general population remains poorly characterised (to date there is no dedicated meta-analysis of its prevalence), but the available data are consistent:

• In the general population, the estimate is below 1 % of isolated presenting complaints; some North American military administrative databases find a diagnostic code in about 1.4 % of patients with non-specific knee pain.²
• In the population with symptomatic knee osteoarthritis, systematic ultrasound finds anserine signs (tendon thickening and/or bursal effusion) in 44-71 % of patients depending on the series; clinical PAPS is therefore a very frequent “satellite comorbidity” of medial knee osteoarthritis.¹
• In the population with type 2 diabetes and knee pain, ultrasound cohorts report anserine tendinobursitis in 24 to 34 % of patients, with a strong female predominance.¹,⁴

What happens in the body, and how does PAPS evolve naturally?

The pathophysiology of PAPS rests mainly on repetitive mechanical stress and friction between the anserine tendons and the underlying structures (MCL, medial tibial condyle).¹,⁵ In acute overuse cases, the bursa can become inflamed (bursal synovitis) with hyperaemia and slight fluid distension, visible on ultrasound as a well-defined hypoechoic collection.² In chronic cases, which account for most consultations, the dominant lesion is an insertional tendinopathy, characterised by tendon thickening, loss of the fibrillar echo-structure and sometimes neovascularisation on colour Doppler.¹,⁵

The typical pain is:

• Localised 5-7 cm below the medial joint line, over the tibial insertion area of the three tendons²;
• Described as a dull ache or tenderness on palpation, sometimes a burning or pulling sensation;⁶
• Made worse by going up and down stairs, sit-to-stand, running (particularly on slopes), and lying on the side with the knees touching (direct compression at night);²,⁶
• Most often unilateral, but bilateral in patients with T2DM or knee osteoarthritis.¹

As for the natural course, acute overload PAPS is self-limiting in most patients once the cause is addressed (change in training volume, weight loss, biomechanical correction). 📈 Symptoms typically settle within 6 to 12 weeks.¹,² However, when the underlying factors are not corrected (persistent obesity, progressive knee osteoarthritis, hip muscle deficit, pronation disorders), PAPS progresses to chronicity with a high risk of recurrence: Hasan's 2025 SR reports recurrence rates after passive treatment (isolated steroid injection) of 20-40 %.³

The diagnosis of PAPS is above all clinical : no single test is sensitive and specific enough to establish it on its own, but the combination of a compatible history and reproducible palpation is enough in the great majority of situations.¹,² Imaging is useful only where the diagnosis is in doubt, where treatment has failed or when looking for an associated condition.²,³

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

History-taking should explore five main dimensions:

• Location and description of the pain : anteromedial aspect of the knee, 5-7 cm below the joint line (much lower than meniscal pain, which is on the joint line); a dull ache, sometimes burning; intensity varying with activity.¹,⁴
• Aggravating factors : key questions to ask systematically: “Does your pain increase when you go up or down stairs? When you get up from a low chair? When you sleep on your side with your knees touching?” Their combination is highly suggestive.¹,²
• Relevant past history : weight and BMI, type 2 diabetes (with duration, glycaemic control, micro- and macrovascular complications), knee osteoarthritis already diagnosed (side, Kellgren-Lawrence severity), previous knee surgery (total arthroplasty: PAPS after TKA is a described entity, and can even be painful).⁵
• Sporting and occupational history : for runners, recent changes in weekly volume (> 10 % per week is a key risk factor, Gabbett 2016), a change of shoes or surface, more elevation gain; for standing occupations, prolonged static standing and hard floors.⁶
• Treatments already tried : rest, NSAIDs, previous injection (steroid? when?), physiotherapy (modalities, duration, response): essential information for deciding on the next strategy.²

Which clinical tests should you perform, and which other conditions should you rule out?

The physical examination aims to reproduce the patient's familiar pain and to rule out the differential diagnoses. 🩺

The reference clinical test is direct, precise palpation of the anserine insertion site: patient supine, hip in abduction and external rotation, knee in 30° of flexion. The thumb locates the medial joint line, then moves 5 to 7 cm down the anteromedial aspect of the tibia. The exquisite reproduction of the patient's usual pain at that precise spot, with no equivalent pain over the joint line or along the course of the MCL, is the most reliable clinical sign.¹,²

What is the place of ultrasound and MRI in confirming the diagnosis?

Musculoskeletal ultrasound 🎯 is the confirmatory investigation of choice: it is accessible, involves no radiation, and directly shows:

• The anserine bursa : normal thickness < 2 mm; a well-defined hypoechoic collection > 2 mm indicates a distended bursitis (rare);²
• The sartorius, gracilis and semitendinosus tendons at their tibial insertion: thickening, loss of the fibrillar echo-structure and focal hypoechogenicity indicate an insertional tendinopathy (by far the majority);¹,²
• The neovascularisation on colour Doppler, a marker of inflammatory activity and a prognostic factor;¹
• The neighbouring structures : joint effusion, an overflowing meniscal cyst, a Baker's cyst, signs of knee osteoarthritis (osteophytes, cartilage degeneration).¹

MRI is reserved for atypical or persistent cases, or where a serious associated condition is suspected (stress fracture not detected on radiographs, complex meniscal lesion, tumour). A retrospective study (Sepulveda 2017, J Clin Rheumatol) of MRI scans performed for medial knee pain found MRI signs of anserine bursitis in only 2.3 % of patients ; this figure is a reminder that “true bursitis” is rare on imaging, whereas insertional tendinopathy is clearly more frequent.²

The “overweight middle-aged woman” profile: why is it dominant?

The landmark publication by Pompan 2016 in American Family Physician is explicit from its title: “Pes Anserine Bursitis: An Underdiagnosed Cause of Knee Pain in Overweight Women ”.¹ This female over-representation is confirmed in all published series:

• In the case-control series of Alvarez-Nemegyei 2007, the 22 consecutive patients were all women (mean age 62 years), with a marked excess risk in overweight patients and those with osteoarthritis.²
• In the ultrasound cohorts of knee osteoarthritis, women account for more than 80 % of the cases of anserine tendinobursitis detected.³

Several pathophysiological hypotheses are offered for this female predominance:

1. Pelvic anatomy : wider pelvis → increased quadriceps Q angle → tendency to dynamic knee valgus under load → increased medial stress.²
2. Body composition and hormones : abdominal and periarticular adiposity, perimenopausal hormonal changes (falling oestrogen affecting tendon quality).¹
3. Associated comorbidities : knee osteoarthritis, obesity and T2 diabetes, which are more frequent in women > 50 years.¹,²

Knee osteoarthritis, type 2 diabetes: how do these comorbidities change management?

The medial knee osteoarthritis and PAPS form a clinical pair: knee osteoarthritis alters knee biomechanics (varus, extension deficit, loss of quadriceps strength), increases friction at the pes anserinus and leads to chronic tendon overload.³ Conversely, PAPS can be the dominant source of the pain perceived by a patient with knee osteoarthritis, sometimes more than the osteoarthritis itself, hence the value of systematically assessing the anserine area in every patient complaining of medial knee pain, even when knee osteoarthritis is already known.¹,³

Having type 2 diabetes 🩸 is an independent and powerful risk factor: the non-enzymatic glycation of collagen alters the mechanical properties of tendons (increased stiffness, cumulative micro-damage), and diabetic microangiopathy compromises tendon healing.² Ultrasound cohorts find a PAPS prevalence of 24 to 34 % in T2DM patients with knee pain.¹,² Clinical implications:

• Optimise glycaemic control in partnership with the endocrinologist;
• Anticipate slower tendon healing when planning the rehabilitation programme (longer duration, more cautious progressive loading);
• Consider corticosteroid injections only sparingly: the risk of post-injection glycaemic imbalance is well documented in T2DM.

The management of PAPS is multimodal and progressive. Current recommendations converge on a 4-tier strategy: start with the least invasive interventions, escalate only if they fail, and always treat the underlying factors in parallel (excess weight, knee osteoarthritis, diabetes, biomechanics).¹,²

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

1. Tier 1 (education + load management) : explanation of the condition (insertional tendinopathy more often than true bursitis), reassurance, temporary modification of the triggering activities, ice in the acute phase, topical or short-course oral NSAIDs if necessary.¹
2. Tier 2 (targeted exercise programme) : the cornerstone of long-term treatment. It comprises strengthening (quadriceps, hamstrings, hip abductors and external rotators) and stretching (hamstrings, adductors).³,⁴
3. Tier 3 (adjunctive modalities) where pain persists despite T1-T2: shockwave therapy (ESWT), high-intensity laser (HILT), kinesio taping, therapeutic ultrasound (weaker evidence), manual therapy.⁴,⁵
4. Tier 4 (ultrasound-guided injections) where pain is disabling or the previous tiers have failed: a choice between corticosteroids (rapid effect but 20-40 % recurrence), PRP, prolotherapy (hypertonic dextrose), oxygen-ozone, the Babaei-Ghazani 2024 multicentre RCT showing all three options to be effective, with an effect that lasts longer for oxygen-ozone and prolotherapy than for the corticosteroid, over 8 weeks of follow-up.⁶,⁷

What is the place of exercise, and is there a superior approach?

Therapeutic exercise is a fundamental and non-negotiable element of PAPS management, particularly in the patient with associated knee osteoarthritis. 💪 Several findings converge:

• The reference RCT by Sarifakioglu 2016 (J Phys Ther Sci, n = 60 patients with knee osteoarthritis and anserine tendinobursitis) compared physiotherapy using physical agents (heat, ultrasound, TENS for two weeks, without exercise) with a corticosteroid injection. At reassessment, at 8 weeks, both groups had improved significantly, with no difference between them ; the authors conclude that injection remains an effective, inexpensive and rapid method. The trial does not go beyond 8 weeks and measures no recurrence.³
• Strengthening should primarily target the hip stabilisers (gluteus medius, external rotators) to correct dynamic knee valgus, a factor of mechanical overload on the pes anserinus.⁸,⁹
• The hamstring and adductor stretches reduce insertional tension on the anserine area and are systematically recommended (Aicale 2024).¹

Manual therapies, shockwave, laser, injections: what does the evidence say?

Extracorporeal shockwave therapy (ESWT) : several RCTs have evaluated ESWT specifically in PAPS:

• The RCT by Gouda 2023 (Adv Orthop, n = 180 patients) compares corticosteroid, PRP and ESWT at 1 and 8 weeks: all three improve pain and function, but the advantage goes to the corticosteroid on the VAS and the WOMAC ; with no follow-up beyond 8 weeks, durability cannot be judged.⁷
• The open-label RCT by Majidi 2023 (Med J Islam Repub Iran, 60 patients randomised, 53 analysed, 3-month follow-up) compares a corticosteroid injection with three sessions of shockwave therapy: pain decreases in both groups, faster with the corticosteroid (lower at 1 month) and more durably with shockwave therapy (lower at 3 months); the thickness of the pes anserinus decreases more with the corticosteroid. This is not a non-inferiority trial. The safety argument in type 2 diabetes (no glycaemic imbalance, no skin atrophy) is a matter of clinical reasoning: the trial does not measure blood glucose.¹⁴
• The systematic review by Korakakis 2018 (Br J Sports Med) on ESWT in lower-limb conditions finds a low to moderate level of evidence overall, with encouraging but heterogeneous results.¹⁰

Ultrasound-guided injections : the multicentre RCT Babaei-Ghazani 2024 published in Am J Phys Med Rehabil (PMID 37752656) is the most recent and most rigorous study:

• Prolotherapy (dextrose 20 %): delayed effect, sharing the advantage with oxygen-ozone at 8 weeks ;
• Oxygen-ozone : effective from the first week and still at 8 weeks, favourable safety profile;
• Corticosteroids : rapid effect but 20-40 % recurrence (Hasan 2025).⁵,⁶,⁷

All three options are effective, and the effect of oxygen-ozone and prolotherapy lasts longer than that of the corticosteroid. This trial nevertheless stops at 8 weeks: no data document these injections beyond that point.⁶

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

Therapeutic education 🧠 is a major determinant of success. It should cover:

• Nature of the condition : it is most often an overload condition of the tendons, not a “serious injury”, a reassuring message that reduces kinesiophobia.¹¹
• Load management : teaching the principle of progression ≤ 10 % per week (Gabbett 2016); the concept of “optimal stress” for tendon tissue; using a diary to identify personal thresholds.¹²,¹³
• Adherence to the exercises : the benefits are cumulative; a programme followed 3-5 times a week for 8-12 weeks is needed for lasting effects.³,¹¹
• Self-assessment of pain : the “24-hour rule” (pain acceptable up to 3/10 maximum during exercise, which must return to baseline within 24 hours), adapted from Silbernagel's model.¹³

The psychosocial factors (yellow flags) are often overlooked in PAPS, even though they strongly predict chronicity:

• Kinesiophobia (Vlaeyen's 2000 fear-avoidance model): fear of movement → avoidance → deconditioning → worsening pain.¹¹
• Catastrophising (“I'll never manage to walk normally”): an independent predictor of poor prognosis.
• Limiting beliefs (“running is bad for my knees”): to be explored and worked on through education and graded exposure.

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

Patient empowerment (self-management) is the cornerstone of preventing recurrence. 🎓 A systematic review by Babatunde 2017 (PLoS One) of musculoskeletal conditions in primary care confirms that self-management interventions combined with exercise are among the most effective for pain control and long-term functional improvement.¹

Key components:

• Self-monitoring of symptoms : recognising the warning signs (morning tenderness, pain after exercise); keeping a diary to correlate them with activities.
• Load management : progression ≤ 10 % per week in volume, intensity and frequency (Gabbett 2016).²
• Home programme : targeted exercises, 3-5 times a week, for at least 8-12 weeks, then maintenance twice a week.
• Optimising systemic factors : weight loss (5-10 % of the initial BMI in overweight women > 50 years), glycaemic control in T2DM, management of associated knee osteoarthritis according to the OARSI recommendations.³

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

The decision to return to sport (RTS) must rest on objective functional criteria, not on a fixed calendar.⁴ The Burgi 2019 review (Br J Sports Med) of post-ACL RTS criteria, which can be extrapolated to other knee conditions, recommends a combination of:

1. Fundamental prerequisites : no pain in ADLs; full and symmetrical range of motion; strength ≥ 90 % of the healthy side (quadriceps, hamstrings, hip abductors).⁴
2. Functional tests : Y-Balance Test (dynamic balance), hop tests (single hop, triple hop, crossover hop), step-down test.
3. Progressive reintegration : resumption in a straight line (jogging) → changes of direction → accelerations/decelerations → jumps → opposition → competition.
4. Pain tolerance : adapted Silbernagel model (pain acceptable ≤ 3/10 during exercise, return to baseline within 24 h, no progressive increase from session to session).⁵

Analysis of a classic case (Allen & Allen 2022): from assessment to resolution

The case report by Allen & Allen 2022 published in Cureus (PMC9674038, PMID 36415475) perfectly illustrates the typical picture of PAPS. The patient presents with medial knee pain of several months' duration, made worse by stairs and running.¹ Clinical examination finds exquisite tenderness on palpation of the anserine insertion site, with no involvement of the joint line or the MCL.

The authors stress a major teaching point: “Without proper physical examination and thorough history taking, the diagnosis of pes anserinus may be delayed”.¹ Resolution was achieved with a multimodal conservative approach (activity modification + targeted exercise + short-course NSAIDs), illustrating the effectiveness of early diagnosis and a well-conducted evidence-based strategy.

The diagnostic challenge: when PAPS mimics another condition

The Corominas 2021 case report in Reumatología Clínica (PMID 34301386) describes an atypical and rare presentation: a giant anserine bursitis appearing as a palpable mass on the medial aspect of the knee.² The authors (Hospital Universitari de Sant Pau, Barcelona) stress that anserine bursae, “clinically frequent, are not always visible on ultrasound or MRI”, hence the diagnostic value of histopathological examination in unusual presentations.²

This case illustrates the phenotypic variability of PAPS and the need to consider differential diagnoses even for a typical location:

• Medial meniscal cyst : can be confused with a palpable anserine bursitis; ultrasound settles the question.
• Baker's cyst that has migrated to the medial aspect.
• Bursitis secondary to an osteochondroma (see the complex case below).
• Stress fracture of the medial tibial plateau, particularly in the endurance runner: a major red flag.

Complex cases: osteochondroma, giant anserine bursitis, septic bursitis

The 2024 case report (PMC11231497) describes a case of chronic PAPS in a 25-year-old patient with recurrent medial knee pain, resistant to all conservative approaches.³ Investigation revealed a proximal tibial osteochondroma (benign exostosis) in mechanical conflict with the pes anserinus tendons. Surgical resection of the exostosis led to complete and definitive resolution of the symptoms.³

Similar cases in the literature:

• Paediatric series of 5 patients (PMC5447900, mean age 13 years) with tibial osteochondromas causing resistant PAPS: 4/5 recovered after surgical excision.
• Isolated cases of septic anserine bursitis in immunocompromised patients or after injection, requiring antibiotic therapy and drainage.
• Giant cell tumour of the anserine tendon sheath (very rare, PMC3114461).

When, and to which other health professionals, should you refer?

Red flags 🚩 : the international IFOMPT framework (Finucane 2020) recommends immediate medical referral in the presence of:

• Exquisite bony pain with inability to bear weight → stress fracture
• Hot, red swelling + fever → septic bursitis
• Painless, growing palpable mass → tumour
• Severe night pain + unexplained weight loss → work-up for malignancy
• Recent history of trauma with instability → fracture / ligament lesion

Yellow flags 💛 : Vlaeyen's fear-avoidance model:

• Marked kinesiophobia (Tampa Scale > 37)
• Catastrophising (“I'll never manage to walk normally”)
• Limiting beliefs (“running is bad for my knees”)
• Associated anxiety and depressive symptoms

→ These justify collaboration with a psychologist, pain neuroscience education (Louw 2016) or CBT.

Interprofessional collaboration 🤝 :

• General practitioner / rheumatologist : diagnostic confirmation, imaging work-up, ultrasound-guided injection, pharmacological optimisation.
• Endocrinologist / diabetologist : optimisation of glycaemic control in T2DM.
• Nutritionist / dietitian : structured weight-loss programme for the overweight patient.
• Podiatrist : analysis of pronation, foot orthoses if there are static disorders.
• Orthopaedic surgeon : if symptoms resist > 6 months or an anatomical cause is suspected (osteochondroma, partial meniscectomy).
• Psychologist / psychiatrist : marked yellow flags, chronic pain with psychosocial comorbidities.

How do you measure outcomes and overcome barriers to implementation?

The systematic use of validated PROMs is a standard of evidence-based practice 📊:

• VAS (Visual Analogue Scale) : pain 0-10, to be measured at every session.
• LEFS (Lower Extremity Functional Scale) : 20 items, score 0-80, validated in French; MCID ≈ 9 points.
• KOOS (Knee injury and Osteoarthritis Outcome Score) : essential in the patient with associated knee osteoarthritis (5 subscales); the “Symptoms” subscale and the “Sport” subscale are the most relevant to PAPS.
• Global Rating of Change (GROC) : “Overall, since the start of treatment, do you feel… better / the same / worse?” on 11 points.

Barriers to evidence-based implementation 🚧 : systematic reviews of EBP in physiotherapy identify recurring barriers:

• Lack of time for reading and critical appraisal.
• Lack of skills in research and in biostatistics.
• Limited access to scientific articles (paywalls).
• Resistance to change on the part of patients (expectations of spectacular “passive techniques”).
• Insufficient organisational support.

Practical strategies for overcoming these barriers:

1. Clinical syntheses in condensed form (such as this article) rather than reading RCTs in full.
2. Journal clubs held monthly or every two months among peers.
3. Targeted continuing education on the most frequent conditions.
4. Digital PROMs built into the practice software (a time saver).
5. Active communication with patients about the available evidence and the expected benefits.