Introduction
Medial knee pain is a common diagnostic challenge in both orthopedic and primary care settings.1–3 While several distinct structures can generate medial knee pain, their overlapping presentations often make the underlying source difficult to identify.3,4 One frequently underrecognized contributor is the pes anserinus,5 a layered complex classically composed of three tendons (sartorius, gracilis, and semitendinosus) that converge as they insert onto the anteromedial surface of the proximal tibia.6,7 The pes anserinus inserts distal to the anteromedial joint line, where it contributes to medial knee stability by resisting valgus stress and rotational forces.8,9 Interposed between the pes anserinus and the underlying tibia is the pes anserine bursa, a fluid-filled sac that minimizes friction during knee motion.10 Pes anserine bursitis (PAB), sometimes termed pes anserine tendino-bursitis, refers to inflammation of the bursa and often the adjacent tendons, producing pain and tenderness along the medial knee.11 PAB is frequently overlooked or misdiagnosed, since its presentation can mimic that of other conditions, particularly medial meniscal tears.12,13 The condition has been associated with several systemic and structural conditions, including knee osteoarthritis, type 2 diabetes mellitus, obesity, and repetitive athletic activity.11,14–16 PAB occurs predominantly in middle-aged and older adults, with a marked female predominance.17,18 It also frequently coexists with medial compartment knee osteoarthritis (OA).15,19 Despite being clinically common, PAB is confirmed on MRI in only about 2.5% of symptomatic knees referred for imaging.12 This low confirmation rate contrasts with the higher prevalence reported in osteoarthritis cohorts assessed by ultrasonography, a discrepancy that remains unresolved and represents a central issue addressed in this review.15,20 The difference reflects current uncertainty in correlating clinical and imaging-based diagnoses rather than confirmation that clinical diagnosis alone suffices. Accurate clinical evaluation is therefore necessary to distinguish PAB from other sources of medial knee pain, after which appropriate treatment can be directed at the underlying contributing factors.12
This review synthesizes current evidence on the anatomy, evaluation, and management of pes anserine bursitis, with particular attention to the discordance between clinical and imaging-based diagnoses and to the comparative durability of nonoperative treatment. The discussion is organized by anatomy, epidemiology, clinical assessment, associated pathology, and treatment. Unlike previous reviews, this article integrates clinical and imaging perspectives to provide a unified approach.21 It also presents a proposed diagnostic approach derived from synthesis of the existing literature, offered as a conceptual framework rather than a validated algorithm.
Anatomy
The pes anserinus is a webbed convergence of three medial-knee tendons, the sartorius, gracilis, and semitendinosus, at the anteromedial surface of the proximal tibia.14,22 On the anteromedial surface of the proximal tibia, the pes anserine inserts roughly 1.5 cm medial to the tibial eminence, about 2 cm distal to the medial joint line, and 2 to 3 cm below the tibial tubercle.23,24 This places the insertion just distal to the proximal tibial growth plate in the skeletally immature.14,22 Although the three tendons converge, they each originate from distinct regions of the pelvis and are innervated by separate nerves (Table 1).14,25 Biomechanically, the pes anserinus is critical for medial knee stability against valgus and rotational loads and supplements the medial collateral ligament during knee flexion by acting as a dynamic restraint.14,19 Deep to the conjoined tendons and superficial to the medial tibial cortex and distal superficial medial collateral ligament lies the anserine bursa. The bursa is a thin synovial-lined sac that facilitates the frictionless movement of tendons over the underlying bone and ligament during knee flexion and extension.6,14,22Table 1The Three Tendons of the Pes Anserinus and Their Anatomic RelationshipsMuscleOriginInsertion Onto Pes AnserinusInnervation/Primary ActionSartoriusAnterior superior iliac spineMost superficial of the three tendons; anteromedial proximal tibiaFemoral nerve (L2-L3); hip flexion, abduction, external rotation; knee flexionGracilisInferior pubic ramusMiddle layer; anteromedial proximal tibiaObturator nerve (L2-L3); hip adduction; knee flexion and internal tibial rotationSemitendinosusIschial tuberosityDeepest of the three; anteromedial proximal tibiaTibial division of sciatic nerve (L5-S2); hip extension; knee flexion and internal tibial rotation
Following their distinct paths down the thigh, these three muscles form a tightly packed, layered supportive complex at their conjoined tibial attachment.14 The sartorius forms the superficial layer, the gracilis forms the intermediate layer, and the semitendinosus forms the deepest layer adjacent to the tibial periosteum.6,14 While each muscle possesses distinct pelvic origins, independent primary actions, and separate nerve pathways, they function synergistically as a unified sheet of dense connective tissue to maintain medial knee stability against valgus and rotational loads.14,25 This close anatomical and functional relationship is a driver of pes anserine bursitis. The bursa lies directly deep to the conjoined layers, so any localized tightness, muscle imbalance, or repetitive strain across these muscles increases frictional and compressive forces on the bursa, leading to irritation and bursitis.14,25
While previous literature describes the pes anserinus as a consistent convergence of three tendons, recent studies have demonstrated anatomical variation in tendon count and bursa morphology. A systematic review by Cavus et al7 pooled data from 19 cadaveric and imaging studies and found that the classic three-tendon configuration was observed in only 62% of specimens, with two- and four-band variants accounting for the remainder of configurations. This review also showed that structural variations in the superficial tendons can influence bursal boundaries.
A cadaveric study by Lee et al24 used a mixed gelatin solution and injected it into 86 legs from 45 cadavers to delineate the bursa cavity. It described the bursa as a consistently present, irregularly circular, synovium-lined sac despite the tendon-count variability. In vivo, Imani et al10 demonstrated sonoanatomic variations in bursa morphology, suggesting that identifying bursal fluid requires clinical correlation.
Consequently, these findings indicate that pes anserine bursa has significant variance in configuration; which makes the diagnosis primarily clinical, with imaging serving a supportive role.14
The pes anserinus is supplied by branches of the inferior medial genicular and saphenous arteries, with sensory innervation from the infrapatellar and sartorial branches of the saphenous nerve, the latter coursing close to the conjoined tendon.14 Iatrogenic injury during hamstring tendon harvest is well documented,26 and the same anatomic proximity has implications on safe surgical bursectomy and accurate palpation.21,22
Epidemiology
The prevalence of PAB is difficult to establish because the condition is defined clinically rather than validated by imaging. It is often misclassified as nonspecific medial or anterior knee pain and has been disproportionately studied in cohorts already presenting with knee OA.5,17,19 A prospective ultrasonographic study by Uysal et al15 examined 170 knees from 85 patients with symptomatic primary knee OA and reported PAB in 20% (34/170), with a significant positive correlation between Kellgren-Lawrence radiographic grade and bursa volume. A cross-sectional study by Mortada et al20 analyzed 245 patients with primary knee OA and identified PAB in 44.9%, with 82.7% categorized as Grade 1 (mild ultrasonographic changes) and 17.3% as Grade 2 (marked changes).
Strikingly, body mass index (BMI) did not differ significantly between patients with and without PAB. Taken together, these cohorts indicate that roughly 20% to 45% of symptomatic knee OA patients develop PAB. Another clinically based study by Kang and Han27 also identified PAB as a contributor in patients with knee OA.
Outside of OA cohorts, a radiology-clinic series by Rennie and Saifuddin12 estimated a 2.5% prevalence of PAB on MRI in symptomatic knees referred for imaging, a rate substantially lower than that reported in OA patients.
Athletes, particularly those who engage in repetitive knee flexion combined with valgus or rotational loading (eg, distance running, cycling, swimming, and cutting sports like basketball and soccer), are at higher risk of PAB.21 Due to the repeated knee flexion under valgus or rotational load during these activities, the conjoined tendons are driven against the medial condyle. This causes friction to exceed the tendons’ capacity to recover, leading to local inflammation and tendon overuse that characterize PAB.16,21
Another high-risk group for PAB includes risk factors like female sex, obesity, and type 2 diabetes. A strong female predominance has been documented across cohorts, as discussed further below.5,15,19,22 Other reported risk factors for PAB include older age and post-arthroplasty mechanics.
Clinical Evaluation
Presently, there is no reliable clinical method to diagnose PAB with a high degree of certainty. One issue in clinical evaluation is the frequent overlap of PAB with other sources of medial knee pain, including medial compartment OA, medial meniscus pathology, and medial collateral ligament injury, all of which may coexist with PAB and confound its identification. Several clinical assessments have been developed to diagnose PAB (Table 2).Table 2Clinical Assessment of Pes Anserine BursitisAssessmentMethodologyHistory and symptom provocationPain localized to anteromedial proximal tibia, exacerbated by stair climbing, rising from seated position, or sitting with crossed legs.Bursal palpationPoint tenderness elicited ~2 cm distal to the medial joint line and 2 to 3 cm below the tibial tubercle at the pes anserine insertion; test is positive if tenderness is reproduced.Pes anserine stress testResisted knee flexion performed with the leg in external rotation; test is positive if pain is reproduced.Hamstring-popliteal angleHip flexed to 90°, leg extended; angle >15–20° indicates hamstring tightness contributing to bursal compression.Diagnostic injectionLocal anesthetic injected into the bursa; test is positive if significant pain relief is achieved, confirming the bursa as the primary pain generator.
Patients with PAB typically report pain at the pes anserine insertion, triggered by activities such as stair climbing or rising from a seated position.22 Pain can present as sudden, stabbing in onset, or as a dull ache that gradually worsens over days to weeks.14 Additional features reported by patients include nocturnal pain and morning stiffness.21 It must be noted that pain may subside spontaneously and recur months before formal presentation, contributing to diagnostic delay.14 A history of knee OA, obesity, diabetes mellitus, valgus deformity, or repetitive lower extremity activity should increase clinical suspicion for PAB, as these are among the most consistently identified risk factors.15
Several physical examination maneuvers can aid in the diagnosis of PAB. The hallmark finding on examination is point tenderness over the anteromedial joint margin at the insertion point of the conjoined pes anserine tendons.22 Localized soft tissue swelling or a palpable fluctuant mass may be present in cases of significant bursal distention, and crepitus indicative of bursitis may also be detected.22 Palpation is critical to distinguish joint line tenderness, as these findings can coexist and require careful comparison with the contralateral knee.22
The pes anserine stress test is performed by applying resistance against knee flexion while the leg is positioned in external rotation. A positive test is indicated by reproduction of medial knee pain.28 In addition to identifying PAB, this maneuver can help detect concurrent hamstring tendinopathy and medial soft-tissue pathology.22 The hamstring popliteal angle is assessed by flexing the patient’s hip to 90 degrees and then extending the leg. A flexion angle greater than 15 to 20 degrees indicates hamstring tightness, which is known to exacerbate bursal inflammation through increased compressive load at the pes anserine insertion.22 The low overall reliability of isolated physical examination findings provides insufficient support for use as a standalone diagnostic method for PAB, and these tests must be performed in conjunction with a thorough clinical history and, when indicated, imaging studies.21,22
Imaging studies are not required for the clinical diagnosis of PAB but may serve as an important adjunctive role in confirming the diagnosis, excluding concurrent intra-articular pathology, and guiding intervention. Plain radiographs are appropriate as a first-line imaging study and should be obtained to evaluate and rule out bony abnormalities, including proximal tibial stress fractures, arthritis, osteochondroma, and exostosis.22 Ultrasonography is useful for locating cystic bursal swellings and distinguishing them from other causes of medial proximal tibial swelling, including joint effusions. However, ultrasound findings are often nonspecific in suspected cases of PAB,15 and diagnosis is qualitative, as normal bursa is not visible until it is distended, with no validated threshold.
Thus, any fluid in the correct plane is abnormal, which is significant because clinical and imaging diagnoses can differ. Ultrasound confirmed bursal fluid in only about 8% of clinically diagnosed cases across OA, diabetic, and rheumatology cohorts,11,18,29 compared with a 20% prevalence in prospective screening.15 Consequently, much of what is labeled pes anserine bursitis likely reflects a pain syndrome without true bursal pathology.
MRI is useful for differentiating PAB from intra-articular pathologies, with characteristic findings including increased signal intensity and fluid formation around the pes anserine bursa on T2-weighted sequences.12,22 Forbes et al described the MR appearance of acute PAB in four patients presenting with presumed internal derangements of the knee, demonstrating fluid collections with low signal intensity on T1-weighted images and homogeneous increased signal on T2-weighted images beneath the pes anserine tendons. The authors emphasized that recognition of these MR findings is important to establish the correct diagnosis and thereby avoid unnecessary intraarticular arthroscopy.13 Axial images are especially helpful for distinguishing fluid in the pes anserine bursa from other medial fluid collections.13,22 A retrospective review by Rennie and Saifuddin of 509 knee MRI studies found a PAB prevalence of 2.5% in symptomatic adult knees and demonstrated that review of axial images resulted in the reclassification of 11 of 24 initially reported pes anserine bursae as other periarticular fluid collections, which supports the use of axial imaging in accurate diagnosis. It must be noted that fluid-filled anserine bursae have been reported in approximately 5% of asymptomatic knees, and MRI findings must therefore be interpreted in conjunction with the clinical presentation rather than in isolation.12
A targeted diagnostic injection of local anesthetic into the pes anserine bursa may serve a dual diagnostic and therapeutic role in the evaluation of PAB. When performing a diagnostic injection, it is critical to assess the patient’s baseline pain level prior to administration.22 A positive diagnostic injection is defined as significant or complete relief of medial knee pain following local anesthetic delivery, which supports the diagnosis of PAB and helps differentiate bursal pain from adjacent sources of medial knee symptoms, including medial knee compartment OA and medial meniscus pathology.14,22 The procedure may be performed using anatomical landmark guidance or under ultrasound guidance, with the latter offering the advantage of real-time visualization of the bursal space and increased precision of needle placement.22 A failure to achieve meaningful pain relief following a technically adequate injection should prompt reassessment of the diagnosis and consideration of alternative or additional sources of medial knee pain.
While a thorough clinical approach in the diagnosis of PAB has been supported in the literature, it is important to recognize that diagnosis is currently limited by the absence of a validated quantitative clinical assessment tool.21,22 Future studies should evaluate the application of advanced dynamic ultrasonography and computational analyses enabled by machine learning and artificial intelligence to develop more reliable diagnostic criteria for PAB. The use of pattern recognition has previously been demonstrated to identify disease characteristics that would otherwise be unappreciable by standard clinical means.21 Evaluation of imaging by AI may provide new insight into the diagnostic criteria for PAB.
The clinical syndrome of pes anserine bursitis and the underlying structural lesion are distinct entities that warrant separate evaluation. Clinical diagnosis remains essential, as PAB may present as medial knee pain regardless of bursal distention and retains clinical significance even when imaging is negative. Many cases labeled as pes anserine bursitis represent a pain syndrome without demonstrable bursal pathology, which underpins the diagnostic framework presented here.
Given the unreliability of individual examination findings, diagnosis should rest on the overall pattern of historical and physical findings rather than on any single test.21,22
Imaging plays a targeted role in the assessment of pes anserine bursitis. Radiographs are the first-line modality to exclude alternative diagnoses such as proximal tibial stress fracture, arthritis, osteochondroma, and exostosis.22 Ultrasound differentiates cystic bursal swelling from joint effusion and other causes of medial proximal tibial swelling, although its findings are qualitative and no validated threshold for bursal distention exists.15 MRI is particularly valuable for identifying intra-articular pathology, with axial images clarifying ambiguous cases and avoiding unnecessary arthroscopy.13 Structural confirmation of bursitis appears to carry more prognostic than diagnostic significance. In one series, only 8 of 17 injected patients reported a good or best global outcome, and the two best responders were the only patients with ultrasonographic evidence of true bursitis.29
The discrepancy between clinical assessment and imaging requires careful interpretation. Ultrasound confirms bursal fluid in only about 8% of clinically diagnosed cases across osteoarthritic, diabetic, and rheumatology cohorts, while prospective screening identifies fluid in 20%.11,15,18,29 MRI detects pes anserine bursitis in just 2.5% of symptomatic knees, and 11 of 24 initially suspected bursae were reclassified as other periarticular fluid collections on further review.12 Approximately 5% of asymptomatic knees demonstrate fluid-filled bursae, so a positive imaging finding alone is insufficient for diagnosis.12 Conversely, a negative study does not exclude pes anserine bursitis in patients with classic clinical features, and incidental fluid collections in asymptomatic individuals should not be overemphasized. These findings support integrating clinical judgment with imaging rather than relying on either in isolation.
When clinical and imaging findings are incongruent, several practical strategies may clarify the diagnosis. A targeted anesthetic injection serves both diagnostic and therapeutic purposes, as significant or complete pain relief supports a diagnosis of pes anserine bursitis and distinguishes it from medial compartment osteoarthritis or meniscal pathology.22 Ultrasound guidance improves the accuracy of intrabursal needle placement over landmark-based technique by providing real-time visualization.30 If a technically sound injection does not yield meaningful relief, the diagnosis should be reconsidered rather than treatment escalated. This stepwise approach is derived from the current literature and is offered as a practical, though not yet validated, clinical algorithm.
Further research is required to establish criteria for its formal validation.
Implications of Associated Pathology
Most conditions commonly cited as predisposing to pes anserine bursitis are supported primarily by cross-sectional and descriptive studies rather than by case-control evidence. The only case-control study to date compared 22 incident cases with 38 age- and sex-matched controls and characterized no significant difference in the prevalence of diabetes, knee osteoarthritis, obesity, knee instability, varus deformity, hindfoot malalignment, or radiographic osteoarthritis severity between groups.17 The sole exposure to reach statistical significance was valgus knee deformity, with an odds ratio of 5.2 (95% CI 1.1–25.5), increasing to 6.0 (95% CI 1.4–26.0) in the presence of collateral instability.17 That study enrolled 22 cases and drew its controls from patients with asymptomatic osteoporosis and rheumatic syndromes, so its null findings represent weak evidence of absence rather than evidence against association. Population-based imaging data nonetheless demonstrate a clear relationship with both radiographic knee osteoarthritis and knee pain, as detailed below.31 Evidence linking obesity to tendinopathy is largely extrapolated from broader musculoskeletal research and does not specifically implicate the pes anserinus.16,32 Anserine tenderness predicts osteoarthritis progression and the need for arthroplasty, which indicates an association with disease outcome rather than with etiology.33 Taken together, current evidence indicates that valgus deformity, particularly when combined with collateral instability, should raise clinical suspicion for pes anserine bursitis, while the contributions of obesity and diabetes remain unresolved.
Studies capable of settling these questions will require adequately powered case-control or prospective cohort designs.
Knee Osteoarthritis
Knee OA is one of the most common conditions associated with PAB and has been identified in approximately 17 to 20% of osteoarthritic knees in ultrasonographic studies, as detailed below.15,22 It is often characterized by progressive cartilage loss and joint space narrowing, which alter the biomechanical environment of the knee and increase load transmission through the medial compartment.21,22 This disruption in medial compartment mechanics produces PAB via altered stress distribution at the pes anserine insertion. These abnormal mechanical forces are characterized by increased medially directed loading, excess tensile demand at the pes anserine insertion, and repetitive microtrauma to the underlying bursa.22
The observed PAB accompanying knee OA shows some association with the degree of structural joint involvement, with Uysal et al reporting a direct correlation between OA severity and bursal size on ultrasonography.15 Kim et al similarly found that PAB was significantly more prevalent among individuals with knee OA (17.5%) than among those without (2.2%) and was more frequently identified in patients with knee pain (14.4%) than in those without (2.5%).31
Obesity
The association between obesity, metabolic conditions, and PAB is less definitive than often assumed. Excess body mass increases compressive and shear forces across the medial compartment of the knee, yet evidence specifically linking obesity to PAB remains inconsistent. One frequently cited descriptive series comprised only women, 93% of whom had radiographic knee osteoarthritis and 75% of whom had a body mass index above 27, an overweight rather than an obese threshold, and it included no comparison group, which limits conclusions about PAB frequency across weight categories.18 The only case-control study identified valgus knee deformity rather than obesity as the exposure associated with PAB.17 In their 245-patient cohort, Mortada et al likewise characterized no significant difference in BMI between knee OA patients with and without PAB (32.1 versus 29.7, P = 0.09).20 Uysal et al observed no significant difference in BMI between patients with and without PAB in their cohort of symptomatic OA patients, and Uson et al similarly documented that, despite 75% of their pes anserine bursitis or tendinitis (PATB) cohort exceeding that threshold, ultrasonographic evidence of true tendinitis or bursitis was found in only a small minority of symptomatic knees (roughly 5 to 8%).
This led the authors to conclude that clinically diagnosed PATB rarely shows structural confirmation on ultrasound.15,18 Obesity therefore co-occurs with PAB without established evidence of an independent causal role, and valgus deformity appears the more robust association.17
Metabolic Conditions
Diabetes mellitus warrants specific mention as an independent risk factor. Cohen et al evaluated 94 patients with non-insulin-dependent diabetes mellitus and identified PAB in 34 individuals, a prevalence of approximately 36% within this diabetic cohort. Notably, bursitis was not observed in any control subjects without diabetes, and 91% of affected individuals were women.34 Unlu et al prospectively evaluated 48 patients with type 2 diabetes mellitus using ultrasonography and found that although 29.1% of patients had pes anserine tendinitis or bursitis syndrome on clinical examination, only 8.3% demonstrated morphologic changes on ultrasonography, and none showed fluid distention of the anserine bursae.
This suggests that clinically diagnosed PAB in diabetic patients may frequently reflect changes related to concurrent OA rather than true isolated bursal inflammation.11
The underlying mechanism connecting obesity and diabetes to PAB most likely involves two complementary pathways. Mechanically, the added medial knee load from obesity and valgus alignment increases stress on the pes anserine tendons, which, in turn, upregulates matrix metalloproteinases and pro-inflammatory cytokines.16 On the other pathway, systemic release of adipokines from visceral fat sustains a chronic, low-grade inflammatory state. In addition, diabetes results in advanced glycation end-products that cross-link and stiffen tendon collagen, and, combined with obesity, impair tendon healing independent of mechanical load.35,36 These same metabolic pathways likely account for why obesity increases the risk of rotator cuff tendinopathy (odds ratio 1.25, 95% CI 1.12 to 1.40), even though the rotator cuff is non-weightbearing.
This implies that the association reflects a shared systemic mechanism rather than a mechanical overload.32 However, despite the mechanistic reasoning, the epidemiologic evidence is not strongly supported as no study has reported a PAB-specific odds ratio for obesity. In the only case-control study to examine these factors (22 cases, 38 controls), there was no significant difference in obesity, diabetes, or knee OA between cases and controls. However, valgus knee deformity was the only identifying significant risk factor (odds ratio 5.2, 95% CI 1.1 to 25.5).17 Therefore, obesity is best regarded as a mechanical contributor, mediated by valgus alignment and medial loading, rather than an independent risk factor.
For this reason, metabolic optimization, including weight management and glycemic control, is considered an important adjunct to local treatment strategies in the management of PAB.21,22
Knee Malalignment and Pes Planus
Knee malalignment and foot deformities are additional contributing factors to PAB.22 Genu valgum increases valgus loading at the knee during ambulation, placing greater stress on the medial stabilizing structures, including the pes anserine complex. A disruption in lower extremity alignment in the presence of genu valgum produces PAB via altered mechanical loading at the pes anserine insertion, specifically through increased medially directed forces and repetitive tensile demand on the conjoined tendons. Pes planus has been specifically identified as a predisposing factor for bilateral PAB, as abnormal lower limb alignment resulting from flatfoot deformity produces increased medially directed pressure at the knee.22 PAB is significantly more prevalent in females, though the underlying mechanisms are multifactorial rather than attributable to a single biomechanical pathway.
While females do have a broader pelvis and greater tendency toward knee valgus angulation, these anatomical differences primarily shift load-bearing forces toward the lateral tibiofemoral compartment rather than directly increasing compressive stress at the medial pes anserine insertion. Instead, the female predisposition to PAB likely results from a combination of factors, including higher rates of obesity, greater prevalence of knee OA, altered medial soft-tissue tension from valgus alignment, which may increase friction at the pes anserine bursa, and potential differences in connective tissue properties. Thus, while female-specific anatomical differences contribute to lower extremity biomechanics, their role in PAB is indirect and part of a broader multifactorial risk profile rather than a straightforward increase in stress at the pes anserine insertion point.15,18,34,37
Sports and Overuse
Athletes, particularly runners, can develop PAB as an overuse injury. Those who engage in activities requiring repetitive knee flexion and extension, lateral movements, or sudden directional changes are at a particularly high risk.38 Among swimmers, the breaststroke kick has been described as a precipitating factor for medial knee pain associated with the pes anserine complex.22 This entity is sometimes termed “breaststroker’s knee” because the whip-kick stroke transmits repetitive valgus and rotational loads through the conjoined tendon with forceful knee extension and external rotation.21 A systematic review of distal hamstring pathology by Koolmees et al identified PAB as the most common chronic medial distal hamstring condition, with mechanical derangement, direct trauma, obesity, and overuse all implicated as contributing factors.39 Athletes with PAB have been observed to frequently demonstrate contributing biomechanical deficiencies, including hamstring tightness and hip abductor weakness, which increase medial compartment loading. It must be noted that PAB in athletes rarely leads to long-term consequences, even in those who continue to engage in physical activity.22 The long-term prognosis of PAB is not well characterized in the literature.
Isolated PAB in athletes is generally benign; however, persistent pes anserine pain in the setting of knee OA tracks with a less favorable outcome. In a knee OA cohort, baseline anserine tenderness independently predicted frequent knee pain (odds ratio 2.28, 95% CI 1.76 to 2.97) and total knee arthroplasty (odds ratio 1.54, 95% CI 1.01 to 2.36). When tenderness persisted for over 4 years, the arthroplasty risk increased further (odds ratio 1.79, 95% CI 1.11 to 2.90).33 Thus, in the setting of knee OA, persistent pes anserine pain possibly serves as a marker of ongoing disease progression rather than an isolated, self-limiting condition.
Treatment Modalities
The main goal of PAB treatment is to reduce bursal inflammation and restore pain-free, functional mobility by addressing the underlying biomechanical and systemic factors that contribute to the condition. The standard of care for the management of PAB is conservative interventions. Physical therapy and corticosteroid injection produce comparable short-term improvement, and the durability of regenerative agents relative to either has not been established.
Surgery is considered only in the presence of refractory symptoms following appropriate nonoperative management and often involves addressing the underlying cause of biomechanical changes leading to pes anserine bursitis.22
Conservative treatment can be divided into two subcategories: therapy aimed at improving flexibility with stretching of the pes anserine tendons, and exercises focused on increasing muscular strength and knee stabilization.22,39 Combining these two approaches reduces tensile loading at the pes anserine insertion and optimizes the biomechanical environment of the medial knee. Proper management of PAB requires determining whether symptoms are secondary to reduced muscle performance or to loss of flexibility in the surrounding soft tissue. If the underlying cause is a lack of muscle control, the patient will be advised to engage in muscle-strengthening and muscle-control exercises.
This will lead to improved proprioception and muscle strength, both of which enhance knee stability. Physical therapy protocols focus on strengthening the adductor and quadriceps muscle groups, with a particular emphasis on exercises performed during the last 30 degrees of knee extension.39 The quadriceps, specifically the vastus medialis oblique through the final 30 degrees of knee extension, aid in stabilization of the medial compartment, while the hip adductors and abductors reduce dynamic valgus loading at the pes anserine insertion during functional activity. It must be noted that, for maximal benefit, the patient must first achieve adequate pain control and active muscular control before the focus shifts to progressive strength training.22 Initial physical therapy typically includes rest, ice, and short-term NSAID use unless contraindicated.39
If the patient’s PAB stems from a lack of soft-tissue flexibility, therapy should be more focused on stretching the pes anserine musculature and surrounding structures. Stretching and mobilization allow for an increased range of motion and may alleviate the pain caused by stiff soft tissue structures.21,22 Muscles targeted during stretching include the hamstrings, hip adductors, and individual components of the pes anserine complex. Stretching of the hamstring tendons is particularly important, as hamstring tightness can exert excessive compressive pressure on the bursa and is a well-recognized contributing factor.22
A randomized trial of 60 patients with knee OA and PAB compared physical therapy to corticosteroid injection. Both groups improved significantly on the VAS, WOMAC, and timed up-and-go test at 8 weeks (all within-group P ≤ 0.001). Additionally, no significant difference was found between the physical therapy and injection groups.40 Median VAS improved from 7 to 4 and 7.5 to 5, and median WOMAC from 43 to 24 and 43.5 to 24, in the physical therapy and injection groups respectively.
Yoon et al examined the correlation between ultrasonographic findings and response to corticosteroid injection in 26 patients with knee OA who were clinically diagnosed with PAB. Among the 17 patients treated with triamcinolone acetonide injection, pain VAS (73.1 to 50.7 mm on a 100-mm scale), WOMAC pain (10.6 to 7.5), and WOMAC physical-function (33.8 to 27.4) scores all improved significantly.29 However, patient-rated global response was more modest, with only 8 of 17 reporting a good or best outcome. Notably, the 2 best responders were the only patients with ultrasonographic evidence of true bursitis.
Taken together, these studies reinforce that clinically diagnosed PAB frequently lacks structural confirmation on imaging. Treatment response, particularly to injection, appears to track more closely with imaging-confirmed bursitis than with clinical diagnosis alone.
Intrabursal injection of local anesthetics, corticosteroids, or a combination of both may be considered for more persistent, severe, or refractory cases.22,30 Ultrasound-guided injection of these agents can provide significant pain relief and offers superior accuracy of intrabursal needle placement compared to landmark-guided technique.30 In Finnoff et al cadaveric study, ultrasound guidance placed the injectate accurately within the bursa in 92% of attempts (11 of 12) compared to only 17% (2 of 12) with the landmark-based technique (P<0.01). However, patients must be counseled on risks including subcutaneous tissue atrophy, skin pigmentation changes, and tendon damage if inadvertently delivered into pes anserine tendons. Injections should therefore be limited to no more than three per year, with an interval of at least one month between administration.22,41 Kang and Han reported clinical remission in 11 of 12 (91.7%) patients with PAB and knee OA who received corticosteroid injections, compared to 7 of 17 (41.2%) who did not, supporting the superiority of injection therapy over observation alone in this population.27 Injectable options differ more in durability than in efficacy.
In the only PAB randomized trial of 72 patients (mean age 61.5 years, 85% female), ultrasound-guided corticosteroid, oxygen-ozone, and 20% dextrose prolotherapy all improved pain and function. This includes VAS (0–10) and WOMAC (0–96) measured at baseline, one week and eight weeks (significant time-by-group interaction, P ≤ 0.05 for both measures).42 However, while corticosteroids led at one week, the regenerative agents had overtaken them by eight weeks. More specifically, the mean VAS in the corticosteroid group fell from 8.0 at baseline to 4.5 at one week but rebounded to 5.1 by eight weeks.
In contrast, the prolotherapy and oxygen-ozone groups continued to improve, reaching their lowest scores at eight weeks (3.5 and 3.9, respectively).
These findings were consistent with those of knee OA, where physical therapy matched or exceeded glucocorticoid injection at one year.43 In this study of 156 patients, the physical therapy group had improved WOMAC scores at one year than the glucocorticoid group (mean 37.0 vs 55.8; between-group differences 18.8 points, 95% CI 5.0–32.6). This suggests that corticosteroid injection manages symptoms rather than the underlying drivers; thus, durable relief depends on addressing them. Autologous platelet-rich plasma (PRP) injections have also proven to be effective in relieving pain caused by this condition.
Rowicki et al reported 28 of 33 patients (84.8%) achieved total or near-total pain relief, as assessed by VAS scale at 6-month follow-up following PRP injection for chronic pes anserine pain syndrome.41 In a randomized controlled trial of patients with PAB, Karabaş et al compared single versus double injections of leukocyte-rich PRP and found significant intragroup improvements in VAS, WOMAC, 6-minute walking test, and Likert scale at 1- and 3-month follow-up in both groups, with no significant between-group differences.44 These findings suggest that a single LR-PRP injection may be sufficient for short-term symptom relief. This is consistent with broader meta-analytic evidence indicating that the benefit of additional PRP may require three rather than two injections.45 However, the absence of a placebo or sham control limits the ability to attribute the observed improvements solely to PRP.46,47 Although these findings are promising, larger trials are required before PRP can be recommended as first-line treatment. A Cochrane review found at most a marginal short-term pain benefit (mean difference 0.95 on a 10-point pain scale, 95% CI 0.48–1.41) and no functional improvement on very-low-quality evidence.48 Currently, there is no direct study comparing PRP against corticosteroid for PAB, leaving it best reserved for refractory cases.
Surgical intervention is rarely required in the management of PAB and is reserved for persistent, treatment-refractory cases. Bursal debridement can relieve symptoms, and the literature has also reported the use of bursal excision in cases where the bursa is large or bony exostosis is present, warranting more definitive removal. It must be noted that underlying conditions, such as bony exostosis, must be identified and addressed at the time of surgery, as failure to do so may increase the risk of recurrence.22 Forbes et al reported that in one of their four acute PAB cases, debridement of the distended bursa resulted in complete resolution of symptoms.13 In rare instances when surgical intervention, such as bursectomy, is performed for refractory pes anserine bursitis, postsurgical care involves a period of immobilization followed by a gradual return to physical activities.
It should be noted that the overwhelming majority of patients respond to conservative management and that the literature strongly supports physical therapy management (including targeted strengthening, flexibility exercises, and manual therapy techniques aimed at restoring normal pes anserine mechanics) as the primary treatment approach. Although quantitative data are limited, in a cohort of 22 post-arthroplasty pes anserine pain syndrome who were managed nonoperatively, 81.8% (18 of 22) responded to a combined NSAID and physical therapy program.49 The remaining 4 responded after an additional corticosteroid injection. Surgical interventions should be considered only in exceptional cases after all conservative measures, including physical therapy and corticosteroid injection, have been thoroughly exhausted.12,13,50,51
Closing Remarks
Pes anserine bursitis is primarily a clinical diagnosis, as structural confirmation is achieved in only a minority of cases. The disconnect between clinical and imaging findings points to the need for evaluation and management strategies grounded in clinical assessment. Valgus knee deformity, alone or with collateral instability, is the only exposure supported by case-control data, while obesity and diabetes co-occur with PAB without established causal roles and knee osteoarthritis shows a consistent association of uncertain direction.
No single examination finding is reliable in isolation, and the diagnosis rests on the combination of point tenderness at the insertion, the pes anserine stress test, and the hamstring popliteal angle, with a targeted anesthetic injection clarifying the picture when clinical and imaging findings diverge. Physical therapy and corticosteroid injection produce comparable outcomes across an eight-week horizon, and regenerative agents may surpass corticosteroid at that interval, although long-term durability remains undetermined. Recognizing pes anserine bursitis as a clinical diagnosis, treating it on that basis, and reserving imaging for the exclusion of alternative pathology together offer the most defensible approach to the patient presenting with medial knee pain on the evidence currently available.