Knee Bursae: A Comprehensive Review of Clinical Evaluation, Imaging Differentiation, and the Expanding Role of Biologic Therapies

Abstract

Background

Knee bursae are potential sources of anterior, medial, lateral, and posterior knee pain, yet many remain under-recognized in clinical practice. Emerging biological therapies offer promising, minimally invasive options for resistant bursitis, but high-level evidence is limited for several bursal types.

Purpose

To systematically review the anatomy, clinical presentation, imaging characteristics, treatment strategies, and outcomes of 11 distinct knee bursae, with emphasis on the role of biologic therapies.

Methods

This systematic review followed PRISMA guidelines. PubMed and Embase were searched (2000-2024) for studies addressing anatomy, diagnosis, imaging, treatment (conservative, injection-based, biologic, or surgical), and outcomes of knee bursae. Studies involving human subjects, published in English, and reporting clinical, imaging, or therapeutic data were included. Levels of Evidence (LOE) were assigned using Oxford criteria.

Results

A total of 76 studies were included. Several randomized controlled trials (LOE I) focused on pes anserine and OA-related bursitis, while additional Level II studies assessed PRP and corticosteroids. Data on rare bursae (e.g., LCL, deep infrapatellar) were primarily derived from imaging reviews and case series (LOE III-IV). Corticosteroid injections showed recurrence rates of 20% to 40%. PRP and PRP+HA demonstrated improved pain relief and reduced recurrence in selected bursae, although protocols remain heterogeneous.

Conclusion

Conservative management remains first-line for most bursae. PRP-based therapies, especially in pes anserine and OA-related bursitis, offer promising alternatives in refractory cases. Although several Level I-II studies support their efficacy, additional high-quality RCTs are warranted—particularly for understudied bursae.

Introduction

Several less-studied bursae around the knee, although rarely symptomatic, may become clinically relevant in cases of persistent or unexplained knee pain. While the popliteal, pes anserine, and prepatellar bursae are well recognized, other bursae—including the superficial and deep infrapatellar, suprapatellar, iliotibial band (ITB), medial and lateral collateral ligament (MCL and LCL), semimembranosus-MCL, and medial gastrocnemius bursae—remain under-recognized despite their potential to mimic intra-articular pathology or tendon injuries.^{1 -5}

These bursae may become inflamed due to repetitive mechanical stress, trauma, systemic disease (e.g., gout, CPPD, rheumatoid arthritis), or infection, with distinct pathophysiological mechanisms. ⁵ - ¹⁰ Diagnosis can be challenging, as symptoms often poorly correlate with imaging findings.^4,11 Ultrasound and MRI are essential tools to differentiate bursitis from meniscal tears, ligament injuries, or cystic lesions.^{1,6,12 -14}

Although corticosteroid injections and aspiration remain standard treatments,^4,15,16 recent years have seen a growing interest in biologic therapies—such as platelet-rich plasma (PRP), PRP combined with hyaluronic acid (PRP+HA), and platelet-rich fibrin matrix (PRFM). Several studies have demonstrated improved pain and function scores with PRP-based therapies in pes anserine and prepatellar bursitis,^{7,17 -21} although high-level randomized trials remain lacking, especially for less-studied bursae like the ITB, LCL, or deep infrapatellar bursa.

This review aims to synthesize current evidence regarding the anatomical, clinical, diagnostic, and therapeutic aspects of 11 distinct knee bursae. Emphasis is placed on the role of biologic therapies, current evidence gaps, and the need for further studies to validate their use in the management of bursitis across these anatomical sites.

Unlike prior narrative reviews, this systematic review was conducted according to PRISMA guidelines, using a predefined search strategy, inclusion criteria, and structured data extraction, and it uniquely integrates clinical, imaging, and biologic treatment perspectives across all 11 anatomically distinct knee bursae, including rare and underreported types.

Methods

This systematic review was conducted in accordance with PRISMA guidelines (see Fig. 1 ). A comprehensive search of PubMed and Embase was performed for studies published between January 2000 and January 2024. Search terms included combinations of anatomical terms (e.g., “prepatellar bursa,” “pes anserine bursa,” “suprapatellar effusion,” “iliotibial band bursa”) and biologic therapies (e.g., “PRP,” “PRFM,” “stem cell therapy”). Titles and abstracts were screened independently by 2 reviewers, with full-text evaluation based on predefined eligibility criteria.

Figure 1.

PRISMA flowchart illustrating the study selection process. The diagram outlines the identification, screening, eligibility assessment, and final inclusion of studies in the review. This structured approach ensures transparency and reproducibility in systematic reviews.

Studies were included if they were peer-reviewed, English-language, human-based, and addressed at least one of the following: anatomy, clinical presentation, imaging, treatment (conservative, injection-based, biologic, or surgical), or outcomes of knee bursae. Eligible designs included randomized controlled trials, cohort studies, imaging reviews, and technical notes. Case reports, cadaveric-only studies, narrative reviews without original data, animal/in vitro studies, and non-English publications without translation were excluded.

Data extraction was performed independently by 2 reviewers and included anatomical location, study design, imaging and treatment modalities, and outcomes (pain, recurrence, function, complications). Methodological quality was assessed using the Oxford Centre for Evidence-Based Medicine Levels of Evidence (LOE). Priority was given to LOE I-II studies; however, in understudied bursae (e.g., LCL, semimembranosus-MCL), selected LOE III-IV studies and imaging reviews were included to ensure anatomical and clinical completeness (see Table 1 ).

Table 1.

Level of Evidence Table.

First author	Year	Study Type	Level of evidence
Perdikakis	2013	Pictorial Review	IV
Sconfienza	2018	Consensus Guideline (ESSR)	IV
Marra	2008	Narrative Imaging Review	IV
McCarthy	2004	Imaging Review	IV
Shikhare	2018	Pictorial Imaging Review	IV
Allen	2021	Educational Imaging Review	IV
Khalil	2024	Pre-experimental clinical study (1 group pre/post)	III
Lalam	2015	Ultrasound Imaging Review	IV
Maricar	2013	Systematic Review + Meta-analysis	I
Morrison	2000	Educational Imaging Review	IV
Liu	2018	Technical Imaging Review	IV
Draghi	2015	Imaging Review with Clinical Correlation	III
Steinbach	2013	Narrative Imaging Review	IV
Liu (K.)	2022	Systematic Review + Meta-analysis	I
Van Nest	2020	Systematic Review	I
Li	2021	Systematic Review + Meta-analysis	I
Zhou	2016	Systematic Review + Meta-analysis	I
Han	2019	Systematic Review + Meta-analysis	I
Naredo	2016	Narrative Review	IV
Yang	2017	Prospective Randomized Study	II
Giard	2014	Narrative Imaging Review	IV
Berkoff	2012	Narrative Review	IV
Herman	2014	Narrative Review	IV
Lueders	2016	Educational Technical Review	IV
Thurlow	2023	Narrative Review with Imaging Focus	IV
Lee (J.H.)	2019	Prospective RCT (ultrasound vs blind injection)	II
Gouda	2023	Prospective RCT (CS vs PRP vs ESWT)	II
Karabaş	2021	Prospective RCT (1 vs 2 PRP doses)	II
Chen (C.P.C.)	2017	Prospective Interventional Study	III
Chen (C.P.C.)	2020	Prospective Interventional (Thermal PRP)	II
Screpis	2021	Surgical Technique Note	V
Adam	2018	Prospective Interventional Study	III

Level of evidence for included studies. This table lists all reviewed studies according to author, year, study design, and corresponding Oxford Level of Evidence (LOE), illustrating the methodological diversity and strength of the included literature.

General Approach to Imaging Evaluation of Knee Bursae

Diagnosis of knee bursitis is primarily clinical, often based on localized swelling and tenderness (see Table 2 ). However, due to the variable depth and overlapping symptoms with intra-articular and periarticular pathologies, imaging plays a central role in confirming the diagnosis and guiding management.^{3 -5}

Table 2.

Evaluation and Imaging Table.

Bursa	Imaging Modalities	Key Diagnostic Features	Notes	Citations
Popliteal Bursa	MRI, ultrasound	Fluid between semimembranosus and medial gastrocnemius	MRI preferred for rupture or septation	McCarthy and McNally, 1 Marra et al., 12 Herman and Marzo, 14 Perdikakis and Skiadas 22
Pes Anserine Bursa	MRI, ultrasound	Hypoechoic area under pes tendons	Ultrasound sensitivity low (~2.5%-7.7%)	Thurlow et al., 11 Herman and Marzo, 14 Lee et al. 16
Prepatellar Bursa	Ultrasound, MRI	Fluid anterior to patella; thick wall in chronic/septic	MRI for severe/septic or differential	McCarthy and McNally, 1 Marra et al. 12
Superficial Infrapatellar	Ultrasound	Fluid over tibial tuberosity, superficial to patellar tendon	Best in longitudinal ultrasound	McCarthy and McNally, 1 Marra et al. 12
Deep Infrapatellar	MRI	Fluid deep to patellar tendon	MRI preferred to distinguish from tendinopathy	Allen and Jacobson, 3 Draghi et al., 4 Flores et al. 5
Suprapatellar Bursa	MRI, ultrasound	Effusion superior to patella	MRI best for joint involvement	McCarthy and McNally, 1 Shikhare et al., 2 Flores et al. 5
MCL Bursa (Voshell’s)	MRI, ultrasound	Calcification/fluid near MCL	Classic in calcific bursitis	Flores et al. 5
ITB Bursa	MRI	Fluid deep to ITB near lateral condyle	MRI best for ITBFS	Allen and Jacobson, 3 Draghi et al., 4 Flores et al. 5
Semimembranosus–MCL Bursa	MRI	Fluid in U-shaped recesses between SM and MCL	Best seen in axial/coronal MRI	Herman and Marzo 14
LCL Bursa	MRI, ultrasound	Thin fluid deep to LCL	MRI preferred	Allen and Jacobson, 3 Draghi et al. 4
Medial Gastrocnemius Bursa	MRI	Fluid adjacent to medial gastrocnemius	MRI essential for confirmation	Thurlow et al., 11 Herman and Marzo 14

Imaging modalities and diagnostic features of knee bursae. This table outlines the preferred imaging techniques (MRI, ultrasound) and key diagnostic findings for each bursa around the knee, aiding in accurate differentiation from adjacent pathologies.

Ultrasound is the preferred first-line tool for most bursae. It allows visualization of fluid accumulation, synovial thickening, septations, or signs of infection, and facilitates guided aspiration or injection. Ultrasound is particularly useful in superficial bursae such as the prepatellar, superficial infrapatellar, and pes anserine.^{4,13 -16} In power Doppler mode, it may detect active inflammation.^4,16 However, sensitivity varies; for example, only 2.5% to 7.7% of clinically diagnosed pes anserine bursitis cases show positive ultrasound findings.^1,16

A specific application of ultrasound in differentiating cystic lesions involves sonopalpation—applying pressure with the probe to assess compressibility. According to Giard and Pineda, ganglion cysts (GCs), which are delineated by dense connective tissue and filled with viscous hyaluronic-rich fluid, typically demonstrate low compressibility, while synovial cysts (SCs), lined by synovium and containing standard synovial fluid, are generally more compressible. ¹⁵ This distinction is valuable in distinguishing para-articular cystic lesions, especially when their content and compressibility are evaluated directly under real-time imaging. ¹⁵

MRI is reserved for complex, deep, or atypical presentations. It offers superior anatomical detail, detects coexisting pathology (e.g., OA, meniscal tears), and is essential in evaluating deeper bursae (e.g., suprapatellar, deep infrapatellar, subpopliteal) or when tumors or crystal deposition are suspected.^{4,5,8,12 -14}

In the specific context of Baker’s cysts, a meta-analysis by Liu et al. demonstrated that ultrasound has excellent diagnostic accuracy compared to both pathology and MRI, with pooled sensitivity and specificity of 97 and 100% versus pathology, and 94 and 100% versus MRI, respectively. Given its ability to detect even small cysts (<4 mm), alongside low cost and wide availability, ultrasound is considered a reliable modality for screening, diagnosis, and follow-up of Baker’s cysts. ²³

Diagnostic injections under ultrasound guidance can aid in confirming bursal involvement when pain relief follows anesthetic administration, particularly in PATB and ITB-related syndromes. Ultrasound-guided injections show higher accuracy (up to 92%) than blind techniques (17%-36%).^6,16,24

Aspiration and laboratory tests are required when infection is suspected—especially in septic or crystal-induced bursitis. Fluid should be analyzed for WBC, Gram stain, culture, and crystals.^9,13,25 ESR, CRP, and CBC may support the diagnosis but are nonspecific.^13,25,26

Radiographs are generally of limited value but may help rule out fractures or detect calcific deposits in crystal-induced or calcific bursitis. ¹³

In summary, ultrasound is the mainstay for routine bursal evaluation and interventions, while MRI is crucial in diagnostically challenging or deep cases. Proper anatomical localization, guided imaging, and selective aspiration significantly enhance diagnostic accuracy across all knee bursa types.^3-5,13,16

Differential Diagnosis

Differential diagnosis of knee bursitis varies by anatomical location and must consider both intra-articular and extra-articular mimics.

Posterior knee swelling, such as that from gastrocnemius-semimembranosus bursitis or popliteal cysts, may resemble deep vein thrombosis (DVT)—a condition termed pseudothrombophlebitis.^1,2,14 Other posterior mimics include popliteal artery aneurysms and venous malformations, both demonstrating internal flow on Doppler or MRI,^6,13 and tumors like schwannomas, sarcomas, or myxomas, which typically enhance with infiltrative margins.^6,12,13 Synovial disorders, including PVNS and osteochondromatosis, may also present as debris-filled or calcified lesions.^1,14

Anterior swelling, especially over the patella, necessitates differentiation from Morel-Lavallée lesions, gouty tophi, CPPD, PVNS, and soft tissue tumors such as lipomas and fibromas.^5,13 Prepatellar and infrapatellar bursitis may be confused with patellar tendinopathy, characterized by tendon thickening without fluid,^4,5 or Hoffa’s fat pad syndrome, which causes deep anterior pain with edema, especially on extension.^3,8 Infrapatellar pain may also result from osteochondromas, synovial cysts, lipomas, or crystal-related disease.^{10,13,25 -28}

Medial knee pain, seen in pes anserine bursitis, overlaps with medial meniscal tears, especially of the posterior horn, MCL sprains, pes anserine tendinopathy, medial tibial stress syndrome, and stress fractures—all distinguishable via MRI and clinical context.^1,2,4,12,29 Referred pain from L3-L4 radiculopathy should be considered in atypical or unresponsive cases. ¹⁶

Suprapatellar bursitis must be differentiated from joint effusion due to OA, RA, or meniscal pathology,^3,25,26 as well as from quadriceps tendon rupture, which presents with superior patellar pain, extension weakness, and a palpable gap.^4,5 Hematomas or abscesses should be ruled out post-trauma,^9,13,25 while tumors and crystal arthropathies like gout or CPPD also mimic acute swelling.^26,28

Lateral knee pain, involving the iliotibial band bursa, may resemble lateral meniscal tears, LCL injuries, or tendinopathies of the popliteus or biceps femoris. Less commonly, referred pain from the lumbar spine or hip, or peroneal nerve entrapment, should be considered in refractory cases.^4,5,16

Precise clinical localization and imaging with ultrasound or MRI are essential to differentiate true bursitis from these mimics and guide appropriate treatment.^4,5,8

Popliteal Bursa

Popliteal cysts (Baker’s cysts) are distentions of the gastrocnemio-semimembranosus bursa, typically linked to osteoarthritis, meniscal tears, and synovitis in adults.^1,11,14 The mechanism involves increased intra-articular pressure with unidirectional synovial fluid flow into the bursa.^14,28 Posterior horn medial meniscal tears are a common MRI finding.^1,11 Prevalence varies (5%-40%), and while sometimes associated with OA symptoms, cysts often reflect secondary synovial inflammation. ¹¹ In children, these bursae are usually asymptomatic and non-communicating. ¹⁴ MRI is the diagnostic gold standard, but ultrasound provides a sensitive and practical tool, including for guiding aspiration or corticosteroid injection. ¹⁴

Etiology

Popliteal bursal distention (Baker’s cyst) is typically a secondary response to intra-articular pathology, especially OA, medial meniscal tears, and synovitis.^1,11,14 A valve-like mechanism allows synovial fluid to enter the gastrocnemius-semimembranosus bursa during flexion but blocks return flow in extension, causing accumulation. ¹⁴ Medial meniscus tears, particularly in the posterior horn, are the most common MRI finding.^1,11 In children, these bursae are usually isolated, non-communicating, and asymptomatic.^11,14 Though rare, other causes include trauma, infection, or crystal arthropathy, ¹⁴ and alternate bursae like the semitendinosus bursa may also be involved. ¹⁴ Some cysts form without joint effusion due to localized irritation.^1,11 Identifying the primary intra-articular driver is essential for effective treatment and recurrence prevention.^4,11,14

Clinical Presentation

Popliteal bursa often cause posterior knee fullness, tightness, or pain, especially in patients with OA or meniscal pathology.^1,12,14,22 A soft mass may be palpable in the medial popliteal fossa during extension and less so in flexion (Foucher’s sign). ¹⁴ Larger bursas can restrict motion due to intracystic pressure.^1,14 However, physical examination alone is frequently insufficient—less than half of imaging-confirmed cases show clear signs. ¹⁴

Bursa rupture may mimic DVT with calf pain, swelling, and bruising—a condition termed pseudothrombophlebitis.^1,13,14,22 Rarely, this may lead to compartment syndrome, especially if misdiagnosed and treated with anticoagulants.^1,13,14 Massive cysts may compress nerves or vessels, causing neuropathy or vascular compromise. ¹⁴ In children, bursas are typically asymptomatic and incidentally found.^1,14 Differential diagnoses include DVT, aneurysm, meniscal cysts, synovial sarcoma, and soft tissue masses^1,13,14 (see Table 3 ).

Table 3.

Clinical Presentation Table.

Bursa	Typical Symptoms	Associated Conditions	Citations
Popliteal Bursa	Posterior knee swelling, tightness, Foucher’s sign	OA, meniscal tears, pseudothrombophlebitis	McCarthy and McNally, 1 Marra et al. , 12 Herman and Marzo, 14 Perdikakis and Skiadas 22
Pes Anserine Bursa	Medial tibial pain, worse with stairs or kneeling	OA, obesity, valgus deformity, diabetes	Thurlow et al., 11 Herman and Marzo, 14 Lee et al. 16
Prepatellar Bursa	Anterior swelling over patella, warm/tender area	Repetitive kneeling, trauma, septic bursitis	McCarthy and McNally, 1 Marra et al. 12
Superficial Infrapatellar	Swelling below patella, tender to pressure	Occupational kneeling, gout, RA	Allen and Jacobson, 3 Marra et al. 12
Deep Infrapatellar	Deep anterior knee pain with movement	Jumping sports, Osgood-Schlatter mimic	Allen and Jacobson, 3 Draghi et al., 4 Flores et al. 5
Suprapatellar Bursa	Swelling above patella, may mimic joint effusion	OA, meniscal tears, synovitis	McCarthy and McNally, 1 Shikhare et al. , 2 Flores et al. 5
MCL Bursa (Voshell’s)	Medial pain, aggravated by valgus stress	Calcific bursitis, OA	Flores et al. 5
ITB Bursa	Lateral knee pain at 20-30° flexion	ITB friction syndrome	Allen and Jacobson, 3 Draghi et al., 4 Flores et al. 5
Semimembranosus–MCL Bursa	Posteromedial pain, worse with flexion and valgus stress	Valgus overload, meniscal pseudotear	Herman and Marzo 14
LCL Bursa	Lateral joint line pain, mimics LCL sprain	LCL strain mimic	Allen and Jacobson, 3 Draghi et al. 4
Medial Gastrocnemius Bursa	Posteromedial pressure sensation or tightness	Repetitive posterior stress	Thurlow et al., 11 Herman and Marzo 14

Clinical characteristics of bursae around the knee. This table summarizes typical symptoms and commonly associated conditions for each of the 11 knee bursae, highlighting key clinical patterns that aid in differential diagnosis.

Treatment and Prognosis

Management of popliteal bursa depends on symptoms and underlying joint pathology. Conservative treatment—such as observation, NSAIDs, and physiotherapy—is often sufficient in children or asymptomatic adults, ¹⁴ though less effective when intra-articular pathology persists. Ultrasound-guided aspiration combined with corticosteroid injection can offer short-term relief, especially in OA-related cysts, though recurrence may reach 40% in septated cases. ³⁰ Sclerotherapy may reduce cyst volume in refractory cases, but evidence is limited and complications such as inflammation may occur. ¹⁴

As in other bursae, PRP used in this context is generally leukocyte-rich and prepared via double-spin centrifugation, concentrating platelets and enhancing both anti-inflammatory and regenerative effects. Biologic therapies are emerging alternatives, particularly in OA-related bursopathy. Ultrasound-guided leukocyte-rich PRP and PRP+HA have shown significant symptom reduction in related conditions such as pes anserine bursitis and knee OA, with over 70% success rates and reduced need for surgery.^14,18,21 Although specific RCTs for popliteal bursae are lacking, their favorable safety profile supports consideration in selected refractory cases.^7,18,19,21

Surgical intervention is indicated when conservative measures fail. Arthroscopic decompression targeting intra-articular lesions and neutralizing the valve-like communication tract has shown improved outcomes and recurrence rates below 10%. ³¹ In contrast, open excision without addressing the communication tract has recurrence rates up to 60% to 70%.^14,27 Prognosis is generally good when treatment targets both the cyst and the underlying joint pathology. In children, cysts are typically non-communicating and often resolve spontaneously ¹⁴ (see Table 4 ).

Table 4.

Treatment.

Bursa	Conservative	Injection-Based Treatment	Biologic Treatment	Surgical Options	Citations
Popliteal Bursa	NSAIDs, PT	Aspiration + CS (ultrasound-guided)	PRP, PRP+HA	Arthroscopy, excision	Herman and Marzo 14 , Karabaş et al., 18 Chen et al., 19 Adam et al. 21
Pes Anserine Bursa	PT, weight loss	CS or PRP (ultrasound-guided)	PRP, PRP+HA, LR-PRP	Rare surgical intervention	Thurlow et al., 11 Herman and Marzo 14 , Lee et al., 16 Gouda et al., 17 Karabaş et al. 18
Prepatellar Bursa	Ice, avoid kneeling	CS injection, aspiration if infected	PRP/PRFM (limited data)	Bursectomy in chronic/septic cases	McCarthy and McNally 1 , Marra et al. , 12 Herman and Marzo 14
Superficial Infrapatellar	Ergonomics, NSAIDs	CS injection (ultrasound-guided)	PRP/PRFM (suggested)	Rare	Allen and Jacobson 3 , Marra et al., 12 Gouda et al., 17 Adam et al. 21
Deep Infrapatellar	PT, quadriceps strengthening	Limited injection data	Not reported	Not indicated	Allen and Jacobson, 3 Draghi et al., 4 Flores et al. 5
Suprapatellar Bursa	NSAIDs, treat OA	CS injection, aspiration	PRP, PRP+HA	Rare (usually non-surgical)	Chen et al., 7 Herman and Marzo, 14 Chen et al., 19 Adam et al. 21
MCL Bursa (Voshell’s)	Valgus unloading brace	CS, ESWT, UGPL	PRP, PRP+HA	Rare excision	Flores et al., 5 Karabaş et al., 18 Adam et al. 21
ITB Bursa	Activity modification	Rarely injected	Not reported	Not indicated	Allen and Jacobson, 3 Draghi et al., 4 Flores et al. 5
Semimembranosus–MCL Bursa	Rest, NSAIDs, PT	Not used	Not reported	Rare documentation	Herman and Marzo 14
LCL Bursa	PT, avoid varus stress	Possibly CS (ultrasound-guided)	PRP (suggested only)	Not commonly required	Allen and Jacobson, 3 Draghi et al., 4 Flores et al., 5 Giard and Pineda, 15 Gouda et al. 17
Medial Gastrocnemius Bursa	Similar to popliteal	CS injection	PRP, PRP+HA (adjacent OA)	Not indicated	Thurlow et al., 11 Herman and Marzo, 14 Adam et al. 21

Treatment approaches for knee bursae. This table summarizes conservative, injection-based, biologic, and surgical treatment options for each of the 11 knee bursae, including relevant citations supporting each modality.

Pes Anserine Bursa

Anatomy, Epidemiology, and Mechanism

The pes anserine bursa lies on the anteromedial proximal tibia between the sartorius, gracilis, and semitendinosus tendons and the medial collateral ligament. ³² It is non-communicating and usually flattened in asymptomatic individuals. ¹⁴ When inflamed, it may appear as a tender swelling, with MRI showing multilobulated fluid beneath the tendons.^14,30

Pes anserine bursitis is common in overweight, middle-aged or elderly women with knee OA and in athletes exposed to repetitive stress, including runners.^14,16,30 A study reported bursitis in up to 17.5% of symptomatic OA patients. ¹⁴

The primary mechanism involves repetitive valgus stress and internal rotation, causing shear forces between tendons and the MCL, leading to friction and inflammation.^14,30 Risk factors include obesity, genu valgum, and overuse syndromes.^14,16,30 Its non-communicating nature distinguishes it from joint-connected cysts like Baker’s cysts. ¹⁴

Clinical Presentation

Pes anserine bursitis (PATB) presents as localized anteromedial knee pain 4 to 5 cm below the joint line, worsened by climbing stairs, rising, or kneeling.^14,16 Tenderness over the pes anserinus insertion is common, with possible warmth or swelling.^1,16 PATB is more frequent in middle-aged women with OA, obesity, diabetes, or valgus alignment, and often coexists with medial OA.^11,16

Prevalence ranges widely: 14% to 20% in OA patients, and 2.5% to 70% in broader populations.^1,11,16 Diagnosis relies on localized tenderness and absence of joint line pain to differentiate from meniscal pathology, ¹⁶ though clinical and tendinous symptoms may overlap.

Ultrasound findings are often absent despite symptoms—detection rates range from 2.5% to 7.7%.^1,16 Still, ultrasound-guided steroid injections yield better pain relief than blind injections, supporting the bursa’s role in symptom generation. ¹⁶

Treatment

Management of PATB typically starts with conservative treatment—activity modification, weight loss, NSAIDs, ice, and physical therapy. ¹⁶ PT programs focusing on hamstring and quadriceps stretching, hip abductor strengthening, gait correction, and neuromuscular retraining have shown long-term benefits and reduced recurrence, particularly in OA-related cases.^10,16 These non-invasive strategies may offer partial relief in chronic bursitis or advanced OA. ¹⁶

For faster symptom control, corticosteroid injection into the bursa is effective. Ultrasound-guided injections provide greater accuracy (92% vs. 17%-36%) and improved pain relief—VAS reductions of 4.5 vs. 2.5 at 1 week and 3.6 vs. 1.9 at 4 weeks.^11,28 Injections also serve a diagnostic role, but repeated use may lead to tissue atrophy or tendon damage. ¹¹ Recurrence within 3 to 6 months occurs in 20% to 30% of patients, especially without addressing biomechanical factors.^11,16 Conservative therapy alone may suffice in mild cases, but adherence is crucial. ¹⁶

Biologic therapies for bursitis most commonly involve autologous platelet-rich plasma (PRP), typically leukocyte-rich and prepared using a double-spin centrifugation technique. This process yields high concentrations of platelets and moderate leukocyte levels, promoting anti-inflammatory and regenerative effects. When combined with hyaluronic acid (PRP+HA), additional viscosupplementation is provided, which may enhance outcomes in osteoarthritis-associated bursitis.

Biological therapies are gaining interest. In a prospective trial of 71 PATB patients, ultrasound-guided leukocyte-rich PRP injections significantly improved WOMAC, VAS, and walking test scores compared to steroids and placebo. ¹⁸ PRP combined with hyaluronic acid (PRP+HA) also reduced pain and improved function in OA-related bursopathy. ²¹ These treatments offer anti-inflammatory and regenerative effects and may reduce recurrence, though PATB-specific high-level data remain limited.

Mesotherapy may offer temporary relief but lacks standardization and strong evidence.^4,16 Surgery is rarely required and reserved for refractory or septic cases. While bursectomy may resolve symptoms, long-term outcomes in PATB are not well established. ¹⁶

Prognosis is generally favorable. Ultrasound-guided injections yield >80% short-term relief, ¹⁶ while sustained outcomes are best achieved through a multimodal strategy combining PT, lifestyle changes, and selective use of injections or biologics.

Prepatellar Bursa

The prepatellar bursa is a superficial, extra-articular, non-communicating synovial sac located between the skin and the anterior patella.^{1 -3,13} It forms part of the anterior trilaminar soft tissue over the patella alongside the infrapatellar bursae.

Prepatellar bursitis is common in professions or sports involving prolonged kneeling, such as carpet layers, roofers, and wrestlers—hence the nickname “housemaid’s knee.”^3,12 It affects adults more often due to cumulative microtrauma and is slightly more frequent in men.^13,29

Repetitive shear and compressive forces lead to synovial hyperplasia and bursal fluid accumulation.^2,3 Chronic inflammation may result in fibrotic thickening, septations, or hemorrhage, especially following trauma.^2,3,9 Imaging studies confirm that prepatellar bursitis is usually isolated, without joint involvement, unlike Baker’s cysts.^1,3

Etiology

Prepatellar bursitis has a multifactorial etiology, most commonly due to chronic mechanical irritation from repetitive kneeling or trauma—seen in occupations like roofers, tile workers, and wrestlers.^1,3 Repeated friction between skin and patella leads to synovial inflammation and bursal fluid accumulation.^1,4

Acute trauma may cause hemorrhagic bursitis, especially in young athletes or post-fall.^2,31 Septic bursitis, often from Staphylococcus aureus, arises from skin breaches or aspiration and is more common in immunocompromised individuals.^10,13

Crystal-induced bursitis may occur in gout or CPPD, with urate or calcium crystals triggering inflammation mimicking infection.^2,3 Autoimmune diseases like RA and lupus can also cause bilateral bursitis, often with systemic signs.^3,6 Differentiating septic, crystal, and autoimmune causes is critical for proper treatment.^2,10,13

Clinical Presentation

Prepatellar bursitis typically presents as visible swelling over the patella with anterior knee pain and tenderness, especially during kneeling or direct pressure.^1,12 Acute cases show soft, fluctuant swelling, often following increased mechanical stress or trauma, without systemic signs or joint involvement. ¹

Chronic bursitis may present as a painless anterior mass without erythema, seen in those with repetitive kneeling and may persist for weeks.^1,5

Septic bursitis is more dramatic, with redness, warmth, severe pain, and possibly fever or lymphadenopathy. It may follow skin trauma or aspiration and must be confirmed via fluid aspiration and culture. ¹⁰

Hemorrhagic bursitis presents with sudden swelling and bruising after trauma or in anticoagulated patients, with possible fluid-fluid levels on imaging. ⁵

Clinical assessment must integrate history, physical examination, and imaging or aspiration to differentiate between etiologies.^1,5

Treatment

Treatment of prepatellar bursitis depends on etiology, severity, and response to prior therapy. Most aseptic cases respond to conservative management including rest, ice, NSAIDs, and avoiding kneeling or direct pressure.^3,12,31 Chronic or recurrent cases may require aspiration and corticosteroid injection, preferably under ultrasound guidance, which improves accuracy and reduces complications.^4,15,16 However, repeated injections may cause skin atrophy, depigmentation, or infection, especially with poor technique.^4,5,15

In septic bursitis, aspiration and culture-guided antibiotics are critical. While many respond to outpatient oral therapy, severe cases may require hospitalization or surgical drainage.^5,9,13,25 Crystal-induced bursitis (gout, CPPD) is treated with aspiration, NSAIDs or colchicine, and long-term metabolic control.^26,28

Surgical bursectomy is reserved for refractory or cosmetically deforming cases. Techniques preserving the anterior bursal wall while excising the posterior reduce risks of scarring, adhesion, and delayed healing.^5,14

Recurrence is common in patients who resume kneeling or high-friction activities without protection. Use of kneepads and patient education are key to prevention. While some chronic cases leave residual swelling, functional outcomes are generally excellent with appropriate treatment.^5,31

Biological Therapies

As in other periarticular bursae, PRP applied in prepatellar bursitis is typically leukocyte-rich and prepared via double-spin centrifugation to enhance its regenerative and anti-inflammatory profile.^18,21 Emerging biological therapies may benefit patients with chronic or recurrent bursitis unresponsive to corticosteroids. A prospective trial on pes anserine bursitis found ultrasound-guided PRP injection more effective than corticosteroids in improving pain and function, with longer-lasting results. ¹⁸ Though data for prepatellar bursitis are limited, anatomical similarities suggest potential use in resistant cases.

PRP combined with hyaluronic acid (PRP+HA) has shown greater pain reduction and improved joint function compared to HA alone in periarticular bursitis, particularly with OA involvement. ²¹ In corticosteroid-restricted patients, such approaches may be valuable.

PRFM (platelet-rich fibrin matrix) offers prolonged local growth factor release. Technical reports support its use in superficial and parameniscal bursae, suggesting possible benefit in prepatellar bursitis, although clinical data remain scarce. ¹⁷

Biologic therapies should be individualized, used adjunctively, and tailored to chronicity and comorbidities. Further studies are needed to clarify their role.

Superficial Infrapatellar Bursa

Anatomy, Epidemiology, and Mechanism

The superficial infrapatellar bursa lies between the skin and anterior patellar tendon, just below the patella, and is distinct from the deeper infrapatellar bursa. ¹³ It reduces friction during kneeling or extension but often remains asymptomatic unless inflamed. ⁵

This bursa is especially prone to irritation from direct pressure or microtrauma, making it susceptible in those with frequent kneeling—such as tilers, floor workers, and volleyball players.^5,31

Although less common than prepatellar or pes anserine bursitis, it may develop from repetitive compression or acute trauma to the anterior tibial region, leading to synovial hyperplasia and fluid accumulation.^5,31

Etiology

This bursitis is typically caused by repetitive mechanical stress or trauma over the anterior tibia, especially in occupations involving kneeling such as carpet laying or athletics.^1,3,12,22 Friction in this region leads to localized inflammation, historically termed “clergyman’s knee.”^3,12

Inflammatory arthropathies—such as RA, gout, and pseudogout—can trigger bursitis via synovial proliferation or crystal deposition.^10,26,28 Septic bursitis may result from superficial trauma or abrasions, most often caused by Staphylococcus aureus.^9,13,25

Biomechanical risk factors include obesity, limb malalignment, patellar tendinopathy, and altered gait, all increasing localized pressure.^8,27,31 Chronic bursitis may arise gradually, while acute onset often follows trauma or infection.

Rarely, iatrogenic factors like repeated steroid injections or nearby procedures may provoke inflammation.^2,30

Clinical Presentation

This condition typically presents with localized pain, swelling, and tenderness below the patellar tendon over the tibial tuberosity, often worsened by kneeling or knee extension.^3,12,22,31 Acute or septic cases may show erythema, warmth, or purulent drainage.^9,13,25

On examination, fluctuant swelling is noted anteriorly, distinct from prepatellar or intra-articular structures.^1,3 Chronic cases may present with firm, fibrotic swelling and mild persistent discomfort.^5,10

Range of motion is generally preserved unless fibrosis or adjacent involvement occurs.^3,28 Differentiation from conditions like prepatellar bursitis, patellar tendinopathy, or fat pad impingement relies on anatomical location, history, and palpation response.^3,4,8

Treatment, Recurrence, and Prognosis

Most acute cases resolve with conservative management, including rest, ice, NSAIDs, activity modification, and physical therapy.^3,12,31 Inflammatory bursitis due to systemic conditions may require prolonged disease control.^10,26,28 For persistent symptoms, ultrasound-guided corticosteroid injection offers both diagnostic and therapeutic benefit, although repeated injections risk skin atrophy or soft tissue damage, especially in fibrotic bursae.^4,5,15,16

Surgical bursectomy is reserved for chronic or refractory cases and generally yields good outcomes when mechanical contributors are addressed, despite potential complications such as scarring or delayed healing.^5,10,13,14 Arthroscopic debridement may be considered if intra-articular pathology coexists.^5,11

Recurrence is common without ergonomic protection, especially in occupations involving kneeling. Misdiagnosis—such as confusing this condition with patellar tendinopathy or deep infrapatellar bursitis—can delay effective treatment.^{3 -5,8,12,31} Prognosis is favorable with accurate diagnosis and preventive measures.

Biologic Therapies

Consistent with its use in other superficial bursae, PRP in this context is prepared using double-spin protocols to optimize its anti-inflammatory and regenerative potential.^18,21 While specific trials for the superficial infrapatellar bursa are lacking, biologic therapies have shown promise in similar superficial bursae. PRP injections led to superior pain and function outcomes compared to corticosteroids in pes anserine bursitis. ¹⁸ PRP combined with hyaluronic acid (PRP+HA) further improved results in OA-associated bursitis, ²¹ and PRFM demonstrated benefit in other superficial sites through sustained growth factor delivery. ¹⁷ These modalities may be considered in select chronic cases, although further targeted studies are needed.

Deep Infrapatellar Bursa

Anatomy, Epidemiology, and Mechanism

This bursa lies between the posterior patellar tendon and the anterior tibia near the tibial tuberosity, reducing friction during knee extension.^3,4,12 Unlike the superficial bursa, it is not externally palpable and is more influenced by tendon-bone mechanics.^{3 -5}

Though less common, it is relevant in athletes engaged in jumping or kneeling, and may mimic or coexist with patellar tendinopathy (“jumper’s knee”).^3,5,31

Inflammation results from repetitive microtrauma, tendon overload, or postoperative scarring. Chronic irritation may cause synovial thickening or fibrosis.^4,5,14,27

Etiology

This condition results mainly from repetitive stress between the patellar tendon and anterior tibia, often in athletes involved in jumping or deceleration sports like volleyball and running.^3,5,31 Poor biomechanics and overuse contribute to microtrauma and bursal inflammation.^4,5

It is frequently confused with patellar tendinopathy due to overlapping symptoms and anatomy.^4,5 Post-surgical changes or tibial procedures may cause tendon misalignment or scarring, increasing bursal friction.^14,27

Direct trauma is rare but possible, particularly in contact sports.^13,25 Systemic conditions such as gout or rheumatoid arthritis may also involve this bursa, especially in bilateral or chronic cases.^10,26,28

Clinical Presentation

This condition presents with deep anterior knee pain beneath the patellar tendon, worsened by activities like running, kneeling, or stair climbing.^3,5,31 Examination reveals deep tenderness over the tibial tuberosity, with no visible swelling or fluctuation due to the bursa’s location.^3,4

Symptoms often develop gradually from repetitive loading or poor biomechanics, though trauma or surgery may trigger acute onset.^4,5,27 It commonly mimics or coexists with patellar tendinopathy, particularly in athletes.^4,5

Functional limitations include pain with squatting or jumping, reduced sports performance, and incomplete relief with NSAIDs.^3,12,31 Chronic cases may involve fibrosis or multiloculated fluid, causing persistent discomfort.^5,14

In inflammatory conditions like gout or RA, bilateral pain, stiffness, and joint effusions may be present.^10,26,28 Diagnosis is often aided by imaging to differentiate from fat pad impingement, tendinopathy, or soft tissue masses.^4,5,8

Treatment

Initial treatment includes activity modification, avoidance of kneeling or jumping, NSAIDs, ice, and physical therapy—generally effective for acute or mild cases.^3,5,12,31 Persistent symptoms may require ultrasound-guided aspiration and corticosteroid injection, which allow targeted delivery and diagnostic evaluation. Repeated injections should be avoided in fibrotic or septated bursae due to risks of subcutaneous atrophy and skin depigmentation.^4,5,15,16

Sclerotherapy has been explored in refractory cases, but results are inconsistent, particularly in complex bursal anatomy.^16,24 Open bursectomy may be needed when fibrosis or infection is present, with favorable outcomes if biomechanical contributors are addressed, though surgery carries risks such as scarring and stiffness.^5,13,14 Arthroscopic debridement is rarely indicated and technically challenging in isolated deep bursitis.^5,11

As in other deep bursae, PRP is typically prepared using a double-spin centrifugation technique to enhance platelet concentration and therapeutic efficacy.^18,21 Biologic therapies are emerging for chronic or steroid-resistant bursitis. PRP injections have shown better outcomes than corticosteroids in infrapatellar and pes anserine bursae. ¹⁸ PRP+HA provides superior symptom relief, especially in cases with degenerative changes. ²¹ PRFM offers sustained local growth factor release and may be a future option in deep bursitis, though data remain limited. ¹⁷

Suprapatellar Bursa

Anatomy, Epidemiology, Mechanism of Formation, and Etiology

The suprapatellar bursa is a synovial-lined structure located between the quadriceps tendon and anterior distal femur, just above the patella.^3,5,12 In most adults, it communicates with the knee joint cavity, making it a common site of effusion in joint pathology.^3,4,12 Embryologically, this connection typically forms by age 2 to 3, but failure of fusion may leave a suprapatellar plica, which can mimic pathology.^3,8

Its main role is reducing friction during knee motion. It is subjected to stress in activities involving squatting, kneeling, or intense quadriceps use—frequent in wrestling, cycling, and certain professions.^5,31 Because of its communication with the joint, inflammation often originates from intra-articular disorders like osteoarthritis, hemarthrosis, or infection.^3,10,25,26

Etiologies include mechanical overload, systemic inflammatory diseases (e.g., RA), or post-traumatic effusion following knee injury.^3,5,13,14,25 In athletes and manual laborers, overuse without joint disease may still provoke bursitis.^5,31 Infection is rare but possible through trauma, iatrogenic procedures, or hematogenous spread—especially in immunocompromised patients—commonly involving S. aureus.^9,13,25

Crystal arthropathies such as gout and CPPD may also involve this bursa, mimicking septic bursitis and requiring aspiration to confirm diagnosis.^26,28

Clinical Presentation

Suprapatellar bursitis presents with swelling and discomfort above the patella, often perceived as a fluctuating mass more prominent in extension and reduced with flexion.^{3 -5} In acute cases, localized tenderness, warmth, and pain during movement are common, especially when related to trauma, infection, or synovitis.^13,25,26 Erythema may appear in infectious or inflammatory forms, while chronic bursitis often manifests as painless, compressible swelling with minimal limitation.^3,5

Because the bursa frequently communicates with the knee joint, symptoms may reflect underlying joint disease such as osteoarthritis or rheumatoid arthritis, with patients reporting stiffness, fullness, or mechanical symptoms like clicking.^3,25,26

In infectious bursitis, systemic signs such as fever, sharp pain, and impaired weightbearing may occur.^9,13,25 Crystal-induced bursitis, including gout and CPPD, may mimic infection with acute swelling and redness but lacks systemic toxicity.^26,28

Examination should assess for suprapatellar swelling, warmth, fluctuation, and range of motion, noting any flexion limitation suggestive of effusion or active inflammation.

Treatment, Complications, and Prognosis

Initial management includes rest, NSAIDs, ice, and physiotherapy to reduce quadriceps overload.^3,12,31 Persistent cases may benefit from ultrasound-guided aspiration and corticosteroid injection, though repeated injections risk atrophy or recurrence.^4,5,15,16 Septic bursitis requires aspiration and targeted antibiotics to prevent joint involvement.^9,13,25 Crystal-induced bursitis is managed with aspiration, anti-inflammatories, and metabolic control.^26,28 Refractory cases may require surgical excision.^5,14

Biologic therapies such as PRP, PRP+HA, and PRFM have shown benefits in peri-bursal and degenerative bursitis, improving pain and function in select patients.^17,18,21 Though RCT-level evidence specific to suprapatellar bursitis is limited, their use may be considered in refractory cases, particularly with OA-related synovial involvement.^18,21 Complications include chronic fibrosis, joint communication, and recurrence—especially when driven by hemarthrosis or underlying arthritis.^3,5,14,25,26 Septic bursitis may lead to necrosis or joint spread, particularly in immunocompromised individuals.^9,13,25 Repeated corticosteroid use may cause soft tissue weakening,^4,15 while crystal deposition can mimic inflammatory arthropathies.^26,28

Prognosis is generally favorable with early diagnosis and management. Conservative care or aspiration resolves most acute cases,^3,4,12 but recurrence is common in the presence of joint pathology or biomechanical overload.^3,5,25,26,31 Chronic or untreated cases may progress to persistent inflammation or joint complications.^{5,9,13,14,25,26,28}

Iliotibial Band Bursa

Anatomy, Epidemiology, and Mechanism of Formation

The ITB bursa is a small potential space between the distal iliotibial band and the lateral femoral epicondyle, reducing friction during knee motion, particularly between 20° and 30° flexion.^{3 -5} It is normally collapsed and becomes distended in pathologic states. ITB friction syndrome (ITBFS), the main clinical manifestation, is common among runners, cyclists, and military recruits, especially with biomechanical issues like genu varum, tight ITB, or poor hip abductor strength.^4,28 Beyond friction, compression forces are now considered central, with increased lateral tissue pressure during knee flexion, leading to bursal irritation, fibrosis, and chronic pain.^5,14

Etiology

ITB bursa inflammation results from repetitive friction between the ITB and lateral femoral condyle, especially during 20° to 30° knee flexion in activities such as running or cycling.^{3 -5} Contributing factors include foot pronation, limb length discrepancy, and ITB tightness. ⁴ Training errors and gluteus medius weakness increase femoral internal rotation, intensifying ITB compression and bursal stress, highlighting the multifactorial pathogenesis. ⁴

Clinical Presentation and Evaluation

Patients with iliotibial band bursa inflammation, often manifesting as ITB friction syndrome (ITBFS), typically present with sharp, localized lateral knee pain aggravated by repetitive flexion-extension—particularly at 20° to 30° knee flexion, where maximal ITB compression occurs.^{3 -5} Symptoms usually have an insidious onset, following increased activity or training changes. Athletes describe burning pain over the lateral knee, often worsening with downhill running or cycling. ⁴

On examination, tenderness 2 to 3 cm above the lateral joint line is common, and pain can be reproduced with palpation or during active knee flexion-extension.^4,5 Swelling may indicate bursal distention. The Noble compression and Ober tests help confirm ITB tightness and symptom provocation.^4,5 Range of motion is preserved, with no locking or instability, distinguishing it from intra-articular pathologies.^4,5

Treatment, Complications, Recurrence, and Prognosis

Management of iliotibial band (ITB) bursa inflammation centers on reducing mechanical stress, controlling inflammation, and correcting biomechanical contributors. Most patients respond well to conservative treatment, including temporary reduction of running or cycling, NSAIDs, ice, and rest.^4,5 Physical therapy is essential, emphasizing ITB stretching, hip abductor strengthening—particularly the gluteus medius—and gait retraining to address dynamic valgus and femoral internal rotation. ⁴ Foam rolling and myofascial techniques may provide additional relief. ⁴

In refractory cases, ultrasound-guided corticosteroid injection into the bursal space offers effective short-term pain relief, though repeated injections are limited due to risks such as tissue atrophy. ¹⁶ Biological therapies like PRP or PRFM have shown promise in other bursae, offering anti-inflammatory and regenerative benefits, but data in ITB bursitis remain limited and preliminary.^7,17,18

Surgical intervention is rare and reserved for chronic, unresponsive cases. Options include bursectomy or ITB release, with good outcomes when non-operative methods fail.^4,5

Complications are uncommon but may include chronic bursal fibrosis or persistent pain from unaddressed biomechanical stress.^4,5 Recurrent symptoms may arise in athletes who resume high-impact activities without correcting training errors or muscular imbalances.^4,5 Despite these risks, prognosis is excellent in most cases, with resolution of symptoms and return to full activity typically achieved through structured rehabilitation and targeted interventions.^4,5,16

Complications of knee bursa

While most knee bursae are benign and self-limiting, several complications may arise if left untreated, misdiagnosed, or improperly managed. Septic bursitis is the most serious complication across multiple bursae and is typically caused by Staphylococcus aureus. It may progress to cellulitis, abscess formation, or even osteomyelitis if aspiration or injection procedures are conducted without strict sterile technique.^5,9,13,16,25 Imaging may reveal bursal wall enhancement, fat stranding, or fluid-fluid levels in cases of infection or hemorrhage.^5,13

Chronic bursitis may result from ongoing mechanical stress or inadequate treatment, leading to fibrosis, septation, or pseudocapsule formation. These changes can mimic soft tissue tumors and limit function, particularly in prepatellar and deep infrapatellar bursae.^5,10,14,16 In anticoagulated patients, even minor trauma may cause hemorrhagic bursitis, with MRI showing characteristic fluid-fluid levels and histology revealing hemosiderin-laden macrophages.^5,14

Repeated corticosteroid injections, especially when not ultrasound-guided, are associated with skin atrophy, depigmentation, tendon weakening, and rarely sterile abscess or post-injection calcification.^4,6,15,16,24 Misguided injections can also damage nearby neurovascular structures, such as the saphenous nerve or geniculate artery, leading to neuropathic pain or bleeding.^6,16

In popliteal bursae, cyst rupture may produce a pseudothrombophlebitis syndrome that mimics DVT, sometimes prompting unnecessary anticoagulation and risking hemorrhage or compartment syndrome.^1,14 Additionally, neurovascular compression due to distended cysts may cause venous thrombosis or neuropathy.^5,14

Finally, recurrence is common across bursae—particularly in patients who return to unmodified mechanical stressors—highlighting the importance of protective measures, biomechanical correction, and tailored rehabilitation strategies to prevent chronic inflammation or surgical escalation.^3,5,12,16,31

Rare or Less-Studied Knee Bursae

In addition to the commonly studied bursae of the knee, several less-characterized bursae may contribute to localized knee pain, particularly in cases of diagnostic uncertainty or treatment resistance. Although rarely presenting as primary sources of pathology, they may become clinically relevant in atypical, persistent, or anatomically complex cases.^3,5

Lateral Collateral Ligament Bursa

Located between the lateral collateral ligament and the biceps femoris tendon, the LCL bursa may become symptomatic with lateral knee pain, snapping, or tightness—especially following repetitive varus stress. MRI typically reveals a localized fluid collection forming an inverted J-shape around the ligament.^{3 -5} Treatment is generally conservative with NSAIDs, physiotherapy, and activity modification. In refractory cases, ultrasound-guided corticosteroid or PRP injection may be considered.^15,17,18

Medial Collateral Ligament Bursa (Voshell’s Bursa)

This bursa lies between the superficial and deep layers of the MCL and may mimic MCL sprain or pes anserine bursitis, presenting as medial knee pain worsened by valgus stress.^3,5 In chronic cases with adjacent OA-related changes, PRP or PRP+HA may offer symptom relief.^18,21

Subpopliteal Bursa

Situated between the popliteus tendon and lateral femoral condyle, the subpopliteal bursa may mimic popliteus tendinopathy, Baker’s cyst, or posterior meniscal pathology. MRI is critical for diagnosis. Management is typically conservative with biomechanical correction; PRP may be considered in persistent cases.^4,5,8,18

Semitendinosus Bursa

This structure, distinct from the pes anserine bursa, may produce posteromedial knee pain in athletes with hamstring overload. It is often misdiagnosed as pes anserine bursitis or sartorius strain. Treatment involves NSAIDs, hamstring unloading, and eccentric strengthening; biologic therapies such as PRP or PRFM may be considered in resistant cases.^3,4,15,17

Deep Anserine Bursa (Subfascial Anserine Bursa)

Located beneath the superficial pes anserinus and adjacent to the tibial cortex,^14,26,28 this bursa can cause deep medial knee pain without visible swelling. Differential diagnoses include deep pes anserine bursitis, medial meniscal tear, or medial tibial stress syndrome. MRI aids diagnosis. Treatment aligns with that of superficial pes anserine bursitis, emphasizing biomechanical correction and conservative pharmacologic therapy.^5,26 In anatomically complex cases, ultrasound-guided PRP+HA injection may offer an adjunctive benefit.^18,21

These bursae, while infrequently diagnosed, should be considered in the differential diagnosis of refractory knee pain. Awareness of their anatomical position, clinical presentation, and relationship to adjacent structures is essential. MRI and ultrasound remain the cornerstone of detection, particularly in complex or non-resolving cases.^4,5,8 Most respond well to non-operative care, though accurate identification can prevent misdiagnosis and improve outcomes.

Discussion

Knee bursae encompass a wide range of anatomical and pathological entities, with varying clinical significance. This review integrates high-level evidence and case series to characterize diagnostic, therapeutic, and prognostic aspects. Superficial bursae (e.g., prepatellar, infrapatellar) are typically related to trauma and compression,^4,24 while deeper bursae (e.g., pes anserine, gastrocnemio-semimembranosus, MCL) are often associated with degenerative changes, overuse, or structural issues such as meniscal tears or malalignment.^12,14,22,23 Imaging—especially ultrasound and MRI—is crucial for distinguishing bursae from cysts, synovial lesions, and soft tissue masses.^5,15,27 MRI-based scoring systems (MOAKS, BLOKS) now incorporate bursal changes as markers of synovitis in osteoarthritis, ¹¹ even when not direct pain sources.

Initial treatment is conservative: rest, NSAIDs, physical therapy, aspiration, and corticosteroid injection.^{25,31 -33} Image-guided injections, particularly for deep bursae, show superior precision and outcomes over blind techniques.^16,17,24,25 A randomized study showed significantly greater pain relief with ultrasound-guided pes anserine injections vs. blind ones. ³⁴ Similar benefit is reported for infrapatellar bursitis.^17,24,25

A key theme emerging is the increasing use of biologic therapies. PRP, PRFM, HA, and MSCs have been studied for refractory bursitis, parameniscal cysts, and OA-related inflammation. These aim to modulate inflammation and promote repair. A prospective cohort using PRP+HA reported >70% lesion resolution and pain relief. ²¹ PRFM has been proposed in surgical protocols to retain growth factors and reduce recurrence. ³⁵ PRFM has also been applied in the surgical management of parameniscal cysts. Screpis et al. ²⁰ described a reproducible technique involving side-to-side suturing of the PRFM into the capsule near the cyst following meniscal repair, aiming to enhance healing and reduce recurrence through localized growth factor delivery. Though clinical data are limited, this method offers a practical, low-cost adjunct to biologically augmented meniscal surgery. ²⁰ However, most data come from low-level studies with non-standardized protocols and limited follow-up.^7,18,19,21

Leukocyte-rich PRP showed superiority over corticosteroids in PATB, with improved WOMAC and VAS scores. ¹⁸ Combined PRP+HA (CM-PRP-HA) was more effective than HA alone for symptom relief and longer duration. ²¹ This supports biologics not only as second-line therapy but possibly preferred options in selecting patients.

Although MSCs remain investigational, early studies show promise. Injections of MSC+PRP into periarticular bursae improved pain and function, with imaging-confirmed regression. ²¹ MSCs’ regenerative potential is significant, but larger trials are needed to define safety and efficacy.^18,21,36

Surgery is reserved for resistant cases, especially persistent popliteal cysts. Arthroscopic decompression with treatment of intra-articular pathology has yielded low recurrence (<10%) and good outcomes.^14,27,31

Anatomical and functional diversity affects diagnosis and management. Suprapatellar and infrapatellar bursae may coexist with fat pad or tendinous conditions, requiring detailed imaging. ⁵ Lateral bursae (e.g., ITB, LCL) are understudied but implicated in chronic lateral pain, especially in athletes.^3,4,20 PRP may be beneficial, though high-quality studies are lacking.

Importantly, asymptomatic bursal enlargement is common, especially in OA patients. ¹¹ Thus, treatment should align with symptoms, not imaging alone. Biologic options may offer local anti-inflammatory effects without systemic risks.

However, despite their potential advantages, biologic therapies such as PRP, PRP+HA, and PRFM remain costly and are not uniformly reimbursed by healthcare systems, limiting their accessibility in standard orthopedic practice and low-resource settings. Cost-effectiveness studies and broader insurance coverage will be crucial to enable their widespread adoption.

Limitations include predominance of level III-IV studies, small samples, variable protocols, and inconsistent outcomes. Nonetheless, findings—especially for PRP, PRFM, and CM-PRP-HA—justify further RCTs, particularly in patients unresponsive to standard care.

Pragmatic Clinical Considerations for Biologic Therapy

While standardized treatment algorithms are lacking, biologic therapies may be considered in chronic bursitis cases that are unresponsive to conventional care, particularly when corticosteroids are contraindicated. Superficial bursae with OA-related inflammation (e.g., pes anserine, prepatellar) may respond well to PRP or PRP+HA, especially when imaging reveals persistent effusion or synovial thickening. Deep bursae (e.g., infrapatellar, suprapatellar) may benefit from image-guided PRP or PRFM injections in degenerative or post-surgical contexts. In rare or anatomically complex bursae, biologics should be considered adjunctively and individually, based on chronicity, response to prior therapies, and comorbidities. Access, cost, and clinician expertise may further shape clinical decision-making (see Box 1 ).

Box 1.

Practical Algorithm for Considering Biologic Therapy in Knee Bursitis.

Clinical Setting	Bursa Type	When to Consider Biologics	Preferred Modality	Notes
Chronic pain unresponsive to NSAIDs / physiotherapy	Superficial (e.g., Pes Anserine, Prepatellar)	Failure of ≥2 steroid injections or contraindication to steroids	PRP or PRP+HA	PRP+HA may offer better outcomes in OA settings 21
Persistent effusion, synovial thickening on imaging	Deep bursae (e.g., Suprapatellar, Infrapatellar)	Refractory cases after mechanical unloading and steroids	Ultrasound-guided PRP or PRFM	PRFM offers prolonged growth factor release 17
Recurrent bursitis with underlying OA	Any bursa (esp. medial side)	Symptom recurrence after steroids or bursectomy	PRP+HA	Consider as adjunct to conservative care18,21
Rare / anatomically complex bursae (e.g., MCL, Subpopliteal)	Variable	On a case-by-case basis when standard treatments fail	PRP (if accessible)	Limited evidence—use individualized approach

This table summarizes suggested clinical indications for initiating biologic therapies such as PRP, PRP+HA, or PRFM across different knee bursae. Recommendations are based on chronicity, failure of standard treatments, imaging findings, and anatomical location. Special considerations are noted for OA-related bursitis, deep or complex bursae, and limited-access settings. The algorithm is intended to support individualized, pragmatic decision-making in the absence of formal guidelines.

In conclusion, while conservative measures remain effective, biologic therapies offer promising alternatives for resistant bursitis and cystic lesions. PRP-based treatments, especially when combined with HA or surgery, may improve outcomes. Future management should integrate precise imaging, biologic advances, and individualized care strategies across the spectrum of knee bursae. In the absence of formal guidelines, biologic therapies may be initiated in chronic or steroid-resistant bursitis, especially in the presence of OA or recurrent effusion. PRP, PRP+HA, or PRFM may serve as adjunctive tools, tailored to bursa location, chronicity, and clinical setting. Superficial bursae often respond to PRP+HA, while deep or complex bursae may benefit from image-guided biologics in select cases.