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  • Author: Kristine M Lohr, MD, MS; Chief Editor: Harris Gellman, MD  more...
Updated: Oct 13, 2015


Bursitis is defined as inflammation of a bursa. Humans have approximately 160 bursae. These are saclike structures between skin and bone or between tendons, ligaments, and bone. The bursae are lined by synovial tissue, which produces fluid that lubricates and reduces friction between these structures.

Bursitis occurs when the synovial lining becomes thickened and produces excessive fluid, leading to localized swelling and pain.[1, 2, 3] It most commonly affects the subacromial, olecranon, trochanteric, prepatellar, and infrapatellar bursae. Symptoms of bursitis may include localized tenderness, pain, edema, erythema, or reduced movement. Pain is aggravated by movement of the specific joint, tendon, or both.

For patient education resources, see the Arthritis Center, as well as Bursitis.



Bursae are flattened sacs that serve as protective buffers between bones and overlapping muscles (deep bursae) or between bones and tendons or skin (superficial bursae). These synovial-lined sacs are filled with minimal amounts of fluid to facilitate movement during muscle contraction. Deep bursae (eg, subacromial and iliopsoas bursae) are located in the fascia. Superficial bursae (eg, olecranon and prepatellar bursae) are located in the subcutaneous tissue.

There are two types of bursae: constant and adventitial. Both types can be involved in acute or chronic bursitis. Constant bursae have the following characteristics:

  • They form during embryologic development
  • They are lined with endothelial cells
  • They are located between bones and tendons or skin
  • They contain synovial cells that secrete a lubricating fluid rich in collagen and proteoglycans

Adventitial bursae have the following characteristics:

  • They form later in life in response to repeated trauma or constant friction and pressure
  • They lack endothelial cells
  • They do not contain synovial fluid
  • Examples include those that develop over a bunion and osteochondroma

All of the approximately 160 bursae in the human body are potentially susceptible to injury. The three upper-extremity bursae that are most commonly affected by bursitis are the subacromial, subscapular, and olecranon bursae.[4]

The subacromial bursa separates the superior surface of the supraspinatus tendon from the overlying coracoacromial arch and the deltoid muscle. It lies between the acromion and the rotator cuff and cushions the coracoacromial ligament from the supraspinatus muscle. When the arm is resting at the side, the bursa protrudes laterally from beneath the acromion; when the arm is abducted, it rolls medially beneath the bone. See the image below.

Subscapular bursae are found between the anterior surface of the scapula and the posterior chest wall. The 2 commonly affected bursae are located superomedially between the serratus anterior and the chest wall. See the image below.

Shoulder anatomy muscle, anterior view. Shoulder anatomy muscle, anterior view.

Two olecranon bursae can become inflamed; one lies between the tendon of the triceps and the posterior ligament of the elbow and the olecranon, whereas the other is more superficial, lying between the attachment of the triceps to the olecranon and the skin.

Various lower-extremity bursae can also be affected by bursitis. The ones most commonly involved are in the hip, the knee, and the ankle.[5, 6, 7]

In the hip, the ischiogluteal bursa lies deep to the gluteus maximus over the ischial tuberosity. The iliopsoas bursa, the largest bursa in the body, lies between the iliopsoas tendon and the lesser trochanter, extending upward into the iliac fossa beneath the iliacus. The trochanteric bursa has superficial and deep components, with the superficial bursa lying between the tensor fascia latae and the skin and the deep bursa located between the greater trochanter and the tensor fasciae latae.

In the knee, bursae commonly affected by bursitis include the medial collateral ligament bursa, the anserine (pes anserinus) bursa (see the image below), the prepatellar bursa (located anteriorly over the patella, between patella and skin), the infrapatellar bursa (containing a superficial component lying between the patellar ligament and the skin and a deep component lying between the patellar ligament and the proximal anterior tibia), and the popliteal bursae, or Baker cysts (located in the posterior joint capsule of the knee).[6]

Location of anserine (pes anserinus) bursa on medi Location of anserine (pes anserinus) bursa on medial knee. MCL=medial collateral ligament.

In the ankle, two bursae are found at the level of insertion of the Achilles tendon. The superficial one is located between the skin and the tendon, and the deep one is located between the calcaneus and the tendon. The latter is the one more commonly affected by bursitis.



Inflammation of the bursa causes synovial cells to multiply and thereby increases collagen formation and fluid production. A more permeable capillary membrane allows entrance of high protein fluid. The bursal lining may be replaced by granulation tissue followed by fibrous tissue. The bursa becomes filled with fluid, which is often rich in fibrin, and the fluid can become hemorrhagic.[8] One study suggests that this process may be mediated by cytokines, metalloproteases, and cyclooxygenases.

In septic arthritis, local trauma usually causes inoculation of bacteria into the bursa, which triggers the inflammatory process.

There are three phases of bursitis: acute, recurrent, and chronic.[9] During the acute phase of bursitis, local inflammation occurs and the synovial fluid is thickened, and movement becomes painful as a result. Chronic bursitis leads to continual pain and can cause weakening of overlying ligaments and tendons and, ultimately, rupture of the tendons. Because of the possible adverse effects of chronic bursitis on overlying structures, bursitis and tendinitis may occur together; the differential diagnosis should include both of these diagnoses.

Upper-extremity bursitis

Subacromial bursitis

The subacromial bursa facilitates movement of the supraspinatus tendon and becomes inflamed secondary to repetitive overuse injury of this tendon. Subacromial bursitis is often coexistent with supraspinatus tendinitis and partial- or complete-thickness tears of the supraspinatus tendon (1 of the 4 tendons comprising the rotator cuff).[10]

Subscapular bursitis

Subscapular bursae become inflamed as a result of abnormal bony structures or soft-tissue changes that affect the movement of the scapula over the posterior chest wall.

Olecranon bursitis

The more superficial of the 2 olecranon bursae commonly involved in bursitis is predisposed to direct trauma or cumulative microtrauma from activities requiring frequent elbow motion (eg, swimming, skiing, gymnastics, and weightlifting). This type of bursitis is often recurrent.[11, 12, 13]

Olecranon bursitis, shown here with elbow flexed. Olecranon bursitis, shown here with elbow flexed. Image courtesy of UMDNJ-New Jersey Medical School,, and

Lower-extremity bursitis

Bursitis of hip

Ischiogluteal bursitis is associated with sedentary occupations and is caused by direct stress on the bursa (hence the nickname “weaver’s bottom”). Patients have pain with sitting and walking and have localized tenderness over the ischial tuberosity. Physical examination often reveals pain with passive hip flexion and resisted hip extension.

Iliopsoas bursitis arises when a defect develops in the anterior part of the hip joint capsule, allowing communication of the joint with the bursa. It is often associated with hip pathology (eg, rheumatoid arthritis or osteoarthritis) or recreational injury (eg, running). Infection of the iliopsoas bursa is rare.

Greater trochanter bursitis is common in overweight middle-aged women and is associated with acute trauma, overuse, and mechanical factors. The clinical presentation is of deep, aching lateral hip pain that may radiate into the buttocks or lateral knee. Pain is worse with activity and stretching and may be worse at night, especially when the patient lies on the affected side. Palpation over the greater trochanter elicits severe tenderness. Physical examination reveals pain with resisted hip abduction and external rotation.[14, 15, 16, 17]

Bursitis of knee

The medial collateral ligament bursa is most commonly injured secondary to a twisting injury with external tibial rotation. Medial joint line pain occurs and may limit knee extension. This may be confused with a meniscal tear on physical examination.

Anserine (pes anserinus) bursitis is not usually associated with overuse but may occur in patients with medial compartmental osteoarthritis. Clinically, patients complain of pain and tenderness over the anteromedial knee that is worse with knee flexion. This condition may be confused with medial meniscal pathology.[18, 19]

Prepatellar bursitis, also known as housemaid’s knee, is associated with trauma or with repetitive kneeling over an extended period. The prepatellar bursa is also a common site for septic (infectious) bursitis, a diagnosis that should be considered when there is skin injury, erythema, warmth, or severe tenderness over the patella. In patients with septic prepatellar bursitis, the patella is not palpable, and knee flexion is painful.

Popliteal bursae (Baker cysts) are associated with local swelling and pain on walking, jumping, and squatting. Magnetic resonance imaging (MRI) or ultrasonography can differentiate an isolated bursitis from intra-articular injury. (See also Baker Cyst.)

Bursitis of ankle

Retrocalcaneal bursitis is generally caused by local trauma from poorly designed shoes. Patients complain of posterolateral heel pain and may have a posterior heel prominence (“pump bump”), as well as local swelling and tenderness over the Achilles tendon. Pain is increased by squeezing the bursa from side to side and anterior to the Achilles. A heel lift and open-back shoes help alleviate pressure.[20]



Bursitis has many causes, including autoimmune disorders, crystal deposition (gout and pseudogout), infectious diseases, traumatic events, and hemorrhagic disorders, as well as being secondary to overuse. Repetitive injury within the bursa results in local vasodilatation and increased vascular permeability, which stimulate the inflammatory cascade.

The following systemic diseases have also been associated with bursitis:

In addition, bursitis and other soft-tissue disorders have been associated with generalized hypermobility. Some rheumatic conditions, such as gout, can predispose patients to bursitis.

Septic (infectious) bursitis is most common in superficial bursae. In the majority (50-70%) of cases, it results from direct introduction of microorganisms through traumatic injury or through contiguous spread from cellulitis (50-70% of cases). Less commonly, infection of deep bursae is due to contiguous septic arthritis or bacteremia (10% of cases).

The most common causative organism is Staphylococcus aureus (80% of cases), followed by streptococci. However, many other organisms have been implicated in septic bursitis, including mycobacteria (both tuberculous and nontuberculous strains), fungi (Candida), and algae (Prototheca wickerhamii).[21] Factors predisposing to infection include diabetes mellitus, steroid therapy, uremia, alcoholism, skin disease, and trauma. A history of noninfectious inflammation of the bursa also increases the risk of septic bursitis.


Epidemiology and Prognosis

Bursitis accounts for 0.4% of all visits to primary care clinics. The most common locations of bursitis are the subdeltoid, olecranon, ischial, trochanteric, and prepatellar bursae.

The incidence of bursitis is higher in athletes, reaching levels as high as 10% in runners. Approximately 85% of cases of septic superficial bursitis occur in men. A French study aimed at assessing the prevalence of knee bursitis in the working population found that most cases occurred in male workers whose occupations involved heavy workloads and frequent kneeling.[22]

Mortality in patients with bursitis is very low. The prognosis is good, with the vast majority of patients receiving outpatient follow-up and treatment.

Contributor Information and Disclosures

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Interim Chief, Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians, American College of Rheumatology

Disclosure: Nothing to disclose.


Janet Kay Talbot-Stern, MD, FACEM, FCEM Emergency Medicine VMO, Ryde and Bankstown Hospitals, Australia Locum Consultant, St Thomas Hospital, UK

Disclosure: Nothing to disclose.

Alita Gonsalves, MD Physiatrist, Private Practice, Vero Orthopaedics and Neurology; Former Staff Physician, Department of Physical Medicine and Rehabilitation, New York Presbyterian Hospital

Alita Gonsalves, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Leon Root, MD Professor of Clinical Surgery, Department of Orthopedics, Weill Medical College of Cornell University; Founder and Director, Pediatric Outreach Program; Emeritus Chief of Osteogenesis Imperfecta Clinic, Attending Orthopedic Surgeon, Medical Director of Rehabilitation, Emeritus Chief of Pediatric Orthopedics, The Hospital for Special Surgery

Leon Root, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, New York Academy of Medicine, American Academy of Cerebral Palsy and Developmental Medicine, Pediatric Orthopaedic Society of North America

Disclosure: Nothing to disclose.

Chief Editor

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine, Clinical Professor, Surgery, Nova Southeastern School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, Arkansas Medical Society

Disclosure: Nothing to disclose.


Ian D Dickey, MD, FRCSC Adjunct Professor, Department of Chemical and Biological Engineering, University of Maine; Consulting Staff, Adult Reconstruction, Orthopedic Oncology, Department of Orthopedics, Eastern Maine Medical Center

Ian D Dickey, MD, FRCSC is a member of the following medical societies: American Academy of Orthopaedic Surgeons, British Columbia Medical Association, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Stryker Orthopaedics Consulting fee Consulting; Cadence Honoraria Speaking and teaching

Gino A Farina, MD, FACEP, FAAEM Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mark Louden, MD Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Department of Medicine, University of Miami, Leonard M Miller School of Medicine

Mark Louden, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Heidi M Stephens, MD, MBA Associate Professor, Department of Surgery, Division of Orthopedic Surgery, University of South Florida College of Medicine; Courtesy Joint Associate Professor, Department of Environmental and Occupational Health, University of South Florida College of Public Health

Heidi M Stephens, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Medical Association, American Orthopaedic Foot and Ankle Society, and Florida Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Olecranon bursitis, shown here with elbow flexed. Image courtesy of UMDNJ-New Jersey Medical School,, and
Olecranon bursitis: aspiration of hemorrhagic effusion. Image courtesy of UMDNJ-New Jersey Medical School,, and
Location of anserine (pes anserinus) bursa on medial knee. MCL=medial collateral ligament.
Acute infectious bursitis upon presentation to emergency department. Image courtesy of Christopher Kabrhel, MD.
Infectious bursitis. Image courtesy of Christopher Kabrhel, MD.
Shoulder anatomy muscle, anterior view.
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