Bursitis: Pathophysiology, Causes, Symptoms, and Progression

What is the Pathophysiology of Bursitis?

Bursitis is an inflammatory condition characterized by the acute or chronic inflammation of a bursa, typically in response to repetitive mechanical stress, direct trauma, infection, or systemic inflammatory diseases, leading to pain, swelling, and restricted movement due to the accumulation of inflammatory fluid and cellular changes within the bursal sac.

Introduction to Bursae

Bursae (plural of bursa) are small, fluid-filled sacs lined with a synovial membrane, similar to joint capsules. Their primary function is to reduce friction and cushion pressure points between bones, tendons, and muscles around joints. They act as gliding surfaces, allowing for smooth movement of adjacent anatomical structures. While there are hundreds of bursae throughout the body, some are consistently present (e.g., subacromial, olecranon), while others develop in response to chronic friction or pressure.

Defining Bursitis

Bursitis is, by definition, the inflammation of a bursa. This inflammation leads to a thickening of the bursal wall, an increase in the volume and viscosity of the synovial fluid within the bursa, and often the infiltration of inflammatory cells. The consequences are pain, tenderness, swelling, and sometimes warmth and redness over the affected area, often exacerbated by movement or direct pressure.

The Pathophysiological Cascade: Mechanisms of Injury

The development of bursitis typically follows an inflammatory response triggered by one or more inciting factors:

• Mechanical Overload and Repetitive Stress: This is the most common cause.
  • Repetitive Friction: Continuous rubbing of a tendon or muscle over a bursa can cause irritation. For example, the iliotibial band repeatedly rubbing over the greater trochanteric bursa.
  • Repetitive Compression: Sustained pressure on a bursa can lead to inflammation. Examples include prolonged kneeling (prepatellar bursitis, "housemaid's knee") or leaning on elbows (olecranon bursitis, "student's elbow").
  • Shear Forces: Forces acting parallel to the surface of the bursa can also induce inflammation.
• Direct Trauma: A sudden, forceful impact to a bursa can cause acute inflammation and sometimes hemorrhage into the bursal sac.
• Infection (Septic Bursitis): Bursae, particularly those close to the skin surface (e.g., olecranon, prepatellar), can become infected.
  • Mechanism: Bacteria (most commonly Staphylococcus aureus) enter the bursa through a break in the skin, a puncture wound, or sometimes hematogenous spread from a distant infection.
  • Response: The body mounts a severe inflammatory response, leading to pus formation (suppurative bursitis), significant pain, redness, warmth, and fever.
• Systemic Inflammatory Conditions: Bursitis can be a manifestation of underlying systemic diseases.
  • Gout and Pseudogout: Deposition of uric acid crystals (gout) or calcium pyrophosphate dihydrate crystals (pseudogout) within the bursa can trigger a potent inflammatory reaction.
  • Rheumatoid Arthritis: Autoimmune inflammation can target bursae, leading to chronic bursitis as part of the systemic disease process.
  • Psoriatic Arthritis, Lupus, Spondyloarthropathies: Other autoimmune conditions can also involve bursae.

Cellular and Biochemical Response

Regardless of the initial trigger, the body's response involves a complex interplay of cellular and biochemical events:

• Inflammatory Mediators: The injured or irritated bursal lining releases pro-inflammatory cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and prostaglandins. These mediators orchestrate the subsequent inflammatory cascade.
• Vascular Changes: These mediators cause vasodilation (widening of blood vessels) and increased capillary permeability in the surrounding tissues. This allows fluid, proteins, and inflammatory cells to leak out of the bloodstream and into the bursal sac.
• Fluid Exudation: The accumulation of this protein-rich fluid (exudate) within the bursa leads to swelling and distention of the bursal sac. This increased pressure contributes to pain.
• Cellular Infiltration:
  • In acute bursitis, there is an influx of neutrophils (a type of white blood cell) to the site.
  • In septic bursitis, neutrophils are abundant, forming pus.
  • In chronic bursitis or bursitis related to systemic inflammatory conditions, macrophages and lymphocytes are more prevalent, indicating a persistent immune response.
• Synovial Membrane Changes: The synovial lining of the bursa can undergo hypertrophy (thickening) and hyperplasia (increase in cell number). This thickened lining produces even more synovial fluid, perpetuating the swelling.
• Pain Generation: The inflammatory mediators directly sensitize nociceptors (pain receptors) in the bursal wall. Additionally, the increased fluid pressure within the distended bursa mechanically stimulates these receptors, contributing significantly to the experience of pain.

Clinical Manifestations and Progression

The pathophysiology of bursitis directly translates into its clinical presentation:

• Pain: Often localized, sharp or aching, worse with movement or pressure.
• Tenderness: Palpable tenderness over the affected bursa.
• Swelling: Visible or palpable distention of the bursa due to fluid accumulation.
• Restricted Range of Motion: Pain and swelling can limit movement of the adjacent joint.
• Warmth and Redness: Especially prominent in septic bursitis, indicating increased blood flow due to inflammation.
• Fever: A systemic sign almost exclusively seen in septic bursitis.

If the inciting factors are not removed, acute bursitis can progress to chronic bursitis. In chronic cases, the bursal wall becomes significantly thickened and fibrotic, and the fluid may become more viscous. Calcification can also occur within the bursa.

Common Sites of Bursitis and Their Specific Pathophysiology

While the general mechanisms are similar, specific anatomical locations predispose bursae to certain types of stress:

• Subacromial (Shoulder) Bursitis: Often caused by shoulder impingement, where the bursa and rotator cuff tendons are compressed between the humerus and the acromion during overhead movements. Repetitive arm elevation leads to friction and compression.
• Olecranon (Elbow) Bursitis: Commonly due to direct trauma or prolonged pressure on the tip of the elbow (e.g., "student's elbow" from leaning on a desk). This superficial bursa is also highly susceptible to septic bursitis.
• Trochanteric (Hip) Bursitis: Typically results from repetitive friction of the iliotibial band or gluteal tendons over the greater trochanter of the femur, often exacerbated by muscle imbalances, gait abnormalities, or prolonged standing.
• Prepatellar (Knee) Bursitis: Caused by repetitive kneeling ("housemaid's knee") or direct trauma to the front of the knee. Like the olecranon bursa, it's superficial and prone to infection.
• Pes Anserine (Knee) Bursitis: Involves the bursa under the insertion of the sartorius, gracilis, and semitendinosus tendons on the medial tibia. Often caused by overuse in runners, obesity, or osteoarthritis of the knee, leading to friction from the overlying tendons.

Healing and Chronic Bursitis

In most cases of non-septic bursitis, removal of the irritant, rest, and anti-inflammatory measures allow the bursa to heal. The inflammatory exudate is reabsorbed, the bursal lining returns to its normal thickness, and symptoms resolve.

However, if the irritant persists or the inflammation is severe, the bursa may undergo fibrotic changes, leading to permanent thickening of the bursal wall and potential calcification. This chronic state can result in persistent discomfort and a higher susceptibility to recurrence. Chronic bursitis may also develop adhesions, further limiting movement and causing pain.

Conclusion

The pathophysiology of bursitis is a dynamic process involving the bursa's response to various stressors, primarily mechanical irritation, trauma, infection, or systemic inflammation. This response manifests as a cascade of cellular and biochemical events—including the release of inflammatory mediators, vascular changes, fluid exudation, and cellular infiltration—culminating in the characteristic symptoms of pain, swelling, and functional limitation. Understanding these underlying mechanisms is crucial for effective diagnosis, treatment, and prevention of this common musculoskeletal condition.