What is the pathophysiology of bursitis?

Updated: Dec 11, 2020
  • Author: Kristine M Lohr, MD, MS; Chief Editor: Herbert S Diamond, MD  more...
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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.

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