Psoriatic arthritis pathophysiology: Difference between revisions
(Created page with "__NOTOC__ {{Psoriatic arthritis}} {{CMG}}; {{AE}} {{CK}} ==Overview== The pathogenesis of psoriatic arthritis (PsA) involves prominent T-lymphocytic infiltrate, particula...") |
No edit summary |
||
| (One intermediate revision by the same user not shown) | |||
| Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
The pathogenesis of psoriatic arthritis | The pathogenesis of psoriatic arthritis involves prominent [[T cell|T-lymphocytic]] infiltrate, particularly [[CD4+ cell|CD4 cells]] in the [[skin]] and [[Joint|joints]]. High levels of [[Tumor necrosis factor-alpha|tumor necrosis factor alpha]] ([[TNF]]), [[Interleukin 8|IL-8]], [[Interleukin 6|IL-6]], [[IL-1]], [[Interleukin 10|IL-10]], and [[Matrix metalloproteinase|matrix metalloproteinases]] are present in the [[synovial fluid]] of [[Patient|patients]] with early psoriatic arthritis.The elevated levels of [[Tumor necrosis factors|TNF]] and various [[Interleukin|interleukins]] lead to a high number of [[Osteoclast|osteoclast precursor cells]] circulating in the [[blood]] which ultimately leads to [[joint]] destruction. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Latest revision as of 14:09, 16 May 2018
|
Psoriatic arthritis Microchapters | |
|
Diagnosis | |
|---|---|
|
Treatment | |
|
Case Studies | |
|
Psoriatic arthritis pathophysiology On the Web | |
|
American Roentgen Ray Society Images of Psoriatic arthritis pathophysiology | |
|
Risk calculators and risk factors for Psoriatic arthritis pathophysiology | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
The pathogenesis of psoriatic arthritis involves prominent T-lymphocytic infiltrate, particularly CD4 cells in the skin and joints. High levels of tumor necrosis factor alpha (TNF), IL-8, IL-6, IL-1, IL-10, and matrix metalloproteinases are present in the synovial fluid of patients with early psoriatic arthritis.The elevated levels of TNF and various interleukins lead to a high number of osteoclast precursor cells circulating in the blood which ultimately leads to joint destruction.
Pathophysiology
The pathogenesis of psoriatic arthritis (PsA) involves the following events:[1]
- In joints there is a prominent lymphocytic infiltrate, limited to the dermal papillae in skin and to the underlying stroma.
- T lymphocytes, particularly CD4 cells, are the most common inflammatory cells in the skin and joints, with a CD4/CD8 ratio of 2:1.
- High levels of tumor necrosis factor alpha (TNF), IL-8, IL-6, IL-1, IL-10, and matrix metalloproteinases are present in the joint fluid of patients with early PsA.
- Collagenase mediated degradation of cartilage collagen begins in early phases of the disease and may be the result of the proteases produced as a result of above mentioned cytokines.
Osteoclast mediated joint destruction
- The elevated levels of TNF leads to a high number of osteoclast precursor cells circulating in the blood.
- Osteoclast precursors migrate to the joint where they encounter increased expression of receptor activator of nuclear factor kappa B ligand ( NF-κB), which favors the differentiation and activation of osteoclasts.
- Osteoclasts eventually lead to the joint destruction seen in psoriatic arthritis.
References
- ↑ Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM (2003). "Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis". J. Clin. Invest. 111 (6): 821–31. doi:10.1172/JCI16069. PMC 153764. PMID 12639988.