Editing Arthritis (section)

=== Rheumatoid arthritis ===
{{Main|Rheumatoid arthritis}}
[[File:X-ray of right fourth PIP joint with bone erosions by rheumatoid arthritis.jpg|thumb|[[Bone erosion]]s by [[rheumatoid arthritis]]<ref>{{cite journal | vauthors = Ideguchi H, Ohno S, Hattori H, Senuma A, Ishigatsubo Y | title = Bone erosions in rheumatoid arthritis can be repaired through reduction in disease activity with conventional disease-modifying antirheumatic drugs | journal = Arthritis Research & Therapy | volume = 8 | issue = 3 | pages = R76 | year = 2006 | pmid = 16646983 | pmc = 1526642 | doi = 10.1186/ar1943 | doi-access = free }}</ref>]]

[[Rheumatoid arthritis]] (RA) is a disorder in which the body's own immune system starts to attack body [[tissue (biology)|tissues]] specifically the cartilage at the end of bones known as articular cartilage.<ref name="niams-ra">{{cite web|url=https://www.niams.nih.gov/health-topics/rheumatoid-arthritis |title=Rheumatoid arthritis|date=November 2022|access-date=30 January 2025|publisher=National Institute of Arthritis and Musculoskeletal and Skin Diseases, US National Institutes of Health}}</ref> The attack is not only directed at the joint but to many other parts of the body. RA often affects joints in the fingers, wrists, knees and elbows, is symmetrical (appears on both sides of the body), and can lead to severe progressive [[deformity]] in a matter of years if not adequately treated. RA usually onsets earlier in life than OA and commonly effects people aged 20 and above. In children, the disorder can present with a skin [[rash]], [[fever]], [[pain]], disability, and limitations in daily activities.<ref name=niams-ra/> With earlier diagnosis and appropriate aggressive treatment, many individuals can obtain control of their symptoms leading to a better quality of life compared to those without treatment.<ref name=niams-ra/><ref>{{cite report |url=https://effectivehealthcare.ahrq.gov/topics/rheumatoid-arthritis-medicine-update/final-report-update-2018 |title=Drug Therapy for Early Rheumatoid Arthritis: A Systematic Review Update |last1=Donahue |first1=Katrina E. |last2=Gartlehner |first2=Gerald |date=2018 |publisher=Agency for Healthcare Research and Quality (AHRQ) |doi=10.23970/ahrqepccer211 |last3=Schulman |first3=Elizabeth R. |last4=Jonas |first4=Beth |last5=Coker-Schwimmer |first5=Emmanuel |last6=Patel |first6=Sheila V. |last7=Weber |first7=Rachel Palmieri |last8=Lohr |first8=Kathleen N. |last9=Bann |first9=Carla|doi-access=free }}</ref>

One of the main triggers of bone erosion in the joints in rheumatoid arthritis is inflammation of the [[synovium]] (lining of the joint capsule), caused in part by the production of pro-inflammatory [[cytokine]]s and receptor activator of nuclear factor kappa B ligand (RANKL), a cell surface protein present in Th17 cells and osteoblasts.<ref name="Chabaud_2000">{{cite journal | vauthors = Chabaud M, Garnero P, Dayer JM, Guerne PA, Fossiez F, Miossec P | title = Contribution of interleukin 17 to synovium matrix destruction in rheumatoid arthritis | journal = Cytokine | volume = 12 | issue = 7 | pages = 1092–1099 | date = July 2000 | pmid = 10880256 | doi = 10.1006/cyto.2000.0681 }}</ref> Osteoclast activity can be directly induced by osteoblasts through the RANK/RANKL mechanism.<ref name="pmid21464945">{{cite journal | vauthors = Won HY, Lee JA, Park ZS, Song JS, Kim HY, Jang SM, Yoo SE, Rhee Y, Hwang ES, Bae MA | display-authors = 6 | title = Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice | journal = PLOS ONE | volume = 6 | issue = 3 | pages = e18168 | date = March 2011 | pmid = 21464945 | pmc = 3064589 | doi = 10.1371/journal.pone.0018168 | bibcode = 2011PLoSO...618168W | doi-access = free }}</ref>
[[File:Lupusfoto.jpg|thumb|160x160px|This is a malar ("butterfly") skin rash that is commonly seen in patients with Lupus.]]