Setyo Purwono Bag.

Farmakologi & Terapi , FK - UGM

PIT PENYAKIT DALAM DESEMBER 2013

Arthritis
(from Greek arthro-, joint + -itis, inflammation) is a form of joint disorder that involves inflammation of one or more joints.
CollinsDictionary.com. Collins English Dictionary Complete & Unabridged 11th Edition.

The most common form :

osteoarthritis

Other arthritis forms :

rheumatoid arthritis,

(degenerative joint disease), is a result of trauma to the joint, infection of the joint, or age.

psoriatic arthritis,
related autoimmune

diseases.
Septic arthritis is caused

by joint infection.

the common symptoms for all arthritis disorders

varied levels of pain,
swelling, joint stiffness,

sometimes a constant ache around the joint(s).

The pain from arthritis is due to inflammation that occurs around the joint, damage to the joint from disease, daily wear and tear of joint muscle strains caused by forceful movements against stiff painful joints and fatigue.

Osteoarthritis Speed of onset Main locations Months

Rheumatoid arthritis Weeks-months[16] Hands (proximal interphalangeal and metacarpophalangeal joint) wrists, ankles and knees Yes

Weight-bearing joints (such as knees, hips, vertebral column) and hands Inflammation May occur, though often mild compared to inflammation in rheumatoid arthritis Radiologic changes Narrowed joint space Osteophytes Laboratory findings None

Local osteosclerosis Anemia, elevated ESR and C-reactive protein (CRP), rheumatoid factor, anticitrullinated protein antibody Ulnar deviation, swan neck- and Boutonniere deformity of the hand Extra-articular features are common

Other features

No systemic signs Bouchard's and Heberden's nodes

Complex cellular interplay in synovial joint.

In osteoarthritic state, aberrantly activated chondrocytes produce ECM-degrading proteases (MMPs, aggrecanases), pro-inflammatory cytokines (e.g. IL-1), and catabolic growth factors (e.g. FGF-2). These proteins can be secreted into synovial fluid, and subsequently act upon synoviocytes. Fragments derived from ECM degradation (e.g. Fn-f) are also present in the synovial fluid as catabolic inducers. In OA, a subpopulation of chondrocytes undergoes hypertrophic changes, as manifested by their expression of type X collagen. Chondrocytes may also upregulate apoptosis, resulting in diminished local cellularity. In response to cartilage loss, pathological remodeling of subchondral bone gives rise to sclerosis and osteophyte formation.

Synoviocytes (fibroblasts and macrophages) also actively synthesize proteases and cytokines which can negatively effect on the articular cartilage and synovium. Pathophysiological changes in synoviocytes pave the way for angiogenesis and innervations, which may account for OA pain. Adapted from S. B. Abramson and M. Attur, Arthritis Res Ther 2009;11(3):227.

Inflammatory mediators in osteoarthritis

Damage-associated molecular patterns (DAMPs) in osteoarthritis.

Molecules implicated in the innate immune response within the damaged joint, each potentially contributing to the chronic inflammation observed in OA

Schematic representation of chronic inflammation as a mediator of osteoarthritis.

damage-associated molecular patterns (DAMPs), cartilage extracellular matrix (ECM), fibroblast-like synoviocytes (FLS)