Arthritis

Rheumatoid arthritis

Rheumatoid arthritis (RA) is classified into several variants:

• Seropositive RA (includes Felty syndrome).
• RA with pulmonary involvement (rheumatoid lung).
• RA with vasculitis (rheumatoid vasculitis).

A distinct category is seronegative RA, in which rheumatoid factor is not detected in the blood. In children under 16 years of age, juvenile rheumatoid arthritis (JRA) is diagnosed—a chronic autoimmune inflammation of uncertain etiology. There is currently no unified classification of JRA, but it is known to be morphologically similar to adult RA. A hallmark of the juvenile form is the frequent development of oligoarthritis (up to 40% of cases). There is a polyarticular seropositive subtype, which is associated with the HLA-DR4 marker, characterized by moderate inflammation and the mandatory presence of rheumatoid factor.

Acquired contractures

Contractures are restrictions of mobility in a joint. By origin, they are classified as traumatic, inflammatory, paralytic, dystrophic, and fixational.

Depending on the primarily affected tissue, the following types are distinguished:

• Dermatodesmogenic: occur after burns and extensive skin trauma due to the formation of coarse scars.
• Tendogenic: associated with tendon damage, adhesion formation, or rupture, when antagonist muscles displace the joint.
• Myogenic: a consequence of ischemia or muscle trauma leading to their cicatricial shortening.
• Arthrogenic: the result of damage to joint structures (cartilage, capsule, bones) from trauma or infections.

Combined forms (arthromyogenic) are frequent, as is Volkmann's ischemic contracture and neurogenic (reflex) contractures, such as Turner's disease.

Infectious arthritides

Based on the character of the exudate, infectious arthritides are divided into serous, serofibrinous, purulent, and putrid. Bacterial and tuberculous arthritides are the most significant.

Bacterial arthritis may be caused by Neisseria gonorrhoeae (gonococcal) or other pathogens: Staphylococcus aureus, streptococci, gram-negative bacteria.

Pathogenesis includes several stages:

1. Acute phase: serous inflammation, edema of the synovial membrane, increase in turbid synovial fluid with fibrin clots. Cartilage is intact.
2. Serous stage: proliferation of synoviocytes, foci of fibrinoid swelling. Changes are reversible with treatment.
3. Purulent synovitis: exudate becomes purulent, leukocyte infiltration occurs, and a pannus forms, destroying the articular cartilage. The joint enlarges, becomes painful, and function is impaired.
4. Purulent panarthritis: spread of pus, destruction of ligaments and bones.

Tuberculous arthritis is a chronic disease resulting from hematogenous seeding of mycobacteria from a primary focus. It most commonly affects a single large joint.

Class and exam questions

What else to study on this topic

• Morphology of synovitis stages in rheumatoid arthritis
• Pathogenesis and complications of rheumatoid lung and vasculitis
• Mechanism of development of Volkmann's ischemic contracture
• The process of pannus formation in purulent arthritis
• Morphological differences between tuberculous and bacterial arthritis

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.