Arthritis

Classification and General Characteristics

The vast majority of joint system pathologies (arthropathies) are accompanied by the development of an inflammatory reaction. Depending on the leading etiological factor and pathogenesis mechanisms, all types of arthritis are traditionally divided into four main groups:

1. Infectious;
2. Autoimmune;
3. Metabolic;
4. Dystrophic (this group includes arthrosis presenting with a secondary inflammatory component).

In addition to classic inflammatory diseases, congenital developmental defects, joint tumors, and pseudosarcomatous proliferations of the ligamentous-muscular apparatus also hold clinical significance in general joint pathology.

Infectious arthritis and enteropathic lesions

The development of infectious arthritis is directly associated with microorganisms entering the joint cavity. Pathogen penetration can occur via a direct route (for example, through an open wound), as well as through lymphogenous or hematogenous pathways from other foci of infection. Usually, the inflammatory process involves only one large joint, forming monoarthritis. Polyarticular involvement occurs in only 10% of cases. Inflammation involves all structural elements of the joint, with active exudation always serving as the initial stage.

A special form is enteropathic arthritis. It manifests suddenly in patients who are positive for the HLA-B27 antigen and suffer from bacterial bowel diseases. Inflammation is most frequently localized in the knee and ankle joints, occasionally affecting the interphalangeal and wrist joints. The disease lasts about a year and, as a rule, resolves without sequelae. In rare cases, the pathology is complicated by the development of ankylosing spondylitis.

Metabolic diseases: Gout

The most striking example of metabolic joint lesions is gout, a chronic disease caused by a systemic disorder of purine metabolism. Epidemiologically, the pathology affects almost exclusively men aged 35 to 50 years.

Primary and secondary forms of the disease are distinguished. Primary (idiopathic) gout arises due to a genetically determined increase in the synthesis of purine bases or their accelerated breakdown. As a result, the concentration of uric acid in the blood increases (hyperuricemia develops), while its excretion in the urine slows down (hyperuricuria). Excessive meat consumption acts as a significant risk factor.

Pathogenesis and morphological changes:

• The leading clinical symptom is acute arthritis with a wave-like course (alternation of prolonged remissions and severe exacerbations).
• Microcrystals of urates are massively deposited in the articular cartilage, bone epiphyses, periarticular tissues, and kidneys.
• Urate crystals act as a trigger activating inflammatory mediators (including kinins and complement system components).
• Foci of necrosis arise in the tissues and an inflammatory reaction develops, accompanied by severe pain. A large number of foreign body giant cells that phagocytose crystals accumulate in the focus.
• Tophi (tophi urici) are formed — gouty nodules representing conglomerates of inflammatory infiltrate and proliferating connective tissue.
• With prolonged chronic gouty synovitis, granulation tissue (pannus) forms. It creeps onto the articular cartilage and subchondral bone, causing their destruction, which ultimately leads to joint ankylosis.

Immune-mediated lesions: Rheumatoid arthritis

Chronically progressive immune-mediated diseases constitute a key link in the pathogenesis of rheumatic diseases. Rheumatoid arthritis (RA) holds the central place among them.

Based on clinical and laboratory features, several variants are distinguished:

• Seropositive RA (rheumatoid factor is detected in serum), which also includes Felty's syndrome.
• Seronegative RA (rheumatoid factor is absent).
• RA with extra-articular manifestations, such as lung involvement (rheumatoid lung) or concomitant vasculitis (rheumatoid vasculitis).

Juvenile rheumatoid arthritis (JRA) is classified separately as a chronic autoimmune inflammation of uncertain etiology developing in children under 16 years of age. Morphological changes in the joints in the juvenile form differ little from lesions in adults, but in children up to 40% of cases present as oligoarthritis. The polyarticular seropositive subtype of JRA is directly associated with the HLA-DR4 immunogenetic marker (as in the adult population), and is accompanied by the mandatory detection of rheumatoid factor and moderate laboratory activity of inflammation.

Class and exam questions

What else to study on this topic

• Pathogenesis and pathological anatomy of tuberculous arthritis
• Osteoarthritis deformans: morphological changes and outcomes
• Benign and malignant tumors of joints and bones
• Rickets and osteomalacia: mechanisms of metabolic disorders
• Morphological picture of Ewing's sarcoma and pathways of metastasis

Other topics in the "Rheumatic Diseases" section

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