Orthopedics - Oleksa A.P. 2006

Joint Diseases
Arthritis of Unknown Etiology
Reactive Arthritides

Reactive Arthritis was previously considered to be a manifestation of aseptic joint inflammation, as neither the CAUSATIVE AGENT OF the inflammatory process nor its Antigens could be detected in the synovial exudate.

However, in recent years, advances in diagnostic Methods (Monoclonal Antibodies, immunoelectron Cell/15.html">Microscopy) have confirmed the presence of Chlamydia antigens and elementary bodies of this microbe in the synovial exudate.

Furthermore, viable microbes have occasionally been isolated from the joints of patients with yersiniosis-associated reactive synovitis (Korzh A.A., Kovalenko V.N., Korzh N.A. et al., 1998).

Thus, reactive arthritis is considered sterile when no microbial factor is detected in the joint exudate, whereas synovitis can develop as a complication of an infection focus located anywhere in the body (urogenital, intestinal, nasopharyngeal, etc.).

Korzh O.O. et al. (1998) suggest that the leading pathogenetic mechanism of reactive arthritis is a HUMAN Immune Response to microbial agents located outside the affected joint, leading to immune complex formation and their deposition in the synovial membrane, thereby causing immune complex synovitis.

The crucial role of genetic factors in the Pathogenesis of reactive arthritis is indicated by its strong association with the HLA-B27 antigen. This antigen is detected in 80–90% of patients with urogenital and enterocolitic reactive arthritis.

Patients carrying the HLA-B27 antigen tend to experience a more severe course of reactive arthritis than those without it. Presumably, susceptibility to reactive arthritis is also influenced by other genetic factors.

Clinically, reactive arthritis can follow an acute, relapsing, or chronic course, largely depending on the localization of the extra-articular infection focus, the biological Properties of the microflora, and the genetic CHARACTERISTICS OF THE Organism.

These same authors outline the Selection/11.html">General features of reactive arthritis:

1. Onset in young individuals.

2. Chronological link to an infection.

3. Acute onset accompanied by pronounced local and systemic signs of inflammation.

4. Mono-, oligo-, or less frequently polyarthritis (asymmetric), predominantly affecting the lower extremities, frequently involving the tendon-ligament apparatus, achillobursitis, and subcalcaneal bursitis.

5. Involvement of the sacroiliac joints and spine.

6. Presence of extra-articular signs of systemic involvement (eyes, Skin, mucous membranes, Internal Organs).

7. Absence of rheumatoid factor in Blood serum.

8. Frequent detection of the HLA-B27 histocompatibility antigen.

9. Relatively benign course with a tendency toward recurrence.

10. Presence of joint exudate.

11. Periarticular tissue Swelling.

12. Tenosynovitis.

13. Elevated local Temperature.

14. Hyperemia or a mottled ("marbled") appearance of the skin.

However, it should be noted that in clinical practice, only some of these features are observed; therefore, diagnosing arthritis requires The Use of additional examination methods.

All patients undergo radiography of the affected joint, which reveals widening of the joint space due to synovitis, without significant alterations in the articular surfaces or Bone tissue destruction.

Laboratory tests reveal neutrophilic leukocytosis with a shift to the left toward band neutrophils, elevated ESR, C-reactive protein, fibrinogen, sialic acid, and uric acid levels, among others. Synovial fluid is analyzed to determine cellular composition, lactic acid content, and bacterial presence, as well as by Polarization Microscopy to detect crystals.

Stool samples are examined for Yersinia, Salmonella, Shigella, etc., and urine and urethral discharge are tested to detect gonococci and chlamydia.

A comprehensive patient evaluation allows for a pathogenetic approach in selecting the optimal Treatment method.