Pathogenesis (disease development)
The pathogenesis of psoriatic arthritis is not yet fully understood. It is thought to be similar to that of psoriasis vulgaris.
Psoriasis is a multifactorial disease in which genetic factors and exogenous factors (infections, smoking, use of certain medications) interact in the pathogenesis. It is considered a systemic autoimmune disease (disease in which the immune system is directed against the body’s own structures), in which endogenous T cells (cells belonging to the lymphocyte cell group) are activated by autoantigens. Subsequently, there are accumulations of leukocytes (white blood cells), which in turn affect the keratinocytes (horn-forming cells). There is an excessive acceleration of proliferation (rapid growth of tissue) (→ acanthosis (thickening of the epidermis) and parakeratosis/dysfunctional keratinization).
Tumor necrosis factor (TNF) plays a central role in the inflammatory process of psoriasis. In patients with psoriatic arthritis, elevated TNF concentrations can be detected in the synovium (synovial fluid) as well as in the psoriatic plaques.
Etiology (Causes)
Biographic Causes
- Genetic burden
The following trigger factors (possible triggers) are suspected:
- Bacterial infections (eg, group A streptococci).
- Inflammatory lesions such as dental granulomas (small nodules in the tooth area).
- Joint trauma (joint injuries), joint stresses.
- Proliferative-destructive inflammation at joint soft tissues, synovium (synovial fluid), bone.
- T-cell-mediated immune response with secretion (release) prophlogistic cytokines (pro-inflammatory messengers).
- Viral infections (e.g., HIV).
