Rheumatism arthritis (RA) is a chronic self-immunological disease that develops in a complex and human-specific manner. The following are typical stages of development and mechanisms for RA: 1. Initial phase – Immuno-system activation: The exact causes of RA ‘ s illness are not yet fully clear, but genetic and environmental factors are considered to work together, leading to anomalous activation of the immune system. Certain trigger factors (e.g., infection, smoking or other environmental factors) may trigger the immune response in the susceptible individuals. Self-activated antibodies: At the early stages of a disease, the immune system begins to produce antibodies against its own organization, such as the rheumatist factor (RF) and the antiacrytic amino acid (ACPA). These antibodies can be detected several years before symptoms occur, suggesting early anomalies in the immune system. Inflammatory stage – Luctile: RA is characterized by chronic inflammation of the joints. The membrane, which is a thin tissue within the joint, produces lubricant to reduce friction. Inflammation leads to a thickening of the membrane, which forms the growth of the membrane, i.e., “pembrane inflammation”. Immunocellination: Multiimmunocellular cells (e.g. T-cells, B-cells and megacormic cells) impregnate and release inflammation media (e.g. cytogens), further exacerbating inflammatory response. Artificial damage phase – cartilage and bone damage: Continued inflammation leads to the growth of the muscular tissue, the formation of an “incremental muscular tissue” and the erosion of joint cartilage and bones. The destruction of the cartilage has led to a narrowing of the joint gap and the erosion of the bone has led to joint malformations and loss of function. Loss of joint function: As the process progresses, the structural impairment of the joint becomes irreversible, resulting in restriction of joint activity, deformity and loss of function. 4. Systemic impact – RA not only affects joints but may also cause systemic symptoms and complications such as fatigue, anaemia, cardiovascular disease, lung problems and osteoporosis. These systemic effects may be related to the whole-body effects of the inflammatory medium. 5. Incidence fluctuations – RA ‘ s pathology is usually expressed in the alternation of activity and mitigation periods. Symptoms increased during the activity period, including joint pain, swelling and rigidity, while symptoms decreased during the mitigation period. Volatile conditions may be affected by a number of factors, such as stress, infection and treatment. 6. Influence factor – (1) Genetic factor: Certain genes (e.g. HLA-DRB1) are associated with RRA susceptibility. (2) Environmental factors: Tobacco use, infection and hormone change may increase the risk of disease. (3) Gender factor: Females are at two to three times the risk of an RA, and hint hormones may play a role in disease development. Diagnosis and treatment – early diagnosis and treatment – are essential to slow RRA progress. The objective is to control inflammation, mitigate joint damage and improve the quality of life. Treatment programmes typically include disease-improvement rheumatist drugs (DMARDs), biological agents, inflammatory drugs (NSAIDs) and sugary cortex hormones.
Rheumatism arthritis
