Childhood arthritis (juvenile arthritis or pediatric rheumatic disease) is an umbrella term used to describe any rheumatic disease or chronic arthritis-related condition which affects individuals under the age of 16. There are several subtypes that differentiate themselves via prognosis, complications, and treatments. Most types are autoimmune disorders, where an individual's immune system may attack its own healthy tissues and cells.

Diagnosis of juvenile idiopathic arthritis is typically considered for children that are below the age of 16 years old and currently experiencing arthritis for at least six weeks with no other evident alternative causes for the symptoms. In 1997 the International League of Associations for Rheumatology (ILAR) presented a classification of juvenile idiopathic arthritis. This was later revised in 2001. In this classification juvenile idiopathic arthritis is the umbrella term and comprises seven categories: systemic arthritis, oligoarthritis, polyarthritis (reumatic factor negative), polyarthritis (reumatic factor positive), psoriatic arthritis, enthesitis related arthritis and undifferntiatied arthritis.

Juvenile arthritis may last for a few months, years, or becomes a lifelong disease that requires treatment as the child becomes an adult. Common complications that can arise include leg-length discrepancy, joint contracture, growth retardation, low bone mineral density, and macrophage activation syndrome.

Some causes or potential risk factors denoting a higher chance of developing childhood arthritis have been identified. However, similar to other autoimmune diseases, the exact cause or mechanism for development is still largely unknown and additional associations are continuously being researched and discovered.

Several types of childhood arthritis exist, including juvenile idiopathic arthritis, juvenile myositis, juvenile lupus, juvenile scleroderma, vasculitis, and fibromyalgia.

The most common type, juvenile idiopathic arthritis (previously known as juvenile rheumatoid arthritis or juvenile chronic arthritis) can be divided into six main forms. The classification is based upon symptoms, number of joints involved and the presence of certain antibodies in the blood. However, some subtypes have overlapping clinical presentation in addition as the child grow older symptoms may change over time. The six subforms of juvenile idiopathic arthritis include:

The cause of this complex disorder is typically idiopathic which can include multiple genes that affects the humoral and cell-mediated immunity in addition to environmental factors. However, Dietary habits and emotional state seem to have no effect on the disease. In most cases, juvenile arthritis is caused by the body attacking its own healthy cells and tissues, i.e. autoimmunity, causing the joint to become inflamed and stiff. Once the joint has become inflamed and stiff, damage is done to the joint and the growth of the joint may by changed or impaired. The underlying cause in the malfunction of the autoimmune system is unknown, however it is common to see an imbalance or abnormality in regulatory T cell levels in a majority of juvenile arthritis cases. Researchers have found that there is an elevation of cytokines like IL-1 and IL-18 in individuals with systemic juvenile idiopathic arthritis. In juvenile idiopathic arthritis (JIA) individuals, it is theorized that a possible environmental trigger for this condition is an infection due to the discovery of elevated heat shock proteins in JIA patients.

Genetic factors play a significant role in the predisposition to juvenile arthritis. Specific genetic markers, such as HLA (human leukocyte antigen) genes, have been associated with an increased risk of developing the disease. The HLA-DRB1 gene, for example, is linked to rheumatoid arthritis in adults and similar associations have been observed in juvenile arthritis, suggesting a genetic overlap between these conditions. Additionally, variations in genes related to the immune system, such as those involved in the production of cytokines and other inflammatory mediators, may contribute to the susceptibility and severity of the disease.