Table 1 Comparison between rheumatoid arthritis and osteoarthritis disease characteristics

From: Arthritis and the role of endogenous glucocorticoids

Characteristics

Rheumatoid arthritis

Osteoarthritis

Major risk factors

Genetics (MHC HLA alleles) and environment (periodontitis, smoking, and gut microbes)

Aging, obesity, female gender, joint biomechanics, injury, and genetics (GDF5)

Age at onset

May occur at any age

Around 65 years +

Symptoms

• Painful, swollen, and stiff joints

• Multiple joints usually in hands, wrists, elbows, and feet, with symmetrical presentation (affects both sides of the body)

• Systemic reaction (fatigue and malaise)

• Tender, aching joints with some swelling/pain

• Usually present on one side of the body in large weight-bearing joints such as the knee, hips, and spine

• No systemic symptoms

Disease onset

Fast (weeks—months)

Slow (years)

Mechanism

Systemic autoimmune reaction (production of autoantibodies e.g., RF and ACPAs)

Local tissue degeneration due to aging, biomechanical, metabolic, and inflammatory changes

Pathological features

• Major synovial reaction (inflammation, hyperplasia, and pannus formation)

• Destruction of cartilage by pannus invasion

• Bone erosion (osteoclast activation)

• Cartilage damage (“wear and tear”)

• Bone sclerosis

• Bone marrow lesions (early stage)

• Osteophytes

• Synovial inflammation

Treatment

Glucocorticoids, NSAIDs and DMARDs (synthetic e.g., methotrexate and biological e.g., anti-TNF-α)

Pain management (NSAIDs, intra-articular glucocorticoid injections), lifestyle modification (exercise and diet), and joint replacement surgery

  1. MHC major histocompatibility complex, HLA human leukocyte antigen, GDF5 growth/differentiation factor 5, RF rheumatoid factor, ACPAs antibodies to citrullinated protein antigens, NSAIDs nonsteroidal anti-inflammatory drugs, DMARDs disease-modifying antirheumatic drugs, TNF tumor necrosis factor