Breaking Points: How OA and RA Challenge the Body in Different Ways

Arthritis encompasses a group of inflammatory conditions that affect the joints and surrounding tissues, leading to pain, swelling, and limited movement. The two most common forms are osteoarthritis (OA) and rheumatoid arthritis (RA).¹

RA is an autoimmune disorder in which the body’s immune system attacks its own joint tissues, causing inflammation that leads to pain, stiffness, swelling, and redness, ultimately impairing joint mobility and function. Notably, RA symptoms often worsen after periods of rest and improve with activity as joint movement helps reduce inflammation and stiffness. The etiology of RA is believed to involve both genetic and environmental factors. Various alleles sharing a common amino acid sequence have been linked to RA development, and polymorphisms in other genes are associated with more severe disease. Cigarette smoking is the strongest environmental risk factor, while others include exposure to silica, asbestos, textile dust, and P. gingivalis. External antigens can trigger an autoimmune response that damages the joints.²

In contrast, osteoarthritis (OA) is a degenerative joint disease characterized by the progressive deterioration of articular cartilage. The loss of cartilage reduces cushioning and lubrication between bones, leading to friction, pain, stiffness, and decreased mobility. In contrast to RA, OA symptoms typically worsen with prolonged use and improve with rest, as mechanical stress aggravates joint pain. Pro-inflammatory mediators and proteolytic enzymes further contribute to joint destruction. As cartilage erosion progresses, chondrocytes proliferate and cluster, resulting in cartilage outgrowths and bone spurs. Continued damage to the collagen matrix triggers chondrocyte apoptosis, while abnormal collagen mineralization promotes subchondral bone thickening. Synovial inflammation and injury to surrounding joint structures, including ligaments, joint capsules, and menisci, may also occur.⁴

OA is classified as either primary or secondary. Primary OA develops with age in the absence of prior trauma or underlying disease, whereas secondary OA arises from joint abnormalities or injury. Major risk factors include advanced age, female sex, obesity, and a history of joint injury.⁵

Both OA and RA are characterized by joint pain, swelling, and reduced mobility. Although their specific causes are not fully understood, a combination of genetic, environmental, and lifestyle factors contributes to their development.