Pathophysiology of Osteoarthritis and Treatments

Osteoarthritis
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Osteoarthritis (OA)
Pathophysiology
The disease is secondary to multiple factors, but the most significant factor is the overuse of the joint, destroying the cartilaginous surfaces that serve as a cushion between the two bones. This begins as microtears, and overuse or increase in weight-bearing on the affected joints leads to progressive destruction that reaches the bone surface. The breakdown of the collagen matrix is facilitated by the matrix metalloproteinases and prostaglandin E and cyclooxygenase-2, which are hydrolytic enzymes. Microscopically, damage to the cartilages affects the collagen matrix, stimulating chondrocytes’ proliferation, resulting in their hypertrophy. Ultimately, this leads to ossifications and outgrowths called osteophytes. Additionally, the joint damage stimulates the recruitment of inflammatory mediators, including prostaglandins, cytokines, leukotrienes, nitric oxide, and growth factors, resulting in synovitis (Sen & Hurley, 2022; Mora et al., 2018).
Treatment
The primary treatment is a non-steroidal anti-inflammatory drug (NSAID). It prevents the formation of cyclooxygenases-1 and -2 (COX-1 and COX-2), which are responsible for the inflammatory reactions in osteoarthritis. COX-1 and COX-2 are the enzymes that transform arachidonic acid into prostaglandin and prostacyclins, which are the inflammatory mediators that are the prerequisites for joint swelling and pain. The nonselective NSAID blocks both COX-1 and COX-2. Because COX-1 is gastroprotective, this type of NSAID may destroy the gastric mucosa, leading to ulcerations or bleeding. Hence, gastric ulcer signs and symptoms should be monitored, such as epigastric pain, vo...