Journal of Clinical & Experimental Pathology
Open Access

Inflammatory arthritis is commonly caused by gout. Gout affects 3.9 percent of the adult population in the United States. The major pathophysiological cause of the condition is Mono Sodium Urate (MSU) crystal deposition. Asymptomatic hyperuricemia, intermittent bouts (flares) of acute arthritis, intercritical gout, and advanced gout, which is defined clinically by tophi, chronic gouty arthritis, and joint destruction in certain people, are typical of the clinical course of gout. The classic clinical presentation of gout is an acute onset of acutely painful monoarthritis, generally affecting the lower leg and most commonly the first metatarsophalangeal joint.

The acute flare's severity generally peaks within 24 hours and subsides over 7–14 days. Concerns regarding other diseases, such as septic arthritis, may demand a histological evaluation of the afflicted tissue in the setting of acute inflammatory monoarthritis. Furthermore, while the symptoms of gout are normally relatively distinct, individuals may have atypical symptoms such as subcutaneous nodules, chronic joint inflammation, or acute inflammation in unusual places. While sophisticated imaging technologies or microscopy of aspirated material for crystal confirmation may aid in the diagnosis, pathological investigation of damaged tissue may be necessary to confirm the diagnosis. The goal of this systematic study was to describe the anatomical pathology of gout in detail, including macroscopic appearances, light (including immunohistochemistry), and electron microscopy.

Most studies addressing the anatomical pathology of gout report involvement of musculoskeletal tissues, with other areas mentioned less frequently, in line with the clinical presentation of gout. MSU crystal deposition was nearly consistently reported in afflicted tissues, indicating that these crystals play a primary pathogenic role in gout. Despite the fact that the pathological presentations of gout varied according on the afflicted tissue, the tophus was described as an organised chronic giant cell granulomatous formation comprised of MSU crystals, innate and adaptive immune cells, and fibrovascular tissue at various sites.

Despite the fact that MSU crystals are regularly seen in synovial fluid in the joint space and within synovial tophi, investigations of synovial pathology during a gout flare detected no free MSU crystals within acutely inflamed synovium. Free MSU crystals interacting with synovial lining cells may cause a gout flare, according to researchers, these lining cells may be quickly discharged into the joint space after MSU crystals are phagocytosed. Historical writings, reporting illness, anatomical aspects can be compared to modern gout sophisticated imaging investigations. The observations of both acute neutrophilic synovitis and chronic synovitis with microtophi and foreign body type giant cells were an interesting observation in the investigations of synovial pathology in gout.

Many individuals with gout exhibit imaging evidence of synovitis throughout the intercritical period, according to recent sophisticated imaging studies, and urate-lowering treatment can diminish MRI synovitis. The 'double-contour sign' described on ultrasonography corresponds to long-standing pathological findings of MSU crystals covering hyaline cartilage. Anatomical pathology investigations have also shown abnormal osteoclast and osteoblast appearances at the tophus-bone interface, confirming the strong relationship between tophi and areas of bone degradation found in dual energy CT imaging.