15-Hydroxyprostaglandin Dehydrogenase in Osteoarthritis and Ankylosing Spondylitis: Associations With Clinical and Musculoskeletal Ultrasound Features.

Osteoarthritis (OA) and Ankylosing Spondylitis (AS) are chronic musculoskeletal disorders with different pathophysiology, clinical manifestations, and management strategies. OA is a degenerative joint disease in which inflammation also contributes to symptom severity and structural progression, while AS is a chronic inflammatory spondyloarthropathy characterized by axial inflammation and, in some patients, peripheral arthritis.

Prostaglandin E2 (PGE2) is a key mediator involved in pain, inflammation, and tissue remodeling in musculoskeletal disease. 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is the major enzyme responsible for degradation of prostaglandins, especially PGE2, and therefore acts as an important regulator of prostaglandin activity in the joint microenvironment. In inflammatory arthritis, synovial studies have shown that 15-PGDH is present in healthy and inflamed synovial tissue, mainly in lining macrophages, fibroblasts, and vessels, supporting a possible role in local inflammatory regulation.

In osteoarthritis, experimental evidence indicates that 15-PGDH is biologically relevant to cartilage degeneration and repair, and inhibition of 15-PGDH may promote cartilage regeneration and reduce OA-associated pain. These findings support the rationale for investigating 15-PGDH as a biomarker in OA and AS.

Musculoskeletal ultrasound is a valuable non-invasive imaging tool in rheumatology and can detect synovial hypertrophy, effusion, and power Doppler activity. EULAR has published recommendations for standardized ultrasound procedures and reporting in rheumatic and musculoskeletal diseases, supporting its use in this study.

Accordingly, this study will assess serum and synovial fluid 15-PGDH levels in patients with OA and AS and examine their correlation with clinical and musculoskeletal ultrasound features.