Targeting CD38 to Suppress Osteoarthritis Development and Associated Pain After Joint Injury in Mice

Gil Alabarse P, Chen LY, Oliveira P, Qin H, Liu-Bryan R · Arthritis & Rheumatology

CD38 was upregulated in human OA cartilage and in IL-1β-stimulated chondrocytes, where it lowered the NAD+:NADH ratio; after joint injury, mean cartilage-damage (OARSI) scores were 6.24 in wild-type vs 1.99 in CD38-knockout mice, and 6.44 untreated vs 2.09 with apigenin, with reduced synovial inflammation and pain-like behavior.

Population

CD38-knockout and wild-type mice with surgically induced (DMM) knee OA; human normal and OA knee cartilage; cultured chondrocytes

Intervention

Genetic CD38 knockout, or the dietary-flavonoid CD38 inhibitor apigenin

Comparator

Wild-type / untreated mice after the same joint injury

Limitations

Mouse joint-injury model. Blocking the NAD+ drain is not the same intervention as supplying more precursor — this paper supports the pathway, not the supplement. Full text read.