Systemic inflammation, a risk factor for OA, may contribute to the risk of developing OA in patients with SD.[14] Apparently, inflammatory cytokines such as IL-1ß, IL-6, IL-17, and TNF-ɑ commonly contribute to the etiopathogenesis of both SD and OA,[4,6,12–14] leading to increased FCT, an early sign of OA, in patients with SD. Here, TNF is linked to Salla disease.