It can exist in the absence of periodontal disease or occur as a sequel to it [1], during which there is loss of periodontal tissue, and the release of cytokines such as IL–1, IL–2, IL–17, TNF-alpha, and PGE2 could promote hipoxia, oxidative stress, relative vasospasm, increased coagulation, and endothelial injury [5, 32]. Here, TNF is linked to periodontal disorder.