It has been hypothesized that the ulcerated periodontal epithelium in periodontitis patients may act as an entrance to the bloodstream of IL-6 and many other pro-inflammatory molecules which evoke an acute-phase response in the liver resulting in the overexpression of systemic inflammatory mediators such as C-reactive protein (CRP), fibrinogen and serum amyloid A1,2 or even specific proteins involved in the process of neurogenic inflammation [i.e., calcitonin gene-related peptide (CGRP)] typically seen in the physiopathology of head pain3. This evidence concerns the gene CRP and periodontitis.