Migraine is a hereditary constitutional base disorder, which is characterized by recurrent episodes of
headache pulsatile characteristics associated with
photophobia/
phonophobia,
nausea and/or
vomiting. The main complication in
migraine is the chronicity of the process, now recognized as a chronic
migraine. Although pathogenic mechanisms that may influence the pathophysiology of
migraine and its possible chronicity are not fully understood, previous studies have shown in patients with
migraine molecular alterations of systemic
inflammation, neurogenic inflammation, endothelial dysfunction, innate immunity, dysfunction of matrix
proteases and blood-brain barrier.
Periodontal disease is an inflammatory lesion caused by bacteria. After the
bacterial infection begins, an immune response that will be responsible for individual susceptibility appears. More advanced forms of
periodontitis have demonstrated molecular alterations of
inflammation, endothelial dysfunction, dysfunction of matrix
proteases and innate immunity, similar to those observed in
migraine. Furthermore, the main molecular mediators of
neurogenic inflammation related to activation of the trigeminovascular system, which are characteristic of
migraine, are overexpressed in gingival crevicular fluid and mucosa in patients with
periodontal disease.
Hypertension,
hypercholesterolemia,
insulin resistance,
stroke or
coronary artery disease are comorbidities that
periodontal disease and
migraine could share. Therefore, several mechanisms and hypotheses could explain the possible association between both diseases. However, epidemiological and molecular studies will be necessary to provide a better understanding of this potential association, which could be implicated in the chronification of
migraine.