Periodontal inflammation is related to increased serum calcitonin gene‐related peptide levels in patients with chronic migraine

Abstract

Background Recently, a relationship was found between periodontitis and chronic migraine. Calcitonin gene‐related peptide (CGRP) is a key element in migraine pathophysiology. However, no information exists of the potential association between periodontal inflammation and CGRP in chronic migraine. The aim of the study was, therefore, to investigate whether there is a link between periodontitis and peripheral levels of CGRP in a cohort of patients with chronic migraine. Methods We included 102 chronic migraineurs and 77 age‐ and sex‐matched individuals free of headache/migraine. Full‐mouth periodontal parameters were recorded and the periodontal inflamed surface area (PISA) was calculated to quantify the periodontal inflammatory status for each participant. Sociodemographic data and comorbidities were assessed by means of a standard questionnaire. We collected blood samples and serum concentrations were done for CGRP, interleukin (IL)‐6 and IL‐10. Results In the chronic migraine group, patients with periodontitis had greater levels of serum CGRP (19.7 ± 6.5 versus 15.3 ± 6.2 pg/mL, P < 0.0001) and IL‐6 (15.1 ± 9.2 versus 9.6 ± 6.3 pg/mL, P < 0.0001) while non‐significant differences were observed with IL‐10 (2.0 ± 1.0 versus 2.8 ± 1.5 pg/mL, P = 0.675) concentrations than those without periodontitis. PISA was independently associated with CGRP in patients with chronic migraine (β = 0.003; 95% confidence interval: 0.001 to 0.006, P = 0.031). PISA correlated positively with CGRP (r = 0.236; P = 0.017) and IL‐6 (r = 0.262; P = 0.008) in chronic migraine. Conclusions Periodontal inflammation is associated with increased circulating levels of CGRP in chronic migraineurs. Elucidating the exact mechanisms through which periodontitis and CGRP are linked in these patients deserves further investigation.

Serotonin and Neuropeptides in Blood From Episodic and Chronic Migraine and Cluster Headache Patients in Case‐Control and Case‐Crossover Settings: A Systematic Review and Meta‐Analysis

“…For comparison group f, ictal vs interictal also refers to the active cluster bout vs remission. In addition to the references from Table 3 with clear blood specimen descriptions (n = 30), 15 references were included 21,26,27,37,39,43,48,125‐132 . Abbreviations: chronic cluster headache (CCH); chronic migraine (CM); control (CTRL); episodic cluster headache (ECH); female/female‐dominated (F/FD); migraine (M); both sexes (M/F); male/male‐dominated (M/MD); migraine with aura (MWA); migraine without aura (MWoA).…”

“…(B) Meta‐analysis of CGRP in episodic and chronic migraine (cases) compared with CTRL. Imputation of missing standard deviation (SD) was done for Leira et al 132 A FD/MD case group means that ≥70.0% of the cases were females/males (case average), thereby sex refers to the sex distribution in the case group. When information was not available for the studies within the subgroup, information from the entire study was used to evaluate sex distribution and age.…”

Mild systemic inflammation enhances response to OnabotulinumtoxinA in chronic migraineurs

“…A recent case-control study showed that subjects with periodontitis had two-fold increased risk for having chronic migraine 15 . On top of that, another clinical study demonstrated that periodontal inflammation was associated with increased circulating levels of CGRP in chronic migraineurs and authors hypothesized that upregulation of IL-6 could mediate this finding 3 . However, whether IL-6 induces CGRP overexpression or vice versa is still unknown as CGRP is capable of producing inflammatory cytokines from lymphocytes and macrophages after lipopolysaccharide infection 28,29 .…”

“…Study design. This is a secondary analysis with a cross-sectional design from previous observational studies from our group, which looked at the clinical and molecular relationship between periodontitis and chronic migraine 3,15 .…”

The presence of leukoaraiosis enhances the association between sTWEAK and hemorrhagic transformation

“…These are mechanisms that are considered to be close to LA development. [14][15][16][17] We compared the results of sTWEAK with other potential biomarkers for predicting hemorrhagic transformation of ischemic stroke 8 ; those related to inflammation and oxidative stress processes namely leukocytes, fibrinogen, C-reactive protein, erythrocyte sedimentation rate, serum levels of interleukin 6 (IL-6), and tumor necrosis factor alpha (TNFa) 25,26 ; those correlating with BBB disruption such as microalbuminuria, matrix metalloproteinase-9 (MMP-9), serum levels of S100-b, neuron-specific enolase (NSE), and neuroserpin 27,28 ; those involved in vasoreactivity including cell fibronectin (c-Fn), endothelin-1 (ET-1), and platelet-derived growth factor-CC isoform (PDGF-CC) 29,30 ; and finally, those related to serum levels of glutamate were determined as an excitotoxicity marker. 31 Blood samples to measure biomarkers were obtained before administering the reperfusion treatment.…”