Yago Leira1,2,3, Pablo Ameijeira4, Clara Domínguez5, Esteban López-Arias6, Paulo Ávila-Gómez6, María Pérez-Mato6, Tomás Sobrino6, Francisco Campos6, Francesco D'Aiuto7, Rogelio Leira5, Juan Blanco4,8. 1. Periodontology Unit, UCL Eastman Dental Institute and Hospital, University College London, 256 Gray's Inn Road, London, WC1X 8LD, UK. y.leira@ucl.ac.uk. 2. Periodontology Unit, Faculty of Medicine and Odontology, University of Santiago de Compostela, Santiago de Compostela, Spain. y.leira@ucl.ac.uk. 3. Medical-Surgical Dentistry (OMEQUI) Research Group, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. y.leira@ucl.ac.uk. 4. Periodontology Unit, Faculty of Medicine and Odontology, University of Santiago de Compostela, Santiago de Compostela, Spain. 5. Department of Neurology, Headache Unit, University Clinical Hospital, Clinical Neurosciences Research Laboratory, Health Research Institute of Santiago de Compostela (IDIS), University of Santiago de Compostela, Santiago de Compostela, Spain. 6. Clinical Neurosciences Research Laboratory, Department of Neurology, Clinical University Hospital, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain. 7. Periodontology Unit, UCL Eastman Dental Institute and Hospital, University College London, 256 Gray's Inn Road, London, WC1X 8LD, UK. 8. Medical-Surgical Dentistry (OMEQUI) Research Group, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Abstract
OBJECTIVES: Periodontitis (PD) and chronic migraine (CM) have been recently linked, and inflammatory processes and vascular endothelial changes are hypothesized as potential mediators of this relationship. The aim of this cross-sectional analysis was to investigate the potential association of PD with vascular systemic inflammation and complement activation in patients with CM. MATERIALS AND METHODS: Ninety-four chronic migraineurs underwent a full-mouth periodontal evaluation and a measure of PD activity and severity, namely the periodontal inflamed surface area (PISA) was calculated for each patient. We divided CM patients according to their periodontal status: mild PD (N = 14), moderate PD (N = 22), severe PD (N = 19), and non-PD (N = 39). Serum levels of C-reactive protein (CRP), pentraxin 3 (PTX3), soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK), and complements C3 and C4 were measured outside of migraine attacks. RESULTS: We found that severe periodontal patients had significantly higher circulating levels of PTX3 and sTWEAK compared with those without PD (2475.3 ± 1646.8 pg/mL vs. 516.6 ± 1193.8 pg/mL, P < 0.0001 and 672.4 ± 118.2 pg/mL vs. 485.7 ± 112.2 pg/mL, P < 0.0001; respectively). For the remaining biomarkers, no significant differences were found between groups. Severe PD was independently associated with higher levels of PTX3 (β = 1997.6, P < 0.0001) and sTWEAK (β = 187.1, P < 0.0001) but not with CRP, C3, and C4. PISA positively correlated to PTX3 (r = 0.475, P < 0.0001) and sTWEAK (r = 0.386, P < 0.0001). CONCLUSIONS: Based on these preliminary results, severe PD was linked with vascular systemic inflammation in patients with CM. However, further longitudinal studies should be performed to confirm these findings. CLINICAL RELEVANCE: sTWEAK and PTX3 measured in serum could be used as biomarkers in the PD-CM link.
OBJECTIVES:Periodontitis (PD) and chronic migraine (CM) have been recently linked, and inflammatory processes and vascular endothelial changes are hypothesized as potential mediators of this relationship. The aim of this cross-sectional analysis was to investigate the potential association of PD with vascular systemic inflammation and complement activation in patients with CM. MATERIALS AND METHODS: Ninety-four chronic migraineurs underwent a full-mouth periodontal evaluation and a measure of PD activity and severity, namely the periodontal inflamed surface area (PISA) was calculated for each patient. We divided CMpatients according to their periodontal status: mild PD (N = 14), moderate PD (N = 22), severe PD (N = 19), and non-PD (N = 39). Serum levels of C-reactive protein (CRP), pentraxin 3 (PTX3), soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK), and complements C3 and C4 were measured outside of migraine attacks. RESULTS: We found that severe periodontal patients had significantly higher circulating levels of PTX3 and sTWEAK compared with those without PD (2475.3 ± 1646.8 pg/mL vs. 516.6 ± 1193.8 pg/mL, P < 0.0001 and 672.4 ± 118.2 pg/mL vs. 485.7 ± 112.2 pg/mL, P < 0.0001; respectively). For the remaining biomarkers, no significant differences were found between groups. Severe PD was independently associated with higher levels of PTX3 (β = 1997.6, P < 0.0001) and sTWEAK (β = 187.1, P < 0.0001) but not with CRP, C3, and C4. PISA positively correlated to PTX3 (r = 0.475, P < 0.0001) and sTWEAK (r = 0.386, P < 0.0001). CONCLUSIONS: Based on these preliminary results, severe PD was linked with vascular systemic inflammation in patients with CM. However, further longitudinal studies should be performed to confirm these findings. CLINICAL RELEVANCE: sTWEAK and PTX3 measured in serum could be used as biomarkers in the PD-CM link.
Authors: Clara Domínguez; Alba Vieites-Prado; María Pérez-Mato; Tomás Sobrino; Xiana Rodríguez-Osorio; Ana López; Francisco Campos; Francisco Martínez; José Castillo; Rogelio Leira Journal: Headache Date: 2017-11-13 Impact factor: 5.887
Authors: Yago Leira; Juan Seoane; Miguel Blanco; Manuel Rodríguez-Yáñez; Bahi Takkouche; Juan Blanco; José Castillo Journal: Eur J Epidemiol Date: 2016-06-14 Impact factor: 8.082
Authors: A Fava; D Pirritano; D Consoli; M Plastino; F Casalinuovo; S Cristofaro; C Colica; C Ermio; M De Bartolo; C Opipari; R Lanzo; A Consoli; D Bosco Journal: Eur J Neurol Date: 2013-11-15 Impact factor: 6.089