Cytokine levels and their role in the etiopathogenesis of Burning Mouth Syndrome: A systematic review

Cephalalgia ◽  
2019 ◽  
Vol 39 (12) ◽  
pp. 1586-1594 ◽  
Author(s):  
Jaimala Kishore ◽  
Fouzia Shaikh ◽  
Sana Mirza ◽  
Muhammad Arsalan Raffat ◽  
Sana Ikram ◽  
...  

Introduction Burning Mouth Syndrome is characterized by variable symptoms that include pain, burning and paraguesia in an otherwise healthy-appearing oral mucosa. Although the etiopathogenesis of Burning Mouth Syndrome is unknown, some studies provide evidence of subclinical inflammation leading to disrupted cytokine levels. Aim To investigate the expression of cytokines and role in the etiopathogenesis of Burning Mouth Syndrome. Methods Online databases (MEDLINE and EMBASE) were searched from November 1986 to November 2018 for case control/cross-sectional studies comparing the levels of cytokines in patients with Burning Mouth Syndrome and healthy controls. Results A total of eight studies were included in the current review. Four studies were of high and four studies were of moderate quality. Seven studies evaluated IL-6, out of which four showed comparable results, two showed higher levels and one study reported lower levels in Burning Mouth Syndrome patients compared to controls. Four studies assessed IL-2, out of which two reported comparable results whereas one study reported higher levels and one study reported lower levels in Burning Mouth Syndrome patients compared to controls. IL-10 levels were measured in three studies that reported no significant differences in the levels between Burning Mouth Syndrome and healthy controls. Discussion and conclusion The etiopathogenesis of Burning Mouth Syndrome is multifactorial. Studies have provided scientific evidence that inflammation plays a key role in Burning Mouth Syndrome pathogenesis. However, whether up-regulation or down-regulation of specific cytokines contribute to the etiopathogenesis of Burning Mouth Syndrome remains debatable. Further high-quality studies with larger sample size and assessing a wider array of cytokines are warranted in order to obtain strong conclusions.

2016 ◽  
Vol 21 (7) ◽  
pp. 2157-2164 ◽  
Author(s):  
Yves Boucher ◽  
Adeline Braud ◽  
Evelyne Dufour ◽  
Scarlette Agbo-Godeau ◽  
Vanessa Baaroun ◽  
...  

Oral Diseases ◽  
2019 ◽  
Vol 25 (6) ◽  
pp. 1634-1644 ◽  
Author(s):  
Lorenzo Azzi ◽  
Giovanni Veronesi ◽  
Angelo Tagliabue ◽  
Fabio Croveri ◽  
Vittorio Maurino ◽  
...  

2010 ◽  
Vol 15 (4) ◽  
pp. 571-575 ◽  
Author(s):  
Frederico Omar Gleber Netto ◽  
Ivana Márcia Alves Diniz ◽  
Soraya Mattos Carmargo Grossmann ◽  
Mauro Henrique Nogueira Guimarães de Abreu ◽  
Maria Auxiliadora Vieira do Carmo ◽  
...  

2020 ◽  
Author(s):  
Luca Bartolini ◽  
Michael P. Moran ◽  
Gina Norato ◽  
Bobbe Thomas ◽  
Alexander D. Dick ◽  
...  

Abstract Background Experimental and clinical findings suggest a crucial role of inflammation in epileptogenesis. We aimed to analyze levels of inflammatory cytokines in plasma and saliva from children with acute seizures and healthy controls and measure their associations with HHV6 and EBV infection. Methods We analyzed plasma from 36 children within 24 hours of acute seizures (cases) and 43 healthy controls and saliva from 44 cases and 44 controls with a multiplex immunoassay. Saliva from all controls and 65 cases and blood from 26 controls and 35 cases were also analyzed by ddPCR for viral DNA. Statistical analysis included Wilcoxon Rank Sum test, Fisher’s exact test, ANOVA and Spearman correlation. Results Compared to controls, children with breakthrough seizures (n=18) had higher levels of CCL11 (p<0.001), CCL26 (p<0.001), IL-8 (p=0.03), CCL4 (p=0.02) in plasma. Children with new onset seizures (n=13) showed higher levels of CCL11 (p=0.05) and IL-6 (p=0.01). Patients with febrile seizures (n=5) had higher levels of IFNγ (p<0.001), IL-6 (p<0.001), IL-10 (p<0.001), CXCL10 (p=0.001). CCL11 was higher with 3 or more seizures (p=0.01), seizures longer than 10 minutes (p=0.001) and when EEG showed focal slowing (p=0.02). In saliva, febrile seizures had higher levels of IL-1β (n=7, p=0.04) and new onset seizures had higher IL-6 (n=15, p=0.02). Plasma and saliva cytokine levels did not show correlation. Frequency of HHV-6 and EBV detection was similar across seizure types and not different than controls. We found no correlation between viral load and cytokine levels Conclusions We showed differential activation of neuroinflammatory pathways in plasma from different seizure etiologies compared to controls, unrelated to HHV-6 infection.


2019 ◽  
Author(s):  
Luca Bartolini ◽  
Michael P. Moran ◽  
Gina Norato ◽  
Bobbe Thomas ◽  
Alexander D. Dick ◽  
...  

Abstract Background: Experimental and clinical findings suggest a crucial role of inflammation in epileptogenesis. We aimed to analyze levels of inflammatory cytokines in plasma and saliva from children with acute seizures and healthy controls and measure their associations with HHV6 and EBV infection. Methods: We analyzed plasma from 36 children within 24 hours of acute seizures (cases) and 43 healthy controls and saliva from 44 cases and 44 controls with a multiplex immunoassay. Saliva from all controls and 65 cases and blood from 26 controls and 35 cases were also analyzed by ddPCR for viral DNA. Statistical analysis included Wilcoxon Rank Sum test, Fisher’s exact test, ANOVA and Spearman correlation. Results: Compared to controls, children with breakthrough seizures (n=18) had higher levels of CCL11 (p<0.001), CCL26 (p<0.001), IL-8 (p=0.03), CCL4 (p=0.02) in plasma. Children with new onset seizures (n=13) showed higher levels of CCL11 (p=0.05) and IL-6 (p=0.01). Patients with febrile seizures (n=5) had higher levels of IFNg (p<0.001), IL-6 (p<0.001), IL-10 (p<0.001), CXCL10 (p=0.001). CCL11 was higher with 3 or more seizures (p=0.01), seizures longer than 10 minutes (p=0.001) and when EEG showed focal slowing (p=0.02). In saliva, febrile seizures had higher levels of IL-1β (n=7, p=0.04) and new onset seizures had higher IL-6 (n=15, p=0.02). Plasma and saliva cytokine levels did not show correlation. Frequency of HHV-6 and EBV detection was similar across seizure types and not different than controls. We found no correlation between viral load and cytokine levels Conclusions: We showed differential activation of neuroinflammatory pathways in plasma from different seizure etiologies compared to controls, unrelated to HHV-6 infection.


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