The Role of Viruses in Pathogenesis of Aphthae
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Date
2021
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Rīgas Stradiņa universitāte
Rīga Stradiņš University
Rīga Stradiņš University
Abstract
Aftozais stomatīts tiek uzskatīts par daudzfaktoru patoloģiju, un tā attīstības pamatā ir dažādi faktori un izraisītāji. Šie faktori ir ģenētiska predispozīcija, sistēmiskas slimības, stress, trauksme, trauma, hormonālas izmaiņas, vitamīnu un mikroelementu deficīts, kā arī vīrusu vai baktēriju izraisītas infekcijas. Ir pārliecinoši pierādījumi, ka gļotādas destrukcija ir saistīta ar imūnās atbildes disregulāciju, ko aktivizē nezināma antigēnu stimulācija. Cēlonis var būt endogēns antigēns (autoimūns) vai eksogēns antigēns (hiperimūns), vai vienkārši trauma, kurā ir iesaistīti ķīmiskie mediatori. Šķiet, ka izšķiroša loma ir T-limfocītiem, TNF-α, gamma interferonam, interleikīniem IL-2, IL-4 un IL-5. Ļoti augsts TNF-α līmenis ir cieši saistīts ar aftu (čūliņu) patoģenēzi, jo tas palielina endotēlija šūnu adhēziju un veicina neitrofilo leikocītu hemotaksi, iesākot čūlu veidošanās procesu. Arī invertētā CD4+/CD8+ šūnu attiecība un pieaugošs CD8+ šūnu skaits šķiet saistīts ar aftu patoģenēzi, jo čūlu veidošanās procesā ir iesaistītas CD8+ šūnas. Procesā var būt iesaistīts arī HLA-B51, kas nosakāms gan Behčeta slimības, gan aftozā stomatīta gadījumā. Šī darba mērķis ir izcelt un izskaidrot vīrusu iespējamo lomu aftu patoģenēzē. Darbs mēģina izskaidrot un atklāt, kurš vīruss pamatā ir iesaistīts slimības patoģenēzē un kā vīrusi var veicināt aftozas čūlas veidošanos mutes dobumā. Šis darbs galvenokārt koncentrējas uz ticamāko vīrusu etioloģiju, taču īsumā izskaidro arī citus iespējamos etioloģiskos faktorus, kas ir recidivējoša aftoza stomatīta pamatā.
Aphthous stomatitis is considered a multifactorial disorder, with different causative factors and agents behind it. These factors are genetics predisposition, systemic disorders, stress, anxiety, trauma, hormonal changes, vitamin and micronutrient deficiencies, and viral or bacterial infections. There is strong evidence that mucosal destruction is connected with immune response dysregulation, activated by unknown antigenic stimulation. The causative factor might be an endogenous antigen (autoimmune) or exogenous antigen (hyperimmune), or simply a trauma where chemical mediators are involved. T-lymphocytes, TNF-α, interferon-gamma, interleukins IL-2, IL-4, and IL-5, seem to play a crucial role. An incredibly high TNF-α level is firmly connected to aphthae's pathogenesis since it increases endothelial cell adhesion and promotes chemotaxis of neutrophils, starting ulcer formation. Inverted CD4+/CD8+ cells ratio, a growing number of CD8+ cells also seems to be associated with aphthae's pathogenesis since CD8+ cells are involved in ulcer formation. HLA-B51 found in both Behcet's disease and aphthous stomatitis may also be involved. This work intends to highlight and explain the possible role of viruses in the pathogenesis of aphthae. Trying to explain and discover which viral agent is primarily involved in the disease's pathogenesis and how they can contribute to oral aphthous ulcer formation. This work focused mainly on the most likely viral etiology, but it briefly explained other possible etiological factors behind recurrent aphthous stomatitis.
Aphthous stomatitis is considered a multifactorial disorder, with different causative factors and agents behind it. These factors are genetics predisposition, systemic disorders, stress, anxiety, trauma, hormonal changes, vitamin and micronutrient deficiencies, and viral or bacterial infections. There is strong evidence that mucosal destruction is connected with immune response dysregulation, activated by unknown antigenic stimulation. The causative factor might be an endogenous antigen (autoimmune) or exogenous antigen (hyperimmune), or simply a trauma where chemical mediators are involved. T-lymphocytes, TNF-α, interferon-gamma, interleukins IL-2, IL-4, and IL-5, seem to play a crucial role. An incredibly high TNF-α level is firmly connected to aphthae's pathogenesis since it increases endothelial cell adhesion and promotes chemotaxis of neutrophils, starting ulcer formation. Inverted CD4+/CD8+ cells ratio, a growing number of CD8+ cells also seems to be associated with aphthae's pathogenesis since CD8+ cells are involved in ulcer formation. HLA-B51 found in both Behcet's disease and aphthous stomatitis may also be involved. This work intends to highlight and explain the possible role of viruses in the pathogenesis of aphthae. Trying to explain and discover which viral agent is primarily involved in the disease's pathogenesis and how they can contribute to oral aphthous ulcer formation. This work focused mainly on the most likely viral etiology, but it briefly explained other possible etiological factors behind recurrent aphthous stomatitis.
Description
Zobārstniecība
Dentistry
Veselības aprūpe
Health Care
Dentistry
Veselības aprūpe
Health Care
Keywords
aphthae, aftozais stomatīts, atkārtots aftozais stomatīts, vīruss, patoģenēze, etioloģija, loma, cilvēka citomegalovīruss, herpes simplex vīruss, COVID-19, cilvēka imūndeficīta vīruss, vējbaku zoster vīruss un Epšteina Barra vīruss., aphthae, aphthous stomatitis, recurrent aphthous stomatitis, virus, pathogenesis, etiology, role, Human Cytomegalovirus, Herpes Simplex Virus, COVID-19, Human Immunodeficiency Virus, Varicella Zoster Virus and Epstein Barr Virus.