One of the urgent problems of modern medicine is the high incidence of herpesvirus infections. The high prevalence of herpesviruses in the human population of the world allow us to consider herpes a common systemic disease of the whole organism. Doctors of any specialty are faced with the clinical manifestations of herpes infection in patients, and they themselves are a risk group of chronic herpes infections formation due to constant patient contacts and frequent professional psycho-emotional overload. Herpes infections are a group of infectious diseases caused by human herpesviruses. Now it is known 8 species of herpesvirus causing various human diseases that occur in the acute (during the initial contact with the infection) or chronic form. The herpesvirus family has a number of common properties that distinguish them from other human pathogenic viruses. There are three subfamilies in the Herpesviridae family. Alpha herpesviruses (Аlphaherpesvirinae) include the two serotypes of the herpes simplex virus (HSV-1 and HSV-2), and the varicella-zoster virus (herpes zoster). Beta herpesviruses (Betaherpesvirinae) include cytomegalovirus, human herpes viruses of types 6 and 7 (HHV-5, HHV-6, HHV-7). Gamma herpes viruses (Gammaherpesvirinae) include the Epstein-Barr virus, human herpesvirus type 8 (HHV-4, HHV-8). Clinical manifestations of herpes infection depend more on the immunity state of the infected organism than on the pathogenic properties of the pathogen itself, and develop only in conditions of immunodeficiency caused by various unfavorable factors. Herpesviruses are able to damage organs, weaken the body's immunity, creating conditions for the attachment of the other infections (fungal, bacterial), which in turn can cause organ damage. The herpesvirus ability to infect all organs and tissues of the body determines a significant clinical polymorphism of diseases, as well as the necessity to study various biological liquids. Herpesviruses can be transmitted from person to person by aerosol, contact, sexual and parenteral transmission, as well as from mother to fetus or newborn, they also can act as mutagens. The pathogenesis of herpesvirus infections is rather complex and not completely understood. For a proper understanding of the disease pathogenesis it is necessary to know the main stages of reproduction of human herpesviruses. Modern laboratory techniques are used for diagnosis of herpes infection and allow obtaining more complete information for an accurate diagnosis: virological method, electron microscopy method, the method of biological sample, the polymerase chain reaction methods for the detection of viral antigens, serological, immunological, cytological and histological methods. Conclusion. The high prevalence of diseases caused by herpes viruses, the complex, not fully understood pathogenesis and high contagiousness of diseases, as well as a variety of clinical manifestations of herpesvirus infections with the possibility of the formation of mixed forms with a blurred clinical picture dictate the need for a detailed study of herpes viruses and knowledge of methods for diagnosing herpes infections
The clinical manifestations of herpes infection depend on the pathogenic properties of the pathogen and on the state of immunity of the infected organism. Herpesviruses type 1-3 are predominantly neurotropic and cause diseases of the nervous system. The reproduction of the virus is carried out in the neurons of the nerve ganglia and epithelial cells, as they have a common ectodermal origin. Herpesviruses type 4, 5 and 8 are predominantly lymphotropic and cause diseases of the immune system. In a latent and persistent state, viruses are found in lymphocytes, monocytes, polymorphonuclear leukocytes, as they exhibit tropism for cells of mesenchymal origin. When the infection is reactivated, the virus is reproduced in cells of ectodermal origin, which leads to characteristic organ lesions. Type 6 and 7 viruses are both neurotropic and lymphotropic. They are capable to infect T-lymphocytes, B-lymphocytes, epithelial cells, endothelial cells, hepatocytes, fibroblasts, glial cells, stem cells, monocytes, macrophages, leukocytes, etc. They are able to promote the reactivation of other viruses, forming mixed forms, which leads to an aggravation of the clinical picture of the disease. Therapy of herpesvirus infections should be scientifically grounded, consistent, gradual, complex and include: specific antiviral treatment; immunotherapy; antibacterial therapy; detoxification therapy; symptomatic treatment and therapeutic measures aimed to eliminate various complications. Antiviral drugs for the treatment of herpes infection are divided into 4 groups: nucleoside analogs; drugs that cause the destruction of viruses located extracellularly; drugs that are active against intracellular viruses; drugs with a double effect. Modern therapy of herpesvirus infections is capable to suppress the reproductive activity of the reactivated virus, modulate the body's immune response, prevent and eliminate various complications of herpes infections, but is unable to affect the latent form of viruses. In the complex therapy of herpes infection, along with the specific treatment methods aimed to destroy the virus and to enhance the body's immunity, it is necessary to apply the entire range of therapeutic measures that help eliminate the accompanying symptoms and complications of diseases caused by herpesviruses
СтоматологіяУкраїнський журнал медицини, біології та спорту -Том 4, № 5 (21) 281Гаймориты одонтогенного происхождения занимают особое место в структуре воспалительных заболеваний челюстно-лицевой области, поскольку их лечение требует междисциплинарного подхода. По данным различных авторов, доля одонтогенного гайморита занимает от 10 до 75,0% среди всех случаев верхнечелюстного синусита.Распространенность стоматогенных гайморитов неуклонно возрастает. Причиной этому может быть сложная анатомическая структура моляров верхней челюсти и необоснованное расширение показаний к их сохранению.Мезиально-щечные корни верхних моляров имеют большое число вариаций строения системы корневых каналов. Упущенный из виду при первичном эндодонтическом лечении канал МБ2 может стать причиной одонтогенного синусита. Каналы МБ1 и МБ2 сообщаются между собой, то есть если МБ1 инфицирован, то МБ2будет инфицирован также. Несмотря на то, что вход в канал находится под слоем дентина и его обнаружение в большинстве случаев затруднено, для успешного эндодонтического лечения апикальной патологии нахождение и обработка МБ2 является необходимым условием.Пациент с одонтогенным гайморитом должен находиться одновременно под наблюдением ЛОРспециалиста и врача-стоматолога-терапевта. Применение компьютерной томографии и увеличения в стоматологии имеют большое значение для идентификации и локализации анатомически сложного канала МВ2, что повышает качество первичного эндодонтического лечения и уменьшает вероятность развития одонтогенных синуситов.Ключевые слова: одонтогенный гайморит, мезиобуккальный канал МБ2, верхнечелюстные моляры, повторное эндодонтическое лечение.Связь работы с научными программами, планами, темами. Представленная публикация является частью НИР «Характер, структура та лікування основних стоматологічних захворювань», № гос. регистрации 0116U004975.Введение. Гаймориты одонтогенного происхождения занимают особое место в структуре воспалительных заболеваний челюстно-лицевой области, поскольку их лечение требует междисциплинарного подхода. По данным различных авторов, доля одонтогенного гайморита занимает от 10 до 75,0% среди всех случаев верхнечелюстного синусита [2,9,10,11].Распространенность стоматогенных гайморитов неуклонно возрастает. Количество больных, поступивших в лор-стационары за последние 4 десятилетия, увеличилось с 4% до 15-40% [8]. Причиной этому может быть сложная анатомическая структура моляров верхней челюсти и необоснованное расширение показаний к их сохранению. Мезиально-щечные корни верхних моляров имеют большое число вариаций строения системы корневых каналов. Во многих исследованиях сообщается о высокой частоте встречаемости второго мезиобуккального канала (МБ2) в верхних молярах. Так, при изучении 1732 стандартно пролеченных верхних моляров [12] было отмечено, что МБ2 был найден в 73,2% случаев в первых молярах, в 50,7% случаев во вторых молярах и в 20% случаев в третьих молярах. Из них оказалось, что МБ2 был отдельным каналом в 54,9% первых моляров и в 45,6% вторых моляров и сливался с другим каналом (МВ1) во все...
Lesions of the oral mucosa may be a sign of systemic human diseases. Most of manifested in the oral cavity diseases are benign, but it is necessary to differentiate them from more serious diseases. Dentists should know the manifestations and recent advances in the diagnosis and treatment of oral diseases, among which are viral infections, especially highly contagious, which include hand-foot-and-mouth disease. In order to prevent its spread and to identify in time possible complications, dentist should have deep knowledge about it. Hand-foot-and-mouth disease is a highly contagious viral infectious disease caused by various enteroviruses. Viruses of the genus Enterovirus are RNA genomic. It is necessary to know the main stages of the reproduction of RNA genomic viruses in the human body. 1. Adsorption on a cell (adhesion) – an interaction between specific receptors of virions and surface molecules of sensitive cells. 2. Penetration into the cell and "undressing" can be carried out in two ways: endocytosis and translocation. 3. The synthesis of viral particles of RNA-viruses (translation) – as a result specific proteins for viral replication are synthesized. 4. Complete assembly of RNA-viruses. 5. Release of daughter virions from the cell. The source of infection can be both a sick person and a virus carrier. Asymptomatic carriage can last for weeks, sometimes months. The most intense pathogen is released in the first days of the disease. The predominant morbidity of children speaks about the high natural susceptibility of a human. For diseases, which are caused by enteroviruses, polymorphism of clinical manifestations is specific. In most cases, the violation of the general condition is insignificant and the course of the disease is benign. The initial phase is usually followed by enanthema and erythematous, papular or vesicular lesions of the skin, localized mainly on the palms and soles, as well as vesicles in the oral cavity. Enanthema usually precedes the appearance of a skin rash. Oral lesions may occur without skin symptoms. Diagnosis of enteroviral vesicular stomatitis is based on anamnestic and clinical data. There are many diagnostic tests available, but PCR of throat and vesicular fluid swabs, if available, is one of the most effective. After an illness, in most cases, immunity is formed, the possibility of developing cross-immunity to other types of the virus is not excluded
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