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In the viral productive cycle, the herpes virus genome is amplified 100- to 1000-fold by the viral replication machinery. El explorador no admite los marcos flotantes o no esta configurado actualmente para mostrarlos.
A proximidade entre a ATM e o ouvido pode ocasionalmente confundir o paciente sobre o local de origem da dor.
Cada indivíduo engole cerca de 2000 vezes por dia, o que gera o contato dos dentes superiores e inferiores. Por que, quando estou mais ansioso e estressado, sinto dores ao mastigar, ao falar e até ao acordar? Se não tiver osso suficiente, existem maneiras de aumentar a quantidade de osso disponível? Sempre que se alimentar, fazer o possível para lavar as dentaduras por meio de escovas macias. A coroa artificial, quando bem executada, corre os mesmos riscos que os dos dentes naturais, estando exposta aos mesmos acidentes. Ao perceber sangramento durante o uso do fio dental, devo suspender esse procedimento de limpeza?
Problemas psiquiátricos (certas psicoses e estados de ansiedade podem causar falta de saliva). Detection of human viruses in patients with chronic periodontitis and the relationship between viruses and clinical parameters. Reduced expression of gamma interferon in serum and marked lymphoid depletion induced by Porphyromonas gingivalis increase murine morbidity and mortality due to cytomegalovirus infection.
Advances in the pathogenesis of periodontitis: Summary of developments, clinical implications and future directions.
The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction.
Activation of interleukin 1b gene transcription by human cytomegalovirus- Molecular mechanisms and relevance to periodontitis. Real-time PCR quantification of cytomegalovirus in aggressive periodontitis lesions using TaqMan technology.
Human herpesvirus 7, Epstein-Barr virus and human cytomegalovirus in periodontal tissues of periodontally diseased and healthy subjects. Effect of prophylactic valacyclovir on the presence of human herpesvirus DNA in saliva of healthy individuals after dental treatment. Valtrex therapy for Epstein-Barr virus reactivation and upper respiratory symptoms in elite runners. O fator principal deve ser acompanhado dos fatores que contribuem, modificam ou perpetuam a doença.
Alguns fatores podem influenciar no sucesso do tratamento, como, por exemplo, o fumo e a diabetes, devendo ser avaliados previamente. Estudos demonstram que implantes de boa procedência apresentam taxas de sucesso acima de 90% no maxilar superior e 97%, no inferior.
Ao ser fixada sobre os dentes do paciente, previamente preparados para recebê-la, reabilita-o para mastigar, falar ou sorrir. Para dar maior resistência, pode-se utilizar estruturas internas de metal (ligas de ouro ou ligas alternativas).

Herpes virus transcription, genome replication, and capsid assembly occur in the host cell nucleus.
Todos esses aspectos fazem parte de um planejamento inicial realizado pelo profissional, que deve ser discutido abertamente com o paciente, antes do início do tratamento. Um bom tratamento de canal para esses casos evitaria problemas futuros que poderiam diminuir a durabilidade da prótese. A porcelana apresenta maior dureza e estabilidade de cor e supre melhor o quesito estético. The herpes virus replication cycle includes binding of viral envelope glycoproteins to cell-membrane receptors, internalization and dismantling of the virus particle, migration of the viral DNA to the cell nucleus, transcription of viral genes, assembly of the virion, and viral egress from the infected cell Herpes viruses destroy infected cells by active lytic replication. After primary infection, herpes viruses remain latent with limited expression of viral genes, albeit retaining the transcriptional and replicational capacity. Psychosocial and physical stress, hormonal changes, infections, immunosuppressive medication, and other events impairing cellular immunity can trigger herpes viral reactivation. Proinflammatory and anti-inflammatory balances controlled by different subsets of lymphocytes are thought to be crucial in the pathogenesis of periodontitis. Transforming growth factor-β1 in saliva seems also to have the potential to reactivate herpesviruses. Increased levels of proinflammatory cytokines in periodontal sites are associated with an enhanced risk of periodontal tissue destruction. The herpes virus-associated proinflammatory cytokines and chemokines can hamper the antibacterial host defence, stimulate bone-resorbing osteoclasts, upregulate matrix metalloproteinase, and downregulate tissue inhibitors of metalloproteinase, thereby impeding tissue turnover and repair and increasing the risk of periodontal tissue breakdown. Studies have reported that these viruses can infect and alter functions of polymorphonuclear leukocytes, lymphocytes, and macrophages and exert diminished ability to defend against bacterial challenge. This may potentiate the virulence of periodontopathogenic microbiota and dysfunction of polymorphonuclear leukocytes in periodontal sites can set the stage for overgrowth of periodontopathic bacteria and subsequent progression of destructive periodontal disease.
Herpes virus infection of periodontal sites may be important in a multistage pathogenesis by altering local host responses. Initially, bacterial infection of the gingival causes inflammatory cells to enter gingival tissue, with periodontal macrophages and T lymphocytes harboring latent HCMV and periodontal B lymphocytes harboring latent EBV.
EBV and cytomegalovirus can also infect and alter the functions of monocytes, macrophages, and lymphocytes in periodontitis lesions. Herpes virus-activating factors are also known risk factors⁄indicators for periodontal disease. Perhaps as result of a herpes virus periodontal infection, aggressive periodontitis lesions contain fewer overall viable cells, more T-suppressor lymphocytes and more B lymphocytes (EBV effect) than chronic periodontitis lesions or healthy periodontal sites.
Herpes virus proteins expressed on eukaryotic cell membranes may act as new bacterial binding sites.
It is conceivable that herpesviruses rely on coinfection with periodontal bacteria to produce periodontitis and, conversely, periodontopathic bacteria may depend on viral presence for the initiation and progression of some types of periodontitis.
EBV active infection can also generate anti-neutrophilic antibodies and neutropenia, and polyclonally stimulate the proliferation and differentiation of B lymphocytes.
Identification of viruses has traditionally been based on cell culture to detect characteristic cytopathic effects, morphologic determination of intracytoplasmic and intranuclear inclusion bodies, immunohistochemical techniques, immunoassays to identify viral antigens in clinical specimens, or the measurement of total or class-specific antibodies against specific viral antigens. The pathogenic mechanisms of herpes viruses cooperate in exacerbating disease, and probably for that reason, a periodontal dual infection with cytomegalovirus and EBV, or with cytomegalovirus and HSV, tends to occur in severe types of periodontitis. The era of relying upon in vitro cell culture for routine laboratory diagnosis of viral infections has truly passed.

Viral isolation indicates an active and possibly disease-producing infection, but isolation of viruses is difficult, costly, and time-consuming.
High-fidelity PCR-based techniques have become the standard for identification and quantification of periodontal herpes viruses, and the transcription of late herpes virus genes for structural proteins is understood to signify productive viral replication and is commonly used to indicate an active herpes virus infection. PCR identification of oral HSV may yield two- to fourfold more positive samples than viral culture.
HCMV and HSV can induce cell-mediated immunosuppression by reducing the cell surface expression of MHC (major histocompatibility complex) class I molecules, thereby interfering with T-lymphocyte recognition. HCMV can suppress antigen-specific cytotoxic T-lymphocyte functions, resulting in decreases in circulating CD4+ cells and increases in CD8+ suppressor cells, which in turn may lead to global impairment of cell-mediated immunity. HCMV infects periodontal monocytes⁄macrophages and T cells, and EBV infects B cells, [14] and since inflammatory cells have a lifespan of up to a few months, an extended periodontal presence of herpesviruses may require repeated influx of infected cells or, possibly, a herpes virus-mediated inhibition of apoptosis. Acute EBV infection and infectious mononucleosis can induce polyclonal B-lymphocyte activation with generation of anti-neutrophil antibodies and neutropenia. EBV-infected B lymphocytes may shed viral structural antigens that result in production of blocking antibodies, immune complex formation, and T-suppressor cell activation.
Mechanical debridement has suppressed subgingival EBV to undetectable levels in 12 of 21 patients, [23] and has decreased subgingival EBV genome copies by sixfold and subgingival cytomegalovirus genome copies by 38-fold. The decrease in post-treatment herpes virus counts is probably caused by a reduction in gingivitis and thus in the numbers of virally infected inflammatory cells. Similarly, the low herpes virus counts in healthy periodontal sites are probably the result of a virtual absence of infected inflammatory cells.Anti-herpes virus chemotherapy can also decrease the salivary viral load.
A short course of valacyclovir, 2 g twice on the day of treatment and 1 g twice the following day resulted in a significant decrease in the salivary occurrence of EBV compared with controls.
Acyclovir types of drugs are acyclic nucleoside analogues that inhibit herpes viral DNA polymerase and replication of the viral genome. The orally administered acyclovir prodrug, valacyclovir, can reach serum concentrations similar to those of intravenously administered acyclovir and is prescribed for a variety of herpes viral diseases. The notion of a herpes viral-bacterial coinfection in periodontitis may turn out to be the pathogenetic Rosetta stone that unlocks many of the intricacies of the disease. Herpes virus-induced periodontitis implies that anti-herpes virus immunity constitutes an important aspect of achieving a long-lasting state of stable periodontal conditions.
The development of herpes virus vaccines in the not too distant future makes the topic of periodontopathic herpes viruses particularly intriguing. Control of herpesviruses by vaccination may foreshadow a future with a diminishing role for the traditional periodontal therapies of surgery and antibiotics and offers hope for low-cost prevention of periodontitis in large groups of individuals. Periodontitis may develop stepwise in a series of simultaneous or sequential infectious disease events, including (i) a high herpes virus load (gingivitis level) in periodontal sites, (ii) activation of periodontal herpesviruses, (iii) an insufficient antiviral cytotoxic T-lymphocyte response, (iv) the presence of specific periodontal pathogenic bacteria, and (v) an inadequate antibacterial antibody response. In most individuals, these five suggested pathogenic determinants of periodontitis may collaborate in a detrimental constellation relatively infrequently and mainly during periods of suppressed cellular immunity.Herpes viruses play a major role as activators of the disease process in this model of periodontitis. Indeed, herpesviruses may be a key missing piece of the periodontopathogenetic jigsaw puzzle that would explain the transition from gingivitis to periodontitis or from stable to progressive periodontitis. It is hoped that the issues raised in this review will help to steer periodontal research into new fertile fields of investigation.

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