【HIV感染口腔表现的免疫学原因:文献综述】。

Revista Cientifica Odontologica Pub Date : 2025-05-16 eCollection Date: 2025-04-01 DOI:10.21142/2523-2754-1302-2025-242
Dayanna Soledad Álvarez Zhapa, Ana Cristina Vásquez Palacios, Magdalena Molina Barahona
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引用次数: 0

摘要

人类免疫缺陷病毒患者由于C型逆转录病毒导致免疫抑制,可导致口腔系统的各种病理。这是由于宿主表现出的免疫缺陷,由全身和口腔细胞的改变引起,从而引起免疫反应的改变。CD4 T细胞、树突状细胞和巨噬细胞与病毒的DNA结合,作为病毒复制的位点和疾病的储存库,并发生凋亡。同样,先天免疫系统的其他细胞也会发生改变。这种免疫抑制导致机会性微生物伺机攻击,改变口腔,出现牙周病、念珠菌病、卡波西氏肉瘤等。方法:通过文献综述来确定2018年至2024年之间的相关信息。目的:本研究旨在描述HIV患者免疫系统的免疫抑制如何产生口腔表现。结论:发生在次级防线的免疫缺陷通常是口腔黏膜完整性丧失、免疫球蛋白等屏障以及牙周组织或上皮损伤的原因。这些可由病毒复制、炎症介质和免疫细胞凋亡引起。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

[Immunological Causes of Oral Manifestations of HIV Infection: A Literature Review].

[Immunological Causes of Oral Manifestations of HIV Infection: A Literature Review].

Introduction: Patients with human immunodeficiency virus experience immunodepression due to type C retrovirus, which can lead to various pathologies in the stomatological system. This occurs due to the immunodeficiency exhibited by the host, resulting from alterations in both systemic and oral cells, thus causing a modified immune response. CD4 T cells, dendritic cells, and macrophages bind to the virus's DNA and act as sites for viral replication and reservoir of the disease, and undergo apoptosis. Similarly, other cells of the innate immune system become altered. This immunosuppression leads to opportunistic microorganisms attacking opportunely, altering the oral cavity and presenting periodontal diseases, candidiasis, Kaposi's sarcoma, and others.

Methodology: A literature review was conducted to identify relevant information available between 2018 and 2024. Objective: The research aims to describe how immunosuppression of the immune system of a patient with HIV generates oral manifestations.

Conclusion: Immunodeficiency occurring in secondary lines of defense is usually the cause of the loss of oral mucosa integrity, barriers such as immunoglobulins, and damage to periodontal tissues or at the epithelial level. These can be caused by virus replication, inflammatory media, and the apoptosis of immune cells.

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