PDF(Pubmed)
Abstract：
The olfactory epithelium (OE) is directly exposed to environmental agents entering the nasal cavity, leaving OSNs prone to injury and degeneration. The causes of olfactory dysfunction are diverse and include head trauma, neurodegenerative diseases, and aging, but the main causes are chronic rhinosinusitis (CRS) and viral infections. In CRS and viral infections, reduced airflow due to local inflammation, inflammatory cytokine production, release of degranulated proteins from eosinophils, and cell injury lead to decreased olfactory function. It is well known that injury-induced loss of mature OSNs in the adult OE causes massive regeneration of new OSNs within a few months through the proliferation and differentiation of progenitor basal cells that are subsequently incorporated into olfactory neural circuits. Although normal olfactory function returns after injury in most cases, prolonged olfactory impairment and lack of improvement in olfactory function in some cases poses a major clinical problem. Persistent inflammation or severe injury in the OE results in morphological changes in the OE and respiratory epithelium and decreases the number of mature OSNs, resulting in irreversible loss of olfactory function. In this review, we discuss the histological structure and distribution of the human OE, and the pathogenesis of olfactory dysfunction associated with CRS and viral infection.
摘要：
嗅觉上皮（OE）直接暴露于进入鼻腔的环境因素，使OSN容易受伤和变性。嗅觉功能障碍的原因多种多样，包括头部外伤，神经退行性疾病，和衰老，但主要原因是慢性鼻-鼻窦炎（CRS）和病毒感染。在CRS和病毒感染中，局部炎症导致气流减少，炎性细胞因子的产生，从嗜酸性粒细胞释放脱颗粒蛋白，细胞损伤导致嗅觉功能下降。众所周知，成年OE中损伤诱导的成熟OSN的丧失会在几个月内通过随后掺入嗅觉神经回路的祖细胞的增殖和分化导致新OSN的大量再生。尽管在大多数情况下受伤后恢复了正常的嗅觉功能，在某些情况下，长期的嗅觉障碍和嗅觉功能缺乏改善是主要的临床问题。OE的持续炎症或严重损伤会导致OE和呼吸道上皮的形态变化，并减少成熟OSN的数量。导致嗅觉功能不可逆的丧失。在这次审查中,我们讨论了人类OE的组织学结构和分布，以及与CRS和病毒感染相关的嗅觉功能障碍的发病机制。
