Some special long tubular glands can be found in the early growth stage of nasal polyps, and their structure, shape and size are completely different from those of normal serous mucus glands. Although there are several hypotheses about the pathogenesis of nasal polyposis, none of them can satisfactorily explain the histological origin of this long tubular gland.
At present, most scholars agree with the theory of epithelial rupture of nasal polyps. Tos et al. [17] have made a series of studies on the pathogenesis of nasal polyps since 1977. He speculated that the formation of polyps was originally due to the increased pressure of edema mucosa lamina propria, which led to epithelial rupture. Mucosal lamina propria protruded from the damaged area of epithelium, and mucosal epithelium grew toward the center through the damaged edge and tended to cover the damaged area. If the growth rate of regenerated epithelium is not enough to cover the protruding part, or the protruding part of the lamina propria of mucosa continues to grow, nasal polyps and their pedicles will be formed. If a small pedicled nasal polyp has been formed, the nasal polyp will not disappear even if the herniated part is completely epithelized. And because of gravity, polyps will continue to grow. In the process of epithelization and growth of nasal polyps, the above-mentioned long tubular glands will be formed at the same time, suggesting that nasal polyps are not just nasal mucosal hernia. In order to understand this hypothesis more thoroughly, Tos divides the formation of polyps into the following stages: ① Infiltration or inflammatory edema of nasal mucosa leads to increased tissue pressure, which in turn leads to epithelial injury, necrosis and rupture, and prolapse of lamina propria of mucosa; ② Epithelialization of hernia site; ③ Gland formation; ④ Polyps are enlarged and glands are elongated due to gravity; ⑤ The epithelium and matrix of mature nasal polyps have changed, such as the transformation from pseudostratified epithelium to stratified epithelium, the density of goblet cells and ciliated cells changed, the types of infiltrating cells changed, and the matrix became edema. The first two stages are difficult to be confirmed in human nose, but Tos et al. proved that epithelial cell necrosis did occur in the process of infection by establishing an experimental model of acute otitis media and long-term nasopharyngeal tube obstruction in rats [18].
Bernstein et al. [19,20] further developed the theory of epithelial rupture and formed a multi-factor theory. The content is that the aerodynamic changes of the lateral wall of the nasal cavity, bacteria, viruses and allergic diseases can all act on the mucosa of the lateral wall of the nasal cavity, causing inflammatory reactions of the mucosa. Then according to Tos et al's "epithelial rupture theory", epithelial rupture, mucosal hernia, re-epithelization, new gland formation and nasal polyps began. At this time, structural cells in nasal polyps, such as epithelial cells and fibroblasts, have the ability to synthesize GM-CSF and G-CSF messenger RNA. These two kinds of cell colony stimulating factors can promote the aggregation of eosinophils, mast cells and neutrophils in tissues. These inflammatory cells secrete a variety of inflammatory mediators, some of which can further promote their own secretion through positive feedback. Inflammatory reaction in nasal polyps can affect Na+, Cl? Ion transport, that is, cell Na+ absorption increases, Cl? Increased secretion. Finally, it leads to the increase of water entering cells and stroma, the edema of cells and stroma, and the maintenance and growth of nasal polyps