Pathogenesis of adhesive otitis media and study of mechanism of development into the pars tensa cholesteatoma

从我们对胆脂瘤中角质瘤（表皮）增殖、终末分化和凋亡的分子生物学研究来看，胆脂瘤是炎症恶性循环的结果。因此，对于胆脂瘤的治疗，要么完全去除胆脂瘤基质和碎片，要么切断恶性循环。首先，收缩袋内的迁移受到感染的干扰，然后炎症持续并导致角化细胞增殖。结果，角蛋白碎片堆积，表皮和上皮下组织被激活。各种细胞因子和其他因素参与了这一反应。除此之外，细胞因子的自分泌和旁分泌调节在胆脂瘤上皮的生长中起着关键作用。然而，胆脂瘤中角质形成细胞（表皮）的终末分化和凋亡与正常皮肤中仅有微小差异。我推测胆脂瘤表皮的过度增生是由终末分化和细胞凋亡的完整功能所补偿的，因此与恶性鳞状瘤相反，这种平衡得以保持。

From our molecular biological studies concerning proliferation, terminal differentiation and apoptosis of keratinocystes (epidermis) in cholesteatoma, cholesteatoma is a result of a vicious circle of inflammations. Therefore, the treatment for cholesteatoma is either complete removal of cholesteatoma matrix and debris or the cutting off of the vicious circle.First of all, migration in retraction pocket is disturbed by infection, then inflammation persists and leads to proliferation of keratinocytes. As a result, keratine debris accumulates and epidermis and subepithelial tissue are activated. Various cytokines and other factors are involved in this reaction. In addition to it, autocrine and paracrine regulation of cytokines plays a key role in the growth of cholesteatoma epithelium.However, there is only a slight difference between the terminal differentiation and apoptosis of keratinocytes (epidermis) in the cholesteatoma and those in the normal skin.I surmise that the hyperproliferation of cholesteatoma epidermis is compensated by the full function of terminal differentiation and apoptosis, thus the balance is retained as opposed to malignant squamous neoplasias.