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[牙源性口腔局部疾病;自身免疫发病机制的胚胎学及临床病因]

[Odontostomatogenic focal disease; embryologic and clinical causes of autoimmune pathogenesis].

作者信息

Bonazzi P, Montanari G, Valentini A F

出版信息

Minerva Stomatol. 1980 Sep-Oct;29(5):363-71.

PMID:7005658
Abstract

The autoimmune pathogenesis of the focal odontostomatogenous disease is investigated and emphasis is laid on the different keys of interpretation: at embryologic, clinic and immunologic level. A special attention is paid to the primary meaning of structured or non structured lymphoid tissue of oropharynx, on account of embryologic identity with thymus and bursa of Fabricius, differentiating into sectors of ecto-entodermic stratification. The clinical evidence of the bursa-equivalent significance of Waldeyer ring, appears to lie in the ascertainment of the tonsillar atrophy in course of agammaglobulinaemia of Bruton type. The active chronic irritant phlogistic stimulus in a primary structure could excite the normal production of intolerant clones, so as to exceed the normal physiological homeostasis (giving rise to the autoimmune disease), or alter the mosiac self, inducing a production of autoantibodies.

摘要

研究了局灶性牙源性口炎的自身免疫发病机制,并强调了在胚胎学、临床和免疫学水平上不同的解释关键。特别关注口咽有结构或无结构淋巴组织的主要意义,因为其与胸腺和法氏囊在胚胎学上具有同一性,可分化为外胚层内胚层分层区域。咽淋巴环具有法氏囊等效意义的临床证据,似乎在于在布鲁顿型无丙种球蛋白血症过程中确定扁桃体萎缩。初级结构中的活性慢性刺激性炎症刺激可激发不耐受克隆的正常产生,从而超过正常的生理稳态(引发自身免疫性疾病),或改变镶嵌自身,诱导自身抗体的产生。

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