Seifert G, Donath K
HNO. 1977 Mar;25(3):81-92.
In view of the etiology and pathogenesis of the so-called Kütter tumor (chronic sialadenitis of the submandibular gland) gland resections of 349 patients (salivary gland register at the Institute of Pathology, University of Hamburg; period 165--1974) were analyzed pathohistologically. In 143 cases (41%) a sialolithiasis of the submandibular gland occurred simultaneously. Regarding the degree of the inflammation 4 stages were distinguished (stage 1 = focal sialadenitis; stage 2= diffuse lymphocytic sialadenitis with salivary gland fibrosis; stage 3 = chronic sclerosing sialadenitis with salivary gland sclerosis; stage 4= chronic progressive sialadenitis with salivary gland cirrhosis). Twenty-five per cent of the cases were classified in stage 1, 19% in stage 2, 38% in stage 3, and 18% in stage 4. A predominance of the male sex (70%) was observed especially in stage 4. The initial stage is characterized by a periductally lymphocytic infiltration, ectasias of the ducts, and alteration of the secret in the duct lumens (spheroliths, microliths). In stages 2--3 an increase of the inflammatory infiltration with lymph follicles, considerable alterations of the ducts (metaplasias, dysplasias, regenerates of the ducts), and a parenchymal reduction were found. This process is combined with an increase of the interstitial connective tissue and a cicatrication of the salivary gland parenchyma. In the final stage, 4, a cirrhotic gland transformation with progressive loss of the parenchyma and considerable duct destruction appeared. From the pathogenetic course of the inflammation and the comparison with other forms of sialadenitis, the conclusion is drawn that two etiologic factors are important in the Küttner tumor: an initial disturbance of secretion with an obstructive electrolyte sialadenitis and an immune reaction of the salivary duct system with the final phase of an obstructive, progressive immunosialadenitis.
鉴于所谓的库特氏瘤（下颌下腺慢性涎腺炎）的病因和发病机制，对349例患者（汉堡大学病理研究所涎腺登记处；1965 - 1974年期间）的腺体切除术进行了病理组织学分析。143例（41%）同时发生下颌下腺涎石病。根据炎症程度分为4期（1期 = 局灶性涎腺炎；2期 = 弥漫性淋巴细胞性涎腺炎伴涎腺纤维化；3期 = 慢性硬化性涎腺炎伴涎腺硬化；4期 = 慢性进行性涎腺炎伴涎腺肝硬化）。25%的病例为1期，19%为2期，38%为3期，18%为4期。尤其在4期观察到男性占优势（70%）。初期的特征是导管周围淋巴细胞浸润、导管扩张以及管腔内分泌物改变（球石、微石）。在2 - 3期，炎症浸润增加伴淋巴滤泡形成，导管出现明显改变（化生、发育异常、导管再生），实质减少。此过程伴有间质结缔组织增加和涎腺实质瘢痕形成。在最后阶段，即4期，出现腺体肝硬化转化，实质逐渐丧失，导管严重破坏。从炎症的发病过程以及与其他形式涎腺炎的比较得出结论，在库特氏瘤中有两个病因因素很重要：最初的分泌紊乱伴阻塞性电解质涎腺炎以及涎腺导管系统的免疫反应，最终发展为阻塞性、进行性免疫性涎腺炎。
