慢性化脓性中耳炎及中耳胆脂瘤术前颞骨CT及耳内镜评估的意义

目的 探讨颞骨CT及耳内镜对慢性化脓性中耳炎静止期及中耳胆脂瘤术前评估的重要性。方法 回顾性分析慢性化脓性中耳炎静止期及中耳胆脂瘤患者42耳病历资料,从CT、耳内镜及术中发现进行分析。结果 ①根据CT结合术中所见,慢性化脓性中耳炎静止期CT分型分为单纯型、硬化灶型、肉芽型、硬化灶肉芽型。胆脂瘤型CT主要表现为听骨链消失或锤砧关节消失,乳突大部分呈硬化型,少部分为板障型,上鼓室鼓窦扩大,上鼓室、中鼓室甚至后鼓室乳突腔为软组织影占据,部分病例外半规管骨质破坏、面神经管水平段骨质破坏,部分病例外耳道后壁骨质破坏;单纯型CT示中耳鼓室乳突呈不完全气化型;硬化灶型CT示中耳鼓室乳突呈硬化型,病变局限于中鼓室,锤骨柄及镫骨周围有“类似骨质影”包裹;肉芽型、硬化灶肉芽型CT相似,示病变累及鼓室及乳突,听骨链基本完整,面神经管水平段骨质完整,但硬化灶型与肉芽型区别之处在于前者鼓室内听骨链周围有“类骨质”样散在高密度影。②耳内镜所见慢性化脓性中耳炎静止期鼓膜紧张部穿孔,鼓膜可有钙化斑;中耳胆脂瘤型则有上鼓室内陷或穿孔、后上象限穿孔、大穿孔、外耳道顶壁或后上壁下塌。结论 慢性化脓性中耳炎静止期及中耳胆脂瘤的术前CT及耳内镜评估,对病变性质、范围、程度及指导手术起重要作用。     

鼓室硬化豚鼠中耳黏膜电镜下超微结构特点

目的了解豚鼠鼓室硬化中耳黏膜电镜下的超微结构特点,以探讨豚鼠鼓室硬化的发病机理。方法健康杂色豚鼠8只为研究对象,其中,6只（8耳）行鼓室硬化造模,2只（4耳）为正常对照。鼓室硬化的造模方法为显微镜下经豚鼠鼓膜紧张部后下象限向鼓室内注射1×10^8个／L金黄色葡萄球菌液100μl,观察6个月以上,观察期间不给任何治疗。以显微镜下可见鼓膜穿孔边缘或鼓室腔有钙化斑为造模成功标准。取鼓室硬化造模成功豚鼠不同部位的中耳黏膜及正常豚鼠相应部位的中耳黏膜分别在电镜下观察其超微结构。结果正常豚鼠中耳黏膜胶原纤维少,纤维细胞形态大小正常,粗面内质网、线粒体形态正常,有线粒体嵴,无溶酶体。鼓室硬化中耳黏膜纤维细胞呈不规则变形、伸长、退变,细胞核深染呈卵圆形,核周的胞浆内有肿胀线粒体和变性溶酶体聚集,内质网扩张成囊状,黏膜下层细胞基质中含大量的胶原纤维,在基质胶原纤维束间有大量无定形的富含高密度电子的小体。结论豚鼠鼓室硬化中耳黏膜电镜下见胶原纤维显著增生,细胞基质小囊泡、胞内溶酶体、脂质颗粒内的磷脂结构均有钙化,但主要发生在细胞基质小囊泡。     

鼓室硬化症

鼓室硬化症是常见的引起传导性听力下降的中耳疾病之一,和慢性中耳感染密切相关,被认为是慢性化脓性中耳炎的后遗症,近年逐步受到关注,但引起鼓室硬化的具体原因、发病机制和预后转归尚不明确.本文主要就鼓室硬化症的临床诊疗现状做一总结.     

保留乳突的改良完壁式鼓室成形术的临床疗效观察

目的 探讨局限于上鼓室区病变的慢性化脓性中耳炎、中耳胆脂瘤行上鼓室径路保留乳突的改良完壁式鼓室成形术的长期临床疗效.方法 诊断慢性化脓性中耳炎、中耳胆脂瘤47例(47耳)患者,结合患者专科检查,依据手术方式不同分A、B两组,A组行上鼓室径路保留乳突的改良完壁式鼓室成形术,B组行完壁式乳突切开+鼓室成形术.术后随访5～7...     

巨噬细胞和骨形成蛋白2在鼓室硬化中的定位和表达

目的：检测巨噬细胞、骨形成蛋白2（BMP2）在鼓室硬化的中耳黏膜中的定位和表达,探讨巨噬细胞、BMP2在鼓室硬化发生机制中的作用。方法：选取17例鼓室硬化患者（鼓室硬化组）,以及17例年龄、性别、病程相匹配的单纯慢性化脓性中耳炎患者（中耳炎组）,应用免疫组织化学的方法检测病变黏膜的巨噬细胞标志CD68以及BMP2蛋白在两组标本的定位和表达情况。结果：两组中CD68阳性染色细胞均主要分布于黏膜下层中,黏膜层中仅有少量分布。两组阳性患者均为12例（70．59％）,两组患者的CD68阳性染色细胞数量无差别（P=0．79）,鼓室硬化组为6．94±6．08,中耳炎组为7．59±7．84。两组均有BMP2阳性染色细胞表达,BMP2蛋白广泛表达于中耳黏膜层、黏膜下层。两组的BMP2阳性染色细胞数及平均吸收度值均有显著差异（P〈0．01）。在鼓室硬化组中,钙化斑周围有巨噬细胞浸润和大量BMP2阳性着色,钙化斑周围的部分细胞同时有CD68和BMP2阳性着色。结论：巨噬细胞参与了鼓室硬化,可能通过分泌BMP2在鼓室硬化形成中起重要作用。     

慢性化脓性胆脂瘤型中耳炎的高分辨CT诊断

目的探讨高分辨CT(HRCT)对慢性化脓性中耳炎(胆脂瘤型)的诊断价值.方法对238例经手术及病理证实的中耳胆脂瘤的CT征象与手术所见进行对照研究.结果(1)CT诊断胆脂瘤的敏感性最高在上鼓室(81.25%),最低在乳突(50%).(2)CT显示胆脂瘤的病理改变为①鼓室乳突腔内胆脂瘤影;②胆脂瘤周低密度环;③鼓室乳突腔边缘骨质硬化;④鼓室乳突腔扩大;⑤听骨链破坏.结论CT检查对于中耳胆脂瘤的诊断及指导手术有很大帮助.     

慢性化脓性中耳炎鼓室硬化的临床分析

目的：探讨鼓室硬化在慢性化脓性中耳炎中的发生率、听力下降类型及听力下降与硬化灶部位和程度间的关系。方法：回顾性分析101例行手术治疗的慢性化脓性中耳炎患者的资料，所有患者均有完整的病史及耳鼻咽喉科体检，均行纯音测听检查，术中病灶均有详细记录。结果：慢性化脓性中耳炎患者鼓室硬化发生率为35．64％，大部分患者（77．78％）长期干耳，听力曲线为传导性聋。鼓膜硬化者中92．86％的患者气骨导间距小于40dB，而鼓膜与鼓室均有硬化者中45．45％的患者气骨导间距大于40dB。结论：鼓室硬化的听力损失与硬化灶的部位和程度直接相关。     

两种鼓室硬化造模方法的比较

目的 应用鼓膜切开法和鼓室接种细菌法构建鼓室硬化动物模型,观察两种方法造模后其鼓膜和鼓室粘膜的组织形态学变化.方法 40只SD大鼠分为4组,每组10只:A1组双耳鼓膜不作处理,作为正常对照;A2组双耳鼓膜紧张部后下象限作2 mm的切口;B1组双侧鼓室不作处理,作为正常对照;B2组双侧鼓室接种1×108 CFU/ml肺炎链球菌0.1 ml.分别于鼓膜切开后第2周及鼓室接种肺炎链球菌后第1、2、4、6、8周时观察各组大鼠鼓膜情况,比较鼓室硬化发生率;分别于造模后第2周和第8周取材行听泡连续切片HE染色,观察鼓膜及鼓室粘膜的组织形态学变化.结果 A2组14耳发生鼓膜钙化(14/20,70%);B2组死亡一只,6耳发生鼓膜钙化(6/18,33.33%),两组的鼓膜及鼓室粘膜均可观察到炎症细胞浸润及纤维组织增生,但B2组的改变更显著.两对照组(A1和B1组)既未发生鼓膜钙化,也未出现组织形态学改变.结论 两种鼓室硬化造模方法均切实可行,但鼓膜切开法操作更简单,成模周期更短,成模率更高.     

鼓室硬化患者中耳黏膜及硬化灶组织病理学特点

目的 了解鼓室硬化患者中耳黏膜及硬化灶的组织病理学特点,以进一步了解鼓室硬化的发病机理.方法 取68例鼓室硬化患者中耳不同位置的黏膜及硬化灶标本,分两组,一组68例予福尔马林固定,苏木精一伊红染色后于光镜下检查,另一组12例于电镜下观察.结果 鼓室黏膜内大量肉芽组织增生并炎症细胞浸润,黏膜下层见纤维化;硬化灶内可见密集的玻璃样变性的胶原纤维束和大量散在分布的钙化区,在某些区域还可见无血管的肉芽组织.电镜下见纤维细胞不规则变形、伸长、退变,嗜锇细胞质含有小囊泡及大量大小不等胶原纤维束,核周的胞浆内有聚集线粒体,胞内的小体中见大量富含高密度电子的钙质沉着,为纤维细胞的变性线粒体或溶酶体.结论 鼓室硬化患者中耳黏膜及硬化灶组织病理学表现为结缔组织纤维化、玻璃样变性、钙化.电镜下见胶原纤维显著增生,在纤维样变性的细胞内可见有富含电子的钙质沉着.     

经耳内镜慢性化脓性中耳炎手术中上鼓室隔分区比较研究

目的通过慢性化脓性中耳炎耳内镜手术中上鼓室隔分区比较研究,探讨以上鼓室隔为界的中耳分区方法对耳内镜下慢性化脓性中耳炎手术的指导意义。方法收集2017年1月至2017年6月于我科就诊的慢性化脓性中耳炎的患者69名(69耳)。所有的患者均进行术前听力学、颞骨HRCT检查,并根据患者术前颞骨HRCT分为中耳腔有阴影组和无阴影组,并对有阴影组的患耳病变区CT值进行测量。所有的患者均在耳内镜下手术。术中分别于以上鼓室隔为界的前下部分和后上部分取0.2×0.2cm2的粘膜标本,术后对收取的粘膜标本进行P物质(SP)免疫组化染色。结果有阴影组和无阴影组术前气骨导差、手术方式、前下部分和后上部分SP表达量均有统计学差异。结论通过对慢性化脓性中耳炎患者的术前颞骨HRCT、耳内镜手术中所见以及对术后不同分区粘膜SP免疫组化的病理学研究发现:以上鼓室隔为界的中耳前下和后上两部分无论是在CT、手术发现还是病理都表现出显著的差异性,为上鼓室隔分区方法在慢性化脓性中耳炎耳内镜手术中的应用提供了一定的指导意义。     

Experimentally induced otitis media with effusion following inoculation with the outer cell wall of nontypable Haemophilus influenzae

Previously, we extracted lipopolysaccaride endotoxin (LPS) from an axenic culture of Haemophilus influenzae and inoculated it into the middle ears of guinea pigs, inducing temporary serous effusions. In the present study, we tried to clarify whether the immunological mechanism responsible for producing the otitis media following outer cell wall inoculation was persistent. We extracted the outer cell wall from nontypable H. influenzae, using Zollinger's method, and inoculated extracts into the middle ears of guinea pigs that had previously received three injections of nonviable H. influenzae in Freund's complete adjuvant. Histological evaluations were performed from day 2 to day 24. Effusions and mucosal changes persisted for a longer time than in the LPS-inoculated model. Hypertrophied mucosae and increased numbers of goblet cells with hypersecretion were visible in the specimens on days 23-24. The condition seemed to show a greater similarity to chronic otitis media with effusion in children than did the LPS-inoculated model. We concluded that both the biological activity of the outer cell wall and immunological mechanisms might induce prolonged otitis media. We speculate that not only single middle ear infection but also general infections and repetitive middle ear infections may contribute to prolonged otitis media.     

Experimentally induced otitis media with effusion following inoculation with the outer cell wall of nontypable Haemophilus influenzae

Summary Previously, we extracted lipopolysaccaride endotoxin (LPS) from an axenic culture of Haemophilus influenzae and inoculated it into the middle ears of guinea pigs, inducing temporary serous effusions. In the present study, we tried to clarify whether the immunological mechanism responsible for producing the otitis media following outer cell wall inoculation was persistent. We extracted the outer cell wall from nontypable H. influenzae, using Zollinger's method, and inoculated extracts into the middle ears of guinea pigs that had previously received three injections of nonviable H. influenzae in Freund's complete adjuvant. Histological evaluations were performed from day 2 to day 24. Effusions and mucosal changes persisted for a longer time than in the LPS-inoculated model. Hypertrophied mucosae and increased numbers of goblet cells with hypersecretion were visible in the specimens on days 23–24. The condition seemed to show a greater similarity to chronic otitis media with effusion in children than did the LPS-inoculated model. We concluded that both the biological activity of the outer cell wall and immunological mechanisms might induce prolonged otitis media. We speculate that not only single middle ear infection but also general infections and repetitive middle ear infections may contribute to prolonged otitis media.     

Influence of nasal allergic reactions on the clearance of middle ear effusion

In order to investigate the influence of nasal allergic reactions on the clearance of middle ear effusion, an animal model of nasal allergy and otitis media with effusion was produced in the same guinea pigs simultaneously by passive sensitization with serum of homologous animals containing IgE antibodies (for nasal allergy) and by inoculation of immunocomplex into the tympanic cavity (for otitis media with effusion). Usually, middle ear effusion appeared within 2 to 3 days and disappeared within 7 to 9 days after the inoculation of immunocomplex. Three days after the inoculation of immunocomplex, intranasal antigen challenge was performed three times daily and continued until the animals were killed. Disappearance of middle ear effusion appeared to be delayed in animals in which nasal allergic reactions were induced. Middle ear effusion was not found in those ears that were not inoculated with immunocomplex. Findings of the present study indicate that IgE-mediated allergic reactions of the mucous membrane lining the nose, nasopharynx, and eustachian tube constitute a factor indicative of a chronic state of disease, rather than a cause of otitis media with effusion.     

Experimental otitis media induced by coagulase negative staphylococcus and its L-forms

In a previous study, we found 15% l-forms of bacteria (predominately coagulase negative staphylococci (CNS)) in ears which gave negative cultures by conventional methods. In this study, we used an animal model to test whether CNS and its l-forms can be pathogenic and whether l-forms have a crucial role in the tendency to secretory otitis media (SOM). We inoculated the tympanic bullas of guinea pigs, in 2 groups, with CNS and its l-forms (revertant forms). We observed that both CNS and its l-forms had the capability of causing infection. However, it was milder for the l-forms than CNS. We clearly noticed that on day 30 60% of the ears inoculated with l-forms had effusion and/or retraction of the tympanic membrane. These ears were histopathologically characterized by hypertrophied pseudostratified epithelium or stratified squamous epithelial metaplasia. The ears inoculated with the original form of CNS had only 16.66% effusion. On day 60 we observed similar findings. Thus, it might be proposed that l-forms could be responsible for chronic irritation to middle ear mucosa leading to SOM.     

Histo-morphological changes of eustachian tube of guinea pigs with effusion after being treated by pulmonary surfactant]

OBJECTIVE: To study the effect of pulmonary surfactant on otitis media with effusion in guinea pigs to find a new way to manage otitis media with effusion. METHODS: Nonviable heat-killed pneumococci (HKP) solution was inoculated into the middle ear cavity in guinea pigs via a transeardrum approach to set up a model of otitis media with effusion in guinea pigs. Seven days after being injected with pulmonary surfactant (PS) by transeardrum approach, ABR threshold and histomorphological changes of eustachian tube mucosa of guinea pigs were examined by light microscopy and scanning microscopy. RESULTS: Five days following inoculation of HKB serous effusion were present in the middle ear cavity of guinea pigs, but disappearance of light cone. Response (mean +/- s) threshold raised from (14.0 +/- 3.1) dB to (45.0 +/- 5.7) dB. The eustachian tube mucosa was thickened and lined eosin-stained structureless matter over mucosa, while cilia of eustachian tube mucosa irregularly arranged. Seven days after being treated by PS, serous effusion of tympanum was reduced or disappeared, and response threshold decreased from (45.0 +/- 5.7) dB to (23.5 +/- 6.3) dB. There was significantly difference between them (P < 0.001). Eustachian tube mucosa was thinned, Cilia of eustachian tube mucosa regularly arranged to the nasopharynx. CONCLUSION: Pulmonary surfactant plays a important role in otitis media with effusion of guinea pigs.     

实验性中耳积液中耳粘膜中纤维粘连蛋白及层粘连蛋白的免疫组化研究

目的探讨细胞外基质成分———纤维粘连蛋白（ｆｉｂｒｏｎｅｃｔｉｎ）和层粘连蛋白（ｌａｍｉｎｉｎ）在中耳积液时中耳粘膜增生中的作用。方法在内窥镜引导下３０只豚鼠行双侧咽鼓管管内烧灼，造成实验性中耳积液动物模型，以过氧化酶标记的链霉卵白素法（ｓｔｒｅｐｔａｖｉｄｉｎｐｅｒｏｘｉｄａｓｅ，ＳＰ）行中耳粘膜中纤维粘连蛋白、层粘连蛋白的检测。结果实验性中耳积液动物模型成功２８耳。免疫组化染色发现，中耳积液豚鼠纤维粘连蛋白和层粘连蛋白在中耳粘膜的表达比正常豚鼠增强，随着病变时间的延长，纤维粘连蛋白在增生中耳粘膜中的成纤维细胞上表达增多，层粘连蛋白在基底膜及新生血管内皮上表达明显。结论实验证实纤维粘连蛋白、层粘连蛋白在中耳积液时参与中耳粘膜的增生反应，这可能对解释中耳粘膜增生、中耳粘连的发生机理有一定意义。     

Topical application of calcium channel blockers to reduce the progression of experimentally induced myringosclerosis and tympanosclerosis

OBJECTIVES: This study aimed to evaluate the ability of topically applied calcium channel blockers (diltiazem) to reduce the progression of experimentally induced myringosclerosis and tympanosclerosis. STUDY DESIGN: Animal model. Experimental prospective study. METHODS: The study included 25 adult albino guinea pigs that were bilaterally myringotomized and inoculated with a suspension of Streptococcus pneumonia type 3. The right ears were treated with topical application of diltiazem, and the untreated left ears served as the control group. Otomicroscopy and remyringotomy were conducted every week. One animal was sacrificed after 1 week and the remaining at the end of 6 weeks. Temporal bones were dissected, and tympanic bullae were analyzed with light microscopy. RESULTS: The untreated control ears showed evidence of extensive myringosclerosis on otomicroscopy, and the ears treated with calcium channel blockers did as well although to a lesser degree. Under light microscopy, the lamina propria of both tympanic membranes and middle ear mucosae of the control group exhibited thicker (P < .1 and P < .05, respectively) and larger (P < .01 and P < .01, respectively) sclerotic tissue in comparison with the treatment group. CONCLUSION: The results suggest that calcium channel blockers had an influence in the prevention of tympanosclerosis.     

实验性中耳积液中耳粘膜中纤维粘连蛋白及层粘连蛋白的 …

探讨细胞外基质成分－纤维粘连蛋和层粘连蛋白在中耳积液时中耳粘膜增生中的作用。方法 在内窥镜引导下３０只豚鼠行双侧咽鼓管管内烧灼，造成实验性中耳积液动物模型以过氧化酶标记的链霉卵白素法行中耳粘膜中纤维粘连蛋白，层粘连蛋白的检测。     

Sensorineural hearing loss in experimental purulent otitis media due to Streptococcus pneumoniae

Sensorineural hearing loss (SNHL) has been described clinically following chronic otitis media with effusion, but to the best of our knowledge, no studies have demonstrated SNHL in an animal model of otitis media. Using the chinchilla model of pneumococcal otitis media, significant SNHL was demonstrated after purulent otitis media, especially at higher frequencies. Animals with otitis media received penicillin G procaine treatment for five days after otitis media with effusion (OME) was first documented; resolution of middle ear infection was confirmed by middle ear effusion culture in all animals. Both the inoculated and uninoculated ears were examined by tone burst-elicited compound action potential at threshold. The inoculated ear showed a marked hearing loss of 13 to 36 dB three to four days after OME was first documented; a hearing loss up to 24 dB persisted two to five weeks after inoculation. The change in the compound action potential was highly significant at all frequencies studied. Conductive losses were largely ruled out because there was no middle ear effusion at death and the tympanogram was normal. Purulent labyrinthitis was ruled out by histopathological study. These results indicate that purulent pneumococcal otitis media in the chinchilla model causes significant SNHL and suggest that the pathogenesis of SNHL associated with chronic OME in humans may be studied in this model.