Norlander T, Fukami M, Westrin K M, Stierna P, Carlsöö B
Department of Otorhinolaryngology, Karolinska Institute, Huddinge Hospital, Sweden.
Otolaryngol Head Neck Surg. 1993 Sep;109(3 Pt 1):522-9. doi: 10.1177/019459989310900322.
Unilateral maxillary sinusitis was experimentally induced in New Zealand White rabbits with Streptococcus pneumoniae serotype 3, Bacteroides fragilis NCTC 9343, and Staphylococcus aureus V8. In another group of rabbits, sinusitis was induced by blocking of the sinus ostium only. Bacteriologic and light microscopic analysis was performed after 5 days to 1 month. Granulation-like polyps developed after deep mucosal inflammatory trauma initiating fibroblast proliferation, angiogenesis, and epithelial migration to cover the polyp. In regions of a more superficial trauma-characterized by epithelial desquamation and fibroblast growth-proliferation and differentiation of basal cells resulted in the formation of microcavities dissecting off edematous polyps. Polyps could be found in all sinusitis groups, irrespective of inducing agent. The cellular events of polyp formation appear to be the result of a continuous inflammatory reaction and are not directly related to the presence of a certain microorganism. Instead, the potential of any microorganism to induce a deep mucosal trauma or epithelial desquamation seems essential for its ability to initiate polyp formation.
用肺炎链球菌3型、脆弱拟杆菌NCTC 9343和金黄色葡萄球菌V8在新西兰白兔中实验性诱发单侧上颌窦炎。在另一组兔子中，仅通过阻塞鼻窦口诱发鼻窦炎。在5天至1个月后进行细菌学和光学显微镜分析。深层黏膜炎性创伤引发成纤维细胞增殖、血管生成和上皮迁移以覆盖息肉后，形成颗粒样息肉。在以浅表创伤为特征的区域——表现为上皮脱屑和成纤维细胞生长——基底细胞的增殖和分化导致形成分离水肿性息肉的微腔。在所有鼻窦炎组中均可发现息肉，与诱发剂无关。息肉形成的细胞事件似乎是持续炎症反应的结果，与特定微生物的存在无直接关系。相反，任何微生物诱发深层黏膜创伤或上皮脱屑的可能性似乎对其引发息肉形成的能力至关重要。
