兔鼻窦炎模型骨质重塑的组织学观察

Histopathological observation of bone remodeling in rabbit sinusitis model

目的评估兔鼻窦炎模型造模不同时段骨质变化的病理学表现及其与时间的相关趋势，探讨骨质重塑在鼻窦炎发病机制中的作用。方法应用慢性鼻-鼻窦炎患者上颌窦穿刺液进行细菌培养，分离出金黄色葡萄球菌制造兔鼻窦炎模型，根据造模时间将实验组分为A（2～4周）、B（6—8周）、C（12周）3组，每组8只，健康对照组4只。在特定造模时间收集鼻窦标本，石蜡包埋、进行HE、Masson和AB—PAS以及碱性磷酸酶和抗酒石酸酸性磷酸酶染色。首先对接种侧和未接种侧上颌窦骨质进行重塑评分；然后以黏膜厚度、黏骨膜厚度、成骨细胞密度和破骨细胞数量为指标对接种侧上颌窦骨质进行定量和半定量评估。结果3组动物接种侧上颌窦骨质重塑评分分别为2．250、2．875、2．875分，未接种侧分别为1．625、2．250、2．500分。A组黏膜厚度、黏骨膜厚度、成骨细胞密度（x^-±s，下同）分别为（143．75±8．76）μm、（15．00±1．31）μm、（42．50±8．45）个／500μm，与对照组的（60．00±2．94）μm、（5．75±0．58）μm、（5．00±0．82）个／500μm相比，差异均有统计学意义（P值均〈0．05）；B组黏膜厚度、成骨细胞密度分别为（268．75±11．26）μm、（135．00±23．90）个／500μm，与A组相比差异具有统计学意义（P值均〈0．05）；C组和B组相比，黏膜厚度、黏骨膜厚度、成骨细胞密度3项指标差异均无统计学意义。结论细菌性鼻窦炎可以引起鼻窦骨质重塑，早期以破坏为主，随时间延长增生逐渐占主要地位，提示骨质重塑为鼻窦炎的基本病理特征之一，且为病变迁延或慢性化的原因。

Objective To observe the histopathological finding of bone remodeling in rabbit sinusitis model at different time and the tendency, and to discuss the effect of bone in the pathogenesis of sinusitis. Methods First, the rabbit sinusitis model was made, then the experimental animals were divided into 3 groups according to the time of infection. There were 8 rabbits in each experimental group, and 4 rabbits in the control group. The sinus specimen were collected, embedded and stained. The bone in the inoculating side and noninoculating side was scored, and the bone in inoculating side was evaluated quantitatively and semiquantitatively. The parameters included the thickness of mucosa, mucoperiosteum, the density of osteoblast, the amount of osteoclast. Results The average bone score in the inoculating side was 2. 250,2. 875,2. 875 ; in the noninoculating side was 1. 625,2. 250,2.500. Between group A and the control group, the difference of all three parameters had statistical significance. Between group B and group A, the difference of the thickness of mucosa and the density of osteoblast had statistical significance. Between group C and group B, none of the three parameters had statistical significance. Conclusions Bacterial sinusitis can lead to bone remodeling, obvious bone destroy can occur at the early phase, then the bone proliferation follows. These results demonstrate that bone remodeling is one of the basic bistopathological characters of CRS and might be the reason to lead CRS to a constant and chronic process of inflammation.