A light microscopic study of odontoblastic and non-odontoblastic cells involved in tertiary dentinogenesis in well-defined cavitated carious lesions
A light microscopic study of odontoblastic and non-odontoblastic cells involved in tertiary dentinogenesis in well-defined cavitated carious lesions
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DOI：
10.1159/000016495
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发表时间：
1999-01-01
期刊：
影响因子：
4.2
通讯作者：
Darvann, T
中科院分区：
文献类型：
--
作者：
Bjorndal, L;Darvann, T
本研究检查了46个空洞病变薄的未矿化切片中的细胞和显微放射学结果，这些病变在临床上明确定义了病变活动性和提取时的估计病变年龄。表面破坏的进行性阶段范围从釉质空化到较大的牙本质暴露，分类为封闭和开放损伤环境。使用计算机图像处理软件测量以下参数：（a）原代成牙本质细胞的细胞质：细胞核比;（B）细胞：牙本质小管比;（c）相邻的前牙本质面积（μ m（2）），和（d）细胞质：非成牙本质细胞和次级成牙本质细胞样细胞的核比率，其中这些细胞类型的估计基于结构标准。在活动性釉质空洞病变中，注意到成牙本质细胞-前牙本质细胞区域减少和不明显的亚成牙本质细胞区域。在最初的牙本质暴露，非成牙本质细胞沿着牙髓牙本质界面观察。第三层牙本质的第一个迹象是在暴露牙本质的陈旧性病变中看到的。封闭/活动性病变中的第三牙本质比开放/进展缓慢的病变中的第三牙本质更不规则。在小的开放性/进展缓慢的病变中，管状三级牙本质中涉及的成牙本质细胞与初级成牙本质细胞相当，然而，也注意到新的牙本质小管呈现反应性和修复性牙本质形成之间的混合物。在闭合/活动性病变中，非初级成牙本质细胞排列在小管状三级牙本质上，而在较大的开放性病变中首先看到次级成牙本质细胞样细胞的明确信号，产生管状三级牙本质。总之，在晚期空洞病变中，外部病变环境与相应的三级牙本质的不同形成之间存在很强的关系。此外，还表明，刺激管状三级牙本质可能是一个密切相关的反应时，一个活跃的病变复杂的变化到一个缓慢进展的病变环境。
This study examines cellular and microradiographic findings in thin, undemineralized sections of 46 cavitated lesions, that were clinically well-defined with respect to lesion activity and estimated lesion age at extraction time. The progressive stages of surface breakdown ranged from enamel cavitation to larger dentine exposures classified as closed and open lesion environments, Measurements of the following parameters were performed using computerized image processing software: (a) the cytoplasm:nucleus ratio of primary odontoblast cells; (b) the cell:dentinal tubule ratio; (c) the adjacent predentine area (mu m(2)), and (d) the cytoplasm: nucleus ratio of non-odontoblastic cells, and secondary odontoblast-like cells, where estimation of these cell types were based on structural criteria. In active enamel cavitated lesions, reduced odontoblast-predentine regions and indistinct subodontoblastic regions were noted. During initial dentine exposures, non-odontoblastic cells along the pulp-dentinal interface were observed as well. The first indication of tertiary dentine was seen in old lesions with exposed dentine. The tertiary dentine appeared more atubular in the closed/active lesions than in the open/slow-progressing lesions. The involved odontoblastic cells in tubular tertiary dentine in small open/slow-progressing lesions were comparable to the primary odontoblast cells, however, new dentinal tubules were also noted presenting a mixture between reactionary and reparative dentinogenesis. In close/active lesions non-primary odontoblastic cells were aligning the atubular tertiary dentine, whereas well-defined sig ns of secondary odontoblast-like cells were fi rst seen in larger open lesions, producing tubular tertiary dentine. In conclusion, a strong relationship between external lesion environments and corresponding different formations of tertiary dentine was noted in advanced cavitated lesions. It is additionally suggested that the stimulation of tubular tertiary dentine could be a closely related reaction when an active lesion complex changes into a slower progressing lesion environment.