de Pizzol Júnior José Paulo, Sasso-Cerri Estela, Cerri Paulo Sérgio
Department of Morphology and Genetics, Federal University of São Paulo (UNIFESP), 04021-001 São Paulo, SP, Brazil.
Laboratory of Histology and Embryology-Araraquara, School of Dentistry, São Paulo State University (UNESP), 1680 Centro, CEP 14801⁻903 Araraquara, SP, Brazil.
Cells. 2018 Nov 10;7(11):206. doi: 10.3390/cells7110206.
The comprehension of dental pathogenesis and disorders derived from eruption failure requires a deep understanding of the molecular mechanisms underlying normal tooth eruption. As intense remodelling is needed during tooth eruption, we hypothesize that matrix metalloproteinase-1 (MMP-1) and acid phosphatase (ACP) play a role in the eruptive pathway degradation. We evaluated MMP-1-immunoexpression and the collagen content in the lamina propria at different eruptive phases. Immunohistochemistry and ultrastructural cytochemistry for detection of ACP were also performed. In the maxillary sections containing first molars of 9-, 11-, 13-, and 16-day-old rats, the birefringent collagen of eruptive pathway was quantified. MMP-1 and ACP-2 immunohistochemical reactions were performed and the number of MMP-1-immunolabelled cells was computed. Data were analyzed by one-way ANOVA and Tukey post-test ( ≤ 0.05). ACP cytochemistry was evaluated in specimens incubated in sodium β-glycerophosphate. In the eruptive pathway of 13- and 16-day-old rats, the number of MMP-1-immunolabelled cells increased concomitantly to reduction of collagen in the lamina propria. Enhanced ACP-2-immunolabelling was observed in the lamina propria of 13- and 16-day-old rats. Fibroblasts and macrophages showed lysosomes and vacuoles containing fragmented material reactive to ACP. MMP-1 degrades extracellular matrix, including collagen fibers, being responsible for the reduction in the collagen content during tooth eruption. The enhanced ACP activity at the mucosal penetration stage indicates that this enzyme plays a role in the degradation of remnant material, which is engulfed by macrophages and fibroblasts of the eruptive pathway. Therefore, enzymatic failure in the eruptive pathway may disturbs tooth eruption.
要理解因萌出失败导致的牙齿发病机制和紊乱，需要深入了解正常牙齿萌出背后的分子机制。由于牙齿萌出过程中需要进行强烈的重塑，我们推测基质金属蛋白酶-1（MMP-1）和酸性磷酸酶（ACP）在萌出途径的降解中发挥作用。我们评估了不同萌出阶段固有层中MMP-1的免疫表达和胶原蛋白含量。还进行了用于检测ACP的免疫组织化学和超微结构细胞化学。在含有9日龄、11日龄、13日龄和16日龄大鼠第一磨牙的上颌切片中，对萌出途径的双折射胶原蛋白进行了定量。进行了MMP-1和ACP-2免疫组织化学反应，并计算了MMP-1免疫标记细胞的数量。数据采用单因素方差分析和Tukey事后检验进行分析（≤0.05）。在β-甘油磷酸钠孵育的标本中评估ACP细胞化学。在13日龄和16日龄大鼠的萌出途径中，MMP-1免疫标记细胞的数量增加，同时固有层中的胶原蛋白减少。在l3日龄和16日龄大鼠的固有层中观察到ACP-2免疫标记增强。成纤维细胞和巨噬细胞显示含有对ACP有反应的碎片物质的溶酶体和液泡。MMP-1降解细胞外基质，包括胶原纤维，导致牙齿萌出过程中胶原蛋白含量减少。在黏膜穿透阶段增强的ACP活性表明该酶在残留物质的降解中起作用，这些残留物质被萌出途径的巨噬细胞和成纤维细胞吞噬。因此，萌出途径中的酶功能障碍可能会干扰牙齿萌出。
