Faloni A P S, Sasso-Cerri E, Katchburian E, Cerri P S
Department of Morphology, School of Medicine, Federal University of São Paulo (UNIFESP/EPM), São Paulo, SP, Brazil.
J Periodontal Res. 2007 Jun;42(3):193-201. doi: 10.1111/j.1600-0765.2006.00932.x.
Bone is a mineralized tissue that is under the influence of several systemic, local and environmental factors. Among systemic factors, estrogen is a hormone well known for its inhibitory function on bone resorption. As alveolar bone of young rats undergoes continuous and intense remodeling to accommodate the growing and erupting tooth, it is a suitable in vivo model for using to study the possible action of estrogen on bone. Thus, in an attempt to investigate the possibility that estrogen may induce the death of osteoclasts, we examined the alveolar bone of estrogen-treated rats.
Fifteen, 22-d-old female rats were divided into estrogen, sham and control groups. The estrogen group received estrogen and the sham group received corn oil used as the dilution vehicle. After 8 d, fragments containing alveolar bone were removed and processed for light microscopy and transmission electron microscopy. Sections were stained with hematoxylin and eosin and tartrate-resistant acid phosphatase (TRAP)-an osteoclast marker. Quantitative analysis of the number of TRAP-positive osteoclasts per mm of bone surface was carried out. For detecting apoptosis, sections were analyzed by the Terminal deoxynucleotidyl transferase-mediated dUTP Nick-End Labeling (TUNEL) method; TUNEL/TRAP combined methods were also used.
The number of TRAP-positive osteoclasts per mm of bone surface was significantly reduced in the estrogen group compared with the sham and control groups. TRAP-positive osteoclasts exhibiting TUNEL-positive nuclei were observed only in the estrogen group. In addition, in the estrogen group the ultrastructural images revealed shrunken osteoclasts exhibiting nuclei with conspicuous and tortuous masses of condensed chromatin, typical of apoptosis.
Our results reinforce the idea that estrogen inhibits bone resorption by promoting a reduction in the number of osteoclasts, thus indicating that this reduction may be, at least in part, a consequence of osteoclast apoptosis.
骨骼是一种矿化组织，受到多种全身、局部和环境因素的影响。在全身因素中，雌激素是一种以抑制骨吸收功能而闻名的激素。由于幼鼠的牙槽骨会持续且剧烈地重塑以适应牙齿的生长和萌出，它是用于研究雌激素对骨骼可能作用的合适体内模型。因此，为了探究雌激素是否可能诱导破骨细胞死亡，我们检查了接受雌激素治疗的大鼠的牙槽骨。
将15只22日龄的雌性大鼠分为雌激素组、假手术组和对照组。雌激素组接受雌激素，假手术组接受用作稀释载体的玉米油。8天后，取出含有牙槽骨的碎片，进行光镜和透射电镜检查。切片用苏木精和伊红以及抗酒石酸酸性磷酸酶（TRAP）染色——一种破骨细胞标记物。对每毫米骨表面TRAP阳性破骨细胞的数量进行定量分析。为了检测细胞凋亡，通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法对切片进行分析；还使用了TUNEL/TRAP联合方法。
与假手术组和对照组相比，雌激素组每毫米骨表面TRAP阳性破骨细胞的数量显著减少。仅在雌激素组中观察到显示TUNEL阳性细胞核的TRAP阳性破骨细胞。此外，在雌激素组中，超微结构图像显示破骨细胞萎缩，细胞核有明显且扭曲的浓缩染色质团块，这是细胞凋亡的典型特征。
我们的结果强化了这样一种观点，即雌激素通过促进破骨细胞数量减少来抑制骨吸收，因此表明这种减少可能至少部分是破骨细胞凋亡的结果。
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