Effects of hypoxia on the proliferation, mineralization and ultrastructure of human periodontal ligament fibroblasts in vitro.
Effects of hypoxia on the proliferation, mineralization and ultrastructure of human periodontal ligament fibroblasts in vitro.
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DOI：
10.3892/etm.2013.1349
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发表时间：
2013-12
影响因子：
2.7
通讯作者：
Li CJ
中科院分区：
文献类型：
--
作者：
Zhang HY;Liu R;Xing YJ;Xu P;Li Y;Li CJ
本研究旨在探讨高原低氧对人牙周膜成纤维细胞（HPLFs）增殖、矿化及超微结构的影响，为高原低氧致牙周病的研究提供实验依据。采用组织培养法培养第5代HPLFs，分别分为轻度低氧组（5%O2）、中度低氧组（2%O2）、重度低氧组（1%O2）和对照组（21%O2）。分别于12、24、48、72 h检测细胞增殖和碱性磷酸酶（ALP）活性。观察重度缺氧组大鼠脑组织超微结构变化。HPLFs在缺氧12和24 h时随缺氧程度的增加生长迅速，重度缺氧组在24 h时增殖明显（P<0.05）。随着缺氧程度的增加，细胞生长在48和72 h受到抑制，中、重度缺氧组细胞生长受到明显抑制（P<0.05）。ALP活性在各时间点随缺氧程度的增加而受到抑制。重度缺氧组24 h、中、重度缺氧组48 h、72 h的限制作用明显（P<0.05）。而重度缺氧组在72 h时，上述限制更为明显（P<0.05）。重度缺氧24 h，线粒体和粗面内质网（RER）数量增多，膜结构完整，但略有扩张; 48 h时，线粒体数量和粗面内质网数量随线粒体体积增大而减少。此外，线粒体嵴模糊，粗面内质网结构紊乱。72 h线粒体嵴断裂，空泡变性，粗面内质网颗粒减少，溶酶体增多，线粒体和粗面内质网数量进一步减少。HPLF增殖和矿化受到抑制。中、重度缺氧组HPLF结构破坏时间较长。这一发现表明缺氧能够损害HPLF的代谢、重建和恢复。因此，缺氧条件下HPLFs的不良状态可能引发或加重牙周病。
This study aimed to investigate the effects of hypoxia on the proliferation, mineralization and ultrastructure of human periodontal ligament fibroblasts (HPLFs) at various times in vitro in order to further study plateau-hypoxia-induced periodontal disease. HPLFs (fifth passage) cultured by the tissue culture method were assigned to the slight (5% O2), middle (2% O2), and severe hypoxia (1% O2) groups and the control (21% O2) group, respectively. At 12, 24, 48 and 72 h, the proliferation and alkaline phosphatase (ALP) activities were detected. The ultrastructure of the severe hypoxia group was observed. HPLFs grew more rapidly with an increase in the degree of hypoxia at 12 and 24 h, and significant levels of proliferation (P<0.05) were observed in the severe hypoxia group at 24 h. Cell growth was restrained with an increase in the degree of hypoxia at 48 and 72 h, and the restrictions were clear (P<0.05) in the middle and severe hypoxia groups. ALP activity was restrained with increasing hypoxia at each time point. The restrictions were marked (P<0.05) in the severe hypoxia group at 24 h and in the middle and severe hypoxia groups at 48 and 72 h. However, the restriction was more marked (P<0.05) in the severe hypoxia group at 72 h. An increase was observed in the number of mitochondria and rough endoplasmic reticula (RER), with slightly expanded but complete membrane structures, in the severe hypoxia group at 24 h. At 48 h, the number of mitochondria and RER decreased as the mitochondria increased in size. Furthermore, mitochondrial cristae appeared to be vague, and a RER structural disorder was observed. At 72 h, the number of mitochondria and RER decreased further when the mitochondrial cristae were broken, vacuolar degeneration occurred, and the RER particles were reduced while the number of lysosomes increased. HPLF proliferation and mineralization was restrained. Additionally, HPLF structure was broken for a relatively long period of time in the middle and severe hypoxia groups. This finding demonstrated that hypoxia was capable of damaging the metabolism, reconstruction and recovery of HPLFs. The poor state of HPLFs under hypoxic conditions may therefore initiate or aggravate periodontal disease.
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影响因子：
3.8
作者：
Park, Hyun-Jung;Baek, Kyung Hwa;Baek, Jeong-Hwa
通讯作者：
Baek, Jeong-Hwa
DOI：
10.1152/ajpregu.00108.2009
发表时间：
2009-10-01
影响因子：
2.8
作者：
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作者：
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作者：
Mylonis, Ilias;Sembongi, Hiroshi;Simos, George
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