Mineral trioxide aggregate (MTA) inhibits osteoclastogenesis and osteoclast activation through calcium and aluminum activities.
Mineral trioxide aggregate (MTA) inhibits osteoclastogenesis and osteoclast activation through calcium and aluminum activities.
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矿物三氧化物骨料（MTA）通过钙和铝活性抑制破骨细胞生成和破骨细胞活化。
DOI：
10.1007/s00784-020-03483-2
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发表时间：
2021-04
影响因子：
3.4
通讯作者：
Kawai, Toshihisa
中科院分区：
文献类型：
--
作者：
Berto Rezende, Taia Maria;Ribeiro Sobrinho, Antonio Paulino;Vieira, Leda Quercia;da Costa Sousa, Mauricio Goncalves;Kawai, Toshihisa
评价MTA对体外rankl介导的破骨细胞依赖骨吸收事件的影响，以及Ca2+和Al3+对MTA抑制破骨细胞生成的影响。两种类型的破骨细胞前体，RAW 264.7 （RAW）细胞系或骨髓细胞（从BALB/c小鼠获得并用重组(r) M-CSF刺激），用或不加RANKL，用或不加MTA刺激6至8天。制备白Angelus MTA和Bios MTA （Angelus, Londrina, paran<e:1>，巴西），分别插入毛细管（直接接触面= 0.50mm2和0.01mm2）。MTA对这些类型破骨细胞前体的影响通过成熟破骨细胞分化的抗酒石酸酸性磷酸酶（TRAP）阳性多核细胞（RAW细胞和骨髓细胞）数量、TRAP酶活性（RAW细胞）、cathepsin K基因表达（RAW细胞）和再吸收坑形成（RAW细胞）来测量。此外，还用Ca2+和Al3+刺激RAW细胞，以评估这些分子对MTA抗破骨细胞潜能的影响。在骨髓和RAW细胞中，与不加MTA的对照rRANKL刺激相比，MTA的存在显著抑制了rRANKL诱导的TRAP阳性成熟破骨细胞数量（p<0.05）， TRAP酶活性降低（p<0.05）， cathepsin K基因表达降低（p<0.05）。而与成熟破骨细胞对照，MTA孵育的成熟破骨细胞牙本质吸收面积显著减少（p<0.05）。Ca2+和Al3+处理的rrankl刺激的RAW细胞减少了破骨细胞的数量。此外，氧化铝是破骨细胞生成过程的主要抑制因子。MTA显著抑制rankl介导的破骨细胞生成、破骨细胞活性，因此似乎能够抑制根尖周围病变中的骨吸收事件。这一过程可能与Ca2+和Al3+活性有关。MTA是一种重要的世界性生物材料。了解其对破骨细胞的分子活性可能有助于提高对其有效临床效果的认识。
To evaluate the effect(s) of MTA on in vitro RANKL-mediated osteoclast dependent bone resorption events and on the influence of Ca2+ and Al3+ on the osteoclastogenesis inhibition by MTA. Two types of osteoclast precursors, RAW 264.7 (RAW) cell line or bone marrow cells (obtained from BALB/c mice and stimulated with recombinant (r) M-CSF), were stimulated with or without RANKL, with or without MTA for 6 to 8 days. White Angelus MTA and Bios MTA (Angelus, Londrina, Paraná, Brazil) were prepared and inserted into capillary tubes (direct contact surface = 0.50mm2 and 0.01mm2). Influence of MTA on these types of osteoclast precursors was measured by the number of differentiated tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells (RAW and bone marrow cells), TRAP enzyme activity (RAW cells), cathepsin K gene expression (RAW cells) and resorptive pit formation (RAW cells) by mature osteoclasts. Besides, RAW cells were also stimulated with Ca2+ and Al3+ to evaluate the influence of these molecules on MTA anti-osteoclastogenic potential. In bone marrow and RAW cells, the number of TRAP-positive mature osteoclast cells induced by rRANKL was significantly inhibited by the presence of MTA compared to control rRANKL stimulation without MTA (p<0.05), along with the reduction of TRAP enzyme activity (p<0.05) and the low expression of cathepsin K gene (p<0.05). In contrast, to control mature osteoclasts, the resorption area on dentin was significantly decreased for mature osteoclasts incubated with MTA (p<0.05). rRANKL-stimulated RAW cells treated with Ca2+ and Al3+ decreased the number of osteoclasts cells. Besides, the aluminum oxide was the dominant suppressor of the osteoclastogenesis process. MTA significantly suppressed RANKL-mediated osteoclastogenesis, osteoclast activity and, therefore, appears able to suppress bone resorptive events in periapical lesions. This process might be related to Ca2+ and Al3+ activities. MTA is an important worldwide biomaterial. The knowledge about its molecular activities on osteoclasts might contribute to improving the understanding of its effective clinical results.
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影响因子：
14
作者：
Granchi, D;Amato, I;Giunti, A
通讯作者：
Giunti, A
影响因子：
5
作者：
De Deus, G;Ximenes, R;Coutinho, T
通讯作者：
Coutinho, T
影响因子：
4.2
作者：
Perez-Amodio, S.;Jansen, D. C.;Everts, V.
通讯作者：
Everts, V.
影响因子：
10.5
作者：
Dougall, WC;Glaccum, M;Schuh, J
通讯作者：
Schuh, J
影响因子：
14
作者：
Granchi, D;Ciapetti, G;Giunti, A
通讯作者：
Giunti, A