Pathways in external apical root resorption associated with orthodontia.

Pathways in external apical root resorption associated with orthodontia.
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DOI:
10.1111/j.1601-6343.2009.01458.x
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发表时间:
2009-08
影响因子:
3.1
通讯作者:
Hartsfield JK Jr
Hartsfield JK Jr
中科院分区:
医学3区
文献类型:
--
作者:
Hartsfield JK Jr

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综述在正畸治疗过程中遗传因素是否在根尖外根吸收(EARR)中起作用的研究。人类同胞的遗传力估计,多个近交系小鼠品系的比较,人类同胞对连锁和亲子三人组关联研究,以及两个基因(Il-1b和P2rx7)敲除小鼠模型。在正畸治疗的同时,上颌中切牙EARR的遗传度为0.8。DBA/2J、BALB/CJ和129P3/J近交系小鼠对与正畸力相关的组织学牙根吸收(RR)高度敏感(p<0.05),而A/J、C57BL/6J和SJL/J小鼠则具有抵抗力。非参数同胞对连锁分析确定了EARR与微卫星D18S64(与TNFRSF11A紧密连锁,也称为RANK)的连锁证据(LOD=2.5;p=0.02)。IL-1B(p=0.0003)、OPG(p=0.003)与EARR存在显著连锁不平衡。与野生型相比,I1b KO(p≤0.013)小鼠的RRAOF增加,而P2rx7 KO(p<0.02)小鼠的RRAOF增加。遗传因素在EARR与正畸力的同时起着显著的作用,占变异的一半到三分之二。这两条途径可能涉及:1)通过ATP/P2XR7/IL-1B炎症调控途径激活破骨细胞;2)RANK/RANKL/OPG激活控制破骨细胞激活。组织学RR发生,通常治愈。如果吸收超过愈合,那么就会发生EARR。正常和副功能的力量,以及正畸力,可能会增加个体的易感性,或与之相互作用,从而通过发生EARR的门槛。
To review studies investigating if genetic factors play a role in external apical root resorption (EARR) during orthodontic treatment. Heritability estimation in human sibpairs, comparison of multiple inbred mouse strains, human sib-pair linkage and parents-child trio association studies, and two gene (Il-1b, and P2rx7) knock out mouse models. Heritability for EARR of the maxillary central incisors concurrent with orthodontic treatment is 0.8. DBA/2J, BALB/cJ, and 129P3/J inbred mouse strains are highly susceptible (p < .05) to histological root resorption (RR) associated with orthodontic force (RRAOF), whereas A/J, C57BL/6J and SJL/J mice are resistant. Non-parametric sibling pair linkage analysis identified evidence of linkage (LOD = 2.5; p = 0.02) of EARR with microsatellite D18S64 (tightly linked to TNFRSF11A, also known as RANK). There is significant linkage disequilibrium of IL-1B (p = 0.0003), and OPG (p = 0.003) with EARR. RRAOF increases in Il1b KO (p ≤ 0.013), and increases in P2rx7 KO (p < 0.02) mice compared to wild-type. Genetic factors play a marked role in EARR concurrent with orthodontic force, accounting for one-half to two-thirds of the variation. Two pathways for this may involve: 1) activation control of osteoclasts through the ATP/P2XR7/IL-1B inflammation modulation pathway; and 2) RANK/RANKL/OPG osteoclast activation control. Histological RR occurs and is typically healed. If resorption outpaces healing, then EARR develops. Normal and parafunctional forces, as well as orthodontic forces, may add to or interact with the individual’s susceptibility to pass the threshold of developing EARR.
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