Departamento de Odontopediatria e Ortodontia, Faculdade de Odontologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Department of Anatomy, University of Otago, Dunedin, New Zealand.
Bone. 2018 May;110:160-169. doi: 10.1016/j.bone.2018.01.032. Epub 2018 Jan 31.
The underlying causes of maxillary bone loss during lactation remain poorly understood. We evaluated the impact of lactation on physiological and mechanically-induced alveolar bone remodeling. Nulliparous non-lactating (N-LAC) and 21-day lactating (LAC) mice underwent mechanically-induced bone remodeling by orthodontic tooth movement (OTM). Micro-computed tomography (microCT) was performed in the maxilla, femur and vertebra. Tartrate-resistant-acid phosphatase (TRAP) and Masson's trichrome labelling was performed in the maxillary bone and gene expression was determined in the periodontal ligament. The effect of prolactin on osteoclast (OCL) and osteoblast (OBL) differentiation was also investigated in N-LAC and LAC mice. Lactation increased alveolar bone loss in the maxilla, femur and vertebra, while OTM was enhanced. The number of OCL and OBL was higher in the maxilla of LAC mice. OTM increased OCL in both groups; while OBL was increased only in N-LAC but not in LAC mice, in which cell numbers were already elevated. The alveolar bone loss during lactation was associated with increased expression of receptor activator of nuclear factor-KappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) in the maxilla. OTM induced the same responses in N-LAC mice, whereas it had no further effect in LAC mice. Lactation enhanced differentiation of OCL and OBL from bone marrow cells, and prolactin recapitulated OCL differentiation in N-LAC mice. Thus, lactation increases physiological maxillary bone remodeling and OTM, and both require activation of RANK/RANKL/OPG system. These findings expand our knowledge of lactation-induced osteopenia and have possible impact on clinical practice regarding orthodontic treatments and dental implants in lactating women.
哺乳期上颌骨丢失的潜在原因仍知之甚少。我们评估了哺乳期对生理和机械诱导的牙槽骨重塑的影响。未产非哺乳期（N-LAC）和 21 天哺乳期（LAC）小鼠通过正畸牙齿移动（OTM）经历了机械诱导的骨重塑。在上颌骨、股骨和椎骨中进行了微计算机断层扫描（microCT）。在上颌骨中进行了抗酒石酸酸性磷酸酶（TRAP）和 Masson 三色染色标记，并在上颌骨牙周韧带中确定了基因表达。还在 N-LAC 和 LAC 小鼠中研究了催乳素对破骨细胞（OCL）和成骨细胞（OBL）分化的影响。哺乳期增加了上颌骨、股骨和椎骨的牙槽骨丢失，同时 OTM 增强。LAC 小鼠上颌骨中的 OCL 和 OBL 数量较高。OTM 增加了两组的 OCL；而 OBL 仅在 N-LAC 中增加，而在 LAC 小鼠中未增加，后者的细胞数量已经升高。哺乳期期间的牙槽骨丢失与上颌骨中核因子-KappaB 受体激活剂（RANK）、RANK 配体（RANKL）和骨保护素（OPG）表达增加有关。OTM 在 N-LAC 小鼠中引起了相同的反应，而在 LAC 小鼠中则没有进一步的作用。哺乳期增强了骨髓细胞中 OCL 和 OBL 的分化，催乳素在 N-LAC 小鼠中再现了 OCL 的分化。因此，哺乳期增加了生理上颌骨重塑和 OTM，两者都需要激活 RANK/RANKL/OPG 系统。这些发现扩展了我们对哺乳期引起的骨质疏松症的认识，并可能对哺乳期妇女的正畸治疗和牙种植体的临床实践产生影响。
