Craniofacial Research Center, Department of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital, Chang Gung University School of Medicine, Taoyuan 33305, Taiwan; Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA; State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Bone. 2018 Jul;112:212-219. doi: 10.1016/j.bone.2018.04.019. Epub 2018 Apr 25.
Aging is associated with a function decline in tissue homeostasis and tissue repair. Aging is also associated with an increased incidence in osteopenia and osteoporosis, but whether these low bone mass diseases are a risk factor for delayed bone healing still remains controversial. Addressing this question is of direct clinical relevance for dental patients, since most implants are performed in older patients who are at risk of developing low bone mass conditions. The objective of this study was to assess how an osteopenic/osteoporotic phenotype affected the rate of new alveolar bone formation. Using an ovariectomized (OVX) rat model, the rates of tooth extraction socket and osteotomy healing were compared with age-matched controls. Imaging, along with molecular, cellular, and histologic analyses, demonstrated that OVX produced an overt osteoporotic phenotype in long bones, but only a subtle phenotype in alveolar bone. Nonetheless, the OVX group demonstrated significantly slower alveolar bone healing in both the extraction socket, and in the osteotomy produced in a healed extraction site. Most notably, osteotomy site preparation created a dramatically wider zone of dying and dead osteocytes in the OVX group, which was coupled with more extensive bone remodeling and a delay in the differentiation of osteoblasts. Collectively, these analyses demonstrate that the emergence of an osteoporotic phenotype delays new alveolar bone formation.
衰老是组织稳态和组织修复功能下降的一个相关因素。衰老是导致骨质减少症和骨质疏松症发病率增加的一个相关因素，但这些低骨量疾病是否是骨愈合延迟的一个风险因素仍存在争议。解决这个问题对牙科患者具有直接的临床意义，因为大多数植入物都是在有发生低骨量疾病风险的老年患者中进行的。本研究的目的是评估骨质疏松/骨质疏松表型如何影响新牙槽骨形成的速度。通过去卵巢（OVX）大鼠模型，比较了拔牙窝和截骨愈合的速度与年龄匹配的对照组。影像学以及分子、细胞和组织学分析表明，OVX 在长骨中产生了明显的骨质疏松表型，但在牙槽骨中仅表现出轻微的表型。尽管如此，OVX 组在拔牙窝和愈合拔牙部位产生的截骨中，牙槽骨愈合明显较慢。最值得注意的是，截骨部位准备在 OVX 组中产生了一个更广泛的死亡和死骨细胞带，这与更广泛的骨重塑和成骨细胞分化延迟有关。综上所述，这些分析表明，骨质疏松表型的出现会延迟新的牙槽骨形成。
