Shigeyama Y, Grove T K, Strayhorn C, Somerman M J
Department of Periodontics/Prevention/Geriatrics, School of Medicine, University of Michigan, Ann Arbor 48109-1078, USA.
J Dent Res. 1996 Sep;75(9):1650-7. doi: 10.1177/00220345960750090601.
Tooth resorption, a common feline dental problem, is often initiated at the cemento-enamel junction and hence is called cat 'neck' lesion. Studies have demonstrated that osteoclasts/odontoclasts are increased and activated at resorption sites, and that areas of resorption are partly repaired by formation of tissues resembling bone, cementum, and possibly dentin. However, the cellular/molecular mechanisms/factors involved in resorption and repair are unknown. In this study of tissues from cats with 'neck' lesions, we used specific antibodies and immunohistochemical analyses to examine adhesion molecules associated with mineralized tissues, bone sialoprotein (BSP) and osteopontin (OPN), and a cell-surface receptor linked with these molecules, alpha v beta 3, for their localization in these lesions. In addition, to determine general cellular activity during repair, we performed in situ hybridization using a type I collagen riboprobe. Results showed OPN localized to resorption fronts and reversal lines, while BSP was localized to reversal lines. However, some osteoclasts and odontoblasts "sat" on mineralized surfaces not associated with OPN. The cell-surface receptor, alpha v beta 3, was localized to surfaces of osteoclasts/odontoclasts. Type I collagen mRNA was expressed where osteoblasts attempted to repair mineralized tissue. In contrast, odontoblasts did not express mRNA for type I collagen. This study suggests that osteoclastic resorption is the predominant activity in 'neck' lesions and that this activity was accompanied, at least in part, by increased concentrations of OPN and an associated integrin, alpha v beta 3, at resorption sites. Lack of collagen expression by odontoblasts indicates that odontoblasts do not play an active role in attempts at repair.
牙齿吸收是一种常见的猫科动物牙齿问题,通常始于牙骨质-釉质界,因此被称为猫的“颈部”病变。研究表明,破骨细胞/破牙细胞在吸收部位增加并被激活,吸收区域部分通过形成类似骨、牙骨质以及可能还有牙本质的组织进行修复。然而,参与吸收和修复的细胞/分子机制/因素尚不清楚。在这项对患有“颈部”病变的猫的组织研究中,我们使用特异性抗体和免疫组织化学分析来检查与矿化组织相关的黏附分子、骨涎蛋白(BSP)和骨桥蛋白(OPN),以及与这些分子相关的细胞表面受体αvβ3在这些病变中的定位。此外,为了确定修复过程中的一般细胞活性,我们使用I型胶原核糖探针进行原位杂交。结果显示,OPN定位于吸收前沿和反转线,而BSP定位于反转线。然而,一些破骨细胞和成牙本质细胞“附着”在与OPN无关的矿化表面上。细胞表面受体αvβ3定位于破骨细胞/破牙细胞表面。I型胶原mRNA在成骨细胞试图修复矿化组织的部位表达。相比之下,成牙本质细胞不表达I型胶原mRNA。这项研究表明,破骨细胞吸收是“颈部”病变中的主要活动,并且这种活动至少部分伴随着吸收部位OPN和相关整合素αvβ3浓度的增加。成牙本质细胞缺乏胶原表达表明成牙本质细胞在修复尝试中不发挥积极作用。