Chen Po-Jung, Wang Ke, Lin Meng-Hsuan, Sharma Radhika, Kalajzic Zana, O'Brien Mara, Yadav Sumit
Department of Growth and Development, University of Nebraska Medical Center, 4000 East Campus Loop South, 68583-0740, Lincoln, NE, US.
Division of Orthodontics, University of Connecticut Health Center, Farmington, US.
Sci Rep. 2025 Jan 2;15(1):88. doi: 10.1038/s41598-024-84756-8.
Osteogenesis imperfecta (OI) is a fairly common generalized connective disorder characterized by low bone mass, bone deformities and impaired bone quality that predisposes affected individuals to musculoskeletal fragility. Periodontal ligament (PDL)-alveolar bone and PDL-cementum entheses' roles under OI conditions during physiological loading and orthodontic forces remain largely unknown. In addition, bisphosphonates (e.g., alendronate) are commonly used therapeutics for the treatment of OI. Our knowledge, in terms of the affects of alendronate treatment on the PDL entheses in OI is also far from complete. In this study, we identified craniofacial skeletal defects in an osteogenesis imperfecta (oim) murine model of OI. Relative to wild-type littermates, oim mice were found to have decreased skull length, cranial height/width/length, nose length, nasal length, and frontal length. Next, we discovered that oim mice exhibited defects in several dental structures, including short roots and decreased volumes of the alveolar bone, dentin, and cellular cementum. Further, we specifically investigated periodontal defects in the oim mice. Alveolar bone loss in oim mice was primarily associated with elevated bone resorption due to an increased osteoclast number, along with reduced bone formation related to increased sclerostin (SOST) expression. PDL fibers in oim mice were disrupted and discontinuous, while Sharpey's fibers at the PDL-bone entheses were reduced. Mechanism-based studies showed that catabolism of the PDL was elevated in oim mice, as revealed by an increase in MMP13 and CTSK expression. Meanwhile, the quality of the collagen fibers were impaired in oim mice due to a large accumulation of uncleaved collagen I fibers. With alendronate treatment, however, we could partially rescue these phenotypes. This study, for the first time, characterized periodontal defects in oim mice, detailed craniofacial defects and demonstrated the effectiveness of alendronate in partially restoring these defects.
成骨不全症(OI)是一种相当常见的全身性结缔组织疾病,其特征为骨量低、骨畸形和骨质量受损,使受影响个体易患肌肉骨骼脆弱症。在生理负荷和正畸力作用下,成骨不全症患者牙周韧带(PDL)-牙槽骨和PDL-牙骨质附着点的作用在很大程度上仍不清楚。此外,双膦酸盐(如阿仑膦酸盐)是治疗成骨不全症的常用药物。就阿仑膦酸盐治疗对成骨不全症患者牙周附着点的影响而言,我们的了解也还很不全面。在本研究中,我们在成骨不全症(oim)小鼠模型中发现了颅面骨骼缺陷。与野生型同窝小鼠相比,发现oim小鼠的颅骨长度、颅高/宽/长、鼻长、鼻腔长度和额长均减小。接下来,我们发现oim小鼠在几个牙齿结构上存在缺陷,包括牙根短以及牙槽骨、牙本质和细胞牙骨质体积减小。此外,我们专门研究了oim小鼠的牙周缺陷。oim小鼠的牙槽骨丢失主要与破骨细胞数量增加导致的骨吸收增加有关,同时与硬化蛋白(SOST)表达增加相关的骨形成减少。oim小鼠的牙周韧带纤维被破坏且不连续,而牙周韧带-骨附着点处的沙比纤维减少。基于机制的研究表明,oim小鼠牙周韧带的分解代谢增加,这通过基质金属蛋白酶13(MMP13)和组织蛋白酶K(CTSK)表达的增加得以体现。同时,由于未切割的I型胶原纤维大量积累,oim小鼠胶原纤维的质量受损。然而,通过阿仑膦酸盐治疗,我们可以部分挽救这些表型。本研究首次描述了oim小鼠的牙周缺陷,详细阐述了颅面缺陷,并证明了阿仑膦酸盐在部分恢复这些缺陷方面的有效性。