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Objective@#To investigate the features of alveolar bone morphology of mandibular central incisors in high-angle adult females using cone-beam computed tomography (CBCT) and evaluate the influence of aging in these patients.@*Methods@# CBCT and lateral cephalometric images of 142 untreated adult female patients were selected and grouped by facial growth pattern. The number of high-angle cases was increased to 164 to further explore the difference within high-angle adult females who were divided into two groups according to age. The indexes of alveolar bone height and thickness in the lower incisor region and inclination of the lower incisors were measured by Dolphin software. The data was statistically analyzed.@*Results@#Compared with the average-angle group, the high-angle group had a lower alveolar bone attachment level (P < 0.05) and less bone thickness at the root apex level (P < 0.05). The thickness of lingual alveolar bone decreased with labial inclination of the lower incisors in both the high-angle and average-angle groups (r = -0.251, P = 0.025; r = -0.428, P = 0.001, respectively). In hyperdivergent female patients, the middle-aged group had a lower attachment level of alveolar bone than the young group (P < 0.05), but no significant difference in bone thickness at the root apex level (P > 0.05) was found between the two groups@*Conclusion @# High-angle adult females had thinner mandibular anterior alveolar bone with significantly lower attachment levels. Aging and inclination of lower incisors influenced bone morphology and should be taken into careful consideration.
RESUMO
@#Mesenchymal stem cells (MSCs) are capable of self-replication and multi-directional differentiation, which are very important for the development and reconstruction of mesenchymal tissue. Bone tissue damage repair involves the participation of various cells and molecules. The recovery of bone mass requires sufficiently many MSCs to migrate to the damaged site to perform the reconstruction function. The local inflammatory response at the injury site can recruit MSCs and promote new bone formation. Simultaneously, niche changes during the migration of MSCs will affect their biological performance and initiate the phase of directed differentiation. This article explores the relevant mechanisms that mediate the migration of MSCs in the process of bone injury repair, including the regulation of immune cells and chemotactic signaling molecules in the inflammatory response in the bone repair stage through signaling pathways such as BMP/Smads. Then, it summarizes the mechanism by which the high matrix stiffness upregulates the expression of the integrin and focal adhesions to promote the MSCs migration and osteogenic differentiation. Simultaneously, the migration ability of MSCs can be regulated through drugs or genetic modification to promote the bone injury repair. The improvement of MSCs migration ability can shorten the time of bone tissue damage repair and improve the bone quality. This article reviews the role of the MSCs migration ability in bone tissue injury repair to provide a reference for the application of MSCs with high migration ability in the fields of stem cell therapy for bone related diseases and bone tissue engineering.