Alveolar bone remodeling in orthodontic tooth movement (OTM) is a highly regulated process that coordinates bone resorption by osteoclasts and new bone formation by osteoblasts. Mechanisms involved in OTM include mechano-sensing, sterile inflammation-mediated osteoclastogenesis on the compression side and tensile force-induced osteogenesis on the tension side. Several intracellular signaling pathways and mechanosensors including the cilia and ion channels transduce mechanical force into biochemical signals that stimulate formation of osteoclasts or osteoblasts. To date, many studies were performed in vitro or using human gingival crevicular fluid samples. Thus, the use of transgenic animals is very helpful in examining a cause and effect relationship. Key cell types that participate in mediating the response to OTM include periodontal ligament fibroblasts, mesenchymal stem cells, osteoblasts, osteocytes, and osteoclasts. Intercellular signals that stimulate cellular processes needed for orthodontic tooth movement include receptor activator of nuclear factor-κB ligand (RANKL), tumor necrosis factor-α (TNF-α), dickkopf Wnt signaling pathway inhibitor 1 (DKK1), sclerostin, transforming growth factor beta (TGF-β), and bone morphogenetic proteins (BMPs). In this review, we critically summarize the current OTM studies using transgenic animal models in order to provide mechanistic insight into the cellular events and the molecular regulation of OTM.

Periodontitis arises from imbalanced host–microbe interactions, leading to dysbiosis and destructive inflammation. The host's innate and adaptive immune responses produce pro‐inflammatory mediators that stimulate destructive events, which cause loss of alveolar bone and connective tissue attachment. There is no consensus on the factors that lead to a conversion from gingivitis to periodontitis, but one possibility is the proximity of the inflammation to the bone, which promotes bone resorption and inhibits subsequent bone formation during coupled bone formation. Conversely, orthodontic tooth movement is triggered by the mechanical force applied to the tooth, resulting in bone resorption on the compression side and new bone formation on the tension side. However, the environment around orthodontic brackets readily retains dental plaque and may contribute to inflammation and bone remodeling. The immune, epithelial, stromal, endothelial and bone cells of the host play an important role in setting the stage for bone remodeling that occurs in both periodontitis and orthodontic tooth movement. Recent advancements in single‐cell RNA sequencing have provided new insights into the roles and interactions of different cell types in response to challenges. In this review, we meticulously examine the functions of key cell types such as keratinocytes, leukocytes, stromal cells, osteocytes, osteoblasts, and osteoclasts involved in inflammation‐ and mechanical force‐driven bone remodeling. Moreover, we explore the combined effects of these two conditions: mechanical force‐induced bone remodeling combined with periodontal disease (chronic inflammation) and periodontally accelerated osteogenic orthodontics (acute transient inflammation). This comprehensive review enhances our understanding of inflammation‐ and mechanical force‐induced bone remodeling.

Objectives: To investigate the role of NF-κB in osteoblast lineage cells and periodontal ligament (PDL) fibroblasts during orthodontic tooth movement (OTM). Materials and Methods: Transgenic mice that expressed a dominant negative mutant of the inhibitor of kB kinase (IKK-DN) with lineage specific expression in osteoblastic cells and PDL fibroblasts driven by a response element in the collagen1α1 promoter and matched wild-type (WT) mice were examined. A 10-12 g force was applied by a NiTi coil and maintained for 5 or 12 days. OTM distance, PDL width, and bone volume fraction were measured using micro computed tomography. Osteoclast numbers were counted in tartrate-resistant acid phosphatase-stained sections. Activation of nuclear factor kappa B (NF-kB) was assessed by nuclear localization of p65, and the receptor activator of nuclear factor-κB ligand (RANKL) was measured by immunofluorescence and compared to control specimens with no orthodontic force. Results: OTM-induced NF-kB activation (p65 nuclear localization) in WT mice was largely blocked in transgenic (TG) mice. OTM was significantly reduced in the TG mice compared to WT mice along with reduced osteoclastogenesis, narrower PDL width, higher bone volume fraction, and reduced RANKL expression. Conclusions: Osteoblast lineage cells and PDL fibroblasts are key contributors to alveolar bone remodeling in OTM through IKKβ dependent NF-κB activation.

The aim of this study is to evaluate the longitudinal transverse growth of the maxillo-mandibular complex in untreated children using the Cone Beam Computed Tomography (CBCT). Two sets of scans on 12 males (mean 8.75 years at T1 and 11.52 years at T2) and 18 females (mean 9.09 years at T1 and 10.80 years at T2) were analyzed using Dolphin 3D imaging. The transverse widths of various maxillary and mandibular skeletal landmarks and the dentoalveolar and dental landmarks at the level of first molars were measured. Overall, there were greater increases in the transverse dimension in the posterior than anterior portions of the maxilla and mandible. The increase in intergonial width of the mandible seems to be primarily due to the lengthening of the mandibular body. The dentoalveolar process at the first molar level increases at an equal rate corono-apically and is independent to the changes in molar inclination. When comparing maxillary dentoalveolar changes with that of the mandible, greater increases were noticed in the maxilla, which might be explained by the presence of sutural growth in the maxilla. Moreover, the first molars maintain their coordination with each other despite the differential increase in the maxillary and mandibular dentoalveolar processes.

This study aims to determine if a large anterior and reduced posterior/superior joint space is highly predictable for disc displacement. From patients with temporomandibular disorders symptoms, fifty-two experimental joints and fourteen control joints were included. The cone beam computed tomography (CBCT) images were used to calculate posterior-to-anterior (P-A) and superior-to-anterior (S-A) joint space ratios, while disc position was determined using magnetic resonance imaging (MRI). One-way analysis of covariance test and receiver operating characteristics analysis were carried out. The results showed that among the 52 experimental joints, 45 were diagnosed as disc displacement and 7 as normal disc positions (N). All 14 control joints showed normal disc positions. The P-A ratio was 1.46 ± 0.21, 0.99 ± 0.23, and 0.86 ± 0.30 in the control, N, and DD groups, respectively (p < 0.001). The S-A ratio was 1.80 ± 0.27, 1.44 ± 0.33, and 1.08 ± 0.35 in the control, N, and DD groups, respectively (p < 0.001). When an altered P-A ratio and/or S-A ratio are observed on the CBCT, the diagnosis of disc displacement is quite predictable with high sensitivity and specificity.