Mechanical stability of orthodontic miniscrew depends on a thread shape.

Background/purpose: Primary stability of orthodontic miniscrew system is of great importance in maintaining stable anchorage during a treatment period. Thus, this study aimed to examine whether the thread shape of orthodontic miniscrew had an effect on its mechanical stability in bone. Materials and methods: Three different types of miniscrews (type A and B with a regular thread shape; type C with a novel thread shape) were placed in artificial bone block with different artificial cortical bone thickness of 1.5, 2.0 and 3.0 mm. Values of maximum insertion torque (MIT), removal torque (RT), torque ratio (TR), screw mobility, static stiffness (K), dynamic stiffness (K∗) and energy dissipation (tan Î´) ability were assessed for each miniscrew system. Results: The MIT, RT, TR and K of type C miniscrew were significantly greater than those of type A and B miniscrews when the miniscrews were placed in the thinner artificial bone. Furthermore, the TR value of type C miniscrew was more than 1, indicating the MRT value was larger than the MIT value in the novel miniscrew. The values of K∗ and tan Î´ were almost similar among the three types of miniscrews. Conclusion: The miniscrew with a novel thread shape showed a higher initial stability compared to those with a regular thread shape. Thus, in order to obtain a sufficient initial stability, it is important to select the type of screw thread that is appropriate for the thickness of the cortical bone.

Thread shape, cortical bone thickness, and magnitude and distribution of stress caused by the loading of orthodontic miniscrews: finite element analysis.

Cortical bone thickness is assumed to be a major factor regulating miniscrew stability. We investigated stress distribution in two miniscrews with different thread shapes (type A and B) and in cortical bone of three different thicknesses using three-dimensional (3D) finite element (FE) models. More specifically, 3D FE models of two different miniscrews were created and placed obliquely or vertically into a cylindrical bone model representing different cortical bone thicknesses. When force was applied to the miniscrew, the stress distribution on the screw surface and in the peri-implant bone was assessed using FE methodology. Miniscrew safety was evaluated using a modified Soderberg safety factor. Screw head displacement increased with a decrease in cortical bone thickness, irrespective of screw type. The smallest minimum principal stresses on the screw surfaces remained constant in type A miniscrews on changes in cortical bone thickness. Minimum principal stresses also appeared on the cortical bone surface. Lower absolute values of minimum principal stresses were seen in type A miniscrews when placed vertically and with upward traction in obliquely placed type B miniscrews. Both miniscrews had acceptable safety factor values. Taken together, orthodontists should select and use the suitable miniscrew for each patient in consideration of bone properties.

HIF-1α controls palatal wound healing by regulating macrophage motility via S1P/S1P1 signaling axis.

OBJECTIVES: To investigate the role of hypoxia-inducible factor 1α (HIF-1α) signaling, the expression profile of M1 and M2 macrophages, and the role of the sphingosine 1-phosphate (S1P)/S1P receptor system in palatal wound healing of heterozygous HIF-1α-deficient (HIF-1α HET) mice. MATERIALS AND METHODS: HIF-1α HET and wild-type (WT) littermates underwent palatal tissue excision at the mid-hard palate. Histological analysis, immunostaining, real-time PCR, Western blotting (WB), and cellular migration assays were performed to analyze wound closure and macrophage infiltration. RESULTS: DMOG pretreatment showed an acceleration of palatal wound closure in WT mice. In contrast, the delayed palatal wound closure was observed in HIF-1α HET mice with diminished production of Col1a1, MCP-1, and MIP-1α, compared with WT mice. Decreased infiltration of M1 macrophage (F4/80+ TNF-α+ , F4/80+ iNOS+ ) and M2 macrophage (F4/80+ Arginase-1+ , F4/80+ CD163+ ) was observed. The numbers of F4/80+ S1P1 + macrophages of HIF-1α HET wounded tissues were significantly lower compared with WT tissues. S1P treatment of bone marrow macrophages (BMMs) significantly upregulated expression of S1P1 in WT mice compared with HIF-1α HET. Phosphorylation of MAPK rapidly decreased in BMMs of HIF-1α HET mice than in BMMs of WT mice by S1P stimulation. Moreover, S1P enhanced HIF-1α expression via S1P1 receptors to affect macrophage migration. CONCLUSIONS: HIF-1α deficiency aggravates M1 and M2 macrophage infiltration and controls macrophage motility via S1P/S1P1 signaling. These results suggest that HIF-1α signaling may contribute to the regulation of palatal wound healing.

Macrophage Motility in Wound Healing Is Regulated by HIF-1α via S1P Signaling.

Accumulating evidence indicates that the molecular pathways mediating wound healing induce cell migration and localization of cytokines to sites of injury. Macrophages are immune cells that sense and actively respond to disturbances in tissue homeostasis by initiating, and subsequently resolving, inflammation. Hypoxic conditions generated at a wound site also strongly recruit macrophages and affect their function. Hypoxia inducible factor (HIF)-1α is a transcription factor that contributes to both glycolysis and the induction of inflammatory genes, while also being critical for macrophage activation. For the latter, HIF-1α regulates sphingosine 1-phosphate (S1P) to affect the migration, activation, differentiation, and polarization of macrophages. Recently, S1P and HIF-1α have received much attention, and various studies have been performed to investigate their roles in initiating and resolving inflammation via macrophages. It is hypothesized that the HIF-1α/S1P/S1P receptor axis is an important determinant of macrophage function under inflammatory conditions and during disease pathogenesis. Therefore, in this review, biological regulation of monocytes/macrophages in response to circulating HIF-1α is summarized, including signaling by S1P/S1P receptors, which have essential roles in wound healing.

Effectiveness of low-intensity pulsed ultrasound on osteoarthritis of the temporomandibular joint: A review.

Loading is indispensable for the growth, development, and maintenance of joint tissues, including mandibular condylar cartilage, but excessive loading or reduced host adaptive capacity can considerably damage the temporomandibular joint (TMJ), leading to temporomandibular joint osteoarthritis (TMJ-OA). TMJ-OA, associated with other pathological conditions and aging processes, is a highly degenerative disease affecting the articular cartilage. Many treatment modalities for TMJ-OA have been developed. Traditional clinical treatment includes mainly nonsurgical options, such as occlusal splints. However, non-invasive therapy does not achieve joint tissue repair and regeneration. Growing evidence suggests that low-intensity pulsed ultrasound (LIPUS) accelerates bone fracture healing and regeneration, as well as having extraordinary effects in terms of soft tissue repair and regeneration. The latter have received much attention, and various studies have been performed to evaluate the potential role of LIPUS in tissue regeneration including that applied to articular cartilage. The present article provides an overview of the status of LIPUS stimulation used to prevent the onset and progression of TMJ-OA and enhance the tissue regeneration of mandibular condylar cartilage. The etiology and management of TMJ-OA are explained briefly, animal models of TMJ-OA are described, and the effectiveness of LIPUS on cell metabolism and tissue regeneration in the TMJ is discussed.