BackgroundMini-implant-assisted rapid palatal expansion (MARPE) appliances have been developed with the aim to enhance the orthopedic effect induced by rapid maxillary expansion (RME). Maxillary Skeletal Expander (MSE) is a particular type of MARPE appliance characterized by the presence of four mini-implants positioned in the posterior part of the palate with bi-cortical engagement. The aim of the present study is to evaluate the MSE effects on the midpalatal and pterygopalatine sutures in late adolescents, using high-resolution CBCT. Specific aims are to define the magnitude and sagittal parallelism of midpalatal suture opening, to measure the extent of transverse asymmetry of split, and to illustrate the possibility of splitting the pterygopalatine suture.MethodsFifteen subjects (mean age of 17.2 years; range, 13.9–26.2 years) were treated with MSE. Pre- and post-treatment CBCT exams were taken and superimposed. A novel methodology based on three new reference planes was utilized to analyze the sutural changes. Parameters were compared from pre- to post-treatment and between genders non-parametrically using the Wilcoxon sign rank test. For the frequency of openings in the lower part of the pterygopalatine suture, the Fisher’s exact test was used.ResultsRegarding the magnitude of midpalatal suture opening, the split at anterior nasal spine (ANS) and at posterior nasal spine (PNS) was 4.8 and 4.3 mm, respectively. The amount of split at PNS was 90% of that at ANS, showing that the opening of the midpalatal suture was almost perfectly parallel antero-posteriorly. On average, one half of the anterior nasal spine (ANS) moved more than the contralateral one by 1.1 mm. Openings between the lateral and medial plates of the pterygoid process were detectable in 53% of the sutures (P < 0.05). No significant differences were found in the magnitude and frequency of suture opening between males and females. Correlation between age and suture opening was negligible (R 2 range, 0.3–4.2%).ConclusionsMidpalatal suture was successfully split by MSE in late adolescents, and the opening was almost perfectly parallel in a sagittal direction. Regarding the extent of transverse asymmetry of the split, on average one half of ANS moved more than the contralateral one by 1.1 mm. Pterygopalatine suture was split in its lower region by MSE, as the pyramidal process was pulled out from the pterygoid process. Patient gender and age had a negligible influence on suture opening for the age group considered in the study.
Blocking transforming growth factor (TGF)β1 signal transduction has been a central strategy for scar reduction; however, this approach appears to be minimally effective. Here, we show that fibromodulin (FMOD), a 59-kD small leucine-rich proteoglycan critical for normal collagen fibrillogenesis, significantly reduces scar formation while simultaneously increasing scar strength in both adult rodent models and porcine wounds, which simulate human cutaneous scar repair. Mechanistically, FMOD uncouples pro-migration/contraction cellular signals from pro-fibrotic signaling by selectively enhancing SMAD3-mediated signal transduction, while reducing AP-1-mediated TGFβ1 auto-induction and fibrotic extracellular matrix accumulation. Consequently, FMOD accelerates TGFβ1-responsive adult fibroblast migration, myofibroblast conversion, and function. Furthermore, our findings strongly indicate that, by delicately orchestrating TGFβ1 activities rather than indiscriminately blocking TGFβ1, FMOD elicits fetal-like cellular and molecular phenotypes in adult dermal fibroblasts in vitro and adult cutaneous wounds in vivo, which is a unique response of living system undescribed previously. Taken together, this study illuminates the signal modulating activities of FMOD beyond its structural support functions, and highlights the potential for FMOD-based therapies to be used in cutaneous wound repair.
Pluripotent or multipotent cell-based therapeutics are vital for skeletal reconstruction in non-healing critical-sized defects since the local endogenous progenitor cells are not often adequate to restore tissue continuity or function. However, currently available cell-based regenerative strategies are hindered by numerous obstacles including inadequate cell availability, painful and invasive cell-harvesting procedures, and tumorigenesis. Previously, we established a novel platform technology for inducing a quiescent stem cell-like stage using only a single extracellular proteoglycan, fibromodulin (FMOD), circumventing gene transduction. In this study, we further purified and significantly increased the reprogramming rate of the yield multipotent FMOD reprogrammed (FReP) cells. We also exposed the ‘molecular blueprint’ of FReP cell osteogenic differentiation by gene profiling. Radiographic analysis showed that implantation of FReP cells into a critical-sized SCID mouse calvarial defect, contributed to the robust osteogenic capability of FReP cells in a challenging clinically relevant traumatic scenario in vivo. The persistence, engraftment, and osteogenesis of transplanted FReP cells without tumorigenesis in vivo were confirmed by histological and immunohistochemical staining. Taken together, we have provided an extended potency, safety, and molecular profile of FReP cell-based bone regeneration. Therefore, FReP cells present a high potential for cellular and gene therapy products for bone regeneration.
Hedgehog (Hh) signaling positively regulates both endochondral and intramembranous ossification. Use of small molecules for tissue engineering applications poses several advantages. In this study, we examined whether use of an acellular scaffold treated with the small molecule Smoothened agonist (SAG) could aid in critical-size mouse calvarial defect repair. First, we verified the pro-osteogenic effect of SAG in vitro, using primary neonatal mouse calvarial cells (NMCCs). Next, a 4 mm nonhealing defect was created in the mid-parietal bone of 10-week-old CD-1 mice. The scaffold consisted of a custom-fabricated poly(lactic-co-glycolic acid) disc with hydroxyapatite coating (measuring 4 mm diameter × 0.5 mm thickness). Treatment groups included dimethylsulfoxide control (n = 6), 0.5 mM SAG (n = 7) or 1.0 mM SAG (n = 7). Evaluation was performed at 4 and 8 weeks postoperative, by a combination of high-resolution microcomputed tomography, histology (H & E, Masson's Trichrome), histomorphometry, and immunohistochemistry (BSP, OCN, VEGF). In vivo results showed that SAG treatment induced a significant and dose-dependent increase in calvarial bone healing by all radiographic parameters. Histomorphometric analysis showed an increase in all parameters of bone formation with SAG treatment, but also an increase in blood vessel number and density. In summary, SAG is a pro-osteogenic, provasculogenic stimulus when applied locally in a bone defect environment.
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