Objective:To investigate whether the changes of anterior arch dimension have an impact on the precision of Bolton analysis. Methods:A mathematic-geometric model was used to evaluate the data. Results:The ideal anterior tooth size ratio may need adjustments, depending on the dimensions in radii of the upper and lower anterior dental arches. The ideal ratio is lower for dental arches with a high anterior curvature. There is a deficiency in the upper arch, a flatter anterior segment may compensate for some of the discrepancy and vice versa. Conclusion:An ideal Bolton value may not guarantee an ideal occlusion. Anterior tooth size ratio is not precise in predicting the anterior inter relationship post-treatment.

BACKGROUND:Previous studies have demonstrated that nano-hydroxyapatite/polyamide 66 (nHA/PA66) composites as a root canal filing material possess the basic physical and chemical properties, have antibacterial properties against the infection of medulary cavity, and have no cytotoxicity. However, it is rarely reported as a direct pulp capping agent.
OBJECTIVE: To observe the histological reaction of nHA/PA66 composites as the pulp capping agent.
METHODS:The first and second molars from 12 Wistar rats were selected to prepare class I cavities by exposing the dental pulp. Then, these rats were randomized into three groups and subjected to dental pulp capping using nHA/PA66 composite, nHA and calcium hydroxide, respectively, folowed by filing with glass ionomer cement. At 7 and 30 days after filing, histological changes of odontoblasts and microvessels in the dental pulp were observed using ink perfusion method.
RESULTS AND CONCLUSION: At 7 days after filing, significant changes in dental pulp fibroblast proliferation, predentin thickening, dilation of blood vessels were observed in the nHA/PA66 group; only dental pulp fibroblast proliferation with no predentin thickening and dilation of blood vessels was found in the nHA group; in the calcium hydroxide group, the pulp tissues in the pulp chamber were mostly damaged, and obvious hyperplasia in dental pulp fibroblasts and certain inflammatory cel infiltration with vascular necrosis were observed. At 30 days after filing, predentin thickness was increased further, dental pulp fibroblasts proliferated, the number of odontoblasts increased, and dilation of blood vessels was observed in the nHA/PA66 group; predentin thickening and dilation of blood vessels were obviously visible in the nHA group; pulp necrosis was found on the pulp surface below the pitting pore, odontoblasts grew actively at the pulp junction, with no obvious thickening of the predentin, and there were dense vessels below the necrotic area. These findings indicate that the nHA/PA66 composite can induce the regeneration of dental pulp cels.

BACKGROUND:The mechanical properties of SonicFil ultrasonic resin are better than those of the traditional light-cured composite resin, but its effect on odontoblasts and dental pulp vessels is unclear.
OBJECTIVE:To study the effect of SonicFil ultrasonic resin on odontoblasts and dental pulp vessels of rats using histological methods.
METHODS:Twenty-five Wistar rats are selected for experiment. Ninety-six teeth from the first and second molars were selected and randomly divided into SonicFil ultrasound resin group and Filtek Z350 nano resin group with 48 teeth in each group. Experimental teeth in each group were equaly subdivided into 7 days group and 30 days group. Besides, randomly selected five teeth with no intervention served as normal control group. After anesthesia and disinfection, class I cavities on the occlusal surface of the maxilary first and second molars were prepared and filed with SonicFil ultrasound resin and Filtek Z350 nano resin group, respectively. The rats were sacrificed by ink perfusion method, and tooth specimens were taken to observe the changes of odontoblasts and pulp microvessels.
RESULTS AND CONCLUSION: At 7 days after filing, two groups had similar changes in the pulp presenting with mild inflammation. Besides, there were scattered inflammatory cels distributing in the cave pulp tissue, and in most of the specimens, odontoblasts arranged disorderly with little vacuoles and microvascular dilatation in the pulp. At 30 days after filing, in the SonicFil ultrasonic resin group, odontoblasts arranged orderly, inflammatory reaction and microvascular dilatation disappeared basicaly. In contrast, in the Filtek Z350 nano resin group, disordered odontoblasts decreased, inflammatory reaction weakened, as wel as microvascular dilatation became less. These results show that under the experimental condition, both of the SonicFil ultrasonic resin and Filtek SonicFil Z350 nano resin play certain roles in the formation of odontoblasts and dental pulp vessels, but over time al of these effects can automaticaly disappear.

BACKGROUND:The mechanism underlying orthodontic-induced external root resorption is not yet clear, and it differs individual y. Kidney deficiency has been proved to be related to bone diseases which mediated by different cytokines. Interleukin-17 is an important cytokine involved in external root resorption. So figuring out whether kidney deficiency and interleukin-17 are related to root resorption wil be helpful for etiological research.
OBJECTIVE:To explore the relationship between kidney deficiency physique, interleukin-17 and root resorption during orthodontic treatment in rats.
METHODS:Thirty-six Wistar rats were selected and equivalently randomized into two groups, fol owed by modeled into kidney deficiency (kidney deficiency group) or injected with normal saline (control group), respectively. Afterwards, the right maxil ary of each rat served as an orthodontic force model, and the left maxil ary as a non-orthodontic force model. Al rats were respectively sacrificed under general anesthesia at the 3, 7 and 14 days after given orthodontic force. Then, the mesial surface of the root of maxil ary first molars and the expression level of interleukin-17 were observed through hematoxylin-eosin staining and immunohistochemical method.
RESULTS AND CONCLUSION:Histological observation showed that significantly increasing root resorption in a time-dependent manner could be observed, and there were various absorbed lacunae of osteoclasts on the enamel in the kidney deficiency orthodontic force group. The alveolar bone resorption and widened periodontal membrane appeared in the control orthodontic force group. While no remarkable root and alveolar bone resorptions were found in the other two non-orthodontic force groups. The expression level of interleukin-17 in the kidney deficiency orthodontic force group was higher than that in the control orthodontic force group;the expression level of interleukin-17 in the kidney deficiency non-orthodontic force group was higher than that in the control non-orthodontic force group. In conclusion, kidney deficiency patients are easy to develop root resorption, the mechanism of which is maybe relevant to the upregulation of interleukin-17.

Collagen is the building component of temporomandibular joint (TMJ) discs and is often affected by inflammation in temporomandibular disorders.The macromechanical properties of collagen are deteriorated by chronic inflammation.However,the mechanism by which inflammation influences disc function remains unknown.The relationship between the ultrastructure and nanomechanical properties of collagen in inflamed discs should be clarified.Seven-week-old female Sprague-Dawley rats were randomly divided into two groups.Chronic TMJ inflammation was induced by intra-articular injection of complete Freund's adjuvant,and samples were harvested after 5 weeks.Picrosirius staining revealed multiple colours under polarized light,which represented alternative collagen bundles in inflamed discs.Using atomic force microscopy scanning,the magnitude of Young's modulus was reduced significantly accompanied with disordered collagen fibril arrangement with porous architecture of inflamed discs.Transmission electron microscopy scanning revealed a non-uniform distribution of collagen fibres,and oversized collagen fibrils were observed in inflamed discs.Fourier transform infrared microspectroscopy revealed a decrease in 1 338 cm-1/amide Ⅱ area ratio of collagen in different regions.The peak positions of amide Ⅰ and amide Ⅱ bands were altered in inflamed discs,indicating collagen unfolding.Our results suggest that sustained inflammation deteriorates collagen structures,resulting in thedeterioration of the ultrastructure and nanomechanical properties of rat TMJ discs.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.