This study aimed to investigate the prevalence and associated factors of malocclusion among children with primary dentition in Xi’an, China. A total of 2,974 subjects were selected from local schools in Xi’an city using a stratified cluster sampling method from January to September 2015. After screening samples according to the inclusion criteria, the final sample size comprised 2,235 pre-school children, with a mean age of 4.82 (SD, 1.76; range, 2.63–6.12) years. Malocclusion traits were assessed by trained clinicians followed by the evaluation of associated factors through clinical examination and a precisely designed questionnaire including data regarding gender, birth place, parental education level, monthly familial income, parental attitude toward the problem of malocclusion, feeding methods of the children, feeding postures, pacifier use, and delivery methods. Data were analyzed using the Chi-square test and logistic regression analysis. The most common type of malocclusion was increased overjet (34.99 %) in the sagittal direction, deep overbite (37.58 %), and midline deviation (25.32 %) in the vertical and transverse directions, respectively. The prevalence of posterior crossbite, anterior crossbite, and anterior open bite was 7.56, 6.80 and 6.98 %, respectively. The prevalence of the anterior edge-to-edge occlusion was the lowest (2.46 %). The variables associated with malocclusion (P < 0.05) were birth place (odds ratio [OR] = 1.741 with 95 % CI of 1.384–2.162), insufficient abrasion of primary canines (OR = 1.465; 95 % CI of 1.153–1.894), caries in primary teeth (OR = 2.045; 95 % CI of 1.665–2.539), tongue thrusting (OR = 2.833; 95 % CI of 1.640–3.649), mandibular prognathism (OR = 2.621; 95 % CI of 1.574–3.689), and finger sucking (OR = 1.573 with 95 % CI of 1.098–2.014). The feeding methods (OR = 3.614 with 95 % CI of 3.087–4.596) along with the method of delivery (OR = 1.847 with 95 % CI of 1.323–2.451) have been observed to play an important role in the morbidity of malocclusion (P < 0.05). The prevalence of malocclusion among pre-school children in Xi’an is higher compared to that in other geographical parts of China. Therefore, early attention to the development of occlusion and necessary interventions toward the associated factors are important to reduce its prevalence and further adverse effects.

Cigarette smoking is one of the high risk factors of adult chronic periodontitis and nicotine is the well established toxic substance in cigarette. However, the mechanism of nicotine induced periodontitis is still unknown. Here we studied whether nicotine impaired the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) through activating α7 nicotinic acetylcholine receptor (α7 nAChR). hPDLSCs with multi differentiation potential and surface makers for mesenchymal stem cells were harvested by limiting dilution technique. The level of mineralized nodule formation was assessed by alizarin red S staining. Expression level of ostegenic related genes and proteins were detected by real-time PCR and western blot analysis. The expression of α7 nAChR and its downstream signaling pathway were examined by western blot. The role of the receptor and related signaling pathway in nicotine impairing the osteogenic potential of hPDLSCs were also studied in different levels. Nicotine deteriorated the ostegenic differentiation of hPDLSCs in a dose dependent manner. Activation of α7 nAChR by nicotine treatment activated wnt/β-catenin signaling pathway, leading to osteogenic deficiency of hPDLSCs. Blockage of α7 nAChR and wnt pathway inhibitor treatment rescued nicotine induced osteogenic differentiation deficiency. These data suggested that nicotine activated α7 nAChR expressed on PDLSCs and further activated wnt signaling downstream, thus deteriorating the osteogenic potential of PDLSCs. The impairment of osteogenic differentiation of PDLSCs by nicotine might lead to cigarette smoking related periodontitis.

Background: To investigate the effects of Er:YAG laser pre-treatment on the dentin structure and shear bond strength of primary teeth. Methods: Dentin specimens were prepared using freshly extracted intact primary molars and divided randomly into four groups based on the surface treatment applied. The control and etchant groups received no treatment and conventional acid etching treatment, respectively, while the energy and frequency groups received laser surface treatment with variable energy (50–300 mJ) and frequency (5–30 Hz) parameters. The morphology was observed using scanning electron microscopy. The surface-treated dentin slices were bonded to resin tablets, followed by thermocycle treatment. The shear strength was determined using a universal testing machine and de-bonded surfaces were observed using a stereomicroscope. Results: SEM observation showed that the surface morphology of the dentin slices changed after etching as well as after Er:YAG laser pre-treatment with different energy and frequency values. The dentin tubules opened within a specific energy (50–200 mJ) and frequency (5–20 Hz) range. Beyond this range, the intertubular dentin showed cracks and structural disintegration. Shear strength tests showed no significant changes after acid etching. The shear strength increased significantly (P < 0.05) after Er:YAG laser pre-treatment compared with that of the control group. The shear strength increased within the same energy (50–200 mJ) and frequency (5–20 Hz) range as the tubule opening, but not significantly (P > 0.05). The most common mode of interface failure was adhesive (interface) failure, followed by mixed and resin cohesive failure. Conclusions: Pre-treatment using Er:YAG laser opens the dentinal tubules without the formation of a smear layer and improves the bonding strength between the primary teeth dentin and the resin composites.

Background/Aims: Tobacco smoking is a major risk factor for the occurrence and progression of periodontitis. We previously demonstrated that nicotine could induce the expression of α7 nicotinic acetylcholine receptors (α7 nAChR) in human and rat periodontal tissues. To further examine the signal pathways mediated by α7 nAChR in periodontal ligament (PDL) cells, we investigated whether nicotine affects interleukin-1β (IL-1β) and interleukin-8 (IL-8) via the α7 nAChR/NF-κB pathway in human PDL cells. Methods: Human PDL cells were pre-incubated with alpha-bungarotoxin (α-BTX) or pyrrolidine dithiocarbamate (PDTC), then cultured with nicotine. Then, we used western blotting, a dual-luciferase reporter, real-time quantitative PCR and an enzyme-linked immunoassay to assess expression of the NF-κB p65 subunit, NF-κB activity and production of IL-1β and IL-8 in human PDL cells. Results: Compared with the control group, nicotine could significantly induce production of IL-1β and IL-8 in human PDL cells and cause the similar effects on the expression of the NF-κB p65 subunit and NF-κB activity. Conclusion: This study demonstrates that nicotine could induce production of IL-1β and IL-8 via the α7 nAChR/NF-κB pathway in human PDL cells, providing data for a better understanding of the relationships among smoking, nicotine, and periodontitis.

Physiological primary teeth exfoliation is a normal phenomenon during teeth development. However, retained primary teeth can often be observed in the patients with cleidocranial dysplasia (CCD) caused by mutation of Runx2. The potential regulative mechanism is still unknown. In the present study, periodontal ligament stem cells (PDLSCs) were derived from different resorbed stages of primary teeth and permanent teeth from normal patients and primary teeth from CCD patient. The proliferative, osteogenic and osteoclast-inductive capacities of PDLSCs from each group were detected. We demonstrated here that the proliferative ability of PDLSCs was reduced while the osteogenic and the osteoclast-inductive capacity of PDLSCs were enhanced during root resorption. The results also showed that PDLSCs from permanent teeth and CCD patient expressed low level of Runx2 and RANKL while high level of OPG. However, expression of Runx2 and RANKL were increased while expression of OPG was decreased in PDLSCs derived from resorbed teeth. Furthermore, Runx2 regulating the expression of RANKL and OPG and the osteoclast-inductive capacity of PDLSCs were confirmed by gain or loss of function assay. These data suggest that PDLSCs promote osteoclast differentiation via Runx2 upregulating RANKL and downregulating OPG, leading to enhanced root resorption that results in physiological exfoliation of primary teeth.