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Background: The purpose of this study was to compare the difference of alveolar bone remodeling between the adolescents and adults in the maxillary incisor area during retraction. Methods: This retrospective study included 72 female patients who needed moderate anchorage to correct the bimaxillary protrusion. Subjects were further divided into the minor group (n=36, 11-16 years old) and adult group (n=36, 18-35 years old). Digital lateral cephalography and cone beam CT scanning were taken in each patient before (T0) and after treatment (T1). Cephalometry was conducted to assess incisor retraction, while alveolar bone thickness (ABT), alveolar bone distance (ABD, and alveolar bone area (ABA) were detected to assess changes in the alveolar bone. Results: No difference in the inclination of upper incisors was observed at both T0 and T1. Changes in the alveolar bone showed a similar tendency with bone apposition on the labial side and resorption on the palatal side. Less increase in the labial ABT (T1-T0) and more decrease in the palatal ABT (T1-T0) was found in the adult group, leading to less total ABT in the adult group. Higher reduction inn ABD (T1-T0) was found in the adult group. Moreover, more decrease in the ABA (T1-T0) was found in the adult group. Conclusion: When compared adolescents, adult patients have less alveolar bone support after orthodontic treatment, showing a through-the-bone remodeling pattern. Orthodontic should take the age into consideration to reduce the potential periodontal risks during treatment planning.

Background/objectives Iron homeostasis plays a crucial role in the combat against pathogen invasion. Ferrous iron can trigger generous production of reactive oxygen species (ROS) by Fenton reaction. Nuclear receptor coactivator 4 (NCOA4), a selective cargo receptor to deliver ferritin to lysosome, may trigger release of ferritin-bound iron into the cytosol. The aim of the present study was to explore whether NCOA4-mediated ferritinophagy participated in the pathogenesis of periodontitis, and its role in promoting the periodontal inflammation. Methods Inflamed and healthy periodontal tissues were harvested for immunobiological staining of ferritinophagy-related genes in the periodontal tissues, while real-time quantitative PCR (qPCR) was utilized to detect mRNA transcription. Periodontal ligament fibroblasts (PDLFs) were isolated and infected with Porphyromonas gingivalis. The mRNA transcription and protein expression of genes involved in the iron metabolism, including NCOA4, transferrin receptor 1 (TFR1), and ferroportin (SLC40A1) were detected by qPCR and western blot. Levels of labile iron pool and ROS production were detected by flow cytometry and confocal endoscopy. Small interference RNA was utilized to knock down NCOA4. Results Elevated expression of NCOA4, ferritin heavy chain, and light chain were observed in the diseased periodontal tissues. P. gingivalis infection promoted expression of TFR1, NCOA4, and microtubule-associated protein 1-light chain 3 B (LC3B), enhanced levels of intracellular labile iron pool and ROS production. NCOA4 knockdown reduced ROS generation in PDLFs in response to P. gingivalis and mitigated production of pro-inflammatory monocyte chemoattractant protein-1 and interleukin 6. P. gingivalis triggered activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase signaling pathway. In addition, inhibitors of JNK, SP600125, and inhibitors of p38, SB203580 blocked NCOA4 transcription. Conclusion NCOA4-ferritinophagy participated in the progress of periodontitis progression. P. gingvalis-triggered ferritinophagy aggravated production of ROS and inflammatory responses in PDLFS. These findings suggest iron homeostasis plays an important role in the pathogenesis of periodontitis.

Cell survival or death is one critical issue in inflammatory responses. Ferroptosis, which is characterized by iron-dependent lethal lipid peroxidation, has been found to participate in the development of cancers, degenerative brain diseases and ischemia-reperfusion injuries. Incorporation of polyunsaturated fatty acids (PUFAs) into cellular membranes represents a vulnerability to invasion of microbials and sterile stimuli. In addition, the competition for iron in the battle between microbials and host cells underlies infection development. Although host cells have been equipped with complex antioxidant systems to combat lethal accumulation of lipid peroxidation, emerging evidence suggests several pathogens may target PUFAs in the cell membrane, and manipulate ferroptosis as a way for pathogen propagation. Moreover, ferroptosis takes part in the progression of sterile inflammations, such as cigarette smoke-induced chronic obstructive pulmonary disease, stroke and ischemia-reperfusion injuries. As iron-dependent oxidative stress and lipid peroxidation are common features for ferroptosis and inflammatory diseases, underlying mechanisms linking such pathological conditions will be discussed in this review. Progress in the research of ferroptosis may shed more light on the etiology and treatment of inflammatory diseases.

Objective Appropriate torque expression contributes to ideal treatment outcomes both clinically and aesthetically. Whether active and passive self-ligating brackets (SLBs) have different torque-control capability in vivo has never been reported. The purpose of present study was to explore whether there was difference in torque expression in active and passive SLBs. Setting and sample population In this retrospective study, 225 patients with four first premolar extractions were enrolled. For each patient, the digital lateral cephalometric radiographs were taken before and after treatment. Materials and methods The study consisted of 2 groups: 111 subjects were treated with passive SLBs (Damon Q, Ormco) and 114 subjects with active SLBs (Empower 2, American Orthodontics). Measurements to determine skeletal changes and incisor inclination were obtained from cephalometric tracings using Dolphin software (version 11.8, USA). Comparisons in both groups and intergroups were compared using t tests and chi-square test. Results Significant differences in the variation of U1-SN(°), U1-NA(°), L1-NB(°) and L1-FH(°) were found between two groups. More labially inclined maxillary incisors were found in active SLB group, while more labially inclined mandibular incisors were observed in passive SLB group. Conclusions With the present prescription set in the two brackets, active SLBs achieved more proclined maxillary incisors and retroclined mandibular incisors. Clinicians should take torque expression of brackets into consideration during orthodontic treatment.

The host innate immune response stands at the first line of defense against the outburst of pathogen invasion and their byproduct release. The balanced and coordinated expression of genes in normal immune responses is compromised in the progress of endotoxemia with exacerbated inflammation and massive cell death. In the present study, we identified cyclin-dependent kinase 9 (CDK9), the functional subunit of the positive transcription elongation factor b, as a master regulator of inflammatory gene transcription in the process of promoter-proximal pausing to productive elongation. Therapeutic pharmacological inhibition of CDK9 by flavopiridol (FVD) rescued mice from death in experimental models of fatal endotoxemia. In addition to alleviation of the cytokine storm in the circulation system following lethal endotoxin injection, FVD treatment significantly dampened the onset of inflammation in the livers and lungs and reduced the necroptosis and pyroptosis in livers. Moreover, CDK9 inhibition reduced inflammatory cytokine release and decreased cell death in the pro-inflammatory pyroptotic and necroptotic cell death pathway in monocytes in responses to lipopolysaccharide. In conclusion, CDK9 inhibition may affect the progress of endotoxemia by dampening inflammation and cell death including necroptosis and pyroptosis.

Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy has been implicated in the ferroptosis in cancer cells and hematopoiesis in the bone marrow. However, the role of iron metabolism, especially NCOA4-mediated degradation of ferritin, has not been explored in the proliferation of mesenchymal stem cells. The present study was designed to explore the role of NCOA4-mediated ferritinophagy in hypoxia-treated dental pulp stem cells (DPSCs). Hypoxia treatment increased ROS generation, boosted cytosolic labile iron pool, increased expression of transferrin receptor 1 and NCOA4. Moreover, colocalization of LC3B with NCOA4 and ferritin was observed in hypoxia-treated DPSCs, indicating the development of ferritinophagy. Hypoxia promoted the proliferation of DPSCs, but not ferroptosis, under normal serum supplement and serum deprivation. NCOA4 knock-down reduced ferritin degradation and inhibited proliferation of DPSCs under hypoxia. Furthermore, the activation of hypoxia inducible factor 1α and p38 mitogen-activated protein kinase signaling pathway was involved in the upregulation of NCOA4 in hypoxia. Therefore, our present study suggested that NCOA4-mediated ferritinophagy promoted the level of labile iron pool, leading to enhanced iron availability and elevated cell proliferation of DPSCs. Our present study uncovered a physiological role of ferritinophagy in the proliferation and growth of mesenchymal stem cells under hypoxia.

To evaluate the effectiveness of periodontal endoscope as an adjuvant therapy for the non-surgical periodontal treatment of patients with severe and generalized periodontitis.Patients (n=13) were divided into three groups: patients treated with conventional subgingival scaling and root planing (SRP) (n=7, 408 sites) (group A), SRP using periodontal endoscope (n=4, 188 sites) (group B) or SRP with periodontal endoscope 3 months after initial SRP (n=2, 142 sites) (group C). Two subgroups were divided into 2 subgroups according to PD at the baseline: 4PD≤6 mm as subgroup 1 and PD6 mm as subgroup 2. Probing depth (PD), attachment loss (AL), gingival recession (GR) and bleeding on probing (BOP) were recorded.The results of 3 months after treatment showed all PD, AL, and GR values in group A1 were less than those in group B1 (P0.05), but no significant difference in BOP was found between the two groups. The decrease in PD, BOP in group B2 was more obvious than those in group A2 (P0.000 1), and the GR values in group B2 were more than those in group A2 (P0.000 1). But the improvement of AL showed no statistical difference between the two groups (P=0.296 8). In group C1, no significant difference in PD, AL, and GR was observed after endoscopy-assisted therapy, but it was more effective for BOP (P0.000 1). In group C2, the improvement in PD and AL was significantly different from the improvement in SRP alone (P=0.000 5, P=0.000 2) and was accompanied by more GR (P=0.000 5).In non-surgical treatment of severe and generalized periodontitis, SRP can achieve good therapeutic effect on sites with 4 PD≤6 mm. For sites with PD6 mm, the application of periodontal endoscopy can increase the effect, reducing PD and GR, which may be an effective supplement to the current non-surgical periodontal treatment.目的 评估牙周内窥镜在辅助治疗年轻患者的重度广泛型牙周炎非手术治疗中发挥的作用。方法 观察了13例重度广泛型牙周炎患者738个位点，在经过牙周非手术治疗前后各项牙周指标的差异。根据所接受的治疗分为3组：A组龈下刮治术+根面平整术（SRP）治疗（n=7，408个位点）；B组内窥镜辅助下行SRP治疗（n=4，188个位点）；C组SRP治疗后3个月在内窥镜辅助下再次行SRP治疗（n=2，142个位点）。根据每个位点的基线PD值再将各组分为2个亚组：4PD≤6 mm记为亚组1，PD6 mm记为亚组2。记录各组的牙周探诊深度（PD）、附着丧失（AL）、牙龈退缩程度（GR）、探诊出血（BOP）。结果 治疗后3个月，A1组PD、AL和GR的改善程度比B1组更明显（P0.05），但2组的BOP值则无明显差异；B2组的PD下降量显著高于A2组（P0.001），并且BOP的改善情况优于A2组（P0.000 1），GR值则大于A2组（P0.000 1），但A2、B2组治疗前后AL的差异无统计学意义（P= 0.296 8）。C1组在内窥镜辅助治疗前后的PD、AL及GR均无明显差异，但治疗有效降低了BOP（P0.000 1）。C2组PD以及AL值在内窥镜辅助治疗后有所改善，并且与仅行SRP治疗时相比，差异有统计学意义（P=0.000 5，P= 0.000 2），同时其GR更为明显（P=0.000 5）。结论 在使用非手术方式治疗年轻患者重度广泛型牙周炎时，对于4~6 mm深的牙周袋，仅采用单纯的SRP治疗已可以获得较好的治疗效果；对于大于6 mm深的牙周袋，采用牙周内窥镜辅助治疗时可以增加其疗效，这可能是对当前牙周非手术治疗方案的一个有效补充。.

Background Periodontal health is of great concern for periodontists and orthodontists in the inter-disciplinary management of patients with bimaxillary protrusion. The aim of present study is to investigate changes in the alveolar bone in the maxillary incisor region and to explore its relationship with displacement of root apex as well as changes in the inclination of maxillary incisors during incisor retraction. Methods Samples in this retrospective study consisted of 38 patients with bimaxillary protrusion. Cone-beam computed tomography (CBCT) images was taken before(T0) and after (T1) treatment. Alveolar bone thickness (ABT), height (ABH) and area (ABA) were utilized to evaluate changes in the alveolar bone, while incisor inclination and apex displacement were used to assess changes in the position of maxillary central and lateral incisors. Correlations between alveolar bone remodeling and apex displacement as well as changes in the inclination were investigated. Results The labial ABT of central and lateral incisors at the mid-root third was increased. In contrast, the palatal ABT at crestal, mid-root and apical third level were consistently decreased. ABH was not altered on the labial side, while significantly decreased on the palatal side. ABA was not significantly increased on the labial side, but significantly decreased on the palatal side, leading to a significantly reduced total ABA. Orthodontic treatment significantly reduced inclination of upper incisors. Changes in the amount (T1-T0) of ABA was remarkably correlated with apex displacement and changes of inclination (T1-T0); in addition, using the multivariate linear regression analysis, changes of ABA on the palatal side (T1-T0) can be described by following equation: Changes of palatal ABA (T1-T0) = − 3.258- 0.139× changes of inclination (T1-T0) + 2.533 × apex displacement (T1-T0). Conclusions Retraction of incisors in bimaxillary protrusion patients may compromise periodontal bone support on the palatal side. An equation that incorporated the displacement of root apex and change in the incisor inclination may enable periodontist-orthodontist interdisciplinary coordination in assessing treatment risks and developing an individualized treatment plan for adult patients with bimaxillary protrusion. Moreover, the equation in predicating area of alveolar bone may reduce the risks of placing the teeth out of the bone boundary during 3D digital setups.

Human β-defensin 3 (hBD3) is a cationic peptide with immunomodulatory effects on both innate and acquired immune responses. Periodontitis, an inflammatory disease that extends deep into periodontal tissues, causes the loss of supporting structures around the tooth. The present study assessed the effects of hBD3 as a monotherapy for periodontitis in mice and explored its potential mechanism. In vivo, hBD3 inhibited the levels of tumour necrosis factor (TNF)-α, interleukin-6, and matrix metalloprotease-9 in periodontium exposed to Porphyromonas gingivalis (P.g) in a mouse periodontitis model; reduced osteoclast formation and lower alveolar bone loss were also observed. In addition, hBD3 was related to the expression of polarization signature molecules in circulating monocytes. In vitro, hBD3 notably suppressed the production of TNF-α and interleukin-6 in RAW 264.7 cells stimulated by the lipopolysaccharide of P.g. Moreover, hBD3 attenuated polarization of RAW 264.7 cells into the M1 phenotype, with reduced activation of nuclear factor-κB signal transduction. In conclusion, hBD3 exhibits potent anti-periodontitis properties both in vitro and in vivo, and this effect may be correlated to inhibition of the nuclear factor-κB pathway and macrophage polarization.

Periodontal tissues are constantly exposed to microbial stimuli. The equilibrium between microbes and host defense system helps maintain the homeostasis in the periodontal microenvironment. Growth of pathogenic bacteria in dental biofilms may induce proinflammatory cytokine production to recruit sentinel cells, mainly neutrophils and monocytes into the gingival sulcus or the periodontal pocket. Moreover, dysbiosis with overgrowth of anaerobic pathogens, such as Porphyromonas gingivalis and Tannerella forsythia, may induce death of both immune cells and host resident cells. Necroptosis is one newly characterized programmed cell death mediated by receptor-interacting protein kinase (RIPK)-1, RIPK3, and mixed lineage kinase like (MLKL). With its release of death-associated molecular patterns (DAMPs) into extracellular environment, necroptosis may help transmit the danger signal and amplify the inflammatory responses. In this review, we present recent advances on how necroptosis influences bacterial infection progression and what a role necroptosis plays in maintaining the homeostasis in the periodontal niche. Until we fully decipher the signals emanated from dying cells, we cannot completely understand the mechanism of disease progression.

Cyclin-dependent kinase 9 (CDK9), one crucial molecule in promoting the transition from transcription pausing to elongation, is a critical modulator of cell survival and death. However, the pathological function of CDK9 in bacterial inflammatory diseases has never been explored. CDK9 inhibition or knock-down attenuated Porphyromonas gingivalis-triggered inflammatory gene expression. Gene-expression microarray analysis of monocytes revealed that knock-down of CDK9 not only affected inflammatory responses, but also impacted cell death network, especially the receptor-interacting protein kinase 3 (RIPK3)-mixed lineage kinase domain-like (MLKL)-mediated necroptosis after P. gingivalis infection. Inhibition of CDK9 significantly decreased necroptosis with downregulation of both MLKL and phosphorylated MLKL. By regulating caspase-8 and cellular FLICE inhibitory protein (cFLIP), key molecules in regulating cell survival and death, CDK9 affected not only the classic RIPK1-RIPK3-mediated necroptosis, but also the alternate TIR-domain-containing adapter-inducing interferon-β-RIPK3-mediated necroptosis. CDK9 inhibition dampened pro-inflammatory gene production in the acute infection process in the subcutaneous chamber model in vivo. Moreover, CDK9 inhibition contributed to the decreased periodontal bone loss and inflammatory response induced by P. gingivalis in the periodontal micro-environment. In conclusion, by modulating the RIPK3-MLKL-mediated necroptosis, CDK9 inhibition provided a novel mechanism to impact the progress of bacterial infection in the periodontal milieu.

Metabolic reprogramming from oxidative phosphorylation to glycolysis have been implicated in the pathogenesis of inflammatory diseases, such as pulmonary hypertension, rheumatoid arthritis and sepsis. Whether metabolic reprogramming participates in the progression of bacteriogenic periodontitis has never been reported. In the present study, we explored metabolic changes in periodontal ligament cells (PDLSCs) in response to Porphyromonas gingivalis. (P. gingivalis)-infected PDLSCs showed distinct metabolomics with metabolic reprogramming from oxidative phosphorylation to glycolysis. In addition, bacteria invasion triggered fundamental changes in glycolysis and tricarboxylate acid (TCA) cycle-related genes, such as the hexokinase (HK), isocitrate dehydrogenase (IDH) and succinate dehydrogenase (SDH). Moreover, P. gingivalis-infected PDLSCs showed accumulation of succinate, elevation in succinate dehydrogenase activity, pileup of reactive oxygen species and activation of hypoxia inducible factor-1α (HIF-1α) pathway. HIF-1α and succinate inhibitors, as well as SDH knockdown alleviated proinflammatory cytokine expression in P. gingivalis-infected PDLSCs. Therefore, targeting metabolic reprogramming by regulating the succinate-SDH–HIF–1α axis may facilitate host modulation therapy of chronic periodontitis.

Glutaraldehyde-fixed pericardium is widely used to replace human heart valves. The lack of endothelialization contributes to calcification and structural-valve deterioration, which is particularly ...

Periodontal homeostasis is maintained by the dynamic equilibrium between cell death, differentiation and proliferation of resident cells in the periodontal microenvironment. Loss of resident periodontal ligament fibroblasts (PDLFs) has been a major challenge in the periodontal treatment. This study aimed to investigate the exact role of necroptotic cell death in periodontal diseases. Elevated levels of receptor-interacting protein serine-threonine kinases -1 (RIPK1), phosphorylated RIPK3, mixed lineage kinase domain-like protein (MLKL), phosphorylated MLKL and FLIPL were observed in gingival tissues collected from patients with untreated chronic periodontitis; whereas no difference in caspase 8 was observed between the periodontitis and healthy control group. In contrast to the high incidence of necroptotic cell death in monocytes during live P. gingivalis infection with a low multiplicity of infection (MOI), necroptosis was only observed in PDLFs with a high MOI. Priming PDLFs with frozen thawed monocytes enhanced proinflammatory responses to P. gingivalis infection; moreover, frozen thawed monocytes stimulation triggered RIPK1, RIPK3 and MLKL-mediated-necroptotic cell death in PDLFs. These results indicated that RIPK3 and MLKL-mediated-necroptotic cell death participated in the pathogenesis of periodontitis, and DAMPs released from monocytes after P. gingivalis stimulation by necroptosis triggered not only inflammatory responses, but also necroptosis of PDLFs.

Objectives The purpose of this study was to investigate whether a novel in situ interdental bone elevation method could achieve vertical bone augmentation around natural teeth. Methods Horizontal periodontal bone defects were created at nine quadrants of mandibles in five dogs. Six weeks later, one of the nine quadrants was randomly chosen as the model control. The remaining mandibles were allocated into two experimental groups: cortical bone removing (CBR) or interdental bone elevation (IBE). For the IBE group, four millimetres of interdental bone blocks were separated and elevated from the base of alveolar bone. Then bone xenografts were implanted beneath the elevated alveolar blocks. Animals were euthanised 12 weeks post‐operation. Cone beam computed tomography (CBCT) examination and histological analysis were performed to evaluate the surgical outcomes. Results Enhanced soft tissue profiles were observed in the two experimental groups as compared to the model control group. CBCT images showed that the height of alveolar bone was significantly higher in the IBE group with bone blocks seated near the cementoenamel junction. Significantly larger area of bone tissues with the highest coronal level of new bone was observed in the IBE group. New bone was observed around the elevated bone blocks with bone remodelling and neovascularisation inside the elevated blocks. Conclusions Vertical bone augmentation at interdental sites may be performed through in situ interdental bone elevation for patients with horizontal alveolar bone resorption.

Objective The purpose of the present study was to explore the sequential changes in the cellular metabolism in gingival fibroblasts (GFs) in response toPorphyromonas gingvalis (P. gingivalis) ATCC33277 infection. Design GFs were treated withP. gingivalis at the MOI of 50 for 4, 24 and 48 h to mimic the early, medium, and late phase in the bacterial infection. LDH assay and cell counting kit-8 were utilized to explore cell death and proliferation. Real-time PCR was utilized to explore the gene transcription of pro-inflammatory genes. The relative levels of biomolecules in GFs were measured by gas chromatography-mass spectrometry. Principal component analysis and orthogonal partial least-squares-discriminant analysis were performed to visualize the metabolic difference among experimental groups. In addition, pathway analysis was conducted regarding differential metabolites in GFs. Results P. gingivalis infection triggered significant gene transcription of IL-1β, IL 6, MCP 1, and MMP 1 in GFs. In addition, P. gingivalis stimulated cell proliferation of GFs at MOI of 10, 50 and 250. Moreover, P. gingivalis triggered significant cell death at higher MOI. 69, 173 and 148 metabolites were qualitatively detected at 4, 24 and 48 h after P. gingivalis infection respectively in GFs, showing a sequential change of different phase. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that ATP-binding cassette transporters, glutathione, purine and pyrimidine metabolism was significantly altered in different phase. Conclusions Human GFs may sequentially rewire metabolomics to shape the inflammatory responses and support the proliferation of host cells during P. gingivalis infection.

To eliminate invading pathogens and keep homeostasis, host employs multiple approaches such as the non-inflammation associated-apoptosis, inflammation associated-necroptosis and pyroptosis, etc. Necroptosis is known as a highly pro-inflammatory form of cell death due to the release of massive damage-associated molecular patterns (DAMPs). For the first time, we reported that Porphyromonas gingivalis induced cellular necroptosis through receptor-interacting protein 1 (RIP1)/RIP3/mixed lineage kinase domain-like (MLKL) signaling pathway in monocytes. Necroptosis in THP-1 cells was induced by MLKL phosphorylation in vitro. P. gingivalis treated-THP-1 cells exhibited lower cell death rate with pretreatment of inhibitors RIP1 and MLKL, accompanied with attenuated TNF-α and IL-6 expressions. Moreover, the necroptosis risk was also reduced via gene silencing by RIP3 or MLKL in the P. gingivalis treated-THP-1 cell lines. We further explored P. gingivalis-induced necroptosis in animal models in vivo. Firstly, C57BL/6 mice were injected with P. gingivalis in the subcutaneous chamber model. Animals pretreated with MLKL inhibitor exhibited significantly enhanced P. gingivalis clearance; in addition, levels of TNF-α and IL-6 were notably decreased by 60% via MLKL inhibition. Secondly, P. gingivalis-induced periodontitis was utilized to investigate necroptosis related-periodontopathogensis. Positive staining of phosphorylated MLKL in mice periodontitis biopsies was detected to a higher degree, while larger amount of alveolar bone loss was observed in MLKL (-) group comparing to those in the MLKL (+) group. These findings may suggest that P. gingivalis play essential roles in necroptosis process during periodontitis, and our research may shed light on the further work on the related periodontopathogenesis investigation.

Rationale: Lymphomas are the second most common non-epithelial malignant tumors in the oral and maxillofacial region. Non-Hodgkin's lymphoma (NHL) develops at extranodal sites, and cases involving the maxilla account for less than 1% of all NHLs. We describe a case of diffuse large B-cell lymphoma (DLBCL) in the maxilla, and highlight the clinical signs, symptoms, differential diagnosis, and appropriate treatment of DLBCL in the oral cavity and maxillofacial region. Patient concerns: A 67-year-old woman was admitted to our surgical department with pain and swelling in her right upper posterior teeth for about six months. She was previously misdiagnosed with periodontal disease and had a history of tooth extraction. Diagnoses: Computed tomography (CT) scan revealed extensive osteolysis in the right posterior part of the maxilla with enhanced neoplasm. A solid mass was found upon incisional biopsy, and immunohistochemistry confirmed the diagnosis of DLBCL. Interventions: The patient was treated with six courses of rituximab, cyclophosphamide, pirarubicin, vincristine, and prednisolone (R-CHOP), followed by external irradiation treatment. Outcomes: The treatment was well tolerated, and the patient is presently alive after two years of follow-up. Lessons: Non-specific symptoms, such as unclear primary dental pain and unresolved periapical swelling, can make an accurate diagnosis of DLBCL difficult, which frequently lead to delayed diagnosis. A CT or cone beam computed tomography (CBCT) scan of the maxilla and immunohistochemical staining of the biopsy specimen is recommended. Combination therapy including radiotherapy and chemotherapy is the optimal treatment for NHL.

To analyze whether upper airway dimensions were influenced by different sagittal skeletal pattern among adolescent patients.Seventy-five adolescent patients were divided into 3 groups based on their ANB angles．The three groups were matched for age and sex． All subjects had a normodivergent skeletal pattern．Airway lengths, cross-sectional measurements and volumes were measured by using cone-beam computed tomography (CBCT) volume scans, and two-dimensional lateral cephalograms were created and analyzed. Airway lengths, cross-sectional measurements and volumes were compared among 3 groups. Statistical analysis was performed using SPSS 22.0 software package.No significant difference among the three groups was found in Anp, Lnp, Lvp, Lgp and Lhp cross-sectional areas of the airway. The glossopharynx volume was smaller in Class II[(2.34±0.79)mL] than in Class Ⅲ[(3.18±0.63)mL] patients(P0.05). Total upper airway volume in Class II[(13.89±2.51)mL] patients was smaller than in Class Ⅰ[(16.48±4.41)mL] and Ⅲ[(17.47±3.55)mL] patients(P0.05).Upper airway volume is significantly reduced in Class II sagittal skeletal pattern, leading to a higher risk of obstructive sleep apnea/hypopnea syndrome.

Background and aim Porphyromonas gingivalis ( P. gingivalis ) lipopolysaccharide (LPS) is reported to be associated with the progression of atherosclerosis (AS). In this study, we explored the potential of human β-defensin-3 (hBD3), an antimicrobial peptide with immunomodulatory properties, to alleviate AS progression accelerated by P. gingivalis LPS and the mechanism underlying this effect. Materials and methods Apolipoprotein E-deficient mice were injected intraperitoneally with hBD3, P. gingivalis LPS, or hBD3 + P. gingivalis LPS. The aorta was assessed immunohistologically and mRNA levels of inflammatory cytokines were determined by quantitative PCR. Macrophages and vascular endothelial cells were stimulated in vitro to investigate the hBD3 target cells. Inflammatory cytokines in serum and cell culture supernatants were detected using cytometric bead arrays. Signaling pathways were investigated by Western blotting. Results In P. gingivalis LPS-treated mice, hBD3 significantly reduced serum IL-6 and TNF-α levels and aortic expression of ICAM-1, IL-6, and MCP-1 (mRNA and protein). The area and severity of atherosclerotic lesions were also diminished, with less advanced plaque formation, more continuous and distinct elastic lamina, and more normal smooth muscle cells arranged along the tunica media layer. In vitro , hBD3 decreased TNF-α, IL-1β, IL-6 secretion and downregulated TNF-α, IL-1β, IL-6, IL-8, VCAM-1, and IL-10 mRNA levels in macrophages. hBD3 did not influence TNF-α, IL-6, and IL-8 levels in HUVECs culture supernatants. Furthermore, hBD3 suppressed P. gingivalis LPS-induced activation of the NF-κB, p38 and JNK pathways. Conclusion hBD3 alleviates AS progression accelerated by P. gingivalis LPS in apolipoprotein E-deficient mice by downregulating the cytokine expression in macrophages via the MAPK and NF-κB signaling pathways.

Human beta-defensin 3 (hBD3) is an antimicrobial peptide showing immunomodulatory effect on both innate and acquired immune response. Atherosclerosis is an inflammatory disease characterized by accumulation of lipids in the vascular wall. In this study, we evaluated whether hBD3 could attenuate the atherosclerosis development accelerated by Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) with apolipoprotein E-deficient (ApoE(-/-)) mice. We observed that, in vivo, hBD3 inhibited serum MCP-1, sICAM-1 levels of ApoE-deficient mice exposed to Pg-LPS in a chronic inflammation model. Serum levels of total cholesterol (TC) and low-density lipoprotein (LDL) were also markedly reduced with hBD3 intervention. In addition, thinned vascular walls, less macrophage infiltration and the formation of atherosclerotic lesions were observed in the hBD3-treated group. Furthermore, in vitro, hBD3 profoundly suppressed the production of TNF-α and IL-6 in RAW 264.7 cells induced by Pg-LPS in a dose-dependent manner. Moreover, hBD3 attenuated the phosphorylation of p38 and ERK1/2 in the mitogen-activated protein kinase (MAPK) pathway. Taken together, our work has revealed that hBD3 exhibits potent anti-inflammatory properties both in vitro and in vivo, and this effect might be correlated with inhibition of MAPK pathway.

To investigate the effects of Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) on apoptotic genes in foam cells.Macrophages from THP-1 monocytes and foam cells from macrophages by oxLDL inducement were treated with oxidized low density lipoprotein (oxLDL) or oxLDL+ Pg-LPS. Cell apoptosis was detected by acridine orange-ethidium bromide (AO-EB) staining. Eleven atherosclerotic related apoptotic genes were examined with polymerase chain reaction (PCR) array, and apoptotic gene p53, c-Myc and caspase-3 were evaluated with real-time PCR.Pg-LPS enhanced cell apoptosis rate during and after foam cells formation [(5.47+/-0.93)% vs. (7.50+/-0.54)%]. PCR array demonstrated that it increased B-cell CLL-lymphoma 2 (BCL2) related protein A1 (BCL2A1) transcription during foam cells formation (2 fold), and promoted BCL2 and BCL2A1 transcription after foam cells formation (2 fold). It promoted p53 and caspase-3 transcription level (4.50x10(-3)+/-4.02x10(-4) vs. 5.30x10(-2)+/-4.58x10(-3)), whereas inhibited c-Myc transcription level (1.53x10(-2)+/-5.77x10(-4)) during foam cells formation. It promoted caspase-3 transcription (6.00x10(-2)+/-6.08x10(-3)), and inhibited p53 transcription (4.23x10(-3)+/-5.85x10(-4)) after foam cells formation.Pg-LPS affected apoptotic gene transcription during and after foam cells formation and enhanced cell apoptosis.