[Changes of parameters associated with anemia of inflammation in patients with stage â ¢ periodontitis before and after periodontal initial therapy].

OBJECTIVE: To investigate the differences and similarities of parameters associated with anemia of inflammation between patients with stage Ⅲ periodontitis and periodontally healthy volunteers, and to explore the influence of periodontal initial therapy on those indicators. METHODS: Patients with stage Ⅲ periodontitis and periodontally healthy volunteers seeking periodontal treatment or prophylaxis at Department of Periodontology, Peking University School and Hospital of Stomatology from February 2020 to February 2023 were enrolled. Their demographic characteristics, periodontal parameters (including probing depth, clinical attachment loss, bleeding index), and fasting blood were gathered before periodontal initial therapy. Three months after periodontal initial therapy, the periodontal parameters of the patients with stage Ⅲ periodontitis were re-evaluated and their fasting blood was collected again. Blood routine examinations (including white blood cells, red blood cells, hemoglobin, packed cell volume, mean corpuscular volume of erythrocytes, and mean corpuscular hemoglobin concentration) were performed. And ferritin, hepcidin, erythropoietin (EPO) were detected with enzyme-linked immunosorbent assay (ELISA). All data analysis was done with SPSS 21.0, independent sample t test, paired t test, and analysis of covariance were used for comparison between the groups. RESULTS: A total of 25 patients with stage Ⅲ periodontitis and 25 periodontally healthy volunteers were included in this study. The patients with stage Ⅲ periodontitis were significantly older than those in periodontally healthy status [(36.72±7.64) years vs. (31.44±7.52) years, P=0.017]. The patients with stage Ⅲ periodontitis showed lower serum hemoglobin [(134.92±12.71) g/L vs. (146.52±12.51) g/L, P=0.002] and higher serum ferritin [(225.08±103.36) µg/L vs. (155.19±115.38) µg/L, P=0.029], EPO [(41.28±12.58) IU/L vs. (28.38±10.52) IU/L, P < 0.001], and hepcidin [(48.03±34.44) µg/L vs. (27.42±15.00) µg/L, P=0.009] compared with periodontally healthy volunteers. After adjusting the age with the covariance analysis, these parameters (hemoglobin, ferritin, EPO, and hepcidin) showed the same trends as independent-sample t test with statistical significance. Three months after periodontal initial therapy, all the periodontal parameters showed statistically significant improvement. The serum hemoglobin raised [(146.05±15.48) g/L vs. (133.77± 13.15) g/L, P < 0.001], while the serum ferritin [(128.52±90.95) µg/L vs. (221.22±102.15) µg/L, P < 0.001], EPO [(27.66±19.67) IU/L vs. (39.63± 12.48) IU/L, P=0.004], and hepcidin [(32.54±18.67) µg/L vs. (48.18±36.74) µg/L, P=0.033] decreased compared with baseline. CONCLUSION: Tendency of iron metabolism disorder and anemia of inflammation was observed in patients with stage Ⅲ periodontitis, which can be attenuated by periodontal initial therapy.

The tendency of anemia of inflammation in periodontal diseases.

Anemia of inflammation (AI) is associated with inflammatory diseases, and inflammation-induced iron metabolism disorder is the major pathogenic factor. Earlier studies have reported a tendency of AI in periodontitis patients, but the explicit relationship and possible pathological mechanisms remain unclear. Here, the analyses of both periodontitis patients and a mouse model of ligature-induced experimental periodontitis showed that periodontitis was associated with lower levels of hemoglobin and hematocrit with evidence of systemic inflammation (increased white blood cell levels) and evidence of iron restriction (low serum iron along with a high serum hepcidin and ferritin levels), in accordance with the current diagnosis criteria for AI. Moreover, periodontal therapy improved the anemia status and iron metabolism disorders. Furthermore, the increased level of hepcidin and significant correlation between hepcidin and key indicators of iron metabolism emphasized the pivotal role of hepcidin in the pathogenesis of periodontitis-related AI. Administration of the signal transducer and activator of transcription 3 (STAT3) inhibitors Stattic suggested that the IL-6-STAT3-hepcidin signaling pathway participated in this regulatory process. Together, these findings demonstrated that periodontitis should be considered an inflammatory disease that contributes to the development of AI; furthermore, IL-6-STAT3-hepcidin signaling pathway plays a key regulatory role in the pathogenesis of periodontitis-related AI. Our study will provide new insights into the systemic effects of periodontitis, while meaningfully expanding the spectrum of inflammatory diseases that contribute to AI.

Human ß-defensins are correlated with the immune infiltration and regulated by vitamin D3 in periodontitis.

OBJECTIVE: Exploring the correlation between human ß-defensins (HBDs) and immune infiltration in periodontitis, and whether it is regulated by vitamin D3 . BACKGROUND: The human body produces essential antimicrobial peptides called HBDs, which are associated with periodontitis. There is a strong link between periodontal tissue destruction and the immune cell infiltration. Moreover, vitamin D3 has been reported to regulate the expression of immune cell chemokines. However, the relationship between vitamin D3 , HBDs, and immune infiltration in periodontitis remains to be investigated. METHODS: The Gene Expression Omnibus database was accessed to obtain transcriptomic information of gingival samples taken from periodontitis patients. The expression value of HBD-2 and HBD-3 was calculated. Additionally, using the online program ImmuCellAl, 10 immune cells were scored for immune infiltration in the high-HBDs-expression group and the low-HBDs-expression group, separately. After that, transcriptome sequencing was done based on human gingival fibroblasts that had received vitamin D3 treatment. Furthermore, hGFs were treated by vitamin D3 , tumor necrosis factor-α (TNF-α), and Porphyromonas gingivalis lipopolysaccharide (Pg-LPS). The expressions of HBD-2, HBD-3, interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) were detected. To seek the potential mechanism, CYP27A1 siRNA was employed to reduce the expression of CYP27A1, and nuclear factor-gene binding protein 65 (NF-κB p65) was examined. RESULTS: In GSE10334, the expressions of HBD-2 and HBD-3 were down-regulated in periodontitis group. Meanwhile, monocyte, macrophage, and CD4_T cell were less infiltrated in low-HBD-2-expression group, while less Gamma-delta T-cell infiltration was found in low-HBD-3-expression group. Transcriptome sequencing found that 21 genes were significantly expressed, of which the function was enriched in response to bacterial origin and TNF signal pathway. Vitamin D3 could significantly up-regulate the expression of HBD-2 and HBD-3, which could be controlled by knocking down CYP27A1 mRNA expression. With prolonged vitamin D3 stimulation, the expression of HBD-2 and HBD-3 increased. TNF-α/Pg-LPS could significantly increase the expression of HBD-2, HBD-3, IL-8, MCP-1, and p65, all of which were reduced by vitamin D3 . CONCLUSION: HBDs are correlated with immune infiltration in periodontitis. Vitamin D3 inhibits the expression of HBDs and chemokines induced by TNF-α/Pg-LPS, possibly through NF-κB pathway, in human gingival fibroblasts.

Application of 3D digital smile design based on virtual articulation analysis in esthetic dentistry: A technique.

A technique for the application of a virtual articulation system in 3-dimensional digital smile design (DSD) during esthetic restoration is described. To acquire stable occlusion and a smooth jaw movement pattern without premature contacts or interference, a digital facebow and a virtual articulator were used to collect and analyze a patient's occlusal data and jaw movement information. The original pattern of occlusal contacts and jaw movements were diagnosed as stable and copied to the digital design of the new prostheses. Preparation of the abutments, crown lengthening surgery, and definitive crown fabrication and cementation were performed according to the design. After 9 months, the occlusion remained stable, and the patient was satisfied with the outcome.

Augmented corticotomy-assisted presurgical orthodontic treatment to prevent alveolar bone loss in patients with skeletal Class III malocclusion.

INTRODUCTION: The objective of this study was to explore the effect of augmented corticotomy (AC) on anterior alveolar bone morphology in presurgical orthodontic treatment for skeletal Class III malocclusion. METHODS: Thirty-six surgical patients with skeletal Class III malocclusion with high-angle were included: 18 (AC group) accepted AC surgery during presurgical orthodontic treatment, and 18 (control group) accepted traditional presurgical orthodontic treatment. Cone-beam computed tomography scans were obtained before treatment (T0) and after presurgical orthodontic treatment (T1). The alveolar bone morphology, root length, dehiscence, and movement of mandibular central incisors were measured by cone-beam computed tomography using Dolphin software. Statistical analyses were performed with independent-sample t tests, paired t tests, and multiple linear regression. RESULTS: After presurgical orthodontic treatment, the whole alveolar bone thickness at each level, alveolar bone area, and alveolar bone height decreased significantly in the control group but increased or remained unchanged in the AC group. In the AC group, the lower the labial alveolar bone height at T0 was, the greater the increase after T1; the change in alveolar bone thickness was related to ΔL1-MP and sex. At T0, the incidences of dehiscence were similar in the 2 groups, ranging from 11.11% to 16.67%. At T1, the labial and lingual incidences of dehiscence in the AC group were 0% and 27.78%, compared with 55.56% and 66.67% in the control group. CONCLUSIONS: During presurgical orthodontic treatment, AC is effective in preventing alveolar bone resorption and dehiscence without additional root resorption. AC can be recommended for high-angle skeletal Class III patients with thin alveolar bone around anterior teeth during presurgical orthodontic treatment.

Three-dimensional measurement of periodontal support during surgical orthodontic treatment of high-angle skeletal Class III malocclusion: A retrospective study.

INTRODUCTION: This study aimed to quantify the periodontal health of incisors during surgical orthodontic treatment in patients with high-angle Class III malocclusion using a cone-beam computed tomography (CBCT) 3-dimensional (3D) reconstruction technique. METHODS: The sample consisted of 30 patients with high-angle Class III malocclusion (mean age, 20.53 ± 2.86 years). CBCT images were taken before treatment (T0), after presurgical orthodontic treatment, and after treatment (T2). In addition, 3D tooth and alveolar bone models were generated. The root surface area, periodontal ligament (PDL)_Area, and vertical bone level (VBL) around the maxillary and mandibular central incisors were measured. RESULTS: The root surface area and PDL_Area of maxillary and mandibular central incisors decreased continuously between T0 and T2 (P <0.01). At T2, mandibular central incisors showed 38.64 ± 13.39% PDL_Area loss, and maxillary central incisors exhibited 21.13 ± 16.48% PDL_Area loss. For mandibular central incisors, the PDL_Area loss caused by VBL loss was significantly greater than that for maxillary central incisors (P <0.01) and significantly greater than the PDL_Area loss caused by root resorption (P <0.01). From T0 to T2, the lingual surface of maxillary central incisors exhibited greater VBL loss than the other 3 surfaces (P <0.01), and the labial and lingual surfaces of mandibular central incisors demonstrated greater VBL loss than proximal surfaces (P <0.01). CONCLUSIONS: The 3D CBCT reconstruction method provides useful information regarding the periodontal defects of incisors in patients with high-angle skeletal Class III malocclusion. The PDL_Area of maxillary and mandibular central incisors decreased continuously during the treatment. Vertical alveolar bone levels at proximal surfaces appeared to be relatively stable.

Association between Osteoprotegerin rs2073618 polymorphism and peri-implantitis susceptibility: a meta-analysis.

OBJECTIVES: Peri-implantitis was an inflammatory progress on the tissue around the implant. The Osteoprotegerin G1181C (rs2073618) polymorphism was reported to be related to the increased risk of the peri-implantitis, whereas another found no relationship. The present study was conducted to research the relationship between Osteoprotegerin rs2073618 polymorphism and peri-implantitis susceptibility. MATERIALS AND METHODS: The meta-analysis was performed according to the Preferred Reporting Items for Systematic reviews. Electronic databases including PubMed, Web of science, Springer Link and Embase (updated to April 15, 2022) were retrieved. The cohort study, case-control study or cross-sectional study focusing on the Osteoprotegerin rs2073618 polymorphism and peri-implantitis were retrieved. The data included basic information of each study and the genotype and allele frequencies of the cases and controls. RESULTS: Three studies were finally included, including 160 cases and 271 controls. Allelic model, homozygote model, recessive model, dominant model, and heterozygous model were established to assess the relationship between OPG rs2073618 polymorphism and peri-implantitis susceptibility. The Osteoprotegerin rs2073618 polymorphism was significantly associated with peri-implantitis in Recessive model and Homozygote model. CONCLUSION: OPG rs2073618 polymorphism in Recessive model and Homozygote model was highly likely related to the risk of peri-implantitis. PROSPERO registration number: CRD42022320812.

Potential links between COVID-19 and periodontitis: a bioinformatic analysis based on GEO datasets.

BACKGROUND: 2019 Coronavirus disease (COVID-19) is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 pandemic has already had a serious influence on human existence, causing a huge public health concern for countries all around the world. Because SARS-CoV-2 infection can be spread by contact with the oral cavity, the link between oral illness and COVID-19 is gaining traction. Through bioinformatics approaches, we explored the possible molecular mechanisms linking the COVID-19 and periodontitis to provide the basis and direction for future research. METHODS: Transcriptomic data from blood samples of patients with COVID-19 and periodontitis was downloaded from the Gene Expression Omnibus database. The shared differentially expressed genes were identified. The analysis of Gene Ontology, Kyoto Encyclopedia of Genesand Genomes pathway, and protein-protein interaction network was conducted for the shared differentially expressed genes. Top 5 hub genes were selected through Maximal Clique Centrality algorithm. Then mRNA-miRNA network of the hub genes was established based on miRDB database, miRTarbase database and Targetscan database. The Least absolute shrinkage and selection operator regression analysis was used to discover possible biomarkers, which were then investigated in relation to immune-related genes. RESULTS: Fifty-six shared genes were identified through differential expression analysis in COVID-19 and periodontitis. The function of these genes was enriched in regulation of hormone secretion, regulation of secretion by cell. Myozenin 2 was identified through Least absolute shrinkage and selection operator regression Analysis, which was down-regulated in both COVID-19 and periodontitis. There was a positive correlation between Myozenin 2 and the biomarker of activated B cell, memory B cell, effector memory CD4 T cell, Type 17 helper cell, T follicular helper cell and Type 2 helper cell. CONCLUSION: By bioinformatics analysis, Myozenin 2 is predicted to correlate to the pathogenesis and immune infiltrating of COVID-19 and periodontitis. However, more clinical and experimental researches are needed to validate the function of Myozenin 2.

Periodontal soft tissue increase induced by periodontally accelerated osteogenic orthodontics surgery.

OBJECTIVES: To quantitatively assess periodontal soft tissue changes, including gingival thickness and keratinized gingiva width after periodontally accelerated osteogenic orthodontics (PAOO) surgery by digital measurements.  METHODS: This study enrolled 15 maxillaries with 89 anterior teeth and 16 mandibles with 94 anterior teeth from Chinese adult patients with skeletal Angle Class III malocclusion for whom PAOO surgery was proposed during orthodontic treatment. Intraoral scanning and cone beam computed tomography (CBCT) examinations were performed before PAOO surgery and 6 months after the surgery. Keratinized gingiva width was measured on the digital model acquired by intraoral scanning. The gingival thickness was measured using a digital three-dimensional (3D) model based on the combination of digital intraoral scanning and CBCT data. RESULTS: The mean gingival thickness before surgery was 0.91 ± 0.32 mm and 1.21 ± 0.38 mm at 6-month after PAOO. Patients showed periodontal soft tissue increase with a mean gingival tissue gain of 0.30 ± 0.33 mm. At 1 mm, 2 and 3 mm apical to cemento-enamel junction (CEJ) levels, the gingival thickness increase of the mandible was higher than that of the maxilla (0.38 ± 0.30 mm vs. 0.24 ± 0.31 mm, 0.43 ± 0.35 mm vs. 0.26 ± 0.41 mm, 0.36 ± 0.27 vs. 0.25 ± 0.32 mm, respectively, all P < 0.05). Moreover, the sites of gingival thickness ≤ 1 mm before surgery showed more tissue gain than the sites > 1 mm (0.36 ± 0.32 mm vs. 0.18 ± 0.31 mm, P < 0.001). The mean keratinized gingiva width at T0 was 3.88 ± 1.22 mm, and increased 1.05 ± 1.24 mm 6 months after PAOO surgery. Moreover, a digital 3D model for gingival thickness measurement based on the combination of digital intraoral scanning and CBCT displayed high reliability and accuracy with an intra-class correlation coefficient (ICC) of 0.897. CONCLUSION: PAOO could improve an insufficient quantity of periodontal soft and hard tissues in patients with skeletal Angle Class III malocclusion, including the gingival thickness and keratinized gingiva width. A digital 3D model based on the combination of digital intraoral scanning and CBCT data could provide a new digital measurement of gingival thickness with high accuracy and reliability.

Calprotectin levels in gingival crevicular fluid and serum of patients with chronic periodontitis and type 2 diabetes mellitus before and after initial periodontal therapy.

BACKGROUND: This study is aimed to compare the total amount of calprotectin in gingival crevicular fluid (GCF) and the concentration of calprotectin in serum among the patients with type 2 diabetes mellitus and chronic periodontitis (DM-P), the patients with chronic periodontitis (CP) and the healthy controls, as well as the variation of these indicators before and three months after the initial periodontal therapy for the DM-P patients. METHODS: 35 patients with DM-P patients, 32 patients with CP patients, and 43 healthy controls were recruited. Calprotectin levels in serum and GCF, periodontal parameters, fasting blood glucose (FBG), and HbA1c were measured at baseline for all the groups and three months after the initial periodontal therapy for the DM-P patients. RESULTS: At baseline, the calprotectin levels in GCF and serum were the highest in DM-P, followed by CP, and the lowest in healthy controls. GCF calprotectin was significantly and positively correlated with serum calprotectin and probing depth (PD), while serum calprotectin had a significant positive correlation with GCF calprotectin and HbA1c. Periodontal parameters, HbA1c, and serum and GCF calprotectin became significantly reduced after the initial periodontal treatment. The reduction of serum calprotectin was consistent with that of HbA1c, while the decrease of GCF calprotectin was in agreement with that of PD, attachment loss (AL), and bleeding on probing (BOP). CONCLUSIONS: The levels of calprotectin in serum and GCF in the DM-P patients are significantly higher than those in CP patients and healthy controls, which significantly reduced 3 months after the initial periodontal therapy. Furthermore, it suggests diabetic patients might exhibit more pronounced inflammation periodontally and systemically.

Pro-inflammatory cytokine interleukin-6-induced hepcidin, a key mediator of periodontitis-related anemia of inflammation.

OBJECTIVES: To investigate whether anemia of inflammation (AI) occurs in periodontitis patients and to further explore underlying pathogenesis of periodontitis-related AI by an experimental periodontitis model. BACKGROUND: Previous studies have reported periodontitis patients could show a tendency toward AI. However, the relationship between periodontitis and AI remains unclear, and the related pathological mechanisms have not been identified. MATERIALS AND METHODS: Periodontal clinical parameters, inflammatory markers, and anemia-related indicators were compared between 98 aggressive periodontitis (AgP) patients and 103 healthy subjects. An experimental periodontitis model was induced by ligature placement in mice. The changes in mice inflammatory markers, anemia indicators, hepcidin mRNA expression, and serum hepcidin concentrations were measured. Human and mouse liver cells were treated with interleukin-6 (IL-6) for analyzing the changes in hepcidin expression based on mRNA and protein levels. RESULTS: AgP patients exhibited higher white blood cell counts, IL-6, and C-reactive protein. Adjusted linear regression analyses showed correlations between AgP and decreased hemoglobin (HGB) and hematocrit (HCT). The ligature-induced periodontitis caused systemic inflammation and elevated IL-6 levels. Lower red blood cell counts, HGB, and HCT were detected, whereas the levels of hepcidin mRNA expression and serum hepcidin concentrations increased. The treatment of hepatocytes with IL-6 induced both hepcidin mRNA expression and hepcidin secretion. CONCLUSIONS: Systemic inflammation induced by periodontitis leads to an increased risk for AI. IL-6-induced hepcidin could play a central mediator role and act as a key pathologic mechanism. Our results demonstrate periodontitis may be considered as an additional inflammatory disease contributing to the development of AI.

Morphometric evaluation of the alveolar bone around central incisors during surgical orthodontic treatment of high-angle skeletal class III malocclusion.

OBJECTIVES: To evaluate morphometric characteristics of alveolar bone around the incisors of high-angle skeletal class III patients receiving surgical orthodontic treatment. SETTING AND SAMPLE POPULATION: Thirty high-angle skeletal class III patients (mean age, 20.94 ± 3.25 years) underwent cone-beam computed tomography before treatment (T0), after pre-surgical orthodontic treatment (T1) and after treatment (T2). MATERIALS AND METHODS: The vertical bone level (VBL), alveolar bone thickness (ABT), alveolar bone area (ABA) and position of upper and lower central incisors (UCIs and LCIs) were evaluated. The ABT included five levels (4, 6, 8 mm from the cemento-enamel junction, midroot and root apex level). One-way repeated measures ANOVA with Bonferroni's multiple-comparison test and matched t test was performed to compare variables. RESULTS: Before treatment, the average labial ABT was approximately 1 mm in UCIs and 0.38 ~ 0.79 mm in LCIs, and the VBL of the LCIs was over 2 mm. After treatment, the VBL increased by 2.19 ± 1.96 mm (P < .001) on the lingual side of UCIs and 2.78 ± 2.29 mm and 3.09 ± 2.52 mm on the labial and lingual sides of LCIs, respectively (all P < .001). ABT at every level decreased significantly, decreasing by 1.66 ± 1.93 mm at the 8 mm level of UCIs and 1.06 ± 1.01 mm at the apex of LCIs (P < .001). The lingual ABA of UCIs and LCIs decreased by over 50% (P < .001). CONCLUSIONS: In high-angle skeletal class III patients, the condition of alveolar bone around UCIs and LCIs was extremely poor before treatment. Further alveolar bone resorption occurred during surgical orthodontic treatment. More attention should be paid to the movement of anterior teeth in cases of severe alveolar bone loss.

Nomogram prediction of vulnerable periodontal condition before orthodontic treatment in the anterior teeth of Chinese patients with skeletal Class III malocclusion.

OBJECTIVE: To establish and verify models predictive of thin periodontal phenotype and alveolar fenestration/dehiscence in the anterior teeth of patients with skeletal Class III malocclusion. MATERIAL AND METHODS: Retrospective data of 669 anterior teeth (305 in maxillae and 364 in mandibles) from 80 patients with skeletal Class III malocclusion before augmented corticotomy were collected. Distribution of thin periodontal phenotype and alveolar fenestration and dehiscence were evaluated and their associations with potential influencing factors were explored using univariate and multivariate analyses. The predictive models were visualized as nomograms, the accuracy of which was tested by receiver operating curve analyses. RESULTS: Thin phenotype was associated with Mazza bleeding index, sex, tooth type, probing depth and width of keratinized gingiva (WKG). Labial dehiscence was associated with age, jaw, labial bone thickness, mandibular plane angle, sagittal root position (SRP), sex, tooth type, and WKG. Labial fenestration was associated with sex, tooth type, SRP, and periodontal phenotype. The areas under the curves of nomogram prediction models for periodontal phenotype, alveolar dehiscence, and alveolar fenestration were 0.84, 0.81, and 0.73, respectively. CONCLUSIONS: Female sex, lateral incisor, and limited WKG may be risk factors for thin periodontal phenotype. Age, canine, male sex, mandible, thin labial bone thickness, and root positioned against the labial plate may be risk factors for labial dehiscence; and female sex, thick phenotype, root positioned against the labial plate, lateral incisor, and canine may be risk factors for labial fenestration. The predictive performance of the models was acceptable.

A digital technique for splinting periodontally compromised mobile teeth in the mandibular anterior region.

A digital technique for fabricating a periodontal splint is presented. The lingual surface of periodontally compromised mandibular anterior teeth is captured and registered to form the emergence profile of the periodontal splint. An accurate periodontal splint is fabricated for mandibular anterior teeth with increased mobility after scaling and root planing.

Prevalence of and risk factors for alveolar fenestration and dehiscence in the anterior teeth of Chinese patients with skeletal Class III malocclusion.

INTRODUCTION: This study investigated the prevalence of and risk factors for alveolar fenestration and dehiscence in the anterior teeth of Chinese patients with skeletal Class III malocclusion. METHODS: This study included clinical and radiographic examinations and intraoperative observations of 460 anterior teeth from 54 patients who underwent corticotomy and periodontal regenerative surgery before orthodontic treatment. Fenestration and dehiscence were detected and recorded during open-flap surgery. Univariate and multivariate analyses were performed to assess relationships between fenestration and dehiscence and age, sex, history of previous orthodontic treatment, mandibular plane angle, dentition, tooth position, sagittal root position, periodontal biotype, gingival recession, width of keratinized gingiva, and width of the basal bone. RESULTS: The prevalence of buccal alveolar bone defects was 16.1% (fenestration) and 20.7% (dehiscence) at the tooth level. Multivariate logistic regressions showed that fenestration was significantly associated with tooth position (canine vs central incisor, odds ratio [OR] = 3.324; P = 0.006; lateral incisor vs central incisor, OR = 5.588; P  <0.001), and sagittal root position (buccally positioned vs centrally positioned, OR = 5.865; P = 0.025). Dehiscence was significantly associated with dentition (mandible vs maxilla, OR = 11.685; P  <0.001), tooth position (canine vs central incisor, OR = 3.863; P = 0.007), age (OR = 1.227; P = 0.010), sex (male vs female, OR = 5.530; P = 0.026), and history of orthodontic treatment (yes vs no, OR = 4.773; P = 0.028). CONCLUSIONS: Buccally positioned teeth in the osseous housing, lateral incisors, and canines were more likely to exhibit alveolar fenestration. Mandibular teeth and canines, patients who were older, were male, and had a history of orthodontic treatment, were more likely to exhibit alveolar dehiscence.

Digital Workflow for Full-Arch Immediate Implant Placement Using a Stackable Surgical Guide Fabricated Using SLM Technology.

The failing dentition of partially edentulous individuals may be used as an initial reference for stackable restrictive surgical guides during full-arch immediate implant placement. The stackable guide option derived from a digital workflow increases the predictability of the performance of bone reduction, immediate implant placement, and immediate loading of provisional implant-supported fixed dental prostheses. The present paper aims to report a practical approach to design and produce a metal framework with occlusal rests to facilitate the use of a tooth-supported surgical guide when full-arch immediate implant placement is indicated in patients with failing dentition.

Platelets as inflammatory mediators in a murine model of periodontitis.

AIM: To investigate the role of platelets during the development of ligature-induced experimental periodontitis in mice. MATERIALS AND METHODS: Experimental periodontitis was induced by placement of sterilized 5-0 cotton ligatures around the maxillary and mandibular second molars of C57BL/6 wild-type mice. Flow cytometry was used to analyse platelet activation and platelet-leucocyte aggregate formation, and histologic analysis was used to evaluate inflammation and localization of platelets and leucocytes in periodontal tissues during the development of experimental periodontitis and in experimental periodontitis with and without antiplatelet drug treatment. RESULTS: Experimental periodontitis induced platelet activation and platelet-leucocyte interaction. Platelets and leucocytes gradually infiltrated in inflammatory gingival tissues during the development of experimental periodontitis. The inhibition of platelet activation via drug therapy led to significant inhibition of leucocyte migration and marked reduction in periodontal inflammation. CONCLUSION: This study revealed that platelets are critical for inflammation and tissue injury in periodontitis and serve as mediators of inflammation in periodontal tissue.

Up-regulated ferritin in periodontitis promotes inflammatory cytokine expression in human periodontal ligament cells through transferrin receptor via ERK/P38 MAPK pathways.

OBJECTIVE: Ferritin, an iron-binding protein, is ubiquitous and highly conserved; it plays a crucial role in inflammation, which is the main symptom of periodontitis. Full-length cDNA library analyses have demonstrated abundant expression of ferritin in human periodontal ligament. The aims of the present study were to explore how ferritin is regulated by local inflammation, and to investigate its functions and mechanisms of action in the process of periodontitis. METHODS: Human gingival tissues were collected from periodontitis patients and healthy individuals. Experimental periodontitis was induced by ligature of second molars in mice. The expression of ferritin light polypeptide (FTL) and ferritin heavy polypeptide (FTH) were assessed by immunohistochemistry. Meanwhile, after stimulating human periodontal ligament cells (HPDLCs) with P. gingivalis-lipopolysaccharide (LPS), interleukin (IL)-6, and tumor necrosis factor-α (TNF-α), the expression of FTH and FTL were measured. Then, IL-6 and IL-8 were measured after incubation with different concentrations of apoferritin (iron-free ferritin) and several intracellular signaling pathway inhibitors, or after knockdown of the transferrin receptor. RESULTS: Both FTH and FTL were substantially higher in inflamed periodontal tissues than in healthy tissues. The location of the elevated expression correlated well with the extent of inflammatory infiltration. Moreover, expression of FTH and FTL were enhanced after stimulation with P. gingivalis-LPS, IL-6, TNF-α. Apoferritin induced the production of IL-6 and IL-8 in a dose-dependent manner partly through binding to the transferrin receptor and activating ERK/P38 signaling pathways in HPDLCs. CONCLUSIONS: Ferritin is up-regulated by inflammation and exhibits cytokine-like activity in HPDLCs inducing a signaling cascade that promotes expression of pro-inflammatory cytokines associated with periodontitis.

The role of platelets in inflammatory immune responses in generalized aggressive periodontitis.

AIM: To investigate the relationship between inflammatory markers and platelet size in generalized aggressive periodontitis (GAgP). MATERIAL AND METHODS: Periodontal, inflammatory and platelet indices were compared between 59 GAgP patients and 59 healthy subjects. Gingival biopsies from five patients and five healthy subjects were examined by immunohistochemistry and electron microscopy. Changes in patient periodontal and platelet indices were re-evaluated at 3 months after periodontal therapy. RESULTS: Platelet size was decreased significantly in GAgP patients compared to healthy subjects (p ≤ 0.003). Weak negative correlations between platelet size and periodontal parameters were found in GAgP patients (p ≤ 0.025). Platelet aggregates and adhesion to the endothelium or leucocytes were found in venules and connective tissues of gingival biopsies from GAgP patients. Mean platelet volume (MPV) and platelet large cell ratio increased after periodontal therapy in GAgP patients (p ≤ 0.038). The increase in MPV was related to the decrease in bleeding index in GAgP patients after periodontal therapy (p < 0.001; r = 0.357). CONCLUSION: Platelet size was reduced in GAgP patients compared to healthy controls, possibly due to the consumption of large platelets at sites of periodontal inflammation. Platelets may be involved in host responses to periodontal infection in GAgP.

Leptin and its receptor expression in dental and periodontal tissues of primates.

Leptin and its receptor (OBR) have attracted much attention since their discovery. They have been reported to play central roles in energy balance, the immune-inflammatory response and bone metabolism. Evidence indicates that leptin and OBR are associated with inflammatory diseases of dental and periodontal tissues. The first step for establishing this is to determine the expression of leptin and OBR in these tissues. Our study is the first to examine systematically the expression of leptin and OBR in dental and periodontal tissues of monkeys (Macaca fascicularis) by immunohistochemistry and in primary cultured cells, isolated from human dental and periodontal tissues, by reverse transcription plus the polymerase chain reaction and immunocytochemistry. Our results show that leptin and OBR are constitutively expressed and widely distributed in dental and periodontal tissues of primates. Their immunoreaction is especially strong in junctional epithelium, a unique front-line defense around teeth and in mineralizing areas of the dental pulp and periodontal ligament. The expression of the long and also functional form of OBR (OBRb) indicates that leptin has a direct effect on these cells. Thus, we can reasonably infer that leptin and OBR exert effects on defense, mineralization and angiogenesis in dental and periodontal tissues of primates.