Mutations of Glu560 within HIV-1 Envelope Glycoprotein N-terminal heptad repeat region contribute to resistance to peptide inhibitors of virus entry.

BACKGROUND: Peptides corresponding to N- and C-terminal heptad repeat regions (HR1 and HR2, respectively) of gp41 can inhibit HIV-1 infection in a dominant negative manner by interfering with refolding of the viral HR1 and HR2 to form a six-helix bundle (6HB) that induces fusion between viral and host cell membranes. Previously, we found that HIV-1 acquired the mutations of Glu560 (E560) in HR1 of envelope (Env) to escape peptide inhibitors. The present study aimed to elucidate the critical role of position 560 in the virus entry and potential resistance mechanisms. RESULTS: The Glu560Lys/Asp/Gly (E560K/D/G) mutations in HR1 of gp41 that are selected under the pressure of N- and C-peptide inhibitors modified its molecular interactions with HR2 to change 6HB stability and peptide inhibitor binding. E560K mutation increased 6HB thermostability and resulted in resistance to N peptide inhibitors, but E560G or E560D as compensatory mutations destabilized the 6HB to reduce inhibitor binding and resulted in increased resistance to C peptide inhibitor, T20. Significantly, the neutralizing activities of all mutants to soluble CD4 and broadly neutralizing antibodies targeting membrane proximal external region, 2F5 and 4E10 were improved, indicating the mutations of E560 could regulate Env conformations through cross interactions with gp120 or gp41. The molecular modeling analysis of E560K/D/G mutants suggested that position 560 might interact with the residues within two potentially flexible topological layer 1 and layer 2 in the gp120 inner domain to apparently affect the CD4 utilization. The E560K/D/G mutations changed its interactions with Gln650 (Q650) in HR2 to contribute to the resistance of peptide inhibitors. CONCLUSIONS: These findings identify the contributions of mutations of E560K/D/G in the highly conserved gp41 and highlight Env's high degree of plasticity for virus entry and inhibitor design.

miR-155 promotes macrophage pyroptosis induced by Porphyromonas gingivalis through regulating the NLRP3 inflammasome.

OBJECTIVE: The aim of this study is to detect pyroptosis in macrophages stimulated with Porphyromonas gingivalis and elucidate the mechanism by which P. gingivalis induces pyroptosis in macrophages. METHODS: The immortalized human monocyte cell line U937 was stimulated with P. gingivalis W83. Flow cytometry was carried out to detect pyroptosis in macrophages. The expression of miR-155 was detected by real-time PCR and inhibited using RNAi. Suppressor of cytokine signaling (SOCS) 1, cleaved GSDMD, caspase (CAS)-1, caspase-11, apoptosis-associated speck-like protein (ASC), and NOD-like receptor protein 3 (NLRP3) were detected by Western blotting, and IL-1ß and IL-18 were detected by ELISA. RESULTS: The rate of pyroptosis in macrophages and the expression of miR-155 increased upon stimulation with P. gingivalis and pyroptosis rate decreased when miR-155 was silenced. GSDMD-NT, CAS-11, CAS-1, ASC, NLRP3, IL-1ß, and IL-18 levels increased, but SOCS1 decreased in U937 cells after stimulated with P. gingivalis. These changes were weakened in P. gingivalis-stimulated U937 macrophages transfected with lentiviruses carrying miR-155 shRNA compared to those transfected with non-targeting control sequence. However, there was no significant difference in ASC expression between P. gingivalis-stimulated shCont and shMiR-155 cells. CONCLUSIONS: Porphyromonas gingivalis promotes pyroptosis in macrophages during early infection. miR-155 is involved in this process through regulating the NLRP3 inflammasome.

Porphyromonas gingivalis can invade periodontal ligament stem cells.

BACKGROUND: Porphyromonas gingivalis is strongly associated with the development, progression, severity and recurrence of periodontitis. Periodontal ligament stem cells (PDLSCs) play an important role in the maintenance of periodontal tissue self-renewal and repair. The purpose of this study was to investigate the ability of P. gingivalis to infect PDLSCs using an in vitro monolayer model. METHODS: We separated and cultured primary PDLSCs using the tissue block with limiting dilution method. The efficiency of P. gingivalis (ATCC 33277) infection of PDLSCs was measured using agar plate culture and quantitative polymerase chain reaction (q-PCR) methods. PDLSCs infected with P. gingivalis were also observed by transmission electron microscopy. RESULTS: We assessed stem cell properties including cell morphology, clone formation, growth activity, cell surface antigens and multiple differentiation capacity. The infection rates of P. gingivalis in PDLSC at MOIs of 50, 100, 200, and 500 were 5.83%, 8.12%, 7.77% and 7.53% according to the agar plate culture method. By q-PCR, the efficiencies of P. gingivalis infection of PDLSCs at MOIs of 50, 100, 200, and 500 were 6.74%, 10.56%, 10.36% and 9.78%, respectively. Overall, the infection efficiency based on q-PCR was higher than that according to agar plate culture. Using transmission electron microscopy, we verified that P. gingivalis (ATCC 33277) could infect and invade PDLSCs after 2 h of incubation, and endocytic vacuoles were not found surrounding the internalized bacteria. CONCLUSIONS: In conclusion, our data demonstrate that P. gingivalis can invade PDLSCs.

Significance of maxillary sinus mucosal thickening in patients with periodontal disease.

AIM: To characterise and measure the Schneiderian membranes of individuals with periodontal diseases in China and to analyse the factors impacting maxillary sinus mucosal thickness using cone-beam computed tomography (CBCT). MATERIAL AND METHOD: A cohort of 221 patients with periodontal disease was subjected to cross-sectional CBCT examination. Various parameters, including age, sex, alveolar bone loss, furcation lesions and vertical infrabony pockets, were analysed as correlates of mucosal thickening (MT). Sinus mucosal thickness ≥ 2 mm qualified as MT. RESULTS: MT was detected in 103 (48.9%) patients, increasing in frequency as the degree of alveolar bone loss advanced (mild, 14.5%; moderate, 29.5%; severe, 87.9%). The association between MT and vertical infrabony pockets was statistically significant (P < 0.001). The likelihood of MT increased with moderate [odds ratio (OR) = 1.02] and severe (OR = 4.62) periodontal bone loss (P < 0.001), as well as with furcation lesions (OR = 2.76) and vertical infrabony pockets (OR = 13.58). CONCLUSIONS: Relative to the case in patients with periodontitis and normal mucosa, the probability of MT increased dramatically as alveolar bone loss worsened. Periodontal pathologies (i.e. furcation lesions and vertical infrabony pockets) were also more likely to coincide with MT.

Expression of histone deacetylase-1 and p300 in aristolochic acid nephropathy models.

Aristolochic acid nephropathy (AAN) is mainly caused by aristolochic acid I (AAI), but the actual mechanism is still uncertain. The current study explored the correlation among the expression of Smad7, p300, histone deacetylase-1 (HDAC1) and the development of AAN using transmission electron microscopy (TEM), RT-PCR, and western blotting in the AAN mouse model and in the AAN cell model. TEM revealed that the renal tubular epithelial cells from the AAI-treated mice presented organelle damages and nuclear deformation. We found that a certain dose of AAI caused renal fibrosis and induced renal tubular epithelial cells to differentiate into myofibroblasts. There was a gradual increase in the expression of HDAC1 mRNA and protein observed using RT-PCR and western blotting in the AAN cell model compared with the control group. Gradual decrease in the expression of Smad7 and p300 mRNA and protein was revealed in the AAN mouse and cell models compared with the control group. These results suggest that AAI dose dependently contributed to the development of AAN, and HDAC1 and p300 participate in the modulation of TGF-ß/Smad pathway-mediated renal interstitial fibrosis.

Evaluation and comparative assessment of clear aligners and conventional appliances on oral health-related quality of life in pediatric populations: a cross-sectional study.

This study was designed to evaluate and compare the usefulness of clear aligners and conventional appliances on Oral Health-Related Quality of Life (OHRQoL) in pediatric population. Emphasis was placed on the relative benefits and implications of employing clear aligners owing to their escalating prevalence and acceptability. The study participants were divided into four groups: Clear Aligner Group (CAG), Conventional Appliance Group (ConAG), Malocclusion Control Group (MCG), and Normal Control Group (NCG). Parameters including sociodemographic indicators and daily routines were assessed. OHRQoL was evaluated via the Child Perceptions Questionnaire (CPQ). Psychological conditions were assessed through the Depression, Anxiety and Stress Scale (DASS). Statistical differences were found between the four groups regarding CPQ subscales and total scores (p < 0.05). CAG was better than ConAG (p < 0.05) regarding the scores of functional limitations, emotional and social well-being, and total score, however no significant difference was discovered in the oral symptoms scores (p = 0.62). Moreover, all the treatment groups had worse OHRQoL compared to NCG (p < 0.05). Malocclusions and their treatments did not increase the psychological distress as per the DASS results. A novel correlation between the excessive tooth brushing and reduced OHRQoL was also observed (p < 0.05). The study herein emphasized the benefits of clear aligners in children and adolescents with OHRQoL. It was highlighted that the clear aligners had potential and were preferred for the adolescent orthodontic treatment.

The pancreatic clock is a key determinant of pancreatic fibrosis progression and exocrine dysfunction.

Chronic pancreatitis (CP) is characterized by progressive fibrosis and exocrine dysregulation, which have long been considered irreversible. As a peripheral oscillator, the pancreas harbors autonomous and self-sustained timekeeping systems in both its endocrine and exocrine compartments, although the role of the latter remains poorly understood. By using different models of CP established in mice with dysfunctional pancreatic clocks, we found that the local clock played an important role in CP pathology, and genetic or external disruption of the pancreatic clock exacerbated fibrogenesis and exocrine insufficiency. Mechanistically, an impaired retinoic acid receptor-related orphan receptor A (Rora)/nuclear receptor subfamily 1, group D, member 1 (Nr1d1)/aryl hydrocarbon receptor nuclear translocator-like (Arntl or Bmal1) loop, called the circadian stabilizing loop, resulted in the deficiency of pancreatic Bmal1, which was responsible for controlling the fibrogenic properties of pancreatic stellate cells (PSCs) and for rewiring the function of acinar cells in a clock-TGF signaling-IL-11/IL-11RA axis-dependent manner. During PSC activation, the antagonistic interaction between Nr1d1 and Rora was unbalanced in response to the loss of cytoplasmic retinoid-containing lipid droplets. Patients with CP also exhibited reduced production of endogenous melatonin. Enhancing the clock through pharmacological restoration of the circadian stabilizing loop using a combination of melatonin and the Rora agonist SR1078 attenuated intrapancreatic pathological changes in mouse models of CP. Collectively, this study identified a protective role of the pancreatic clock against pancreatic fibrosis and exocrine dysfunction. Pancreatic clock-targeted therapy may represent a potential strategy to treat CP.

A highland-adaptation mutation of the Epas1 protein increases its stability and disrupts the circadian clock in the plateau pika.

The Qinghai-Tibet Plateau (QTP) harbors hundreds of species well adapted to its extreme conditions, including its low-oxygen (hypoxic) atmosphere. Here, we show that the plateau pika-a keystone mammal of the QTP-lacks robust circadian rhythms. The major form of the plateau pika Epas1 protein includes a 24-residue insert caused by a point mutation at the 5' juncture site of Intron14 and is more stable than other mammalian orthologs. Biochemical studies reveal that an Epas1-Bmal1 complex with lower trans-activation activity occupies the E1/E2 motifs at the promoter of the core-clock gene Per2, thus explaining how an Epas1 mutation-selected in the hypoxic conditions of the QTP-disrupts the molecular clockwork. Importantly, experiments with hypoxic chambers show that mice expressing the plateau pika Epas1 ortholog in their suprachiasmatic nucleus have dysregulated central clocks, and pika Epas1 knockin mice reared in hypoxic conditions exhibit dramatically reduced heart damage compared with wild-type animals.

Identification of PCBP1 as a Novel Modulator of Mammalian Circadian Clock.

The circadian clock governs our daily cycle of behavior and physiology. Previous studies have identified a handful of core clock components and hundreds of circadian modifiers. Here, we report the discovery that poly(C)-binding protein 1 (PCBP1), displaying a circadian expression pattern, was a novel circadian clock regulator. We found that knocking down PCBP1 resulted in period shortening in human U2OS cells, and that manipulations of PCBP1 expression altered the activity of CLOCK/BMAL1 in an E-box-based reporter assay. Further mechanistic study demonstrated that this clock function of PCBP1 appears to work by enhancing the association of Cryptochrome 1 (CRY1) with the CLOCK/BMAL1 complex, thereby negatively regulating the latter's activation. Co-immunoprecipitation of PCBP1 and core clock molecules confirmed the interactions between PCBP1 and CRY1, and a time-course qPCR assay revealed the rhythmic expression of PCBP1 in mouse hearts in vivo. Given that the RNA interference of mushroom-body expressed (mub), the poly(rC) binding protein (PCBP) homolog of Drosophila, in the clock neurons also led to a circadian phenotype in the locomotor assay, our study deemed PCBP1 a novel clock modifier whose circadian regulatory mechanism is conserved during evolution.

The dimension and morphology of alveolar bone at maxillary anterior teeth in periodontitis: a retrospective analysis-using CBCT.

The morphology of the alveolar bone at the maxillary anterior teeth in periodontitis patients was evaluated by cone-beam computed tomography (CBCT) to investigate the distribution of alveolar defects and provide guidance for clinical practice. Ninety periodontitis patients and 30 periodontally healthy individuals were selected to determine the morphology of the alveolar bone at the maxillary anterior teeth according to the degree of bone loss, tooth type, sex and age. The differences in the dimensions between periodontitis patients and healthy individuals were compared, and the distribution of alveolar bone defects was analyzed. A classification system was established regarding the sagittal positions and angulations of the teeth. The buccal residual bone was thicker and the lingual bone was thinner in the periodontitis patients than in the periodontally healthy individuals, and there were differences between the different tooth types, sexes and age subgroups. The buccal undercut was close to the alveolar ridge, while fenestration was reduced and the apical bone height was higher in periodontitis patients than in periodontally healthy individuals. The apical bone height increased with the aggravation of bone loss and age. The proportions of different sagittal positions changed with the aggravation of bone loss. Moreover, the teeth moved more buccally regarding the positions of the maxillary anterior teeth. The morphology of the alveolar bone at the maxillary anterior teeth differed between periodontitis patients and healthy individuals, and the differences were related to the degree of bone loss, tooth type, sex and age.

Effects of xipayi mouth rinse combined with minocycline on localized aggressive periodontitis' therapeutic effect and the levels of CRP, TNF-α, IL-6 in serum.

BACKGROUND: Localized aggressive periodontitis is rare periodontitis in clinical practice, which often occurs in young adults under 35 years old, seriously affecting patients' quality of life. As a tetracycline antibacterial drug, minocycline is also considered an essential choice to treat periodontal disease. However, few reports focused on the effect of xipayi mouth rinse combined with minocycline on periodontal pathogens. The goal of this study was to investigate the clinical effect of xipayi mouth rinse combined with minocycline in the treatment of localized aggressive periodontitis and its effect on the levels of CRP, TNF-α, and IL-6. METHODS: Ninety-six patients with limited aggressive periodontitis were selected and randomly divided into two groups. Forty-eight patients in the control group were treated with xipayi mouth rinse after primary periodontal treatment. Then, 48 patients in the experimental group were treated with xipayi mouth rinse combined with minocycline after primary periodontal treatment. The periodontal probe was applied to detect periodontal plaque index (PLI), periodontal pocket depth (PD), sulcus bleeding index (SBI), gingival index (GL), and clinical attachment loss (CAL) before and after treatment in both groups of patients. ELISA was used for detecting the expression levels of CRP, TNF-α, and IL-6 in the serum of patients in two groups before and after treatment. We compared the recurrence rates of the two groups after a 1-year follow-up. RESULTS: Compared with the control group, the PLI, PD, SBI, GL, CAL, and total masticatory efficiency of the experimental group were significantly better than those of the control group. The levels of inflammatory factors CRP, TNF-α, and IL-6 were significantly declined, and the total effective rate of treatment was significantly elevated. After follow-up, it was found there was no noticeable difference in the recurrence rate between the two groups. CONCLUSIONS: Xipayi mouth rinse, combined with minocycline in the treatment of localized aggressive periodontitis, can significantly improve the periodontal gingival condition and reduce the level of inflammatory factors. Also, the efficacy of the treatment was significant. This experiment has provided ideas for improving the clinical treatment of patients with localized aggressive periodontitis.

Chemical perturbations reveal that RUVBL2 regulates the circadian phase in mammals.

Transcriptional regulation lies at the core of the circadian clockwork, but how the clock-related transcription machinery controls the circadian phase is not understood. Here, we show both in human cells and in mice that RuvB-like ATPase 2 (RUVBL2) interacts with other known clock proteins on chromatin to regulate the circadian phase. Pharmacological perturbation of RUVBL2 with the adenosine analog compound cordycepin resulted in a rapid-onset 12-hour clock phase-shift phenotype at human cell, mouse tissue, and whole-animal live imaging levels. Using simple peripheral injection treatment, we found that cordycepin penetrated the blood-brain barrier and caused rapid entrainment of the circadian phase, facilitating reduced duration of recovery in a mouse jet-lag model. We solved a crystal structure for human RUVBL2 in complex with a physiological metabolite of cordycepin, and biochemical assays showed that cordycepin treatment caused disassembly of an interaction between RUVBL2 and the core clock component BMAL1. Moreover, we showed with spike-in ChIP-seq analysis and binding assays that cordycepin treatment caused disassembly of the circadian super-complex, which normally resides at E-box chromatin loci such as PER1, PER2, DBP, and NR1D1 Mathematical modeling supported that the observed type 0 phase shifts resulted from derepression of E-box clock gene transcription.

Porphyromonas gingivalis degrades integrin ß1 and induces AIF-mediated apoptosis of epithelial cells.

Background:Porphyromonas gingivalis, a major pathogen of chronic periodontitis, adheres to and invades epithelial cells via an interaction between fimbriae and integrin. P. gingivalis proliferation and infection may affect the survival of cells. In this study, we further examined alternative signaling pathways mediating epithelial-cell death induced by P. gingivalis and the role of the cell-adhesion molecule integrin. Methods: Human epithelial KB cells interacted with P. gingivalis to evaluate cell death by Annexin V-propidium iodide (PI) staining. JC-1 staining was used to measure mitochondrial membrane potential (MMP). The mRNA and protein of integrin ß1, apoptosis-inducing factor (AIF) and caspase-3 were detected by real-time PCR and western blot. Caspase-3 activity was analyzed by spectrophotometry. Results:P. gingivalis infection downregulated integrin ß1 and led to cell detachment in a dose and time-dependent manner. Large amount of P. gingivalis induced MMP depolarization and apoptosis in KB cells. Moreover, P. gingivalis up-regulated AIF, but not activate caspase-3 during apoptosis. In addition, AIF inhibitor N-Phenylmaleimide almost inhibited the P. gingivalis-induced apoptosis. Conclusions:P. gingivalis disrupts epithelial-cell adhesion by degrading integrin ß1 and induces caspase-independent, AIF-mediated mitochondrial apoptosis, which may promote the damage of oral tissue.

The Additional Effect of Autologous Platelet Concentrates to Coronally Advanced Flap in the Treatment of Gingival Recessions: A Systematic Review and Meta-Analysis.

BACKGROUND: To improve the efficacy of regenerative treatment for gingival recessions, the autologous platelet concentrates (APCs) combined with coronally advanced flap (CAF) have been investigated. However, few studies systematically assess the complementary effect of APCs in periodontal regeneration. The present study aims to evaluate the additional effect of different types of APCs to CAF in the treatment of gingival recessions. METHODS: Electronic databases (EMBASE, MEDLINE, and Cochrane Central Register of Controlled Trails) and relevant journals were searched until May 15, 2019. Only randomized controlled trials (RCTs) in English were included. Outcome variables include root coverage (RC), recession depth (RD), clinical attachment level (CAL), keratinized tissue width (KTW), and gingival thickness (GT). Data were analyzed with Revman5.3. The estimate of effect sizes was expressed as the mean differences and the 95% confidence interval. RESULTS: 8 RCTs involving 170 patients (328 sites) were included. Our meta-analysis indicated RC, RD, CAL, KTW, and GT were better improved in the CAF plus APCs groups than the CAF alone. The subgroup analyses revealed that platelet-rich fibrin (PRF) brought significant improvement in RC, RD, CAL, and GT. Concentrated growth factors (CGF) lead clinic beneficial in CAL, KTW, and GT. No significant effect of platelet-rich plasma (PRP) could be found in any clinical parameters when combined with CAF. CONCLUSIONS: PRF could exert additional effect to CAF; the preferred treatment for gingival recessions was considered. Based on the limited studies, it seemed that PRP failed to show any additional effect and it was not suggested for gingival recessions. Given the limited research and high risk of bias, it is still needed to confirm the additional effect of CGF by more high-quality studies.

Identification of entacapone as a chemical inhibitor of FTO mediating metabolic regulation through FOXO1.

Recent studies have established the involvement of the fat mass and obesity-associated gene (FTO) in metabolic disorders such as obesity and diabetes. However, the precise molecular mechanism by which FTO regulates metabolism remains unknown. Here, we used a structure-based virtual screening of U.S. Food and Drug Administration-approved drugs to identify entacapone as a potential FTO inhibitor. Using structural and biochemical studies, we showed that entacapone directly bound to FTO and inhibited FTO activity in vitro. Furthermore, entacapone administration reduced body weight and lowered fasting blood glucose concentrations in diet-induced obese mice. We identified the transcription factor forkhead box protein O1 (FOXO1) mRNA as a direct substrate of FTO, and demonstrated that entacapone elicited its effects on gluconeogenesis in the liver and thermogenesis in adipose tissues in mice by acting on an FTO-FOXO1 regulatory axis.

Persistent Exposure to Porphyromonas gingivalis Promotes Proliferative and Invasion Capabilities, and Tumorigenic Properties of Human Immortalized Oral Epithelial Cells.

Recent epidemiological studies revealed a significant association between oral squamous cell carcinoma (OSCC) and Porphyromonas gingivalis, a major pathogen of periodontal disease. As a keystone pathogen of periodontitis, P. gingivalis is known not only to damage local periodontal tissues, but also to evade the host immune system and eventually affect systemic health. However, its role in OSCC has yet to be defined. To explore the underlying effect of chronic P. gingivalis infection on OSCC and to identify relevant biomarkers as promising targets for therapy and prevention, we established a novel model by exposing human immortalized oral epithelial cells (HIOECs) to P. gingivalis at a low multiplicity of infection (MOI) for 5-23 weeks. The P. gingivalis infected HIOECs were monitored for tumor biological alteration by proliferation, wound healing, transwell invasion, and gelatin zymography assays. Microarray and proteomic analyses were performed on HIOECs infected with P. gingivalis for 15 weeks, and some selected data were validated by quantitative real-time PCR and (or) western blot on cells infected for 15 and 23 weeks. Persistent exposure to P. gingivalis caused cell morphological changes, increased proliferation ability with higher S phase fraction in the cell cycle, and promoted cell migratory and invasive properties. In combining results of bioinformatics analyses and validation assays, tumor-related genes such as NNMT, FLI1, GAS6, lncRNA CCAT1, PDCD1LG2, and CD274 may be considered as the key regulators in tumor-like transformation in response to long-time exposure of P. gingivalis. In addition, some useful clinical biomarkers and novel proteins were also presented. In conclusion, P. gingivalis could promote tumorigenic properties of HIOECs, indicating that chronic P. gingivalis infection may be considered as a potential risk factor for oral cancer. The key regulators detected from the present model might be used in monitoring the development of OSCC with chronic periodontal infection.

Reciprocal Regulation between the Circadian Clock and Hypoxia Signaling at the Genome Level in Mammals.

Circadian regulation is critically important in maintaining metabolic and physiological homeostasis. However, little is known about the possible influence of the clock on physiological abnormalities occurring under pathological conditions. Here, we report the discovery that hypoxia, a condition that causes catastrophic bodily damage, is gated by the circadian clock in vivo. Hypoxia signals conversely regulate the clock by slowing the circadian cycle and dampening the amplitude of oscillations in a dose-dependent manner. ChIP-seq analyses of hypoxia-inducible factor HIF1A and the core clock component BMAL1 revealed crosstalk between hypoxia and the clock at the genome level. Further, severe consequences caused by acute hypoxia, such as those that occur with heart attacks, were correlated with defects in circadian rhythms. We propose that the clock plays functions in fine-tuning hypoxic responses under pathophysiological conditions. We argue that the clock can, and likely should, be exploited therapeutically to reduce the severity of fatal hypoxia-related diseases.

[Evaluation of the degree and pattern of alveolar bone defect inaggressive periodontitis using cone-beam CT].

OBJECTIVE: To evaluate the degree and pattern of alveolar bone defect in aggressive periodontitis (AgP) using cone-beam CT (CBCT), and to investigate the distribution of alveolar bone defects in aggressive periodontitis. METHODS: Forty AgP patients (age: 14-36 years, male: 15 cases, female: 25 cases) were selected by simple random method and scanned by CBCT. NNT software was applied to measure the average degree of alveolar bone defects and bone loss types in different regions. RESULTS: In forty AgP patients, 86.6% (3,769/4,352) sites presented moderate and severe alveolar bone defects. In the maxilla, the molar areas presented the heaviest alveolar bone defect [(6.3±0.7) mm], the canine areas showed the lightest bone loss [(4.8±0.8) mm]. In the mandible, the incisal areas presented the heaviest alveolar bone defect [(5.9±0.9) mm], the canine areas showed the lightest bone loss[(5.1±0.7) mm]. The degree of alveolar bone defect in the areas of maxillary canine, maxillary molars, mandibular premolar was significantly different (P<0.05). The degree of alveolar bone defect in mandibular canine and mandibular molars was significantly differenct (P<0.01). The most serious alveolar bone defect was in the mesial side of maxillary molar [(6.9±0.7) mm] and the mesial side of mandibular incisor [(6.5±1.1) mm]. The oblique bone defects were found in the mesial part of the first molars in mandibula [13.6% (42/308)], the first molars in maxilla [12.0% (39/316)] and the first premolar in maxilla [10.8% (34/316)]. CONCLUSIONS: The alveolar bone defects of generalized AgP patients were serious. The most serious areas were located in the mesial side of maxillary molars and the mesial side of mandibular incisor.

Assessment of Alveolar Bone Status in Middle Aged Chinese (40-59 Years) with Chronic Periodontitis--Using CBCT.

OBJECTIVE: This study used con-beam computed tomography (CBCT) to investigate the prevalence and severity of alveolar bone loss in middle-aged (40-59 years) Chinese with chronic periodontitis. MATERIALS AND METHODS: The study group comprised 145 dentate individuals aged 40 to 59 years residing in China who suffered from chronic periodontitis. CBCT and the application of NNT software were used to examine the level and location of alveolar bone loss. RESULTS: The study revealed that 40-59 year old patients with chronic periodontitis had severe bone loss. At 5,286 sites (34.7%), alveolar bone loss was mild; severe alveolar bone loss was found at 5,978 sites (39.2%). A comparison of bone loss in different jaws revealed that the area with the highest degree of bone loss was on the lingual side of the maxillary molar (56.3 ± 7.2%), and that the area with the lowest degree was primarily on the lingual side of the mandibular canine (27.5 ± 6.3%). There was a lower degree of alveolar bone loss in males than females. Differences were observed when comparing the incidence of bone loss between males and females (P < 0.05). Menopause in females and smoking in both genders may affect the level of bone loss. Male smokers experienced a greater degree of bone loss (41.67 ± 5.76%) than male non-smokers (32.95 ± 4.31%). A 42.23 ± 6.34% bone loss was found in menopausal females versus 31.35 ± 3.62% in non-menopausal females. CONCLUSIONS: The study revealed that different sites and teeth exhibited a diverse degree of bone loss. In middle-aged patients with chronic periodontitis, the highest degrees of bone loss in the incisors, premolars, and molars were on the lingual side, mesial side and lingual side, respectively. Menopause in females and smoking may affect the level of bone loss.

[Evaluation of alveolar bone defect in chronic periodontitis by cone-beam computed tomography].

OBJECTIVE: To evaluate the morphological characteristics of alveolar bone defects of the patients with chronic periodontitis using cone-beam CT (CBCT). METHODS: Sixty patients with chronic periodontitis were included in this study. CBCT was used to scan the alveolar bone and NNT software to measure the alveolar bone defects and bone loss types in different regions. RESULTS: Seventy-five percent (45/60) of the alveolar bone defect was the generalized type, 25% (15/60) was the localized type. In incisor and canine area, the defect of the mandibular alveolar bone was more severe than in the same sites of maxilla. There was less bone loss in the premolar area of mandible than in the same site of maxilla. In the mesial and buccal sites of mandibular molars and in the lingual site of maxillary molars, the most severe alveolar bone loss was found. CONCLUSIONS: The obvious alveolar bone defect areas in chronic periodontitis were the palatal side of maxillary molars and the lingual side of mandibular incisors. CBCT can clearly demonstrate the degree of alveolar bone defects in different regions of chronic periodontitis.