Successful treatment of nasopalatine duct cyst after maxillary anterior implant surgery: a case report.

BACKGROUND: Sporadic studies have reported the occurrence of nasopalatine duct cysts after maxillary anterior implant surgery, and the treatment methods still have clinical uncertainty. PURPOSE: We report a potential therapy method that successfully treated a nasopalatine duct cyst that developed and expanded one year after maxillary anterior implant placement following periodontally hopeless teeth extraction. MATERIALS AND METHODS: The nasopalatine cyst was treated surgically without removing implants. During flap surgery, the cyst was removed intact, and the exposed implant's surface was debrided thoroughly by hydrogen peroxide (H2O2) rinsing, glycine air polishing, and saline rinsing. To deal with the significant bone defect caused by the cyst, a bovine porous bone mineral injected platelet-rich fibrin (BPBM-i-PRF) complex was applied to fill the defect, following a resorbable collagen membrane to cover. RESULTS: 7 years after surgery, no cyst recurrence was observed, and bone regeneration in the bone graft area was stable. The implants functioned well without mobility. CONCLUSIONS: For nasopalatine duct cysts associated with dental implant placement, complete surgical debridement and longitudinal stable bone regeneration are possibly accessible by regenerative surgery without implant removal.

The long-term effect of periodontitis treatment on changes in blood inflammatory markers in patients with generalized aggressive periodontitis.

BACKGROUND: Periodontitis is characterized by local inflammatory conditions in the periodontium, its severe form has been associated with elevated systemic inflammatory markers. However, the long-term effects of periodontal inflammation control on systemic inflammatory markers are unclear. OBJECTIVE: This study aimed to investigate the long-term effects of periodontal therapy on the levels of peripheral venous blood inflammatory markers in patients with generalized aggressive periodontitis (GAgP), all of whom were now diagnosed as Stage III or IV Grade C periodontitis. METHODS: Patients with GAgP were consecutively recruited from April 2013 to August 2014 (T0). Active periodontal treatment (APT) was provided, and follow-ups were conducted over a 3- to 5-year period (T1). Clinical parameters were assessed and fasting venous blood was collected at T0 and T1. Complete blood cell counts were obtained, and biochemical analyses were performed to evaluate the levels of serum components. The correlations between probing depth (PD) and hematological parameters were analyzed. RESULTS: A total of 49 patients with GAgP completed APT and follow-ups. Probing depth (PD) reduced from 5.10 ± 1.07 mm at T0 to 3.15 ± 0.65 mm at T1. For every 1-mm reduction in PD after treatment, the neutrophil count, neutrophil-lymphocyte ratio, and total protein concentration were reduced by 0.33 × 109/L, 0.26, and 1.18 g/L, respectively. In contrast, the albumin/globulin ratio increased by 0.10. CONCLUSION: This study indicated that periodontal therapy may have beneficial effects on peripheral venous blood inflammatory markers in patients with GAgP during long-term observation.

Population pharmacokinetic/pharmacodynamic modeling of nifekalant injection with varies dosing plan in Chinese volunteers: a randomized, blind, placebo-controlled study.

Nifekalant hydrochloride is a class III antiarrhythmic agent which could increase the duration of the action potential and the effective refractory period of ventricular and atrial myocytes by blocking the K+ current. Nifekalant is used to prevent ventricular tachycardia/ventricular fibrillation. QT interval prolongation is the main measurable drug effect. However, due to the complicated dosing plan in clinic, the relationship among dosage, time, drug concentration and efficacy is not fully understood. In this study, a single-center, randomized, blind, dose-ascending, placebo-controlled study was conducted to explore the intrinsic characteristics of nifekalant injection in healthy Chinese volunteers by a population pharmacokinetic (PK)-pharmacodynamic (PD) model approach. 42 subjects were enrolled in this study and received one of three dose plans (loading dose on Day 1 (0.15, 0.3 or 0.5 mg/kg), loading dose followed by maintenance dose (0.2, 0.4 or 0.8 mg/kg/h) on Day 4) or vehicle. Blood samples were drawn for PK evaluation, and ECGs were recorded for QTc calculation at the designed timepoints. No Torsades de Pointes occurred during the study. The popPK model of nifekalant injection could be described by a two-compartment model with first-order elimination. The population mean clearance (CL) was 53.8 L/h. The population mean distribution volume of the central (Vc) and peripheral (Vp) compartments was 8.27 L and 45.6 L, respectively. A nonlinear dose-response (Emax) model well described the pharmacodynamic effect (QTc interval prolongation) of nifekalant. The Emax and EC50 from current study were 101 ms and 342 ng/mL, respectively.

Glucose and lipid metabolism indexes and blood inflammatory biomarkers of patients with severe periodontitis: A cross-sectional study.

BACKGROUND: To investigate the relation of established glucose and lipid metabolism indexes and blood inflammatory biomarkers with severe periodontitis in systemically healthy patients. METHODS: Systemically healthy Stage III/IV periodontitis patients (case group) (n = 397), Stage II periodontitis patients (n = 36), and periodontally healthy subjects (control group) (n = 285) were recruited. A periodontal examination, complete blood cell examination, and blood biochemical examination were conducted for all participants. Full-mouth apical films were taken for the case group. Both the case and control groups were divided by age into younger (≤ 35 years) and elder subjects. Multiple logistic regression analysis and Pearson correlation analysis were conducted. A logistic least absolute shrinkage and selection operator (LASSO) model was constructed for the younger subgroups. RESULTS: Various glucose and lipid metabolism indexes and blood inflammatory biomarkers significantly differed between severe periodontitis patients and healthy controls, and the younger subgroups presented a greater degree of statistical differences than the elder ones. More pairs of periodontal parameters and blood indexes with significantly fair linear correlations were found in the younger patient subgroup. A logistic LASSO regression model containing eight blood indexes to assess a severe periodontitis outcome in younger subgroups showed satisfactory predictive ability. CONCLUSION: The present study revealed various glucose and lipid metabolism indexes and blood inflammatory biomarkers significantly differ between severe periodontitis patients and healthy controls, especially in the younger subgroups. A LASSO regression model could be a viable option to assess severe periodontitis risk for younger patients.

A double-edged sword: Role of butyrate in the oral cavity and the gut.

Butyrate, a four-carbon short-chain fatty acid (SCFA), is a metabolite of anaerobic bacteria. Butyrate has primarily been described as an energy substance in the studies on the digestive tract. The multiple mechanisms of its protective function in the gut and on underlying diseases (including metabolic diseases, diseases of the nervous system, and osteoporosis) via interaction with intestinal epithelial cells and immune cells have been well documented. There are many butyrogenic bacteria in the oral cavity as well. As essential components of the oral microbiome, periodontal pathogens are also able to generate butyrate when undergoing metabolism. Considerable evidence has indicated that butyrate plays an essential role in the initiation and perpetuation of periodontitis. However, butyrate is considered to participate in the pro-inflammatory activities in periodontal tissue and the reactivation of latent viruses. In this review, we focused on the production and biological impact of butyrate in both intestine and oral cavity and explained the possible pathway of various diseases that were engaged by butyrate. Finally, we suggested two hypotheses, which may give a better understanding of the significantly different functions of butyrate in different organs (i.e., the expanded butyrate paradox).

Comparison of the Effects of Low-Molecular-Weight Heparin and Fondaparinux on Liver Function in Patients With Pulmonary Embolism.

Hepatotoxicity with low-molecular-weight heparin (LMWH) or fondaparinux is a relatively common adverse reaction. This study assessed the effects of LMWH and fondaparinux on liver function in patients with pulmonary embolism based on a retrospective cohort. As a result, a total of 463 patients with pulmonary embolism and treated with LMWH (enoxaparin sodium or nadroparin calcium) or fondaparinux sodium were included. Liver dysfunction was identified in 79 patients (17.1%), of whom 97.5% had grade 1 drug-induced liver injury (DILI) and 2.5% had grade 2 DILI. The results showed that liver dysfunction usually occurred in the first week after anticoagulant administration, and the liver tests of all patients with liver dysfunction gradually recovered or alleviated at discharge. The multivariable logistic regression analysis indicated that a longer treatment course and hepatitis B surface antigen-positive (HBsAg+) were risk factors for liver dysfunction (P < .05). Moreover, nadroparin calcium had the highest risk of liver dysfunction, approximately 2.2 times (95% confidence interval [CI], 1.1740-4.224; P = .015) that of enoxaparin sodium. In conclusion, nearly one-fifth and 10% of patients prescribed with LMWH or fondaparinux, respectively, for pulmonary embolism had liver dysfunction, mainly with mild liver injury and characterized by self-limited elevated serum transaminase levels. Hence, during the 3 anticoagulant applications, we should pay more attention to the monitoring of liver function in the first week and transit to oral anticoagulants if possible, especially for patients who are HBsAg+ or suffering from other liver diseases.

Plasma α1-antitrypsin: a neglected predictor of angiographic severity in patients with stable angina pectoris.

BACKGROUND: As an acute phase protein, α1-antitrypsin (AAT) has been extensively studied in acute coronary syndrome, but it is unclear whether a relationship exists between AAT and stable angina pectoris (SAP). The purpose of the present study was to investigate the association between AAT plasma levels and SAP. METHODS: Overall, 103 SAP patients diagnosed by coronary angiography and clinical manifestations and 118 control subjects matched for age and gender were enrolled in this case-control study. Plasma levels of AAT, high-sensitivity C-reactive protein (hsCRP), lipid profiles and other clinical parameters were assayed for all participants. The severity of coronary lesions was evaluated based on the Gensini score (GS) assessed by coronary angiography. RESULTS: Positively correlated with the GS (r = 0.564, P < 0.001), the plasma AAT level in the SAP group was significantly higher than that in the control group (142.08 ± 19.61 mg/dl vs. 125.50 ± 19.67 mg/dl, P < 0.001). The plasma AAT level was an independent predictor for both SAP (odds ratio [OR] = 1.037, 95% confidence interval [CI]: 1.020-1.054, P < 0.001) and a high GS (OR = 1.087, 95% CI: 1.051-1.124, P < 0.001) in a multivariate logistic regression model. In the receiver operating characteristic curve analysis, plasma AAT level was found to have a larger area under the curve (AUC) for predicting a high GS (AUC = 0.858, 95% CI: 0.788-0.929, P < 0.001) than that of hsCRP (AUC = 0.665, 95% CI: 0.557-0.773, P = 0.006; Z = 2.9363, P < 0.001), with an optimal cut-off value of 137.85 mg/dl (sensitivity: 94.3%, specificity: 68.2%). CONCLUSIONS: Plasma AAT levels correlate with both the presence and severity of coronary stenosis in patients with SAP, suggesting that it could be a potential predictive marker of severe stenosis in SAP patients.

The relationship between serum amyloid A and apolipoprotein A-I in high-density lipoprotein isolated from patients with coronary heart disease.

BACKGROUND: Alteration in the protein composition of high-density lipoprotein (HDL) has been proposed as a mechanism for the development of coronary heart disease (CHD). In HDL, an increase in serum amyloid A protein (SAA) accompanying the decrease in apolipoprotein A-I (apoA-I) has been found during the acute inflammation period. However, whether this phenomenon persists in CHD patients, a disease related to inflammation, is unknown. The purpose of the present study was to explore the relationship between SAA and apoA-I in HDL isolated from CHD patients. METHODS: Overall, 98 patients with confirmed stable CHD and 90 control subjects matched for age and gender were enrolled in this case-control study. Potassium bromide (KBr) density gradient ultracentrifugation was used to isolate HDL from plasma. The levels of SAA and apoA-I in the HDL samples were detected by enzyme-linked immunosorbent assay kits. Pearson's correlation and general linear models were used in the analysis. RESULTS: Compared with controls, patients with CHD had a significant decrease in the amount of apoA-I ((14.21 ± 8.44) µg/ml vs. (10.95 ± 5.95) µg/ml, P = 0.003) in HDL and a significant increase in the amount of log SAA (1.21 ± 0.46 vs. 1.51 ± 0.55, P < 0.00001). Differences were independent of age, body mass index (BMI), HDL cholesterol (HDL-C), and other factors. An independently and statistically significant positive correlation between log SAA and apoA-I in HDL was observed only in the CHD group (ß = 2.0, P = 0.026). In the general linear model, changes in log(SAA), age, age2, gender, BMI and HDL-C could explain a statistically significant 43% of the variance in apoA-I. CONCLUSIONS: This study provides direct evidence for the first time that there was an independent positive correlation between log SAA and apoA-I in the HDL of CHD patients, indicating the alteration of protein composition in HDL. However, the question of whether this alteration in HDL is associated with impairment of HDL functions requires further research.