Gingival crevicular fluid lactoferrin levels in adult per iodontitis patients

The present study was designed to determine in a cross-sectional study whether there was any relationship between the levels of lactoferrin in gingival crevicular fluid and clinical periodontal parameters. Crevicular fluid was collected from individual sites using standardized filter paper strips (clinically healthy sites, N=23; periodontitis sites, n=66) and evaluated for lactoferrin by enzyme-linked immunosorbent assay. The data showed that: (1) the total amounts of lactoferrin were 0.003-0.021 ng (30 second sample) (average 0.009±0.005 ng) in a clinically healthy periodontium group and 0.016-3.847 ng (30 second sample) (average 0.575±0.069 ng) in adult periodontitis patients (statistically significantly higher in adult periodontitis patients); and (2) the total amounts of lactoferrin were significantly correlated with clinical parameters,     

Serum neutralizing activity against Actinobacillus actinomycetemcomitans leukotoxin in juvenile periodontitis

A relatively high incidence of infection by Actinobacillus actionomycetemcomitans can be shown in subgingival plaque samples obtained from patients with juvenile periodontitis. These organisms possess a potent leukotoxin(s) which rapidly destroys isolated human polymorphonuclear leukocytes (PMNs) and monocytes. If such leukotoxins operate in vivo, they could deprive the gingival crevice area of an essential antibacterial defense mechanism. We have found that sera from juvenile periodontitis patients consistently (greater than 90%) contain antibodies which neutralize Actinobacillus actinomycetemcomitans leukotoxin(s). On the other hand, sera from normal individuals or patients with other types of periodontal disease usually amplified rather than inhibited the leukotoxic reaction. Many patients with juvenile periodontitis have demonstrable defects in PMN or monocyte chemotaxis and this may place them at risk to gingival infection by Actinobacillus actinomycetemcomitans. The immune response against these organisms could be a crucial determinant in the course of juvenile periodontitis. While this disease is relatively rare, it does cause immeasurable emotional, physical and economic hardship for patients and their families. The identification of Actinobacillus actinomycetemcomitans as a potential pathogen in this disorder may eventually lead to specific forms of therapy to prevent and eliminate infection by this organism in these patients.     

Activation of the complement system by some gram-positive oral bacteria.

Actinomyces viscosus 19246, T₁₄V and T₁₄AV, Streptococcus mutans and Streptococcus sanguis consumed complement in vitro. Complement (C) profile analysis revealed that C₄ and C_3–9 were consumed concomitantly in unadsorbed human serum. In serum from which naturally occurring agglutinating antibodies had been removed, the same microorganisms caused C_3–9 consumption in the absence of a demonstrable loss of C₄ activity. Congenitally C₄-deficient guinea-pig serum (C₄D) supported a similar consumption of C_3–9. The Gram-positive plaque microorganisms tested activated serum complement by the classical as well as the alternate pathways. Dental plaque microorganisms may cause a similar activation of gingival crevicular fluid complement in vivo, thus resulting in complement-mediated inflammatory processes.     

Relationship between periodontal furcation involvement and molar cervical enamel projections

A total of 78 individuals ages 21 to 61 years with periodontal furcation involvement was examined for the presence of cervical enamel projections on the buccal surfaces of molar teeth. The furcal defects and cervical enamel projections (CEPs) of molars were diagnosed by probing, periapical roentgenographs, flap operation and inspection. Plaque index (PlI) and gingival index (GI) were recorded for the buccal and lingual surfaces of molars examined. The percentage of CEPs in the 78 individuals examined was 67.9%. The prevalence of CEPs in all molars examined was 45.2%. The prevalence of CEPs in molars with and without furcal involvements were 82.5% and 17.5%, respectively. The frequency of CEP in molars occurred in the following order: mandibular first molars, maxillary first molars, mandibular second molars and maxillary second molars. Statistical analyses (Chi-square test) revealed a significant difference between periodontal furcation involvements and the presence of CEPs. Results of this study also indicated that the furcal involvements with CEPs were associated with poor oral hygiene as measured by GI and PlI.     

The up-regulation of heme oxygenase-1 expression in human gingival fibroblasts stimulated with nicotine

BACKGROUND: Cigarette smoking is a major risk factor in the development and further progression of periodontal diseases. Heme oxygenase-1 (HO-1) is known as a stress-inducible protein and functions as an antioxidant enzyme. There is limited information on the expression of HO-1 in smoking-associated periodontal disease. OBJECTIVES: The aim of the present study was to investigate the effects of nicotine on the expression of HO-1 protein in cultured human gingival fibroblasts in vitro and further to compare HO-1 expression in gingival tissues obtained from cigarette smokers and non-smokers in vivo. METHODS: Western blot assay was used to investigate the effects on human gingival fibroblasts exposed to nicotine. In addition, antioxidants catalase, superoxide dismutase (SOD), and N-acetyl-l-cysteine (NAC) were added to test how they modulated the effects on nicotine-induced HO-1 expression. Gingival biopsies taken from the flap surgery of 20 male patients with periodontal disease (10 cigarette smokers and 10 non-smokers) were examined by immunohistochemistry. RESULTS: The exposure of quiescent human gingival fibroblasts to 10 mm nicotine resulted in the induction of HO-1 protein expression in a time-dependent manner (p < 0.05). The addition of glutathione (GSH) precursor NAC inhibited the nicotine-induced HO-1 protein expression (p < 0.05). However, SOD and catalase did not decrease the nicotine-induced HO-1 protein expression (p > 0.05). The results from immunohistochemistry demonstrated that HO-1 expression was significantly higher in cigarette smokers (p < 0.05). HO-1 was noted in the basal layers of epithelium, inflammatory cells, and fibroblasts in specimens from cigarette smoking. CONCLUSIONS: Taken together, these results suggest that HO-1 expression is significantly up-regulated in gingival tissues from cigarette smokers, and nicotine may, among other constituents, be responsible for the enhanced HO-1 expression in vivo. The regulation of HO-1 expression induced by nicotine is critically dependent on the intracellular GSH concentration.     

Fracture resistance of compomer and composite restoratives

This study evaluated and compared the fracture toughness of compomers and composites. Three compomer (Compoglass F [CG], Vivadent; F2000 [FT], 3M-ESPE; Dyract Posterior [DP], Dentsply) and three composite (Tetric Ceram [TC], Vivadent; Z250 [ZT], 3M-ESPE; Esthet X [EX], Dentsply) restoratives were selected for the study. Single-edged notched specimens (25 x 2 x 2 mm) were fabricated according to manufacturers' instructions and conditioned in distilled water at 37 degrees C for one week prior to testing. Seven specimens were made for each material. The specimens were loaded to failure using an Instron microtester with a crosshead speed of 0.5 mm/minute. Data were subjected to ANOVA/Scheffe's test and Independent Samples T-test at significance level 0.05. The mean fracture toughness (K(IC)) ranged from 0.97 to 1.23 MPam 1/2 for compomers and 1.75 to 1.92 MPam 1/2 for composites. The fracture toughness of compomers was significantly lower than their composite counterparts. No significant difference in K(IC) values was observed among the different composites. When the compomers were compared, FT had significantly higher fracture toughness than DP and CG. In view of their poorer resistance to crack propagation, compomers are not recommended for use in stress-bearing areas.     

Mutation analysis of Crouzon syndrome in Taiwanese patients

Crouzon syndrome is an autosomal-dominant disorder that causes premature fusion of the cranial suture. Crouzon, Pfeiffer, and Apert syndromes are caused by mutations in the extracellular, third immunoglobulin-like domain, and adjacent linker regions (exons IIIa and IIIc) of the fibroblast growth factor receptor 2 (FGFR2) gene. We screened 12 Crouzon syndrome patients for mutations in exons IIIa and IIIc of the FGFR2 gene by polymerase chain reaction (PCR) and direct sequencing. Mutations were detected in nine of 12 patients at amino acid positions 278, 281, 289, 342, and 354. More than half of the studied Crouzon patients carried a mutation resulting in either the loss or gain of a cysteine residue. A novel missense Ser354Phe substitution at exon IIIc of the human FGFR2 gene was found. According to our results, sequencing analysis of IgIII domain of the FGFR2 gene can lead to a genetic diagnosis of Crouzon syndrome.