Impact of orthognathic surgery on quality of life of patients with dentofacial deformity: a systematic review and meta-analysis.

The aim of this study was to evaluate the impact of orthognathic surgery on the quality of life (QoL) of patients with dentofacial deformity. This systematic review was performed through the survey of observational studies that had evaluated the impact of orthognathic surgery on the QoL of patients with dentofacial deformity. The article databases included PubMed, Scopus, Web of Science, LILACS, BBO, Cochrane Library, and grey literature. The risk of bias was analysed according to the Newcastle-Ottawa Scale for quality assessment. The meta-analysis was performed considering the exposure before and after orthognathic surgery using the Oral Health Impact Profile (OHIP-14) versus the Orthognathic Quality of Life Questionnaire (OQLQ). A total of 2,263 articles were identified. Twelve studies remained in the qualitative synthesis and seven studies were included in the meta-analysis. The impact of QoL both preoperatively and postoperatively with the OHIP-14 questionnaire was 7.63 (95% confidence interval (CI) = 1.62 to 13.65; p = 0.01) and the OQLQ questionnaire was 20.53 (95% CI = 14.27 to 26.79; p < 0.0001). Overall impact of QoL was 16.01 (95% CI = 10.50 to 21.52; p < 0.0001), which showed that orthognathic surgery has an influence on the QoL. Orthognathic surgery generates positive impact on the QoL of patients with dentofacial deformity.

MSX1 is differentially expressed in the deepest impacted maxillary third molars.

An impacted third molar is one of the most common dental abnormalities. Among the reasons for impaction the most common are: insufficient space, time of eruption, improper position of the tooth bud, and genetic disruptions. To investigate if runt-related transcription factor 2 (RUNX2), bone morphogenetic protein 2 (BMP2), and msh homeobox 1 (MSX1) are differently expressed depending on the position of the molar, we studied 32 patients who had been referred for surgical removal. An orthopantomogram was used to separate them according to Winter's, and Pell & Gregory's, classifications. Bone samples were harvested during the operation for gene expression assay. The Kruskal-Wallis, Dunn's post hoc, and Spearman's correlation, tests were used to assess the significance of differences. No correlations were found in expression of the genes, and no differences between expression in maxillary and mandibular third molars, nor were they expressed differently according to Winter's or Pell and Gregory's classifications or in relation to impaction of the mandibular ramus. However, MSX1 was expressed differently when account was taken of the depth of impaction in maxillary third molars (p = 0.029), but there was no difference in expression of RUNX2, BMP2, and MSX1 for the Pell and Gregory classification of depth of impaction (p > 0.05). We conclude that MSX1 is expressed differently depending on the depth of maxillary impaction phenotypes.

Association between facial measurements and polymorphisms in human epidermal growth factor and transforming growth factor ß1.

The aim of the study was to evaluate the association between genetic polymorphisms in human epidermal growth factor (EGF) (rs4444903) and transforming growth factor ß1 - (TGF-ß1) (rs1800470) with facial measurements in patients with dentofacial deformities. A total of 144 adult patients with dentofacial deformities were included. Facial linear and angular measurements were traced in lateral cephalometric radiographs used Dolphin 2D software. Cells from oral mucosa were collected for DNA to be extracted. The polymorphisms were genotyped using real-time polymerase chain reaction (PCR). Probabilites of less than 0.05 were accepted as significant. The rs4444903 heterozygous patients had a decrease in the mandibular length (p=0.043) and the length of the mandibular base (p=0.008), and homozygous A patients also had a reduction in the length of the mandibular base (p=0.013) compared with homozygous G patients. Patients AG had an increase in measurement of the anterior facial height (p=0.032) and in ANS-Me distance (p=0.022) when compared with homozygous A. To the rs1800470, heterozygous patients had an increase in the length of the mandibular base (p=0.043) when compared with homozygous A. Heterozygous AG patients had an increase in angular measurements in TGF-ß1 polymorphism for the upper gonial angle, when compared with the homozygous AA (p=0.032). Genetic polymorphisms in EGF and TGF-ß1 are associated with facial measurements in a Brazilian population of patients with dentofacial deformities.

Evaluation of functional relationships for predicting mainstream smoke constituent machine yields for conventional cigarettes from the Japanese market.

The objective of this study was to predict mainstream smoke constituent yields for conventional filter cigarette brands on sale in Japan between 2004 and 2005. Mainstream smoke was generated under ISO machine smoking conditions. Developed functional relationships indicate the validity of benchmarking even for a market which is characterized by a diversity of tobacco blend types. Smoke yields were in general well predicted by linear regression with "tar" (R2>or=0.7). Blend-type-sensitive analytes like tobacco-specific nitrosamines showed improved prediction relationships after blend stratification or regressing against nitric oxide (NO, R(2)>0.7). Relationships calculated from 83 exploratory brands were validated with a subset of 23 validation brands. Seventy-five to one-hundred percent of the validation brand yields were inside the 95% prediction intervals. The mean-relative prediction error over all analytes was 24% after stratification. Smoke constituents yields analyzed in 2002 from 96 Japanese market products were well predicted and indicate the model validity over time. Similar relationships were observed when comparing American blended filter cigarette yields from Japan and worldwide markets. Consistent with reported results from previous benchmark studies and market surveys mainstream smoke constituent yields are well predictable when "tar" (and NO) yields are known.

Assessment of the exposure of children to environmental tobacco smoke (ETS) by different methods.

1. In order to elucidate the role of exposure to environmental tobacco smoke (ETS) in various acute and chronic illnesses in children, it is important to assess the degree of exposure by suitable methods. For this purpose, we determined the exposure to ETS in 39 children (4-15 years) and 43 adults (16+ years) by questionnaires, personal diffusion samplers for nicotine, and cotinine measurements in saliva and urine. In addition, the influence of the smoking status and the location of the home (urban or suburban) on the benzene exposure of the children was investigated. 2. On average, the 24 children living in homes with at least one smoker were exposed to ETS for 3.1 h/d. This is significantly longer (P<0.001) than the daily exposure time of the 15 children from nonsmoking homes (0.3 h/d). The nicotine concentrations on the personal samplers worn over 7 days were 0.615 and 0.046 microg/m3 for children from smoking and nonsmoking homes, respectively (P<0.001). Average salivary cotinine levels were 1.95 ng/ml in children from smoking homes and 0.11 ng/ml in children from nonsmoking homes (P< 0.01). The corresponding urinary cotinine levels were 29.4 and 4.5 ng/mg creatinine (P< 0.001). There was no difference in the extent of ETS exposure between children and adults from smoking households. Adults from nonsmoking homes tended to have higher ETS exposure than children from nonsmoking homes. 3. Exposure to benzene, which was determined by means of personal samplers, measurements of benzene in exhaled air and of the urinary benzene metabolite trans, trans-muconic acid, was not significantly related to the smoking status of the home but primarily dependent on the location of the home.

Metabolism and disposition of 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanone (NNK) in rhesus monkeys.

Metabolism and disposition of the tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent rodent lung carcinogen, were studied in rhesus monkeys. In three males receiving a single i.v. dose of [5-3H]NNK (0.72 mCi; 4.6-9.8 microg/kg), urine was collected for 10 days. Within the first 24 h, 86.0 +/- 0.7% of the dose was excreted. NNK-derived radioactivity was still detectable in urine 10 days after dosing (total excretion, 92.7 +/- 0.7%). Decay of urinary radioactivity was biexponential with half-lives of 1.7 and 42 h. Metabolite patterns in urine from the first 6 h closely resembled those reported previously for patas monkeys; end products of metabolic NNK activation represented more than 50% of total radioactivity. At later time points, the pattern shifted in favor of NNK detoxification products (60-70% of total radioactivity in urine), mainly 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its O-glucuronide conjugates. One female rhesus monkey received a single i.v. dose of [5-3H]NNK (1.72 mCi; 28.4 microg/kg) under isoflurane anesthesia; biliary excretion over 6 h (0.6% of the dose) was 10 times less than predicted by our previously reported rat model. No preferential excretion of NNAL glucuronide was observed in monkey bile. Collectively, these results suggest that the rhesus monkey could be a useful model for NNK metabolism and disposition in humans.

Analysis and evaluation of trans,trans-muconic acid as a biomarker for benzene exposure.

Benzene is an important industrial chemical and, due to its occurrence in mineral oil and its formation in many combustion processes, a widespread environmental pollutant. Since benzene is hematoxic and has been classified as a human carcinogen, monitoring and control of benzene exposure is of importance. Although trans,trans-muconic acid (ttMA) was identified as a urinary metabolite of benzene at the beginning of this century, only recently has its application as a biomarker for occupational and environmental benzene exposure been investigated. The range of metabolic conversion of benzene to ttMA is about 2-25% and dependent on the benzene exposure level, simultaneous exposure to toluene, and probably also to genetic factors. For the quantitation of ttMA in urine, HPLC methods using UV and diode array detection as well as GC methods combined with MS or FID detection have been described. Sample pretreatment for both HPLC and GC analysis comprises centrifugation and enrichment by solid-phase extraction on anion-exchange sorbents. Described derivatization procedures prior to GC analysis include reaction with N,O-bis(trimethysilyl)acetamide, N,O-bis(trimethylsilyl)trifluoroacetamide, pentafluorobenzyl bromide and borontrifluoride-methanol. Reported limits of detection for HPLC methods range from 0.1 to 0.003 mg l(-1), whereas those reported for GC methods are 0.03-0.01 mg l(-1). Due to its higher specificity, GC methods appear to be more suitable for determination of low urinary ttMA levels caused by environmental exposure to benzene. In studies with occupational exposure to benzene (>0.1 ppm), good correlations between urinary ttMA excretion and benzene levels in breathing air are observed. From the reported regressions for these variables, mean excretion rates of ttMA of 1.9 mg g(-1) creatinine or 2.5 mg l(-1) at an exposure dose of 1 ppm over 8 h can be calculated. The smoking-related increase in urinary ttMA excretion reported in twelve studies ranged from 0.022 to 0.2 mg g(-1) creatinine. Only a few studies have investigated the effect of exposure to environmental levels of benzene (<0.01 ppm) on urinary ttMA excretion. A trend for slightly increased ttMA levels in subjects living in areas with high automobile traffic density was observed, whereas exposure to environmental tobacco smoke did not significantly increase the urinary ttMA excretion. It is concluded that urinary ttMA is a suitable biomarker for benzene exposure at occupational levels as low as 0.1 ppm. Biomonitoring of exposure to environmental benzene levels (<0.01 ppm) using urinary ttMA appears to be possible only if the ingestion of dietary sorbic acid, another precursor to urinary ttMA, is taken into account.