Combination injuries 2. The risk of pulp necrosis in permanent teeth with subluxation injuries and concomitant crown fractures

Abstract – Background: The reported risk of pulp necrosis (PN) is generally low in teeth with subluxation injuries. A concomitant crown fracture may increase the risk of PN in such teeth. Aim: To analyse the influence of a concomitant trauma‐related infraction, enamel‐, enamel–dentin‐ or enamel–dentin–pulp fracture on the risk of PN in permanent teeth with subluxation injury. Material and Methods: The study included 404 permanent incisors with subluxation injury from 289 patients (188 male, 101 female). Of these teeth, 137 had also suffered a concomitant crown fracture. All the teeth were examined and treated according to a standardized protocol. Statistical Analysis: The risk of PN was analysed separately for teeth with immature and mature root development by the Kaplan–Meier method, the log‐rank test and Cox regression analysis. The level of significance was set at 5%. Risk factors included in the analysis were gender, patient age, crown fracture type, mobility and response to an electric pulp test (EPT) at the initial examination. Results: Teeth with immature root development: The risk of PN was increased in teeth with a concomitant enamel fracture (log‐rank test: P = 0.002), enamel–dentin fracture (log‐rank test: P < 0.0001), enamel–dentin–pulp fracture (log‐rank test: P < 0.0001) and in teeth with no response to EPT at the initial examination [hazard ratio: 21 (95% confidence interval, CI: 2.5–172.5), P = 0.005]. Teeth with mature root development: the risk of PN was increased in teeth with an enamel–dentin fracture [hazard ratio: 12.2 (95% CI: 5.0–29.8), P < 0.0001], infraction [hazard ratio: 5.1 (95% CI: 1.2–21.4) P = 0.04] and in teeth with no response to EPT at the initial examination [hazard ratio: 8 (95% CI: 3.3–19.5), P < 0.0001]. Conclusion: A concomitant crown fracture and no response to EPT at the initial examination may be used to identify teeth at increased risk of PN following subluxation injury.     

Microduplication of 15q13.3 and Xq21.31 in a family with tourette syndrome and comorbidities

Tourette syndrome (TS) is a childhood onset neurodevelopmental disorder. Although it is widely accepted that genetic factors play a significant role in TS pathogenesis the etiology of this disorder is largely unknown. Identification of rare copy number variations (CNVs) as susceptibility factors in several neuropsychiatric disorders such as attention deficit‐hyperactivity disorder (ADHD), autism and schizophrenia, suggests involvement of these rare structural changes also in TS etiology. In a male patient with TS, ADHD, and OCD (obsessive compulsive disorder) we identified two microduplications (at 15q13.3 and Xq21.31) inherited from a mother with subclinical ADHD. The 15q duplication included the CHRNA7 gene; while two genes, PABPC5 and PCDH11X, were within the Xq duplication. The Xq21.31 duplication was present in three brothers with TS including the proband, but not in an unaffected brother, whereas the 15q duplication was present only in the proband and his mother. The structural variations observed in this family may contribute to the observed symptoms, but further studies are necessary to investigate the possible involvement of the described variations in the TS etiology. © 2013 Wiley Periodicals, Inc.     

Early treatment with inhaled antibiotics postpones next occurrence of Achromobacter in cystic fibrosis

ObjectivesIn this nationwide retrospective study, we analysed species distribution, antimicrobial susceptibility and time to next occurrence of Achromobacter in Danish cystic fibrosis (CF) patients from 2000 to 2011.MethodsThirty-four primary isolates were identified to species level and subjected to antimicrobial susceptibility testing. Effectiveness of early antimicrobial treatment was assessed by a Kaplan–Meier estimation of time to recurrence.ResultsAchromobacter xylosoxidans accounted for 13 (38%) of the isolates, and an unnamed species accounted for 11 (32%) of the isolates. Meropenem, piperacillin–tazobactam and trimethoprim–sulfamethoxazole were highly active against chemotherapy-naïve Achromobacter, while ceftazidime, colistin and tobramycin were judged adequate for inhalation therapy. Fifty-five percent of 25 patients treated with inhaled ceftazidime, colistin, or tobramycin remained free of Achromobacter three years after acquisition, in contrast to 17% of 22 patients who did not receive inhaled antibiotics (P < 0.01).ConclusionsEarly treatment with inhaled antibiotics may prevent or postpone chronic infection with Achromobacter in CF patients.     

Carry-over of host nutrients during sampling enhances undesired growth of Staphylococcus aureus in liquid Amies transport medium

Optimal transportation of bacteria is important for accurate clinical interpretation, quantitative assays, and microbiome studies. A transport medium should ideally keep the bacteria alive without supporting growth or altering the relative proportions of the constituent species. We investigated the effect of nasal mucus and mucin on the growth and survival of two Staphylococcus aureus strains in liquid Amies transport medium at room temperature and 4?°C for 14?days. The study showed that the presence of nasal mucus in microbiological samples stimulated undesired S. aureus growth at room temperature in a dose-dependent manner. These findings underscore that microbiological samples from humans and animals should be stored at 4?°C until analysis to avoid undesired S. aureus growth.     

Clues for early detection of autoimmune Addison's disease – myths and realities

Background

Early detection of autoimmune Addison's disease (AAD ) is important as delay in diagnosis may result in a life‐threatening adrenal crisis and death. The classical clinical picture of untreated AAD is well‐described, but methodical investigations are scarce.

Objective

Perform a retrospective audit of patient records with the aim of identifying biochemical markers for early diagnosis of AAD .

Material and Methods

A multicentre retrospective study including 272 patients diagnosed with AAD at hospitals in Norway and Sweden during 1978–2016. Scrutiny of medical records provided patient data and laboratory values.

Results

Low sodium occurred in 207 of 247 (84%), but only one‐third had elevated potassium. Other common nonendocrine tests were largely normal. TSH was elevated in 79 of 153 patients, and hypoglycaemia was found in 10%. Thirty‐three per cent were diagnosed subsequent to adrenal crisis, in whom electrolyte disturbances were significantly more pronounced (P < 0.001). Serum cortisol was consistently decreased (median 62 nmol L^?1 [1–668]) and significantly lower in individuals with adrenal crisis (38 nmol L^?1 [2–442]) than in those without (81 nmol L^?1 [1–668], P < 0.001).

Conclusion

The most consistent biochemical finding of untreated AAD was low sodium independent of the degree of glucocorticoid deficiency. Half of the patients had elevated TSH levels. Only a minority presented with marked hyperkalaemia or other nonhormonal abnormalities. Thus, unexplained low sodium and/or elevated TSH should prompt consideration of an undiagnosed AAD , and on clinical suspicion bring about assay of cortisol and ACTH . Presence of 21‐hydroxylase autoantibodies confirms autoimmune aetiology. Anticipating additional abnormalities in routine blood tests may delay diagnosis.

     

DNA methylation is altered in B and NK lymphocytes in obese and type 2 diabetic human

Objective

Obesity is associated with low-grade inflammation and the infiltration of immune cells in insulin-sensitive tissues, leading to metabolic impairment. Epigenetic mechanisms control immune cell lineage determination, function and migration and are implicated in obesity and type 2 diabetes (T2D). The aim of this study was to determine the global DNA methylation profile of immune cells in obese and T2D individuals in a cell type-specific manner.

Material and methods

Fourteen obese subjects and 11 age-matched lean subjects, as well as 12 T2D obese subjects and 7 age-matched lean subjects were recruited. Global DNA methylation levels were measured in a cell type-specific manner by flow cytometry. We validated the assay against mass spectrometry measures of the total 5-methylcytosine content in cultured cells treated with the hypomethylation agent decitabine (r = 0.97, p < 0.001).

Results

Global DNA methylation in peripheral blood mononuclear cells, monocytes, lymphocytes or T cells was not altered in obese or T2D subjects. However, analysis of blood fractions from lean, obese, and T2D subjects showed increased methylation levels in B cells from obese and T2D subjects and in natural killer cells from T2D patients. In these cell types, DNA methylation levels were positively correlated with insulin resistance, suggesting an association between DNA methylation changes, immune function and metabolic dysfunction.

Conclusions

Both obesity and T2D are associated with an altered epigenetic signature of the immune system in a cell type-specific manner. These changes could contribute to the altered immune functions associated with obesity and insulin resistance.