Measurement of tooth displacement.

The periodontium is a biological structure that supports the tooth in the jaw and behave as a developmental, biological, and functional unit. Teeth may be considered to be 'suspended' in their tooth sockets which provides teeth the ability to move in response to an applied load. In terms of the protection the suspension effect of the periodontal ligament may offer dental restorations, movement in an axial direction is of interest. No device or system to measure this movement is readily available, thus a novel approach had to be developed to address the questions of this research. The device developed allowed images to be taken of the participants teeth before, during and after a participant bit down on the tooth and used to measure the displacement of the tooth in image processing software. Average maximum tooth displacement from all participants of 73.8 µm (sd = 22.5 µm) were recorded. Longer application time of bite force was associated with greater cumulative tooth displacement, for a given level of force, and female participants experienced approximately 2 µm more displacement per Newton than males. The device and methods utilised in this study has shown good potential as a measurement protocol for measurement of vertical tooth movements in vivo. The response to load the teeth in this study has shown, highlighted the visco-elastic properties of the periodontal ligament and the amount of movement recorded supports the protection that controlled tooth movement offers teeth.

Development of a bite force transducer for measuring maximum voluntary bite forces between individual opposing tooth surfaces.

Bite forces are studied in order to understand a wide range of factors pertaining to the mastication system. Various strain gauge transducers have been employed to measure bite forces, with several descriptions of these available in the literature; unfortunately, many reports provide insufficient detail to enable accurate reproduction. The aim of this project was to develop a bite force transducer with the capability of measuring maximum voluntary bite forces between individual opposing tooth surfaces. Furthermore, in an attempt to address the issue of vague device descriptions in the available literature, a detailed account of the transducer development has been included. A novel strain gauge transducer was designed and built. Bite forces of forty individuals were measured to verify the capabilities and clinical application of the device.

Missense Pathogenic variants in KIF4A Affect Dental Morphogenesis Resulting in X-linked Taurodontism, Microdontia and Dens-Invaginatus.

The etiology of dental anomalies is multifactorial; and genetic and environmental factors that affect the dental lamina have been implicated. We investigated two families of European ancestry in which males were affected by taurodontism, microdontia and dens invaginatus. In both families, males were related to each other via unaffected females. A linkage analysis was conducted in a New Zealand family, followed by exome sequencing and focused analysis of the X-chromosome. In a US family, exome sequencing of the X-chromosome was followed by Sanger sequencing to conduct segregation analyses. We identified two independent missense variants in KIF4A that segregate in affected males and female carriers. The variant in a New Zealand family (p.Asp371His) predicts the substitution of a residue in the motor domain of the protein while the one in a US family (p.Arg771Lys) predicts the substitution of a residue in the domain that interacts with Protein Regulator of Cytokinesis 1 (PRC1). We demonstrated that the gene is expressed in the developing tooth bud during development, and that the p.Arg771Lys variant influences cell migration in an in vitro assay. These data implicate missense variations in KIF4A in a pathogenic mechanism that causes taurodontism, microdontia and dens invaginatus phenotypes.

Diagnosing tuberculous pericarditis.

BACKGROUND: Definitive diagnosis of tuberculous pericarditis requires isolation of the tubercle bacillus from pericardial fluid, but isolating the organism is often difficult. AIM: To improve diagnostic efficiency for tuberculous pericarditis, using available tests. DESIGN: Prospective observational study. METHODS: Consecutive patients (n = 233) presenting with pericardial effusions underwent a predetermined diagnostic work-up. This included (i) clinical examination; (ii) pericardial fluid tests: biochemistry, microbiology, cytology, differential white blood cell (WBC) count, gamma interferon (IFN-gamma), adenosine deaminase (ADA) levels, polymerase chain reaction testing for Mycobacterium tuberculosis; (iii) HIV; (iv) sputum smear and culture; (v) blood biochemistry; and (vi) differential WBC count. A model was developed using 'classification and regression tree' analysis. The cut-off for the total diagnostic index (DI) was optimized using receiver operating characteristic (ROC) curves. RESULTS: Fever, night sweats, weight loss, serum globulin (>40 g/l) and peripheral blood leukocyte count (<10 x 10(9)/l) were independently predictive. The derived prediction model had 86% sensitivity and 84% specificity when applied to the study population. Pericardial fluid IFN-gamma >or=50 pg/ml, concentration had 92% sensitivity, 100% specificity and a positive predictive value (PPV) of 100% for the diagnosis of tuberculous pericarditis; pericardial fluid ADA >or=40 U/l had 87% sensitivity and 89% specificity. A diagnostic model including pericardial ADA, lymphocyte/neutrophil ratio, peripheral leukocyte count and HIV status had 96% sensitivity and 97% specificity; substituting pericardial IFN-gamma for ADA yielded 98% sensitivity and 100% specificity. DISCUSSION: Basic clinical and laboratory features can aid the diagnosis of tuberculous pericarditis. If available, pericardial IFN-gamma is the most useful diagnostic test. Otherwise we propose a prediction model that incorporates pericardial ADA and differential WBC counts.

The role of histopathology in establishing the diagnosis of tuberculous pericardial effusions in the presence of HIV.

AIMS: To establish the influence of human immunodeficiency virus (HIV) infection on the histopathological features of patients presenting with tuberculous pericarditis. METHODS AND RESULTS: A prospective study was carried out at Tygerberg Academic Hospital, South Africa; 36 patients with large pericardial effusions had open pericardial biopsies under general anaesthesia and were included in the study. Patients underwent pericardiocentesis, followed by daily intermittent catheter drainage; a comprehensive diagnostic work-up (including histopathology of the pericardial tissue) was also performed. Histological tuberculous pericarditis was diagnosed according to predetermined criteria. Tuberculous pericarditis was identified in 25 patients, five of whom were HIV+. The presence of granulomatous inflammation (with or without necrosis) and/or Ziehl-Neelsen positivity yielded the best test results (sensitivity 64%, specificity 100% and diagnostic efficiency 75%). CONCLUSIONS: Co-infection with HIV impacts on the histopathological features of pericardial tuberculosis and leads to a decrease in the sensitivity of the test. In areas which have a high prevalence of tuberculosis, the combination of a sensitive test such as adenosine deaminase, chest X-ray and clinical features has a higher diagnostic efficiency than pericardial biopsy in diagnosing tuberculous pericarditis.

Hydatid cyst fistula into the aorta presenting with massive hemoptysis. Case report and literature review.

Hydatid involvement of the aorta is extremely uncommon. We present a case where a hydatid cyst of the lung eroded into the thoracic aorta, causing massive hemoptysis. Successful repair was performed by resection (including left lower lobectomy) and graft interposition.