Gingival thickness assessment at the mandibular incisors with four methods: A cross-sectional study.

BACKGROUND: This study was conducted to determine accuracy, precision and repeatability of four different methods for assessing gingival thickness METHODS: This cross-sectional study evaluated gingival thickness on 200 consecutively included orthodontic patients. Gingival thickness was assessed at both central mandibular incisors with: 1) transgingival probing with a standard periodontal probe, 2) transgingival probing with a stainless-steel acupuncture needle, 3) ultrasound, and 4) a color-coded periodontal probe. Intra-examiner reproducibility and method error were also evaluated. RESULTS: Transgingival measurements with the standard periodontal probe were found to be more accurate than those with the acupuncture needle, after method error assessment. Acupuncture needle and ultrasound device yielded higher values than the probe. Expected differences between the two methods were 22% more for the mandibular left central incisor (95% confidence interval (CI) = 11% to 32%) and 26% more (95% CI = 13% to 39%) for the mandibular right central incisor when measured with the needle. Ultrasound measurements exceeded probe measurements on average by 0.16 mm at mandibular left central incisor (95% CI = 0.14 to 0.18) and by 0.11 mm for mandibular right central incisor (95% CI = 0.08 to 0.13). Intraclass correlation coefficient concluded good agreement for the color-coded periodontal probe (0.624). CONCLUSIONS: Within the inherent limit of the uncertainty about the true value of gingival thickness, the present results demonstrate the differences between the tested methods, as far as accuracy and reproducibility are concerned. Based on the reproducibility, the transgingival probing with the periodontal probe as well as the ultrasound determination, seem to present an adequate choice for every day practice.

Matrix metalloprotease 1a deficiency suppresses tumor growth and angiogenesis.

Matrix metalloprotease-1 (MMP1) is an important mediator of tumorigenesis, inflammation and tissue remodeling through its ability to degrade critical matrix components. Recent studies indicate that stromal-derived MMP1 may exert direct oncogenic activity by signaling through protease-activated receptor-1 (PAR1) in carcinoma cells; however, this has not been established in vivo. We generated an Mmp1a knockout mouse to ascertain whether stromal-derived Mmp1a affects tumor growth. Mmp1a-deficient mice are grossly normal and born in Mendelian ratios; however, deficiency of Mmp1a results in significantly decreased growth and angiogenesis of lung tumors. Coimplantation of lung cancer cells with wild-type Mmp1a(+/+) fibroblasts completely restored tumor growth in Mmp1a-deficient animals, highlighting the critical role of stromal-derived Mmp1a. Silencing of PAR1 expression in the lung carcinoma cells phenocopied stromal Mmp1a-deficiency, thus validating tumor-derived PAR1 as an Mmp1a target. Mmp1a secretion is controlled by the ability of its prodomain to facilitate autocleavage, whereas human MMP1 is efficiently secreted because of stable pro- and catalytic domain interactions. Taken together, these data demonstrate that stromal Mmp1a drives in vivo tumorigenesis and provide proof of concept that targeting the MMP1-PAR1 axis may afford effective treatments of lung cancer.

Colonization and infection by colistin-resistant Gram-negative bacteria in a cohort of critically ill patients.

In recent years there has been renewed interest in colistin for the treatment of infections by multidrug-resistant Gram-negative bacteria, causing concern that increasing use may be accompanied by the emergence of resistance. This is a retrospective cohort study of colonization and infection by colistin-resistant (CR) gram-negative bacteria in critically ill patients. Colonization data were based on surveillance culture results. Among 150 patients, 78 (52%) were colonized by CR Gram-negative bacteria. Among them, 30 (20%) were colonized by Klebsiella pneumoniae isolates and 51 (34%) were colonized by intrinsically resistant to colistin (CIR) enterobacteriaceae. Seven cases of infection were caused by CR K. pneumoniae and 12 cases by CIR strains. The main risk factor for colonization by CR pathogens was colistin treatment.