Tetracycline demineralization of dentin: the effects of concentration and application time

Abstract The current investigation was initiated to study the effect concentration and application time has on the rate of tetracycline demineralization of dentin. Buccal and lingual surfaces of extracted bovine molars were ground to a smooth flat dentin surface using wetted silicon carbide discs. Standardized depressions were made in the dentin surface with a #909-055 diamond round wheel. Fresh tetracycline HCl (TTC-HCl) (Flavine Int. Inc.) solutions, i.e., 0, 25, 50, 75, 100, 125 and 150 mg/ml were prepared. A 30% citric acid solution was used as a positive control. The pH of each solution was recorded. 7 μl of each solution were pipetted into a depression and remained undisturbed for 1, 3, or 5 min. At the end of each application time period a fresh #3 cotton pellet was placed in the depression, once every 20 s for 1 min, to soak up the solution. The 3 pellets were placed in a 2.00 ml of 18 Mω H₂O sample. As a measure of the rate of demineralization the parts per million calcium (ppm Ca⁺⁺) found in each sample were determined using atomic absorption spectrophotometry. Two-way analysis of variance was used to determine effects of TTC-HC1 concentration and time on the rate of demineralization. No significant differences were found in the mean ppm Ca⁺⁺ released at 1-, 3- and 5-min application times for 0, 25, or 50 mg/ml TTC. No significant differences were found in the mean ppm Ca⁺⁺ released (i) between 3- and 5-rmn application times for 75, 100, 125 and 150 mg/ml TTC-HCl solutions and (ii) between 75, 100, 125 and 150 mg/ml TTC-HCl solutions within either the 3- or 5-min application times. The mean ppm Ca⁺⁺ released at 3- and 5-min application times for 75, 100, 125 and 150 mg/ml TTC-HCl solutions were all significantly greater than the respective readings at the 1-min application time. The mean ppm Ca⁺⁺ recorded for the 30% citric acid solution for all 3 application times were 3 to 5.5 × greater than the highest mean ppm Ca⁺⁺ recording for TTC-HCl. The results of this study show that a 3-min application time of 75 mg/ml TTC-HCl solution is equally as effective at demineralizing dentin as is higher concentrations and/or longer application times, but was far less effective than a 30% citric acid solution.     

Hepatitis B virus and primary hepatocellular carcinoma: Family studies in Korea

Chronic infection with hepatitis B virus (HBV) is closely associated with the etio-pathogenesis of primary hepatocellular carcinoma (PHC). It has been proposed that infection with HBV early in life, frequently transmited by an HBV-carrier mother, leads to persistent infection with HBV, which in turn is associated with the development of chronic active hepatitis (CAH), post-necrotic cirrhosis and PHC. If this view is correct, then there should be clustering of chronic carriers of HBV in families of patients with chronic liver disease. We tested this hypothesis in Korea by collecting serum from 132 patients with these chronic liver diseases admitted to the Seoul National University Hospital and 664 of their first-degree relatives. Controls (636) were members of two churches in Seoul and a rural village population; 261 of the controls were between the ages of 30 and 59, the age range that included 95% of the cases of chronic liver disease. Sera were assayed for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs) and antibody to hepatitis B core antigen (anti-HBc). Almost all cases showed evidence of present or past infection with HBV; 80% were HBsAg(+) and 14% were anti-HBs(+); 100% of 47 cases of PHC, 100% of 35 cases of cirrhosis, and 94% of 50 cases of CAH were anti-HBc(+); 6% of males and 4% of females in the control population (30–59 years of age) were HBsAg(+), 71% were anti-HBc(+), and 51% were anti-HBs(+), HBsAg(+) patients with chronic liver disease tended to be younger than HBsAg(?) patients with anti-HBs or anti-HBc antibodies. Mothers of patients were more frequently HBsAg(+) (9 of 33) than agematched women in the control population (0 of 34) or wives of patients (5 of 68). Five of 23 fathers were also HBsAg(+) compared with 1 of 25 age-matched controls. As first observed in Africa, there was a deficit of anti-HBs in the fathers of cases compared with the controls. Siblings of patients were frequently HBsAg(+) (45% of 154), with the highest prevalence in brothers (53%). Family history shows that five fathers, two mothers and five brothers of cases have died of PHC. These data are compatible with the hypothesis tested and lend further support to the view that prevention of infection with HBV will lead to a marked decrease in the incidence of CAH, cirrhosis and PHC in areas where these diseases are endemic. Members of the families of patients with these diseases are at high risk of developing persistent infection with HBV and chronic liver disease. It would be appropriate to focus preventive strategies on infants and children in such families.     

Changes in serum iron levels due to infection with hepatitis B virus

We found in two previous studies (Down syndrome patients and end-stage kidney patients receiving renal dialysis) that total serum iron is higher on average in carriers of the hepatitis B virus than in those who are not. The elevation of the serum iron is independent of elevations of serum L-alanine:2-oxoglutarate aminotransferase, EC 2.6.1.2) (SGPT), an indicator of liver cell damage. We have followed for 10 yr a large number of patients with end-stage renal disease receiving renal dialysis. In this paper we describe studies of serum iron and SGPT levels in patients (i) 1 mo before infection, (ii) after infection but within the month of infection, and (iii) 6-12 mo after infection. Comparisons of serum iron levels were made between those infected who retained the virus (carriers) and those who rejected the infection (transients). There were no differences between these groups before infection. Serum iron remained high in the carrier group and dropped in the transients. However, not all of the carriers retained high levels, although this was the case in general. Individual changes in the pre- and postconversion period were then considered. All carriers who had a preconversion decline in iron had an increase after infection, whereas this occurred in only some of the transients. Those carriers who had a decline after infection had raised levels before infection, and the decline was generally less than the increase. Consideration of the SGPT and the iron levels together led to the same conclusion as the previous studies, that elevation of iron may be independent of rise in SGPT. Several hypotheses were derived from these findings. Individuals who are carriers in general have higher iron levels and, therefore, are more likely to become infected with bacteria; this may contribute to increased morbidity and mortality. From experimental evidence, iron is required for the growth of tumor cells. Carriers with elevated iron levels may be more likely to develop detectable cancer of the liver than those who do not.