Randomized Clinical Trials on Deep Carious Lesions: 5-Year Follow-up.

Deep caries presents a dilemma in terms of which treatment that will render an optimal prognosis by maintaining pulp vitality with absence of apical pathology. Previously, 2 randomized clinical trials were performed testing the short-term effects of stepwise carious tissue removal versus nonselective carious removal to hard dentin with or without pulp exposure. The aim of this article was to report the 5-y outcome on these previously treated patients having radiographically well-defined carious lesions extending into the pulpal quarter of the dentin but with a well-defined radiodense zone between the carious lesion and the pulp. In this long-term study, 239 of 314 (76.2%) patients were analyzed. The stepwise removal group had a significantly higher proportion of success (60.2%) at 5-y follow-up compared with the nonselective carious removal to hard dentin group (46.3%) ( P = 0.031) when pulp exposures per se were included as failures. Pulp exposure rate was significantly lower in the stepwise carious removal group (21.2% vs. 35.5%; P = 0.014). Irrespective of pulp exposure status, the difference (13.3%) was still significant when sustained pulp vitality without apical radiolucency and unbearable pain was considered (95% confidence interval, 3.1-26.3, P = 0.045). After pulp exposure, only 9% ( n = 4) of the analyzed patients were assessed as successful, indicating that the prognosis is highly dubious following conventional pulp-capping procedures (direct pulp capping or partial pulpotomy) in deep carious lesions in adults. In conclusion, the stepwise carious removal group had a significantly higher proportion of pulps with sustained vitality without apical radiolucency versus nonselective carious removal of deep carious lesions in adult teeth at 5-y follow-up ( ClinicalTrials.gov NCT00187837 and NCT00187850).

High levels of salivary lactobacilli in Estonian schoolchildren.

AIM: This was to assess oral salivary lactobacilli levels compared with oral health in a group of 12-year-old schoolchildren in Tartu, Estonia. METHODS: Whole saliva samples were collected and transferred to dip-slides (Dentocult LB) and incubated at 37 degrees C for 3 days. Dental caries, dental plaque, and data concerning the general health, dental habits and eating patterns were recorded. RESULTS: Salivary lactobacilli were found in all children, with a quarter of them having high or very high lactobacilli counts. Caries prevalence of 75% and 2.6 DMFT were recorded. A positive correlation was found between the DMFS counts and the lactobacilli counts. CONCLUSION: High levels of salivary lactobacilli were found in Estonian schoolchildren. Caries indicators of these children were slightly higher than in the same age group in Nordic countries.

The reproducibility of ultrasonic enamel thickness measurements: an in vitro study.

OBJECTIVES: The diagnosis of tooth wear is mostly based on visual scoring systems. Recently, methods measuring ultrasonic enamel thickness have been proposed. The aim of this study was to evaluate the reproducibility and evaluate factors affecting variation of ultrasonic enamel thickness measurements in an in vitro set up. METHODS: Four observers (1-4) in two institutes (G and S) performed ultrasonic enamel thickness measurements at buccal and palatal surfaces of extracted teeth placed in a phantom jaw. A Panametrics 25DL thickness gauge (Panametrics, Waltham MA, USA), with a 15 MHz transducer, covered by a plexi-glass delay line with a tip diameter of 2 mm was used, coupled to a laptop computer. After one week these measurements were repeated. Subsequently four selected teeth were measured 20 times at a fixed buccal site by one observer. Finally, two observers made ink marks with the instrument probe tip on the buccal and palatal surfaces of all teeth. This was repeated after one week. Digital images were made of the marked teeth and analysed to determine variation in positioning. The underlying enamel thickness variation was subsequently estimated. Results were analysed by calculating the 95% range of measurement variation (RMV, 4 x standard deviation) for each experiment. RESULTS: The main reproducibility experiment showed a 95% RMV of 0.79 mm (observer 1G), 0.64 mm (observer 2G), 0.63 mm (observer 3S), 0.71 mm (observer 4S), 0.51 mm (observer 1S). The repeatability experiment showed a mean 95% RMV of 0.26 mm. The probe position variation in the cervical-incisal direction resulted in an estimated thickness 95% RMV of 0.10 mm (1G) and 0.09 mm (2G). CONCLUSIONS: It was concluded that, due to measurement variation, thickness changes of less than 0.33 mm cannot be detected reliably. Probe positioning and a poor repeatability were responsible for only a small part of the total variation. Hence other factors influencing variation in enamel thickness are still to be identified.

Increased release of tissue plasminogen activator and its inhibitor in human parotid saliva upon stimulation.

Parotid saliva from 12 healthy volunteers was collected prior to and after 5 and 25 min of stimulation at a constant flow rate of 0.25 or 1.0 ml min-1. In the salivary samples the concentrations of tPA (tissue-type plasminogen activator), PAI-1 (plasminogen activator inhibitor type-1), albumin and total protein were determined and the activity of amylase, tPA and PAI assessed. Presence of both tPA and PAI-1 antigen was demonstrated in all samples, and in unstimulated saliva the ratio between the activator and its inhibitor was 1:7. Upon stimulation we found a significantly increased concentration of PAI-1, a less pronounced increase in tPA concentration, unchanged amylase and total protein levels and significantly decreased albumin concentration. tPA activity was significantly reduced after prolonged stimulation which had no effect on PAI activity. In stimulated saliva a significant positive correlation between concentration of tPA and PAI-1 was demonstrated. Stimulation with citric acid had no effect on output of albumin which is passively filtered from blood, whereas the increase in flow rate corresponded to the significantly increased secretion rate of total protein and amylase which is secreted by gland cells. The secretion pattern of tPA and PAI-1 differed significantly from that of albumin in showing markedly increased output rate during the stimulation period, and the relative increase in output of PAI-1 was significantly higher than that of amylase and total protein. Thus, the results from this study suggest an active release of both tPA and its main inhibitor PAI-1 into saliva.

Presence of a fast-acting specific inhibitor of plasminogen activator in human parotid saliva.

The plasminogen activator in parotid saliva has recently been characterized as a tissue-type plasminogen activator (t-PA). In this study stimulated parotid saliva from 21 healthy volunteers was analysed for (a) t-PA activity using the fibrin plate assay or a bioimmunoassay coupled to the plasmin-specific chromogenic substrate S-2251, (b) t-PA antigen using an enzyme-linked immunospecific assay and (c) activity of the specific fast-acting plasminogen activator inhibitor (t-PA inhibitor) assayed by its inhibitory effect on one-chain t-PA added to the samples. In parotid saliva the median t-PA activity was 0.2 IU ml-1 (normal range 0.05-0.35 IU ml-1), but activity of free t-PA could not be demonstrated by bioimmunoassay in any sample. The mean antigen concentration of t-PA was 2.2 IU ml-1 in the 10 samples with levels above the detection limit (0.5 IU ml-1). High activity of t-PA inhibitor was demonstrated in all parotid salivas, and the mean inhibitory effect on t-PA was 13.2 IU t-PA quenched per millilitre. This study thus demonstrates a fibrinolytic system in parotid saliva characterized by high t-PA inhibitor activity and relatively low concentration of inactive, probably complex-bound, t-PA which is activated in the presence of fibrin.

Effect of flow rate on tissue plasminogen activator activity in human parotid saliva.

Parotid saliva from 10 healthy volunteers was collected at rest and at constant flow rates of 0.25, 0.5 and 1.0 ml/min, and its tissue plasminogen activator (tPA) activity assayed on fibrin plates containing plasminogen. In unstimulated salivas the median tPA activity was 0.26 (range 0.03-2.0) IU/ml. During the first 15 min of stimulation, a continuous decrease in tPA activity was found at the three flow rates; thereafter a steady state was obtained. No significant differences in activity were found between the three rates. The initial decrease was on average 0.15 IU/ml, and the activity during the steady state was 38% of the prestimulatory level. Thus, stimulation with citric acid causes a significant decrease in tPA activity of parotid saliva but this decrease, as well as the reduction rate, appears to be independent of flow rate.

Immunological characterization of plasminogen activators in human parotid saliva.

These were characterized in stimulated saliva from 21 healthy volunteers using antibodies specific for human tissue-type plasminogen activator (t-PA) or urokinase. After pre-incubation with immunoglobulins, with and without specific antibodies, the fibrinolytic activity was assayed on fibrin plates containing plasminogen. Fibrinolytic activity was demonstrated in all salivas but one; it was completely quenched by antibodies against t-PA, but antibodies against urokinase-like plasminogen activator had no effect. The fibrinolytic activity was expressed in international units (IU) using a standard curve obtained by serial dilution of the international tissue-plasminogen standard. The normal range was 0.05-0.35 IU/ml, and the maximal value 2 IU/ml. There is thus considerable individual variation in fibrinolytic activity in parotid saliva, where it is regulated by t-PA under physiological conditions.

In vitro stimulation of plasminogen activator release from vein walls by adrenaline.

The effect of adrenaline on plasminogen activator release was studied in vitro in human vein biopsy specimens, in which the fibrinolytic activity was determined according to the fibrin slide technique. The tissue slides were covered with a thin fibrin film containing 10(-9) and 10(-7) M adrenaline and exposed for 30 to 60 minutes. In both concentrations highly significant (p less than 0.001) enhancement of fibrinolytic activity was shown, and the enhancement of fibrinolysis was most pronounced during the first 30 minutes of exposure. Stimulation of fibrinolysis was maximal after exposure to the physiological concentration of 10(-9) M, while no further increase was seen using the pharmacological concentration. These results show that adrenaline has a stimulant effect on tissue fibrinolysis in vitro, and this effect may account for the direct stimulation of fibrinolysis by adrenaline in vivo.

Immunological characterization of plasminogen activators in human mixed saliva.

In mixed saliva obtained from six healthy volunteers, the plasminogen activators were characterized immunologically using antibodies specific for human tissue plasminogen activator and urokinase, which were raised in goats immunized with low molecular weight urokinase and tissue-type activator from melanoma cells. The fibrinolytic activity in mixed saliva upon stimulation was assayed on fibrin plates containing plasminogen after preincubation with immunoglobulins with and without specific antibodies. In both centrifuged and uncentrifuged saliva, antibodies against tissue plasminogen activator completely quenched the fibrinolytic activity. By contrast, antibodies against urokinase had no suppressive effect, neither did non-immunized goat serum influence the fibrinolytic activity in mixed saliva. In conclusion, during physiological conditions tissue plasminogen activator appears to regulate fibrinolytic activity in mixed saliva, in which no activity of urokinase-like plasminogen activators could be demonstrated.