Survival of composite restorations after selective or total caries removal in primary teeth and predictors of failures: A 36-months randomized controlled trial.

OBJECTIVES: The aim of this study was to assess the survival of composite restorations after selective (SCR) or total caries removal (TCR) and determine predictors of failures after 36 months. METHODS: 120 teeth with deep occlusal or occlusal-proximal carious lesions were randomly divided into control (TCR; n = 54; 69% Class II) and test (SCR; n = 66; 63% Class II) groups. Clinical evaluation was applied using the USPHS criteria, and the presence of Charlie or Delta scores at the marginal integrity were considered as a failure. RESULTS: The overall survival rate of restorations was 68% after 36 months, 81% for TCR and 57% for SCR (p = 0.004). The multivariable Cox Regression model demonstrated that restorations performed after SCR had 3.44 times greater probability of failure compared to TCR (p = 0.006). The other two predictors for failure of restorations were teeth with Class II cavities (hazard ratio = 3.3) and children with gingival bleeding over 20% (hazard ratio = 2.5). CONCLUSIONS: Performing composite restorations after SCR in primary teeth had success rate significantly lower than restorations performed after TCR. Complex cavities and worst patient´s oral hygiene were found to be predictors of failure of restorations. CLINICAL SIGNIFICANCE: Although SCR has been demonstrating high rates of pulp preservation, clinicians should consider that composite restorations fail in a higher frequency compared to TCR in primary teeth and, in some circumstances, may be preferable in terms of restoration longevity.

Randomized controlled clinical trial of the 24-months survival of composite resin restorations after one-step incomplete and complete excavation on primary teeth.

OBJECTIVE: This randomized clinical trial aimed to compare the 24-months survival of composite restorations in primary molars after partial caries removal (PCR) and total caries removal (TCR). METHODS: Forty-eight children aged 3-8 years with at least one molar with a deep carious lesion were included (PCR; n=66; TCR; n=54). For PCR, excavation was stopped when dentine with a leathery consistency was achieved; in the TCR group, total absence of carious tissue was confirmed using a blunt-tipped probe. Pulpotomy was performed in cases of pulp exposure. Success was assessed by modified USPHS criteria with Alpha and Bravo scores recorded as success. RESULTS: Pulp exposure occurred in 1 and 15 of the teeth treated with PCR and TCR respectively (p<0.01). The restorations survival rate after 24 months was 66% (PCR) and 86% (TCR) (p=0.03). When teeth that received pulpotomy were analyzed separately, the survival rate was 92% (p=0.09). PCR performed in occlusoproximal restorations demonstrated the lowest success rate (p=0.002). PCR increases 2.90 times the probability of having a restorative failure compared to TCR (p=0.03), after adjusting for cavity type. When pulp exposure and restoration failure were considered as the outcome, there was no significant difference between the two groups (p=0.10) with success rates of 64% (PCR) and 61% (TCR). CONCLUSION: Collectively, deciduous teeth submitted to PCR prevented pulp exposure and, consequently, more invasive treatments; otherwise, PCR yielded lower longevity for composite restoration compared to TCR, suggesting that PCR restorations need to be followed over time, especially when multi-surface restorations are involved. CLINICAL SIGNIFICANCE: Composite restorations on carious remaining tissue require monitoring over time, especially those performed in more than one surface. Even if the restorations present shortcomings over the time, the majority of them are subject to repair, allowing more conservative approaches for teeth with deep caries lesions.

Dentin rehardening after indirect pulp treatment in primary teeth.

PURPOSE: The purpose of this study was to investigate dentin rehardening in the remaining carious dentin after indirect pulp treatment (IPT) using microhardness analysis after 37 to 71 months. METHODS: Eighteen teeth submitted to IPT and capped with calcium hydroxide (CH) or gutta-percha (GP) were evaluated (treated group). Ten sound molars and 10 molars with deep acute carious lesions were selected to serve as positive and negative control groups, respectively. In the treated group, restorations and pulp-capping materials were removed. In the positive control group, 3- to 4-mm deep cavities were prepared. In the negative control group, the carious tissue was removed. Microhardness analysis was performed at 10-, 35-, 60-, 85-, and 110-microm depths. Data were analyzed using 1-way analysis of variance (P<.05). RESULTS: Microhardness values for sound, carious, and treated groups at 10-, 35-, 60-, 85-, and 110-microm depths showed a statistically significant difference (P

Nitric oxide synthase inhibition by L-NAME prevents the decrease of Na+,K+-ATPase activity in midbrain of rats subjected to arginine administration.

In the present study we investigated the effect of acute administration of L-arginine on Na(+),K(+)-ATPase and Mg(2+)-ATPase activities and on some parameters of oxidative stress (chemiluminescence and total radical-trapping antioxidant parameter-TRAP) in midbrain of adult rats. We also tested the effect of L-NAME on the effects produced by arginine. Sixty-day-old rats were treated with an acute intraperitoneal injection of saline (group I, control), arginine (0.8 g/kg) (group II), L-NAME (2 mg/kg) (group III) or arginine (0.8 g/kg) plus L-NAME (2 mg/kg) (group IV). Na(+),K(+)-ATPase activity was significantly reduced in the arginine-treated rats, but was not affected by other treatments. In contrast, Mg(2+)-ATPase activity was not altered by any treatment. Furthermore, chemiluminescence was significantly increased and TRAP was significantly decreased in arginine-treated rats, whereas the simultaneous injection of L-NAME prevented these effects. These results demonstrate that in vivo arginine administration reduces Na(+),K(+)-ATPase activity possibly through free radical generation induced by NO formation.

Inhibition of Na+,K+-ATPase activity from rat hippocampus by proline.

Na+,K+-ATPase and Mg2+-ATPase activities were determined in the synaptic plasma membranes from hippocampus of rats subjected to chronic and acute proline administration. Na+,K+-ATPase activity was significantly reduced in chronic and acute treatment by 33% and 40%, respectively. Mg2+-ATPase activity was not altered by any treatment. In another set of experiments, synaptic plasma membranes were prepared from hippocampus and incubated with proline or glutamate at final concentrations ranging from 0.2 to 2.0 mM. Na+,K+-ATPase, but not Mg2+-ATPase was inhibited (30%) by the two amino acids. In addition, competition between proline and glutamate for the enzyme activity was observed, suggesting a common binding site for these amino acids. Considering that Na+,K+-ATPase activity is critical for normal brain function, the results of the present study showing a marked inhibition of this enzyme by proline may be associated with the neurological dysfunction found in patients affected by type II hyperprolinemia.

Inhibition of rat brain Na+, K+-ATPase activity induced by homocysteine is probably mediated by oxidative stress.

The objective of the present study was to investigate the effects of preincubation of hippocampus homogenates in the presence of homocysteine or methionine on Na+, K+-ATPase and Mg2+-ATPase activities in synaptic membranes of rats. Homocysteine significantly inhibited Na+, K+-ATPase activity, whereas methionine had no effect. Mg2+-ATPase activity was not altered by the metabolites. We also evaluated the effect of incubating glutathione, cysteine, dithiothreitol, trolox, superoxide dismutase and GM1 ganglioside alone or incubation with homocysteine on Na+, K+-ATPase activity. Tested compounds did not alter Na+, K+-ATPase and Mg2+-ATPase activities, but except for trolox, prevented the inhibitory effect of homocysteine on Na+, K+-ATPase activity. These results suggest that inhibition of this enzyme activity by homocysteine is possibly mediated by free radicals and may contribute to the neurological dysfunction found in homocystinuric patients.

Factors affecting fasting urinary calcium excretion in stone former patients on different dietary calcium intake.

The effects of variable calcium content on daily and fasting urinary calcium and other lithogenic solutes excretion, on the bone turnover index (fasting hydroxyproline urinary excretion) and on the calciotropic hormones were studied in 312 stone former patients with an outpatient protocol and 15 stone former patients in an inpatient study. Furthermore in 60 of these patients, 30 while on a low calcium diet (LCD) and 30 on a free calcium home diet (FCD), the effects of an oral calcium load (OCL) on bone turnover index, calciotropic hormones and calcium excretion were evaluated. The results demonstrate that an LCD is effective in reducing daily calcium excretion. Fasting calcium excretion is apparently not affected by changes in dietary calcium content. On the other hand, LCD induces a marked increase in bone resorption, without apparent signs of increased parathyroid activity. This may explain the failure to reduce fasting urinary calcium excretion by the LCD. The OCL greatly reduced bone resorption rate, without any change in calciotropic hormones, especially in patients on LCD. In conclusion, the LCD induces a reduction in the lithogenic factors in the urine of stone formers, but induces a marked increase in bone resorption. The lack of any change in fasting urinary calcium excretion in conditions of different dietary calcium intake may be due to an opposite change in the intestinal and osseous components that affect this parameter, and is therefore of little value.

Radiolabelled semisolid test meal clearance in the evaluation of esophageal involvement in scleroderma and Sjogren's syndrome.

Esophageal involvement by scleroderma is frequent. Investigation by manometry or radiography is invasive and nonphysiological. Scintigraphy of the clearance of small radiolabelled liquid boluses in the supine position, while sensitive and noninvasive, may also be nonphysiological and does not allow the simultaneous determination of gastric emptying. We thus studied the esophageal clearance of a semisolid test meal ingested in the upright position. Forty-seven patients with scleroderma and 24 with Sjogren's syndrome were compared with ten normal controls and ten patients with gastric emptying abnormalities but no esophageal involvement. Results of scintigraphy were also correlated with manometry and contrast radiography. Quantitative evaluation of esophageal tracer retention at ten minutes postingestion was: (mean +/- SD), 2.8 +/- 1.0% in normals, 2.9 +/- 0.9% in gastric dysmotility, 4.8 +/- 2.9% in Sjogren's syndrome, and 22.3 +/- 25.0% in scleroderma; similar results were found at 20 and 60 minutes. The T 1/2 of gastric emptying was 47.1 +/- 5.7 minutes in normals, 95.9 +/- 25.3 minutes in gastric dysmotility, 62.9 +/- 19.5 minutes in Sjogren's syndrome, and 52.9 +/- 13.5 minutes in scleroderma. We conclude that esophageal clearance of a semisolid test meal is a sensitive index of esophageal dysmotility and correlates well with results from manometry and contrast radiography but is noninvasive and quantifiable. The simultaneous measurement of gastric emptying is also possible in many cases.