The presence of osteocalcin, osteopontin and reactive oxygen species-positive cells in pulp tissue after dental bleaching.

AIM: To analyse the influence of H2 O2 on pulp repair through osteocalcin and osteopontin immunolabelling and in cellular defence by using the antireactive oxygen species (ROS) antibody. METHODOLOGY: The maxillary molars of 50 rats were treated with 35% H2 O2 (Ble groups) or placebo gel (control groups). At 0 h and 2, 7, 15 and 30 days (n = 10 hemimaxillae), the rats were killed and pulp tissue was evaluated using inflammation and immunolabelling scores (osteocalcin/osteopontin); ROS-positive cells were counted. Paired t-test and Wilcoxon signed-rank test were used (P < 0.05). RESULTS: The Ble group had necrosis in the coronal pulp at 0 h and in the occlusal third of the coronal pulp at 2 days; at 7, 15 and 30 days, no inflammation was noted similar to the controls (P > 0.05). Osteocalcin was absent in the Ble at 0 h, moderate at 2 days and increased thereafter, differing from the controls at all two periods (P < 0.05). Osteopontin was higher principally at 7 and 15 days in Ble groups, but differing with control groups from 2 days after bleaching (P < 0.05). The Ble group had more ROS-positive cells in the pulp at 7 and 15 days (P < 0.05). Tertiary dentine was observed at 7 days, increasing thereafter (P < 0.05). CONCLUSIONS: Post-bleaching pulp repair was associated with increased osteocalcin over time. Osteopontin also participated in this process, and anti-ROS was involved in cellular defence against H2 O2 .

In vivo analysis of the presence of heme oxygenase-1, transcription factor Jun-D and CD90+/CD73+/CD105+/CD45- cells in the pulp of bleached teeth.

AIM: To investigate hydrogen peroxide (H2 O2 )-induced responsiveness in pulp cells using heme oxygenase-1 (HO-1) immunolabelling, Jun-D immunolabelling to study the effects of H2 O2 on odontoblastic differentiation and CD90+/CD73+/CD105+/CD45- cell counting for in vivo identification of mesenchymal stem cells in the pulp. METHODOLOGY: The maxillary molars of 50 rats were treated with a bleaching gel (35% H2 O2 , 1 × 30 min) or placebo gel (control groups). At 2, 3, 7, 15 and 30 days after the treatment (n = 10), inflammation in pulp tissue was analysed by haematoxylin-eosin staining, HO-1- and Jun-D-immunolabelled cells were counted in each third of the pulp chamber, and the number of CD90+/CD73+/CD105+/CD45- cells was quantified by immunofluorescence. The results were assessed using the Paired t-test or Wilcoxon signed-rank test (P < 0.05). RESULTS: Significant H2 O2 -induced inflammation was noted at 2 and 3 days (P < 0.05), with tertiary dentine formation occurring from 7 days. The bleached specimens had greater HO-1 immunolabelling in the middle and cervical thirds of the coronal pulp at 2 and 3 days, in all thirds at 7 days, and in the occlusal third at 15 days (P < 0.05), and significant nuclear Jun-D immunolabelling in the cervical third at 2 and 3 days and in the occlusal and middle thirds at 7 days (P < 0.05). Bleached and control groups had low numbers of CD90+/CD73+/CD105+/CD45- cells in the pulp at all periods (P > 0.05). CONCLUSIONS: Pulp cells responded to oxidative stress by expressing HO-1 during the post-bleaching inflammation phase until the beginning of the repair phase. Jun-D expression occurred during the reduction of inflammation and the beginning of tertiary dentine production. The presence of oxidative stress did not influence the number of CD90+/CD73+/CD105+/CD45- cells identified in vivo in the dental pulp.

The effect of dental bleaching on pulpal tissue response in a diabetic animal model: a study of immunoregulatory cytokines.

AIM: To evaluate the influence of tooth bleaching on immunoregulatory cytokines production (IL-6, Tumour necrosis factor (TNF)-α and IL-17) in the pulp tissue of normoglycaemic and diabetic rats. METHODOLOGY: Twenty-eight rats were divided into normoglycaemic and diabetic rats (n = 14). Diabetes mellitus (DM) was induced with a single dose of alloxan diluted in citrate buffer via intramuscular injection. After DM confirmation, all rats were sedated and tooth bleaching was performed using 35% hydrogen peroxide on the right maxillary molars for 30 min. Left molars were used as controls. Bleaching resulted in four hemimaxillae groups: normoglycaemic (N), N-bleached (NBle), diabetic (D) and D-bleached (DBle). After 2 and 30 days, rats were euthanized and hemimaxillae processed for analysis by haematoxylin and eosin and immunohistochemistry. Results within and between animals were submitted to Wilcoxon signed-rank and Mann-Whitney tests (P < 0.05). RESULTS: At 2 days, the NBle group had mild, and the DBle had severe inflammatory infiltration in the pulpal tissue (P < 0.05). TNF-α and IL-6 cytokines were associated with increased immunolabelling in the bleached groups compared to nonbleached (P < 0.05). However, IL-17 had increased immunolabelling in the NBle compared to the N and DBle group (P < 0.05). At 30 days, reactionary dentine was observed in the coronal pulp of all bleached teeth and no inflammation was present (P > 0.05). TNF-α cytokines had increased immunolabelling in the DBle group compared to the D group (P < 0.05). However, for IL-6 and IL-17, no difference was observed in this period (P > 0.05). CONCLUSIONS: Tooth bleaching increased IL-6 and TNF-α in the pulp tissue regardless of diabetes mellitus; however, diabetic rats had higher TNF-α levels for longer periods. Tooth bleaching influenced the increase in IL-17 in the early periods in normoglycaemic rats.

Waiting for a kidney transplant: association with anxiety and stress.

BACKGROUND: The pretransplantation period is characterized by many stressful events that can result in symptoms of anxiety and stress and ultimately can have a negative impact on graft outcome. Our objective was to evaluate the association between symptoms of anxiety and stress in patients awaiting kidney transplantation. METHODS: This was a transversal study describing 50 randomly selected patients undergoing hemodialysis and waitlisted for kidney transplantation. We collected social and demographic data, and adopted the Beck Anxiety Inventory and the Lipp Stress Symptoms for Adults Inventory to respectively evaluate anxiety and stress. RESULTS: The mean age was 50.2 ± 11.7 years, 54% of patients were female, time on dialysis was 6.5 ± 4.5 years, and transplant waitlist time was 5.9 ± 4.4 years. Forty-six percent of patients were married or had a stable relationship, 50% were illiterate or had only finished primary school, and 64% were pensioners. Stress was documented in 60% of patients, of which 30% had severe stress, whereas 56% of patients showed symptoms of anxiety. The presence of stress was associated with longer waitlist time (P = .006) and longer time on dialysis (P = .052). Less severe stress was associated with higher education level (P = .031), whereas patients in more advanced phases of stress showed higher levels of anxiety. After a multivariate analysis, stress was 3.6 times (CI 1.34 to 9.89) more frequent among individuals with anxiety. CONCLUSIONS: Stress and anxiety were prevalent in patients on a waitlist and were associated with social and chronic kidney disease-related patterns. This observation can stimulate the adoption of strategies for the prevention of stress and anxiety, avoiding posttransplantation complications, such as nonadherence to treatment.

Body mass index in the first year after kidney transplantation.

INTRODUCTION: Kidney transplant recipients (KTR) experience better appetite, partly due to the use of steroids, and are subjected to less severe dietetic restrictions, hence they tend to increase the uptake of calories, which favors weight gain posttransplantation. In this study, we evaluate the profile of body mass index (BMI) in the first year posttransplantation. METHODS: This was a retrospective study including 131 patients who received transplants between 1991 and 2011. We collected demographic and clinical data such as body weight and height, and calculated BMI pretransplantation and at 6 and 12 months posttransplantation. RESULTS: Mean age was 47.1 ± 13.1 years, 64.9% were male, and 29% of patients were diabetic. Pretransplantation mean BMI was 23.04 ± 4.08 kg/m(2), and at 6 and 12 months posttransplantation it increased to 24.55 ± 4.2 kg/m(2) and 24.65 ± 4.16 kg/m(2), respectively (P < .001). At 6 months, this significant weight gain occurred in all patients, even those malnourished, eutrophic, overweight, and obese at pretransplantation. Looking at pretransplantation malnourished patients, 30.8% remained malnourished 1 year after transplantation. Otherwise, 28.6% of pretransplantation overweight patients and 100% of pretransplantation obese patients could be classified as obese at 1 year posttransplantation. CONCLUSIONS: Increase in BMI is common in obese and nonobese KTR. This study highlights the importance of identifying subjects at risk for excessive weight gain posttransplantation, thus allowing an early nutritional intervention to prevent its complications.

Excessive immunosuppression in kidney transplant patients: prevalence and outcomes.

BACKGROUND: Death with a functioning graft is currently one of the main causes of kidney graft loss. A large proportion of cases is attributed to infectious complications that can be related to overimmunosuppression. We retrospectively studied 80 kidney transplant patients, grafted from January 2005 to December 2009, to assess the prevalence of excessive immunosuppression, and its possible correlation with infections and infection-related death. METHODS: Excessive immunosuppression was defined by a prescribed dosage above the expected to the time point or an elevated drug blood level according to the Kidney Disease: Improving Global Outcomes (2009) recommendations at 1, 3, 6, and 12 months, and then annually. RESULTS: Death with a functioning graft accounted for 76.5% of losses. Overall, 53.8% of deaths were from infections, and 38.5% from cardiovascular causes. Acute rejection episodes were noted in 8.8% of patients. Only 10% of patients had adequate immunosuppression throughout the follow-up. Seventy-two percent of patients showed adequate immunosuppression at least half of the 18 evaluated points, although 50% showed between 1 and 3 drugs administered above recommended dosages during the whole period. Infections were recorded in 78.8% patients, with a median of 3 episodes per patient. Any level of excessive immunosuppression was associated with infections (odds ratio, 11.2; P < .001), but not with death caused thereby. CONCLUSION: Excessive immunosuppression among this cohort was associated with a greater incidence of infections, but not with death from this cause.

Urinary tract infection caused by extended-spectrum beta-lactamase-producing bacteria in kidney transplant patients.

Urinary tract infection (UTI) is a common complication among kidney transplant patients. UTI caused by multi-resistant extended-spectrum beta-lactamase producing bacteria (ESBL) have largely increased among the hospitalized patient population and especially kidney transplant recipients. We retrospectively studied 83 kidney transplant patients to evaluate the incidence and possible causative conditions of ESBL-related UTI over the last 6 years. ESBL production was determined by the antibiotic susceptibility profile of urine cultures. We compared the incidence in two 3-year periods, 2003-2005 (period 1) and 2006-2008 (period 2). An high incidence of ESBL-related UTI (16.8%) was observed in the posttransplant period performing 31% of the overall UTI incidence, with an increase over the last 3 years from 23.8% to 37.5%. ESBL-related UTI was related to previous episodes of UTI (78.6% vs 29.0%; P < .01) and reoperations (50.0% vs 12.9%; P < .05). We observed a progressively increasing incidence of 13%, 38%, and 45% of ESBL-related UTI among first, second, and third episodes, respectively. Age, gender, HLA mismatches, etiology of chronic kidney disease, diabetes mellitus, acute rejection, induction treatment, and type/level of immunosuppressants were similiar between the groups with or without ESBL-related UTI. We observed a high increased incidence of ESBL-related UTI among kidney transplant recipients, and particularly patients with recurrent UTI.