Relationship between apical periodontitis and atherosclerosis in rats: lipid profile and histological study.

AIM: To investigate the relationship between apical periodontitis and atherosclerosis in rats by lipid profile and carotid artery intima tunic measurement, and histological and histometric evaluation of periapical lesions. METHODOLOGY: Forty male Wistar rats were allocated into four groups: control (C), with apical periodontitis (AP), with atherosclerosis (AT) and with AP and AT (AP + AT). Atherosclerosis was induced using a high-lipid diet associated with a surgical ligature in the carotid artery and a super dosage of vitamin D3 . AP was induced via pulp exposure to the oral environment. At 45 and 75 days, serum levels of total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were measured. The maxillary and mandibular jaws and carotid artery were collected and processed for histological analysis. The Kruskal-Wallis or Mann-Whitney test was performed for nonparametric data, and the Tukey's or Student's t-test was performed for parametric data (P < 0.05). RESULTS: In nonatherosclerotic animals, the induction of apical periodontitis increased TG levels significantly, from 63.1 ± 11.4 mg dL-1 in group C to 88.2 ± 7.9 mg dL-1 in the AP group (P < 0.05). The induction of AP was associated with a trend for higher TC and LDL-C levels in atherosclerotic animals (P > 0.05); however, it only significantly increased TG levels, from 93.2 ± 18.0 mg dL-1 in AT group to 121.9 ± 14.5 mg dL-1 in the AP + AT group (P < 0.05). Animals in the AP + AT group had a 36.5% increase in the thickness of the carotid intima tunic when compared with the AT group (P < 0.05). The intensity of the inflammatory infiltrate was significantly larger in the AP + AT group when compared with AP group (P < 0.05). The AP + AT group exhibited significantly greater alveolar bone loss, with a periapical lesion size of 206.4 ± 56.3 × 104 µm2 , compared with 151.4 ± 49.1 × 104 µm2 in the AP group (P < 0.05). CONCLUSION: Apical periodontitis influenced triglyceride levels, increasing them even in the absence of atherosclerosis, and influenced the increase in the thickness of the carotid artery intima tunic in the presence of atherosclerosis. Atherosclerosis intensified the inflammatory reaction and increased bone resorption in periapical lesions.

Relationships between oral infections and blood glucose concentrations or HbA1c levels in normal and diabetic rats.

AIM: To measure glycosylated haemoglobin (HbA1c) in a diabetic model as a means of investigating apical periodontitis and periodontal disease for their effects on both blood glucose concentrations and long-term glycaemic control. METHODOLOGY: Wistar rats (n = 80) were assigned to one of eight groups (10 animals/group): control (G1), apical periodontitis (G2), periodontal disease (G3), apical periodontitis and periodontal disease (G4), diabetic (G5), diabetic with apical periodontitis (G6), diabetic with periodontal disease (G7) and diabetic with apical periodontitis and periodontal disease (G8). A diabetic state was induced with streptozotocin. Apical periodontitis was induced by dental exposure to the oral environment. Periodontal disease was induced by periodontal ligature. Blood glucose concentrations were measured at 0, 6, 30 and 60 days. After euthanization, rat maxillae were excised and processed for histopathology and for measurement of HbA1c levels by ion exchange chromatography. Data were tabulated and subject to statistical analysis (P < 0.05). RESULTS: The inflammatory infiltrate and alveolar bone resorption were more severe in diabetic rats (P < 0.05). Diabetic rats exhibited higher levels of HbA1c independent of apical periodontitis or periodontal disease (P < 0.05). However, the presence of oral infections in diabetic rats was associated with increased blood glucose concentrations (P < 0.05). CONCLUSIONS: Oral infections affect glycaemic conditions in diabetic rats and increase HbA1c levels in normoglycaemic or diabetic rats.

Qualidade espermática de sêmen de cães naturalmente infectados por leishmania sp / Semen quality of dogs naturally infected by leishmania sp

Avaliaram-se alterações espermáticas associadas à infecção por leishmaniose no sêmen de cães naturalmente infectados, utilizando-se, durante oito semanas consecutivas, ejaculados de seis cães soronegativos e seis cães soropositivos. As amostras foram colhidas uma vez por semana e avaliadas quanto ao volume, concentração, motilidade, vigor, morfologia espermática, integridade da cromatina, avaliação simultânea da integridade da membrana plasmática, acrossoma e potencial mitocondrial. Concomitantemente foram dosadas a proteína total do plasma seminal e sanguíneo. A leishmaniose visceral causou aumento dos defeitos maiores e menores nos espermatozoides dos animais acometidos pelo estágio moderado a severo da doença. Em estágios mais avançados da enfermidade, a integridade das membranas acrossomal e plasmática foi afetada negativamente. Não foi possível estabelecer um critério quanto à avaliação do potencial mitocondrial. A incidência de alterações morfológicas nos animais acometidos não promoveu aumento de injurias à cromatina. Todos os animais com leishmaniose apresentaram hiperproteinemia do sêmen.

The spermatic changes associated with the natural infection in dogs by Leishmania sp was evaluated during eight consecutive weeks, using ejaculates of six seronegative and six seropositive dogs. The samples were collected once a week and evaluated for volume, concentration, motility, vigor, sperm morphology, chromatin integrity, simultaneous evaluation of the plasmatic membrane integrity, acrosome, and mitochondrial potential. The total proteins of the seminal plasma and blood were measured. The visceral leishmaniasis caused increase of major and minor defects in spermatozoa of animals attacked by moderate to severe stages of the disease. In more advanced stages of the illness, the acrosomal and plasmatic membranes integrity was adversely affected. It was not possible to establish a pattern refering the evaluation of the mitochondrial potential. The incidence of morphological changes in the seropositive animals did not promote an increase of injuries to the chromatin. All animals with leishmaniasis presented hyperproteinemia of the semen.

Bone healing in critical-size defects treated with platelet-rich plasma activated by two different methods. A histologic and histometric study in rat calvaria.

BACKGROUND AND OBJECTIVE: The purpose of this study was to analyze histologically the influence of platelet-rich plasma (PRP) coagulated with two different activators on bone healing in surgically created critical-size defects (CSD) in rat calvaria. MATERIAL AND METHODS: Forty-eight rats were divided into three groups: C, PRP-C and PRP-T. An 8 mm diameter CSD was created in the calvarium of each animal. In group C, the defect was filled by a blood clot only. In groups PRP-C and PRP-T, the defect was filled with PRP activated with either calcium chloride or thromboplastin solution, respectively. Each group was divided into two subgroups (n = 8 per subgroup) and killed at either 4 or 12 weeks postoperatively. Histologic and histometric analyses were performed. The amount of new bone formed was calculated as a percentage of the total area of the original defect. Percentage data were transformed into arccosine for statistical analysis (analysis of variance, Tukey's post hoc test, p < 0.05). RESULTS: No defect completely regenerated with bone. Group PRP-C had a statistically greater amount of bone formation than groups C and PRP-T at both time points of analysis. No statistically significant differences were observed between groups C and PRP-T. CONCLUSION: It can be concluded that the type of activator used to initiate PRP clot formation influences its biological effect on bone healing in CSD in rat calvaria.

Bone healing in critical-size defects treated with platelet-rich plasma: a histologic and histometric study in rat calvaria.

BACKGROUND AND OBJECTIVE: The purpose of this study was to analyze histologically the influence of autologous platelet-rich plasma on bone healing in surgically created critical-size defects in rat calvaria. MATERIAL AND METHODS: Thirty-two rats were divided into two groups: the control group (group C) and the platelet-rich plasma group. An 8-mm-diameter critical-size defect was created in the calvarium of each animal. In group C the defect was filled by a blood clot only. In the platelet-rich plasma group, 0.35 mL of platelet-rich plasma was placed in the defect and covered by 0.35 mL of platelet-poor plasma. Both groups were divided into subgroups (n = 8) and killed at either 4 or 12 wk postoperatively. Histometric (using image-analysis software) and histologic analyses were performed. The amount of new bone formed was calculated as a percentage of the total area of the original defect. Percentage data were transformed into arccosine for statistical analysis (analysis of variance, Tukey, p < 0.05). RESULTS: No defect completely regenerated with bone. The platelet-rich plasma group had a statistically greater amount of bone formation than group C at both 4 wk (17.68% vs. 7.20%, respectively) and 12 wk (24.69% vs. 11.65%, respectively) postoperatively. CONCLUSION: Within the limits of this study, it can be concluded that platelet-rich plasma placed in the defects and covered by platelet-poor plasma significantly enhanced bone healing in critical-size defects in rat calvaria.