RESUMO
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.
Assuntos
Aterosclerose , Periodontite Periapical , Animais , Aterosclerose/etiologia , Humanos , Inflamação , Lipídeos , Masculino , Ratos , Ratos WistarRESUMO
AIM: To evaluate the morphology and impact of root canal preparation in maxillary incisors with palatogingival grooves (PGG). METHODOLOGY: Twenty extracted human maxillary incisors with PGG were subjected to macroscopic analysis and scanning electron microscopy analysis (SEM). The following characteristics of the PGG were evaluated: depth, point of origin in the cingulum, extension and position on the lingual surface. Furthermore, the presence of calculus, communications between the root canal system and the PGG, and root resorptions were investigated. The root canals were subsequently instrumented with K-files of three consecutive sizes. The teeth were sectioned, and the axial plane of each tooth section was imaged using SEM before and after instrumentation. The distance between the root canal walls and the PGG was calculated according to the location. Additionally, the distance between canal walls and cementum was measured at three different sites, to verify if instrumentation influenced dentine removal on a specific wall in teeth with PGG. Statistical analysis was performed using the Mann-Whitney or Student's t-test (P < 0.05). RESULTS: Macroscopic analysis revealed that a deep groove was most frequently observed (75%), followed by a depression/shallow groove (25%) (P < 0.05). PGG typically originated in the distal margin ridge of the cingulum (65%) (P < 0.05), extending only to the middle (45%) or up to the apical (50%) third of the root (P < 0.05). Additionally, PGGs were typically located on the distal aspect of the lingual surface (70%) (P < 0.05). Calculus was concentrated on the surface of the crown and cementum-enamel junction (P < 0.05). Communication between the root canal and PGG was present in 35% of teeth, and root resorptions were noted in 50% of teeth. The distance between the external root surface and the pulp cavity was significantly narrower after instrumentation (P < 0.05); however, root canal preparation did not influence dentine removal on the specific wall associated with the groove (P > 0.05). CONCLUSIONS: Palatogingival grooves were characteristically deep and originated from the distal margin of the cingulum. Although it has been associated with a thinner root wall, root canal preparation did not influence the thickness of the specific wall in the maxillary incisors with PGG.
Assuntos
Cavidade Pulpar , Camada de Esfregaço , Cemento Dentário , Dentina , Humanos , Incisivo , Irrigantes do Canal Radicular , Preparo de Canal Radicular , Tratamento do Canal RadicularRESUMO
The aim of this review was to examine current knowledge of the role of interleukin-6 (IL-6) in apical periodontitis (AP) pathogenesis as an inflammatory or pro-inflammatory cytokine. It also looked at whether IL-6 could serve as a measure for differential diagnosis or as a biomarker that can further predict the progression of bone resorption. A systematic review relating to AP and IL-6 was made via PubMed, BIOSIS, Cochrane, EMBASE and Web of Science databases using keywords and controlled vocabulary. Two independent reviewers first screened titles and abstracts and then the full texts. The reference lists of the identified publications were examined for additional titles. Eighteen papers were studied in total. In vitro studies (n = 6) revealed that IL-6 is present in AP, and its levels are proportional to the size of the periapical lesions. Neutrophils and macrophages resident in these lesions can produce IL-6 in vitro after a bacterial stimulus. Animal studies (n = 5) showed that IL-6 is present in AP and that osteoblasts can produce IL-6 in vivo. On the other hand, two studies using IL-6 knockout mice revealed larger periapical lesions when compared with control groups, demonstrating IL-6's role as an anti-inflammatory cytokine. In human studies (n = 7), IL-6 was identified in AP, and its levels were higher in symptomatic, epithelialized and large lesions than in asymptomatic and small lesions. These data lead to the conclusion that IL-6 may play a pro-inflammatory role, increasing its levels and reabsorbing bone in the presence of infections. When IL-6 is not present, other cytokines such as IL-1 and TNF-α induce bone resorption. Further studies about the relationship between AP development and the cytokine network must be performed to establish the exact role of each cytokine in the inflammatory process.