The relationship between severity of periapical periodontitis and next-generation systemic inflammatory biomarkers in children with early childhood caries.

INTRODUCTION: Early childhood caries (ECC) is closely associated with poor oral hygiene and cariogenic diet. Untreated ECC results in recurrent odontogenic infections and local and systemic consequences. In this study, our goal is to assess the relationship between the intensity of odontogenic infection-associated periapical periodontitis and new generation of systemic inflammatory markers (SII, NLR, PLR) in ECC-affected children. MATERIAL AND METHOD: 95 healthy patients in early childhood and demonstrating periapical periodontitis who underwent dental treatment under general anesthesia (GA) in the last two years were included in the present study. Their periapical statuses were dichotomized as mild and severe. Periapical Index (PAI) scores of 2 and 3 were regarded as "mild" whereas 4 and 5 as "severe". Of the complete blood test (CBC) parameters, systemic inflammatory index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), neutrophilic granulocyte (NEUT), lymphocyte (LYMPH) and platelet (PLT) were recorded. The relationship between the degree of periapical pathology and the evaluated markers was assessed using Receiver Operating Characteristic (ROC) analysis. RESULTS: Results of the present study revealed that mean NLR, SII and NEUT index scores of the patients having severe periapical periodontitis were statistically higher than those of the ones with mild pathology (p < 0.05). A positive, statistically significant interrelationship was found between the number of teeth demonstrating a PAI score of severe periapical periodontitis with the signs of exacerbation (PAI 5) and NLR and SII values (p < 0.05). Area under the ROC curve (AUC) values for NLR and SII were determined as 66.8% and 66.6% respectively, indicating that classification performance was sufficient and statistically significant (p < 0.05). CONCLUSION: Postponing the management of odontogenic infections will induce some complications such as, infective endocarditis and cause the systemic inflammatory process to continue by aggravating the systemic effects of local lesions. Thus, underlying mechanism should be eliminated and oral hygiene should be maintained, also novel biomarkers may be recommended to be used for the decision-making process for the teeth with persistent periapical lesions unresponsive to treatment.

Is there any association between the presence of biomarkers and apical periodontitis? A systematic review.

This systematic review aimed to verify whether there is evidence of an association between apical periodontitis and the presence of systemic biomarkers. This study adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses - PRISMA. For this, the acronym PECO was used; population (P) of adult humans exposed (E) to the presence of apical periodontitis, compared (C) to adult humans without apical periodontitis, and the outcome (O) of the presence of biomarkers was observed. The articles were searched in PubMed, Scopus, Web of Science, LILACS, Cochrane Library, OpenGray, and Google Scholar grey databases. Subsequently, studies were excluded based on title, abstract, and full article reading, following the eligibility criteria. The methodological quality of the selected studies was evaluated using the Newcastle-Ottawa qualifier. After exclusion, 656 studies were identified, resulting in 17 final articles that were divided into case-control, cross-sectional, and cohort studies. Eight studies were considered to have a low risk of bias, one had a medium risk of bias, and eight had a high risk of bias. In addition, 12 articles evaluated biomarkers in blood plasma, four evaluated them in saliva, and only one evaluated them in gingival crevicular fluid. The results of these studies indicated an association between apical periodontitis and the systemic presence of biomarkers. These markers are mainly related to inflammation, such as interleukins IL-1, IL-2, and IL-6, oxidative markers, such as nitric oxide and superoxide anions, and immunoglobulins IgG and IgM. Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier (CRD42023493959).

Omega 3 Fatty Acids Reduce the Triglyceride Levels in Rats with Apical Periodontitis.

The aim of this study was to evaluate the influence of the prophylactic and therapeutic supplementation with omega 3 polyunsaturated fatty acids (w-3 PUFAs) on the lipid profile and periapical bone resorption in rats with apical periodontitis. Forty male rats were divided into groups: control rats (C), rats treated with w-3 PUFAs (C+O), rats with pulp exposure-induced apical periodontitis (AP), and rats with AP treated with w-3 PUFAs (AP+O). The administration of w-3 PUFAs was carried out orally once a day for 15 days before pulp exposure and, subsequently, for an additional 30 days after pulp exposure. AP was induced by exposing pulpal tissues to the oral environment. The samples were collected after 30 days. Triglycerides and cholesterol levels were enzymatically measured using the Trinder method. The jaws were collected and submitted for histological analysis. Two-way analysis of variance and Kruskal-Wallis tests were used for statistical analysis, and the significance was set at p<0.05. The triglyceride levels of the AP group were significantly higher than those of the C, C+O and AP+O groups (p<0.05). However, the difference in the cholesterol levels among the groups was not significant (p>0.05). Rats with AP showed larger areas of bone resorption as well as higher inflammatory intensity compared with rats with AP supplemented with w-3 PUFAs. It may be concluded that the presence of multiple AP foci increased the triglyceride levels. In addition, omega 3 supplementation might reduce these levels in rats with AP, as well as the bone resorption areas of periapical tissues.

Omega 3 fatty acids reduce the triglyceride levels in rats with apical periodontitis

Abstract The aim of this study was to evaluate the influence of the prophylactic and therapeutic supplementation with omega 3 polyunsaturated fatty acids (w-3 PUFAs) on the lipid profile and periapical bone resorption in rats with apical periodontitis. Forty male rats were divided into groups: control rats (C), rats treated with w-3 PUFAs (C+O), rats with pulp exposure-induced apical periodontitis (AP), and rats with AP treated with w-3 PUFAs (AP+O). The administration of w-3 PUFAs was carried out orally once a day for 15 days before pulp exposure and, subsequently, for an additional 30 days after pulp exposure. AP was induced by exposing pulpal tissues to the oral environment. The samples were collected after 30 days. Triglycerides and cholesterol levels were enzymatically measured using the Trinder method. The jaws were collected and submitted for histological analysis. Two-way analysis of variance and Kruskal-Wallis tests were used for statistical analysis, and the significance was set at p<0.05. The triglyceride levels of the AP group were significantly higher than those of the C, C+O and AP+O groups (p<0.05). However, the difference in the cholesterol levels among the groups was not significant (p>0.05). Rats with AP showed larger areas of bone resorption as well as higher inflammatory intensity compared with rats with AP supplemented with w-3 PUFAs. It may be concluded that the presence of multiple AP foci increased the triglyceride levels. In addition, omega 3 supplementation might reduce these levels in rats with AP, as well as the bone resorption areas of periapical tissues.

Resumo O objetivo deste estudo foi avaliar a influência da suplementação profilática e terapêutica com os ácidos graxos ômega-3 no perfil lipídico e na reabsorção óssea, em ratos com periodontite apical. Quarenta ratos machos foram divididos em grupos: ratos controle (C), ratos tratados com ácidos graxos ômega-3 (C+O), ratos com periodontite apical induzida por meio de exposição pulpar (PA), ratos com PA tratados com ácidos graxos ômega-3 (PA+O). A administração do ômega-3 foi realizada oralmente, uma vez ao dia durante 15 antes da exposição pulpar e, subsequentemente, por mais 30 dias depois da exposição pulpar. A PA foi induzida por meio da exposição do tecido pulpar ao ambiente oral. Após 30 dias, os ratos foram mortos e os níveis de triglicérides e colesterol foram mensurados pelo método enzimático de Trinder. As mandíbulas foram coletadas e submetidas à análise histológica. Análise de variância de dois fatores e teste de Kruskal-Wallis foram utilizados para análise estatística, e o nível de significância foi de p < 0,05. Os níveis de triglicérides do grupo PA foram significativamente maiores que dos grupos C, C+O e PA+O (p<0,05). Entretanto, não houve diferença significativa nos níveis de colesterol entre os grupos (p>0,05). Ratos com PA apresentaram maior área de reabsorção óssea bem como maior intensidade no infiltrado inflamatório comparados aos ratos com PA suplementados com ômega-3. Pode-se concluir que a presença de múltiplos focos de PA aumentou os níveis de triglicérides. Além disso, a suplementação com ômega-3 pode reduzir estes níveis em ratos com PA, bem como a área de reabsorção óssea dos tecidos periapicais.

Assessment of C-reactive Proteins, Cytokines, and Plasma Protein Levels in Hypertensive Patients with Apical Periodontitis.

INTRODUCTION: Chronic apical periodontitis (CAP) manifests mostly as periapical radiolucency. Various inflammatory mediators play a significant role in the pathogenesis of apical periodontitis. In acute inflammatory conditions, C-reactive proteins (CRP) and fibrinogen show a rise in their concentrations. In chronic diseases with high inflammatory components, an increased prevalence of hypertension has been observed. Hence, we assessed the association of CAP and plasma levels of various inflammatory markers (CRP, interleukin 6 [IL-6], and fibrinogen) in severely hypertensive patients. MATERIALS AND METHODS: This study was conducted in the conservative wing of the institute and included assessment of 250 hypertensive patients with apical periodontitis. With the help of periapical radiographs and clinical examination, the assessment of following parameters was done: Amount of teeth present, visible plaque index, periodontal pocket probing depth, clinical attachment level, bleeding on probing, presence/absence of carious lesions, which included assessment of caries in crown portion, in the root portion, and residual tooth roots (RR), presence of CAP from each patient; 8 mm of venous blood was collected in the morning for the assessment of plasma levels of IL-6, CRP, and fibrinogen levels. Immediate collection and processing of the samples were done in the hospital laboratory. All the results were analyzed by Statistical Package for the Social Sciences software. RESULTS: Out of 250, 155 patients were females. Mean plasma levels of CRP observed in our study were 0.8 mg/dL. Mean plasma levels of IL-6 and fibrinogen were found to be 3.3 and 337.1 mg/dL respectively. A significant correlation was observed while comparing mean body mass index (BMI), RR, and CAP in hypertensive patients. While comparing the mean plasma IL-6 levels, mean BMI, and CAP in the patients, significant results were obtained. Significant correlation was observed while comparing the mean BMI and CAP in hypertensive patients. CONCLUSION: Systemic levels of CRP, IL-6, and fibrinogen levels are influenced by the presence of CAP in hypertensive patients. CLINICAL SIGNIFICANCE: In hypertensive patients, CAP alters the systemic levels of various inflammatory markers.

FSH aggravates bone loss in ovariectomised rats with experimental periapical periodontitis.

Periapical bone loss is one of the prominent pathological and clinical features of periapical periodontitis. Previous studies have demonstrated that follicle­stimulating hormone (FSH) could directly affect skeletal remodelling by stimulating the formation and the function of osteoclasts in vitro and in vivo. However, the effect of FSH on periapical bone loss remained to be fully elucidated. In the current study, a rat model was established in order to verify the effect of FSH in experimental periapical lesions. It was identified that FSH aggravated the bone loss of periapical lesions. In addition, RANKL­, TRAP­, TNF­α­ and IL­1ß­positive cells were increased significantly in FSH­treated groups, which indicated that the function of FSH in bone loss may be mediated through the increasing activity of osteoclasts and the increased secretion of inflammatory cytokines. The results of the current study suggested that FSH, independent of oestrogen, may aggravate periapical bone loss by FSH receptors, which may serve an important role in the immune and inflammatory response of the host to root canal and periradicular infection during menopause.

Multiple Apical Periodontitis Influences Serum Levels of Cytokines and Nitric Oxide.

INTRODUCTION: This study evaluated whether apical periodontitis (AP) in a single tooth or in multiple teeth affected serum levels of inflammatory mediators and influenced blood homeostasis. METHODS: Thirty male Wistar rats were divided into 3 groups of 10 rats each: control group, healthy rats; 1AP group, rats with AP in 1 tooth; and 4AP group, rats with AP in 4 teeth. After 30 days, the rats were anesthetized, and their blood was collected through cardiac puncture to quantify tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-6, IL-17, IL-23, and nitric oxide (NO) levels. The rats were then sacrificed by administering an anesthetic overdose. Their maxillary and mandibular molars were collected and processed for histologic analysis with hematoxylin-eosin and for immunohistochemical staining of the cytokines and NO-producing enzyme nitric oxide synthase. Results of these analyses were statistically analyzed; P < .05 was considered statistically significant. RESULTS: Rats in the 1AP and 4AP groups showed increased IL-6, IL-17, IL-23, TNF-α, IFN-γ, and NO synthase expression; inflammatory cell infiltration; and moderate bone resorption in affected teeth. Serum TNF-α, IL-6, IL-17, and IL-23 levels were higher in rats in the 4AP group than in those in the control group (P < .05). Serum NO levels were significantly lower in rats in the 1AP and 4AP groups than in those in the control group (P < .05). Serum IFN-γ levels were not different among rats in the 3 groups (P > .05). CONCLUSIONS: These results suggested that AP affected blood homeostasis by altering the serum levels of inflammatory cytokines and NO.

Association between apical periodontitis lesions and plasmatic levels of C-reactive protein, interleukin 6 and fibrinogen in hypertensive patients.

AIM: To test the null hypothesis of association between chronic apical periodontitis (CAP) and plasmatic levels of the C-reactive protein (CRP), interleukin-6 (IL-6) and fibrinogen in a population of severely hypertensive patients. METHODOLOGY: One hundred and seventy patients with severe refractory hypertension were selected. All patients were submitted to radiographic, clinical and periodontal evaluation. Plasmatic levels of CRP, IL-6 and fibrinogen were measured on the morning of the first periodontal appointment using commercially available kits. Multiple linear regression analyses were carried out to appraise the effect of the co-variables on the plasmatic levels of the inflammatory markers assessed. RESULTS: Of the 170 subjects who participated, 105 (61.8%) were females and the median age of the participants was 53 years (range: 40-78). The adjusted multiple linear analyses demonstrated that plasmatic levels of CRP levels were associated with the body mass index (BMI) (r = 0.259, P < 0.001) and residual tooth roots (RTR) (r = 0.191, P = 0.041). IL-6 and fibrinogen levels showed associated with BMI (r = 0.400, P < 0.001 and r = 0.214, P = 0.002 respectively). CAP correlated weakly with CRP (r = 0.250, P = 0.005), IL-6 (r = 0.174, P = 0.020) and fibrinogen (r = 0.393, P < 0.001) levels. CONCLUSION: The null hypothesis was rejected in favour of the alternative hypothesis. In other words, the presence of chronic apical periodontitis was associated with higher plasmatic levels of CRP, IL-6 and fibrinogen, in a population of severely hypertensive patients. However, the weak association between CAP and each dependent variable suggests a modest participation of endodontic infection on the plasmatic levels of biomarkers.

Can apical periodontitis affect serum levels of CRP, IL-2, and IL-6 as well as induce pathological changes in remote organs?

OBJECTIVES: The aim of this study was to investigate whether apical periodontitis (AP) could cause systemic cytokine elevation and pathological changes in remote organs in an experimental animal model. MATERIALS AND METHODS: AP was induced in 36 Sprague Dawley (SD) rats. Serum levels of C-reactive protein (CRP), interleukin 2 (IL-2), and interleukin 6 (IL-6) were measured by enzyme-linked immunosorbent assays at different time intervals (0, 6, 12, 24, 48, and 96 h and 1, 2, 3, 4, 5, and 6 weeks) after pulp exposure. Multiple organs (the aortic arch, myocardium, liver, and spleen) were collected for histological observation. The results were analyzed by one-way analysis of variance (ANOVA). RESULTS: Serum levels of CRP, IL-2, and IL-6 were significantly elevated at all time points assessed after 6, 24, and 96 h, respectively. The peak values of serum cytokines (CRP 6.363 ± 0.05 ng/ml, IL-2 21.997 ± 0.15 ng/L, and IL-6 2.406 ± 0.02 ng/L) were reached at 1, 4, and 2 weeks, respectively, followed by a decline. Time-dependent reversible histopathological changes were detected in the aortic arch, myocardium, and spleen, whereas irreversible changes were found in the liver. CONCLUSIONS: AP elevated the levels of CRP, IL-2, and IL-6 in rat blood serum, causing reversible changes in the aortic arch, myocardium, and spleen as well as irreversible changes in the liver. CLINICAL RELEVANCE: AP may trigger a systemic immune response, impair remote organs, and affect the general health of patients.

Lipids and lipoproteins and inflammatory markers in patients with chronic apical periodontitis.

BACKGROUND: Since chronic apical periodontitis (CAP) appears to be a risk factor for coronary heart disease, the aim of the study was to determine the relationship between the size of CAP lesion and inflammatory markers (hsCRP, IL-6, TNF-α), as well as lipids and lipoproteins (LpPLA2, apoAI, apoB level) in blood serum of patients with CAP. METHODS: The patients studied (n = 43) were divided into groups: patients under 50 and over 50 years of age, and a separate subgroup of the oldest age with the largest size of CAP lesions. Apolipoprotein AI (apoAI) above 150 mg/dL and below 150 mg/dL was used as an important criterion for the division of patients into groups. The CAP lesion size was measured using the Kodak digital imaging system software. The control group consisted of clinically healthy volunteers (n = 20) without CAP. Lipids were measured on a Siemens analyzer (Germany), apoAI, apoB, hsCRP levels were determined by immunonephelometric method, using the Health Care Diagnostic Product (Siemens GmbH, Germany), and IL-6, TNF-α and LpPLAG7 assay kits (ELISA, R&D Systems) were used. RESULTS: The findings suggested that in patients with CAP and their age increase, the CAP lesion size, the concentration of inflammatory markers and LpPLA2 mass increased. Correlations between the CAP lesion size and LpPLA2 mass and between the CAP lesion size and TG level in patients with apoAI 150 ≤ mg/dL showed increase TG in atherogenic apoB-containing triglyceride-rich lipoprotein and TC in cholesterol-rich lipoprotein. The patients with a low apoAI and high LpPLA2 level can have a higher risk of odontogenic disease and progression of atherosclerosis and coronary heart disease. CONCLUSION: We have found a positive correlation between apoAI level and the CAP lesion size and a negative correlation between LpPLA2 level and the CAP lesion size. The results suggest that apoAI and LpPLA2 in HDL particles have antiinflammatory action and together can limit the CAP lesion size in patient with a higher apoAI level. The literature data on the distribution of lipoprotein particles in subjects are still insufficient, so this problem requires further studies.

Effect of raloxifene on periapical lesions in ovariectomized rats.

INTRODUCTION: The aim of this study was to evaluate the effect of raloxifene (RLX) during progression of periapical lesions in ovariectomized (OVX) rats. METHODS: Female Wistar rats were OVX or subjected to sham surgery and received vehicle or RLX by gavage for 90 days. The treatment groups were as follows: sham surgery and treated with vehicle (SHAM-veh), OVX and treated with vehicle (OVX-veh), and OVX and treated with RLX (OVX-RLX). During treatment, the pulp of lower first molar was exposed to the oral environment for induction of periapical lesion that was analyzed 7 or 30 days after procedure. Blood samples were taken from jugular vein for measurement of estradiol, and the mandibles were removed and prepared for radiographic, histopathologic, histometric, and immunohistochemical analysis. RESULTS: Estradiol plasma concentration showed hypoestrogenism in OVX rats. The histopathologic analysis of the OVX/RLX group was similar to that of the SHAM-veh group, whereas OVX-veh group showed larger periapical lesions with more intense inflammatory response and more cells positive for tartrate-resistant acid phosphatase. Radiographically, the groups were similar, but lesions on day 7 were smaller than lesions on day 30. CONCLUSIONS: The results suggest that hypoestrogenism potentiates the progression of periapical lesions, and such condition was reversed by treatment with RLX.

Blood profile and histology in oral infections associated with diabetes.

INTRODUCTION: We aimed to investigate the relationship between blood profile and histologic findings in both apical periodontitis (AP) and periodontal disease (PD) associated with diabetes. METHODS: Wistar rats (N = 80) were assigned to the following 8 groups: control, AP, PD, AP associated with PD, diabetes, diabetes with AP, diabetes with PD, and diabetes with AP and PD. Diabetes mellitus (DM) was induced with streptozotocin, AP was induced by exposure to the oral environment, and PD was induced using periodontal ligature. After 30 days, blood samples were collected, and the rats were euthanized. Subsequently, the maxillae were processed for light microscopy. Hematologic examinations were conducted to determine the total number of erythrocytes and leukocytes, erythrocyte constant, and blood glucose level. One-way analysis of variance and Kruskal-Wallis tests were used for statistical analysis, and the significance was set at P < .05. RESULTS: A significant correlation was found between the histologic findings and blood parameters. CONCLUSIONS: In conclusion, diabetes accelerated the development and progression of AP and PD in the rats and caused an increase in the average erythrocyte volume as well as the leukocyte and neutrophil counts. Oral infections increase the total number of leukocytes, the number of neutrophils and lymphocytes, and blood glucose concentrations in DM rats.

Apical periodontitis and periodontal disease increase serum IL-17 levels in normoglycemic and diabetic rats.

OBJECTIVES: This study aimed to evaluate the influence of apical periodontitis (AP) and/or periodontal disease (PD) on serum interleukin-17 (IL-17) levels in a rat model of diabetes mellitus (DM). METHODS: Eighty male Wistar rats were divided into eight groups of ten animals each: normoglycemic, AP, PD, AP+PD, DM, DM+AP, DM+PD, and DM+AP+PD. DM was induced using streptozotocin, AP by dental pulp exposure to the oral environment, and PD by periodontal ligature. The animals were sacrificed after 30 days, and venous blood samples were collected via cardiac puncture to determine the serum IL-17 and neutrophil levels. The maxillae were dissected and processed for radiographic analysis. The periapical lesion areas were quantified in pixels. The total assessed values were tabulated according to each experimental group and were statistically analyzed using Spearman's correlation and Kruskal-Wallis test (p < 0.05). RESULTS: A significant difference in the serum IL-17 levels was observed between the groups without oral infections and the groups with AP+PD-associated lesions, regardless of the presence of DM (p < 0.05). Diabetes increased the neutrophil levels, regardless of the presence of oral infection. However, a combination of two oral infections increased the neutrophil levels in DM rats (p < 0.05). The level of bone resorption lesions was greater in DM rats than in normoglycemic rats (p < 0.05). CONCLUSION: The combination of AP and PD increased the serum IL-17 levels in DM and normoglycemic rats and increased the neutrophil levels in DM rats. Diabetes increased the neutrophil levels and bone resorption in rats. CLINICAL SIGNIFICANCE: AP is capable of potentiating systemic inflammatory changes when associated with PD, and increases in blood glucose can accelerate the pathogenesis of oral infections.

The recurrence of leprosy reactional episodes could be associated with oral chronic infections and expression of serum IL-1, TNF-alpha, IL-6, IFN-gamma and IL-10.

The aim of this study was to determine whether the presence of leprosy reactional episodes could be associated with chronic oral infection. Thirty-eight leprosy patients were selected and divided into 2 groups: group I - 19 leprosy patients with oral infections, and group II - 19 leprosy patients without oral infections. Ten patients without leprosy, but presenting oral infections, were assigned to the control group. Leprosy patients were classified according to Ridley and Jopling classification and reactional episodes of the erythema nodosum type or reversal reaction were identified by clinical and histopathological features associated with serum IL-1, TNF-alpha, IL-6, IFN-gamma and IL-10 levels. These analyses were performed immediately before and 7 days after the oral infection elimination. Patients from group I presenting oral infections reported clinical improvement of the symptoms of reactional episodes after dental treatment. Serum IL-1, TNF-alpha, IL-6, IFN-gamma and IL-10 levels did not differ significantly before and after dental treatment as determined by the Wilcoxon test (p>0.05). Comparison of the 2 groups showed statistically significant differences in IL-1 and IL-6 at baseline and in IL-1, IL-6 and IL-10 on the occasion of both collections 7 days after therapy. Serum IL-6 and IL-10 levels in group I differed significantly at baseline compared to control (Mann-Whitney test; p<0.05). These results suggest that oral infection could be involved as a maintenance factor in the pathogenesis of leprosy reactional episodes.

The recurrence of leprosy reactional episodes could be associated with oral chronic infections and expression of serum IL-1, TNF-á, IL-6, IFN-ã and IL-10

The aim of this study was to determine whether the presence of leprosy reactional episodes could be associated with chronic oral infection. Thirty-eight leprosy patients were selected and divided into 2 groups: group I - 19 leprosy patients with oral infections, and group II - 19 leprosy patients without oral infections. Ten patients without leprosy, but presenting oral infections, were assigned to the control group. Leprosy patients were classified according to Ridley and Jopling classification and reactional episodes of the erythema nodosum type or reversal reaction were identified by clinical and histopathological features associated with serum IL-1, TNF-?, IL-6, IFN-? and IL-10 levels. These analyses were performed immediately before and 7 days after the oral infection elimination. Patients from group I presenting oral infections reported clinical improvement of the symptoms of reactional episodes after dental treatment. Serum IL-1, TNF-?, IL-6, IFN-? and IL-10 levels did not differ significantly before and after dental treatment as determined by the Wilcoxon test (p>0.05). Comparison of the 2 groups showed statistically significant differences in IL-1 and IL-6 at baseline and in IL-1, IL-6 and IL-10 on the occasion of both collections 7 days after therapy. Serum IL-6 and IL-10 levels in group I differed significantly at baseline compared to control (Mann-Whitney test; p<0.05). These results suggest that oral infection could be involved as a maintenance factor in the pathogenesis of leprosy reactional episodes.

O objetivo deste estudo foi determinar se os episódios reacionais da hanseníase podem estar associados a infecções orais crônicas. Trinta e oito pacientes com hanseníase foram selecionados e divididos em dois grupos: grupo I & 19 pacientes com hanseníase apresentando infecções orais, e grupo II & 19 pacientes com hanseníase sem infecções orais. Os pacientes foram classificados, quanto à forma clínica da doença, de acordo com Ridley and Jopling, e os episódios reacionais, tipo eritema nodoso e reação reversa, foram identificados pelas características clínicas, histopatológicas associadas à quantificação no soro de IL-1, TNF-?, IL-6, IFN-? e IL-10. Estas analises foram realizadas imediatamente antes e 7 dias após a resolução dos focos de infecção. Pacientes do grupo I aprentando infecções orais relataram melhora clínica dos sintomas dos episódios reacionais após o tratamento odontológico. Os níveis séricos de IL-1, TNF-?, IL-6, IFN-? e IL-10 não diferiram significantemente antes e após o tratamento odontológico, como determinado pelo teste Wilcoxon (p>0,05). As comparações entre os grupos mostrou diferenças estatisticamente significantes nos níveis de IL-1 e IL-6 na coleta inicial e nos níveis de IL-1, IL-6 e IL-10 nas duas coletas 7 dias após o tratamento (teste Mann-Whitney; p<0,05). Estes resultados sugerem que infecções orais estão envolvidas na patogênese dos episódios reacionais da hanseníase, como fatores mantenedores.

The correlation between serum immunoglobulin A and immunoglobulin G levels and the presence of Treponema denticola in human periapical lesions.

The aim of this study was to compare the serum immunoglobulin A (IgA) and immunoglobulin G (IgG) levels and the presence of Treponema denticola in the root canals in a group of teeth with/without periapical lesion. A total of 66 children aged 8 to 13 years old were involved in this study. Five milliliters of blood samples were taken to detect the serum IgA and IgG levels. Sixty-six endodontic samplings were also obtained to determine the presence of T. denticola by polymerase chain reaction. The presence of T. denticola between the groups with/without periapical lesion was statistically significant (p = 0.026). A significant negative correlation was found between serum IgG and IgA levels and the presence of T. denticola (p = 0.023 and 0.038, respectively). This study may support the hypothesis that the presence of T. denticola in the root canals is mainly related to the periapical lesions, and the higher levels of serum IgG and IgA levels may protect against T. denticola.

C-reactive protein and serum amyloid A in a canine model of chronic apical periodontitis.

Increased levels of systemic inflammatory markers have been observed in patients with chronic dental diseases, such as marginal periodontitis. A canine model was used to determine if a systemic inflammatory response was evident during chronic apical periodontitis (CAP). Dental pulps in 10 dogs were exposed and infected with dental plaque to induce CAP. Blood samples were drawn preoperatively and postinfection when CAP was seen radiographically. In three of the 10 dogs, an intravenous challenge of Porphyromonas gingivalis A7436 was given subsequent to the development of CAP. An ELISA assay was used to measure the levels of C-reactive protein (CRP) and serum amyloid A (SAA) as markers of systemic inflammation. During CAP the levels of CRP and SAA were not statistically different from the preoperative values as determined by the Friedman test (p < 0.05). One dog, which had an unplanned trauma-induced laceration of the paw 2 days before blood sampling, showed a 40-fold increase in CRP. The 3 dogs challenged by intravenous P. gingivalis A7436 showed elevated levels of CRP, consistent with an acute phase response. These data demonstrate that the canine model provides a useful means for studying the systemic effects of apical periodontitis, and show that CAP is not associated with elevated CRP or SAA.

Inflammatory cytokine production and specific antibody responses to lipopolysaccharide from endodontopathic black-pigmented bacteria in patients with multilesional periapical periodontitis.

We examined the induction of the cytokines interleukin (IL)-1 beta, IL-6, and IL-8 by lipopolysaccharides (LPSs) from several species of possible endodontopathic black-pigmented bacteria. Studies were conducted in human whole blood cultures from six patients (two from each group) with differing numbers of periapical periodontitis lesions (i.e. patients with radiographically clear periapical lesions in 10 or more teeth (high-lesion group, n = 4), in one or two teeth (low-lesion group, n = 6), and six healthy volunteers with no periapical lesions (no lesion group)). LPS from Prevotella intermedia ATCC 25611, Porphyromonas gingivalis 381, and Prophyromonas endodontalis ATCC 27067 induced a higher IL-8 response in the subjects of the high-lesion group, compared with the subjects of the other two groups. To ascertain the degree of sensitization by test bacteria, we examined the reactivities of antibodies in serum and saliva from the subjects to different bacterial species. LPS from P. gingivalis reacted strongly with sera from the high-lesion group. Thus, LPS from black-pigmented bacteria may be involved in multilesional periapical periodontitis by inducing particular cytokines and/or humoral immune responses.

Influence of surgical treatment of periapical lesions on serum and blood levels of inflammatory mediators.

Changes in the serum levels of immunoglobulin IgA, IgG, IgM, positive acute phase proteins and complement activity, as well as the lymphocyte subpopulations and the neutrophil leucocyte-related chemiluminescence in the blood of patients with apical granuloma as related to endodontic and surgical treatment were investigated. Measurements were performed on admission, and 7 days and 3 months after the treatment. Elevated IgM concentration, positive acute-phase protein levels and spontaneous whole-blood chemiluminescence were noted at admission. However, a significant decrease in the serum level of each of the six investigated acute-phase proteins, and in the spontaneous chemiluminescence of blood was observed during the 3-month follow-up period. The significant increase in serum complement activity following therapy suggests that complement fixation might have occurred in these patients. A significant increase in the ratio of early sheep erythrocyte rosette-forming lymphocytes was also observed. The results of this study provide evidence for complete recovery after elimination of local inflammation by proper endodontic treatment and apicectomy in patients with apical granuloma.

[The characteristics of the development of experimental apical periodontitis in irradiation-induced immunodeficiency]. / Osobennosti razvitiia éksperimental'nogo verkhushechnogo periodontita na fone immunodefitsita, vyzvannogo oblucheniem.

Apical periodontitis was induced in 24 mongrel dogs (16 experimental and 8 reference ones) over the course of total x-ray exposure. Analysis of clinical and physiologic data, hematologic parameters, and roentgenograms of the jaws of the two animal groups has shown the development of immunodeficiency state in the experimental animals due to exposure to ionizing irradiation in a dose of 1.5 Gy and an earlier development of destruction foci in bone tissue with diffuse involvement of the dental apexes.