Fluoride-modified implant surfaces improves osseointegration in the tibias of rats with induced diabetes.

This study evaluated the influence of a fluoride-modified titanium surface on osseointegration in rats with induced diabetes. One hundred and eighty rats were randomly allocated into 3 groups with 60 animals each: Control group (C): Animals without diabetes; Diabetes Group (D): Animals with uncontrolled induced diabetes; Controlled Diabetes Group (CD): Animals with diabetes induced controlled by the insulin administration. Diabetes was induced by streptozotocin injection. Each animal received 2 implants in the proximal tibial metaphysis, one with the machined surface (M) and the other one with a fluoride-modified titanium surface (F), after 4 weeks of induction of diabetes. The animals were submitted to euthanasia 2, 4, and 6 weeks after the implant placement (n = 20 animals/group). The osseointegration was evaluated by the implant removal torque test and the histometric analysis of the non-decalcified histological sections: 1) Contact bone/implant (%BIC); 2) Bone tissue area between implant threads (%BBT). Implants with F surface showed a higher removal torque than implants with surface M in all groups. There was no difference in %BIC between the groups regardless of the surface used. The F surface showed a tendency to present higher %BBT values for the 3 evaluation periods in the D group. The fluoride-modified implant surface has no impact on the %BIC and %BBT. However, the fluoride-modified implant surface increases the locking of the implants with the bone. The hyperglycemia was associated with lower removal torque values despite the surfaces of the implant used.

Fluoride-modified implant surfaces improves osseointegration in the tibias of rats with induced diabetes

Abstract This study evaluated the influence of a fluoride-modified titanium surface on osseointegration in rats with induced diabetes. One hundred and eighty rats were randomly allocated into 3 groups with 60 animals each: Control group (C): Animals without diabetes; Diabetes Group (D): Animals with uncontrolled induced diabetes; Controlled Diabetes Group (CD): Animals with diabetes induced controlled by the insulin administration. Diabetes was induced by streptozotocin injection. Each animal received 2 implants in the proximal tibial metaphysis, one with the machined surface (M) and the other one with a fluoride-modified titanium surface (F), after 4 weeks of induction of diabetes. The animals were submitted to euthanasia 2, 4, and 6 weeks after the implant placement (n = 20 animals/group). The osseointegration was evaluated by the implant removal torque test and the histometric analysis of the non-decalcified histological sections: 1) Contact bone/implant (%BIC); 2) Bone tissue area between implant threads (%BBT). Implants with F surface showed a higher removal torque than implants with surface M in all groups. There was no difference in %BIC between the groups regardless of the surface used. The F surface showed a tendency to present higher %BBT values for the 3 evaluation periods in the D group. The fluoride-modified implant surface has no impact on the %BIC and %BBT. However, the fluoride-modified implant surface increases the locking of the implants with the bone. The hyperglycemia was associated with lower removal torque values despite the surfaces of the implant used.

Resumo Este estudo avaliou a influência de uma superfície de titânio modificada com flúor na osseointegração em ratos com diabetes induzida. Cento e oitenta ratos foram distribuídos aleatoriamente em 3 grupos com 60 animais cada: Grupo controle (C): Animais sem diabetes; Grupo Diabetes (D): Animais com diabetes induzida descompensada; Grupo Diabetes Controlado (CD): Animais com diabetes induzido controlado pela administração de insulina. O diabetes foi induzido por injeção de estreptozotocina. Cada animal recebeu 2 implantes na metáfise proximal da tíbia, um com superfície usinada (M) e outro com superfície de titânio modificado com flúor (F), após 4 semanas de indução do diabetes. Os animais foram submetidos à eutanásia 2, 4 e 6 semanas após a colocação do implante (n = 20 animais/grupo). A osseointegração foi avaliada pelo teste de torque de remoção do implante e pela análise histométrica dos cortes histológicos não descalcificados: 1) Contato osso-implante (%BIC); 2) Área de tecido ósseo entre as roscas do implante (%BBT). Os implantes com superfície F apresentaram maior torque de remoção do que os implantes com superfície M em todos os grupos. Não houve diferença no %BIC entre os grupos independente da superfície utilizada. A superfície F mostrou tendência a apresentar maiores valores de %BBT para os 3 períodos de avaliação no grupo D. As superfícies de implantes modificadas com flúor não influenciaram nos dados de %BIC e %BBT. Entretanto, essas superfícies aumentaram o travamento dos implantes no tecido ósseo. A hiperglicemia foi associada a menores torques de remoção dos implantes independentemente do tipo de superfície de implante utilizada.

The Role of Dyslipidemia in Periodontitis.

Studies have suggested an important role of dyslipidemia, a condition with alterations in blood lipid levels, in promoting an additional effect on periodontal breakdown. Thus, this study aimed to explore the theoretical pathways associated with dyslipidemia and periodontitis. We used data from 11,917 US adults with complete periodontal examinations participating in the Third National Health and Nutrition Examination Survey (NHANES III). Our hypothesis was tested using structural equation modelling (SEM). Dyslipidemia was defined according to the National Cholesterol Education Program (NCEP-ATP III) and periodontitis as a latent variable reflecting the shared variance of the number of surfaces with periodontal pocket depth [PPD] = 4 mm, PPD = 5 mm, PPD ≥ 6 mm, clinical attachment level [CAL] = 4 mm, CAL = 5mm, CAL ≥ 6 mm, and furcation involvement. The model also considered distal determinants (age, sex, and socioeconomic status) and proximal determinants (HbA1c, smoking and alcohol consumption, and obesity). The model showed sufficient global fit (Root Mean Squared Error of Approximation = 0.04, 90%CI = 0.04−0.05, Tucker−Lewis Index = 0.93, Comparative Fit Index = 0.95). Age, sex, socioeconomic status, obesity, and smoking were directly associated with periodontitis (p < 0.01). Dyslipidemia revealed a significant direct effect on periodontitis (standardized coefficient [SC] = 0.086, SE 0.027; p < 0.01), also mediated via an indirect pathway through HbA1c (SC = 0.021; SE 0.010; p = 0.02) and obesity (SC = 0.036; SE 0.012; p < 0.01) and resulted in a total effect on periodontitis. Dyslipidemia was associated with periodontitis through a direct pathway and indirectly through HbA1c and obesity in the US population. These results support the need for a multi-professional approach to tackling oral and noncommunicable diseases (NCDs), directed at their common risk factors.

Long-term evaluation of alendronate treatment on the healing of calvaria bone defects in rats. Biochemical, histological and immunohistochemical analyses.

OBJECTIVE: The aim of this study was to investigate the effects of the long-term alendronate administration on bone healing in defects created in rat calvarias. MATERIALS AND METHODS: Female Wistar rats were randomly distributed into 2 groups: Control (CTL): animals received saline solution once a week; and Alendronate (ALD): rats underwent alendronate treatment (1 mg/kg/weekly). After 120 days from the commencement of treatment, a critical size defect was created in all animals, and 10 animals from each group were sacrificed at 5, 10, 15, 20, 25, 30, 45 and 60-days after the defect creation. On the day of sacrifice, urine and blood samples were collected for determination of the serum levels of bone resorption and formation markers by enzyme linked immunosorbent assay, and the urinary concentration of deoxypyridinoline. Bone mineral density (BMD) in the femurs, descriptive histology, tartrate-resistant acid-phosphatase staining and immunohistochemical analyzes were assessed in the calvaria. RESULTS: Alendronate group showed increased BMD compared to the test group. The concentration of C-terminal telopeptide of type I collagen and deoxypyridinoline decreased significantly, and the concentration of aminoterminal propeptide of procollagen type 1 and osteocalcin were significant lower in the alendronate group. Immunohistochemical analysis showed significant downregulation in the inducible nitric oxide synthase, runt-related transcription factor-2, cathepsin-K and receptor activator of nuclear factor kappa-B ligand expression in the alendronate group. Vascular endothelial growth factor and osteopontin were upregulated in the later periods of alendronate group. CONCLUSIONS: Our results suggest that long-term treatment with alendronate did not compromise the repair processing of critical size defects in rat.

Expression Profile of Genes Potentially Associated with Adequate Glycemic Control in Patients with Type 2 Diabetes Mellitus.

Despite increasing research in type 2 diabetes mellitus (T2D), there are few studies showing the impact of the poor glycemic control on biological processes occurring in T2D. In order to identify potential genes related to poorly/well-controlled patients with T2D, our strategy of investigation included a primary screen by microarray (Human Genome U133) in a small group of individuals followed by an independent validation in a greater group using RT-qPCR. Ninety patients were divided as follows: poorly controlled T2D (G1), well-controlled T2D (G2), and normoglycemic individuals (G3). After using affy package in R, differentially expressed genes (DEGs) were prospected as candidate genes potentially relevant for the glycemic control in T2D patients. After validation by RT-qPCR, the obtained DEGs were as follows-G1 + G2 versus G3: HLA-DQA1, SOS1, and BRCA2; G2 versus G1: ENO2, VAMP2, CCND3, CEBPD, LGALS12, AGBL5, MAP2K5, and PPAP2B; G2 versus G3: HLA-DQB1, MCM4, and SEC13; and G1 versus G3: PPIC. This demonstrated a systemic exacerbation of the gene expression related to immune response in T2D patients. Moreover, genes related to lipid metabolisms and DNA replication/repair were influenced by the glycemic control. In conclusion, this study pointed out candidate genes potentially associated with adequate glycemic control in T2D patients, contributing to the knowledge of how the glycemic control could systemically influence gene expression.

Dyslipidemia rather than Type 2 Diabetes Mellitus or Chronic Periodontitis Affects the Systemic Expression of Pro- and Anti-Inflammatory Genes.

A high percentage of type 2 diabetes mellitus (T2D) patients are also affected by dyslipidemia and chronic periodontitis (CP), but no studies have determined the gene expression in patients that are simultaneously affected by all three diseases. We investigated the systemic expression of immune-related genes in T2D, dyslipidemia, and CP patients. One hundred and fifty patients were separated into five groups containing 30 individuals each: (G1) poorly controlled T2D with dyslipidemia and CP; (G2) well-controlled T2D with dyslipidemia and CP; (G3) normoglycemic individuals with dyslipidemia and CP; (G4) healthy individuals with CP; (G5) systemic and periodontally healthy individuals. Blood analyses of lipid and glycemic profiles were carried out. The expression of genes, including IL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1, and IRF1, was investigated by RT-qPCR. Patients with dyslipidemia demonstrated statistically higher expression of the IL10 and IFNA genes, while IFNG, IP10, IRF1, JAK1, and STAT3 were lower in comparison with nondyslipidemic patients. Anti-inflammatory genes, such as IL10, positively correlated with parameters of glucose, lipid, and periodontal profiles, while proinflammatory genes, such as IFNG, were negatively correlated with these parameters. We conclude that dyslipidemia appears to be the primary disease that is associated with gene expression of immune-related genes, while parameters of T2D and CP were correlated with the expression of these important immune genes.

Glycemic control protects against trabecular bone microarchitectural damage in a juvenile male rat model of streptozotocin-induced diabetes.

PURPOSE: To determine which features of the bone microarchitecture are affected by established diabetes mellitus (DM) and the effectiveness of glycemic control in the protection of bone tissue. MATERIAL AND METHODS: Sixty juvenile Wistar male rats were divided into three groups of 20 animals: a control group (C) that included healthy animals, a diabetic group (D) that included animals with induced diabetes, and a controlled diabetic group (CD) that included animals with induced diabetes that were treated with insulin. The animals were euthanized at the periods of 6 and 8 weeks after the induction of diabetes (10 animals per group/period). Vertebral L4 specimens were submitted to µCT analysis to assess the following parameters of the bone microarchitecture: bone volume fraction (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), and trabecular spacing (Tb.Sp). RESULTS: The D group exhibited lower values of BV/TV (%) and numbers of trabeculae compared with the C group at 6 and 8 weeks and compared with the CD group at 8 weeks. The CD group exhibited higher trabecular thickness values compared with the D group at 8 weeks. There were no differences between the groups regarding the spaces between the trabeculae. CONCLUSION: Induced diabetes affected the microarchitecture of the trabecular bone of the vertebrae by reducing the values of the majority of the parameters in relation to those of the control group. Glycemic control with insulin appears to protect bones from the effects of the hyperglycemia.

Diabetes and increased lipid peroxidation are associated with systemic inflammation even in well-controlled patients.

BACKGROUND: The effect of the interaction between type 2 diabetes and dyslipidemia on inflammation and lipid peroxidation (LPO) has not been assessed. AIM: To investigate whether diabetes coupled with dyslipidemia alters oxidative metabolism leading to increased LPO products and inflammatory status. METHODS: 100 patients were divided into four groups based upon diabetic and dyslipidemic status: poorly controlled diabetes with dyslipidemia (DM-PC/D), well-controlled diabetes with dyslipidemia (DM-WC/D), normoglycemic individuals with dyslipidemia (NG/D), and normoglycemic individuals without dyslipidemia (NG/ND). Plasma was evaluated for an LPO product (MDA), antioxidant levels and inflammatory cytokines. RESULTS: Diabetics presented significantly higher levels of LPO (p<0.05) and the DM-PC/D had higher levels of proinflammatory cytokines and MDA in the plasma in comparison with normoglycemics (p<0.05). Interestingly IL1-ß, IL-6, and TNF-α in DM-WC/D were not statistically different from those in DM-PC/D. Normoglycemic individuals with dyslipidemia presented significantly increased levels of IL-6 and TNF-α when compared to normoglycemic without dyslipidemia (p<0.05). MDA levels were also positively correlated with the presence of DM complications (r=0.42, p<0.01). CONCLUSIONS: These findings show that dyslipidemia is associated with an increased inflammatory status, even in well-controlled diabetics and in normoglycemics. Our results suggest that lipid metabolism and peroxidation are important for the development of inflammation, which is elevated in several complications associated with diabetes.

Modulation of cell proliferation, survival and gene expression by RAGE and TLR signaling in cells of the innate and adaptive immune response: role of p38 MAPK and NF-KB.

OBJECTIVE: The aim of this study was to evaluate a possible synergism between AGE-RAGE and TLR4 signaling and the role of p38 MAPK and NF-kB signaling pathways on the modulation of the expression of inflammatory cytokines and proliferation of cells from the innate and adaptive immune response. MATERIAL AND METHODS: T lymphocyte (JM) and monocyte (U937) cell lines were stimulated with LPS and AGE-BSA independently and associated, both in the presence and absence of p38 MAPK and NF-kB inhibitors. Proliferation was assessed by direct counting and viability was assessed by a biochemical assay of mitochondrial function. Cytokine gene expression for RAGe, CCL3, CCR5, IL-6 and TNF-α was studied by RT-PCR and RT-qPCR. RESULTS: RAGE mRNA expression was detected in both cell lines. LPS and AGE-BSA did not influence cell proliferation and viability of either cell line up to 72 hours. LPS and LPS associated with AGE induced expression of IL-6 and TNF-α in monocytes and T cells, respectively. CONCLUSIONS: There is no synergistic effect between RAGE and TLR signaling on the expression of IL-6, TNF-α , RAGE, CCR5 and CCL3 by monocytes and lymphocytes. Activation of RAGE associated or not with TLR signaling also had no effect on cell proliferation and survival of these cell types.

Microbiological changes after periodontal therapy in diabetic patients with inadequate metabolic control.

The present study investigated the effect of non-surgical periodontal treatment (SRP) on the composition of the subgingival microbiota of chronic periodontitis (CP) in individuals with type 2 diabetes (DM2) with inadequate metabolic control and in systemically healthy (SH) individuals. Forty individuals (20 DM2 and 20 SH) with CP underwent full-mouth periodontal examination. Subgingival plaque was sampled from 4 deep sites of each individual and tested for mean prevalence and counts of 45 bacterial taxa by the checkerboard method. Clinical and microbiological assessments were performed before and 3 months after SRP. At baseline, those in the DM2 group presented a significantly higher percentage of sites with visible plaque and bleeding on probing compared with those in the SH group (p<0.01). Those in the DM2 group presented significantly higher levels of C. rectus and P. gingivalis, and lower prevalence of P. micra and S. anginosus, compared with those in the SH group (p≤0.001). At the 3-month visit, both groups showed a significant improvement in all clinical parameters (p<0.01). Those in the DM2 group showed significantly higher prevalence and/or levels of A. gerencseriae, A. naeslundii I, A. oris, A. odontolyticus, C. sputigena, F. periodonticum, and G. morbillorum compared with those in the SH group (p≤0.001). However, those in the DM2 group showed a significant reduction in the levels of P. intermedia, P. gingivalis, T. forsythia, and T. denticola (p≤0.001) over time. Those in the SRP group showed improved periodontal status and reduced levels of putative periodontal pathogens at 3 months' evaluation compared with those in the DM2 group with inadequate metabolic control.

Modulation of cell proliferation, survival and gene expression by RAGE and TLR signaling in cells of the innate and adaptive immune response: role of p38 MAPK and NF-KB

Objective: The aim of this study was to evaluate a possible synergism between AGE-RAGE and TLR4 signaling and the role of p38 MAPK and NF-kB signaling pathways on the modulation of the expression of inflammatory cytokines and proliferation of cells from the innate and adaptive immune response. Material and Methods: T lymphocyte (JM) and monocyte (U937) cell lines were stimulated with LPS and AGE-BSA independently and associated, both in the presence and absence of p38 MAPK and NF-kB inhibitors. Proliferation was assessed by direct counting and viability was assessed by a biochemical assay of mitochondrial function. Cytokine gene expression for RAGe, CCL3, CCR5, IL-6 and TNF-α was studied by RT-PCR and RT-qPCR. Results: RAGE mRNA expression was detected in both cell lines. LPS and AGE-BSA did not influence cell proliferation and viability of either cell line up to 72 hours. LPS and LPS associated with AGE induced expression of IL-6 and TNF-α in monocytes and T cells, respectively. Conclusions: There is no synergistic effect between RAGE and TLR signaling on the expression of IL-6, TNF-α , RAGE, CCR5 and CCL3 by monocytes and lymphocytes. Activation of RAGE associated or not with TLR signaling also had no effect on cell proliferation and survival of these cell types. .

Prevalence of Candida spp. during radiographic examination in Diabetes mellitus patients / Prevalência de Candida spp. durante o exame radiográfico em pacientes diabéticos

Introdução: Relata-se que indivíduos diabéticos são mais susceptíveis a infecções por Candida que indivíduos saudáveis, especialmente se doença periodontal estiver associada. Objetivo: Este estudo propôs avaliar a prevalência de colonização por Candida spp. durante o exame radiográfico em pacientes diabéticos e não diabéticos. Material e Método: Vinte e seis pacientes com Diabetes mellitus do tipo 2 e 20 pacientes sem Diabetes mellitus, apresentando periodontite crônica e Candida spp. na saliva, foram avaliados. Durante o exame radiográfico, amostras de saliva foram coletas: da mucosa oral, do filme radiográfico periapical convencional, sensor radiográfico digital (CDR) e bloco de mordida do posicionador de filmes. Unidades formadoras de colônia (cfu/mL) e identificação das leveduras do gênero Candida foram avaliadas. Resultado: A mucosa oral de ambos os grupos mostrou maior colonização por Candida spp. quando comparada com outras superfícies coletadas (p < 0.05). Nos pacientes diabéticos, a mucosa da região esquerda superior mostrou níveis mais altos de colonização. Nos pacientes não diabéticos, a região de molar superior direito mostrou o nível mais alto de colonização durante o exame no posicionador, no sensor e no lado do filme periapical que não fica voltado para a radiação X. Os níveis de Candida spp. na saliva foram similares entre diabéticos (média = 3.0 × 10(6)) e não diabéticos (média = 3.8 × 10(6)). Conclusão: Nenhuma diferença na colonização por Candida spp. (cfu/mL) em pacientes diabéticos e não diabéticos foi observada nas cinco superfícies coletadas e nas regiões radiográficas simuladas. Candida albicans foi a espécie prevalente de Candida spp. encontrada em todas as amostras.

Introduction: It is suggested that individuals with diabetes are more susceptible to Candida infections than healthy people, especially if periodontal infection is associated. Objective: This study evaluated the prevalence of colonization by Candida spp. during radiographic examination in diabetic and non-diabetic patients. Material and Methods: Twenty-six patients with type 2 diabetes mellitus and 20 patients without diabetes mellitus, presenting chronic periodontitis and presence of Candida spp. in saliva were evaluated. During radiographic examination, samples of saliva were collected from: oral mucosa, conventional radiographic periapical film, digital x-ray sensor (CDR), and bite block of the receptor-positioning device. Colony forming units (cfu/mL) and identification of Candida yeasts were assessed. Result: Oral mucosa from both groups showed the highest colonization with Candida spp. if compared with others surfaces collected (p < 0.05). In diabetic patients, the mucosa of the upper left regions showed higher levels of colonization. In non-diabetic patients, the upper right molar region showed the highest level of colonization during the examination of the receptor-positioning device, the sensor and the non-sensitive film. Candida spp. levels in saliva were similar between diabetics (mean = 3.0 × 10(6)) and non-diabetics (mean = 3.8 × 10(6)). Conclusion: No difference in Candida spp. colonization (cfu/mL) in diabetics and non-diabetic patients was observed for the five collected surfaces and the simulated radiographic region. Candida albicans was the prevalent species of Candida spp. found on all the samples.

Lipid profile of people with diabetes mellitus type 2 and periodontal disease.

The objective of this study was to evaluate improvement of lipids and periodontal disease in patients with type 2 Diabetes mellitus, by means of the relationship between blood levels of total cholesterol and its fractions, triglycerides and clinical periodontal parameters. Twenty patients, in age-range 18-70 years, were selected and divided into 2 groups: (1) conventional periodontal scaling and root planing+controlled mechanic; (2) conventional periodontal scaling and root planing+controlled mechanical+maintenance therapy. The analyses were performed on day 0, 180 and 720 days, including plaque index, gingival index, probing depth and clinical attachment level, and evaluation of total cholesterol and its fractions, and triglycerides. The 2 groups presented significant reduction in clinical periodontal parameters, however, probing depth did not diminish significantly only in Group 1. There was significant improvement in all blood parameters in both groups. It was concluded that after 720 days of the experiment, there were significant improvements in clinical and blood parameters, in general. The group that received maintenance therapy also showed a more expressive improvement in clinical periodontal parameters, in general, suggesting that this therapy is important and necessary in patients with type 2 Diabetes mellitus and periodontal disease.

Associação da raspagem com antibioticoterapia em um caso de periodontite agressiva generalizada / Association of manual scaling with antibiotic therapy in a case of generalized aggressive periodontitis. Case report

O tratamento da periodontite agressiva é um desafio ao clínico, e por isso a busca por protocolos efetivos no controle dessa doença é de extrema importância. O objetivo deste trabalho foi, a partir do relato de um caso clínico, demonstrar a efetividade da associação de antibioticoterapia sistêmica com o tratamento periodontal não cirúrgico no tratamento da periodontite agressiva generalizada. A paciente RCS, 27 anos, fumante há 11 anos (dez cigarros/dia), sistemicamente saudável, compareceu à clínica de Periodontia com queixa principal de má posição dentária. Após o exame clínico foi definido o diagnóstico de periodontite agressiva generalizada. Foi executado o tratamento periodontal não cirúrgico associado à administração de amoxicilina e metronidazol por dez dias. Parâmetros clínicos (nível de inserção, nível gengival, profundidade de sondagem, sangramento a sondagem, índice de placa visível e índice de sangramento marginal) e radiográficos (distância junção cemento-esmalte ao topo da crista óssea) foram avaliados antes e após o tratamento periodontal não cirúrgico, após a antibioticoterapia e três, seis e 12 meses após o término do tratamento. Após um ano de acompanhamento, os resultados demonstraram melhora nos parâmetros clínicos e radiográficos da paciente, com estabilização do quadro e diminuição da mobilidade dentária, além de ausência de perdas dentárias. Concluiu-se que a associação do tratamento periodontal não cirúrgico com a administração da associação amoxicilina/metronidazol foi eficaz no tratamento da periodontite agressiva generalizada.

Doença periodontal em pacientes com Diabetes Mellitus:influência de polimorfismos genéticos? / Periodontal disease in patients with Diabetes Mellitus:influence of genetic polymorphisms?

Nos últimos anos, evidenciou-se que, em muitas patologias, há fatores que não causam diretamente a doença, mas podem modificá-la, tornando o quadro clínico mais grave e a progressão mais rápida. Observa-se um número crescente de estudos investigando a relação entre Diabetes Mellitus (DM) e Doença Periodontal (DP), com alguns enfoques sobre a influência de fatores genéticos nesse processo. Existem polimorfismos genéticos cuja expressão está associada a fatores de risco. Portanto, para que as variantes genéticas afetem a severidade da doença ou aincidência de forma significativa, os polimorfismos genéticos devem agir cumulativamente ou pela interação com outros fatores, como a presença do diabetes. O objetivo deste estudo foi verificar, por meio de revisão sistemática da literatura, a influência de polimorfismos genéticos no perfil inflamatório da DP em pacientes com diabetes. Foram utilizadas as bases de dados BIREME e PubMed com os termos Periodontitis ou Periodontal disease, Polymorphism e Diabetes Mellitus. Realizando-se um refinamento na pesquisa bibliográfica, foram selecionados cinco referênciasque relacionavam DP crônica com DM e polimorfismos em genes de citocinas, especialmente Interleucina 1 (IL1) e IL6. Estudos associaram a presença de polimorfismos em pacientes portadores de diabetes à maior concentração de citocinas pró-inflamatórias no fluido gengival, quando comparados a pacientes sem diabetes. Conclui-se que, para confirmar essa associação, é necessária a realização de estudos longitudinais, investigando um maior número de genes para compreender melhor as relações causa-efeito entre polimorfismos genéticos, DM e DP.

Currently it is clear that there are several factors that can act as modifiers of diseases, without causing them directly, but having the potential to make these conditions to progress faster and more severe. There is a growing number of studies investigating the relationship between Diabetes Mellitus (DM) and Periodontal Disease (PD), includingsome studies focusing on the influence of genetic factors in this process. The aim of this study was to verify through a literature review, the influence of genetic polymorphisms in the development of PD in patients with DM. PubMed and BIREME were used as databases and the terms Periodontitis or Periodontal Disease, Polymorphism, Diabetes Mellitus were searched. After a refinement in the literature, five studies were selected and they were related to chronic PD with DM and polymorphisms in cytokine genes, especially interleukin 1 (IL1) e IL6. Polymorphismswere associated with a higher concentration of pro-inflammatory cytokines in the gingival crevicular fluid of diabetic patients when compared to non-diabetic. In conclusion, it is necessary to confirm this association with longitudinal studies that must investigate a larger number of cytokine genes in order to understand the cause-effectrelationship between genetic polymorphisms, DM and PD.

Influence of estrogen deficiency on bone around osseointegrated dental implants: an experimental study in the rat jaw model.

PURPOSE: The aim of this study was to evaluate the influence of estrogen deficiency on bone around osseointegrated dental implants in a rat jaw model. MATERIALS AND METHODS: This study used 16 female rats that had the first molars bilaterally extracted and were allowed to heal for 30 days before implant placement. Sixty days after implant placement, the animals were randomly subjected to sham surgery or ovariectomy (OVX). The animals were euthanized 90 days after OVX. Bone-to-implant contact, bone area fraction occupancy between implant threads, mineral density, turnover markers, and cells positive for tartrate-resistant acid phosphatase were assessed for the 2 groups. RESULTS: The results showed that OVX group presented a decrease of systemic bone density, alterations in bone turnover markers, and an increase of cells positive for tartrate-resistant acid phosphatase compared with the sham-surgery group. However, no difference relative to bone-to-implant contact and bone area fraction occupancy was observed between groups. CONCLUSIONS: The findings of this study demonstrate that estrogen deficiency may not be considered a risk factor for osseointegrated implant failure in jaw bone.

Diabetes mellitus and oral mucosa alterations: prevalence and risk factors.

AIMS: To investigate the prevalence of oral mucosa alterations in patients with type 2 diabetes and to identify possible risk factors related to oral mucosa alterations. METHODS: 146 patients with type 2 diabetes and 111 age- and gender-matched healthy controls subjects were consecutively recruited from Araraquara School of Dentistry to answer a structured questionnaire designed to collect demographic data as well as current and former history of diabetes. Clinical examination of the oral mucosa was carried out by a stomatologist. RESULTS: A higher prevalence of oral mucosa alterations was found in patients with diabetes than in patients without diabetes (p<0.001), with significant difference to development conditions (p<0.0001), potentially malignant disorders (p<0.0001) and fungal infections (p<0.05). In the multiple logistic regression, diabetes (odds ratio 9.9 IC 5.11-19.16) and smoking habit (odds ratio 3.17 IC 1.42-7.12) increased the odds of oral mucosa alterations significantly. CONCLUSIONS: Patients with diabetes mellitus not only showed an increased prevalence of oral mucosa alterations but also a significant percentage of potentially malignant disorders. These findings elucidate the necessity of regular clinical examination to ensure early diagnosis and prompt management of oral mucosa lesions in patients with diabetes.

Effects of magnesium intake deficiency on bone metabolism and bone tissue around osseointegrated implants.

OBJECTIVES: This study evaluated the effect of magnesium dietary deficiency on bone metabolism and bone tissue around implants with established osseointegration. MATERIALS AND METHODS: For this, 30 rats received an implant in the right tibial metaphysis. After 60 days for healing of the implants, the animals were divided into groups according to the diet received. Control group (CTL) received a standard diet with adequate magnesium content, while test group (Mg) received the same diet except for a 90% reduction of magnesium. The animals were sacrificed after 90 days for evaluation of calcium, magnesium, osteocalcin and parathyroid hormone (PTH) serum levels and the deoxypyridinoline (DPD) level in the urine. The effect of magnesium deficiency on skeletal bone tissue was evaluated by densitometry of the lumbar vertebrae, while the effect of bone tissue around titanium implants was evaluated by radiographic measurement of cortical bone thickness and bone density. The effect on biomechanical characteristics was verified by implant removal torque testing. RESULTS: Magnesium dietary deficiency resulted in a decrease of the magnesium serum level and an increase of PTH and DPD levels (P ≤ 0.05). The Mg group also presented a loss of systemic bone mass, decreased cortical bone thickness and lower values of removal torque of the implants (P ≤ 0.01). CONCLUSIONS: The present study concluded that magnesium-deficient diet had a negative influence on bone metabolism as well as on the bone tissue around the implants.

The effect of oestrogen and alendronate therapies on postmenopausal bone loss around osseointegrated titanium implants.

OBJECTIVES: This study evaluated the influence of oestrogen deficiency and its therapies on bone tissue around osseointegrated implants. METHODS: Implants were placed in 66 female rats tibiae. The animals were assigned into five groups: control (CTL), sham, ovariectomy (OVX), oestrogen (EST), and alendronate (ALE). While CTL was sacrificed 60 days after implant placement, other groups were subjected to ovariectomy or sham surgery according to group and euthanized after 90 days. Blood and urine samples were collected at sacrifice day for osteocalcin (OCN) and deoxypyridinoline (DPD) quantification. Densitometry of femur and lumbar vertebrae was performed in order to evaluate rats' skeletal impairment. Non-decalcified sections were referred to fluorescent and light microscopy for analyses of mineral apposition rate (MAR), eroded and osteoclastic surfaces, bone-to-implant contact (BIC), and bone area fraction occupancy (BAFO). RESULTS: Results from the OVX group showed significantly lower bone mineral density (BMD), BIC, BAFO, and MAR, while OCN, deoxipiridinoline, eroded surface and ostecoclastic surface were increased compared with the other groups of the study. ALE reduced OCN and DPD concentrations, MAR, osteoclastic and eroded surfaces, and no difference was in BIC and BAFO relative to SHAM. EST and CTL showed similar results to SHAM for measurements. CONCLUSIONS: Oestrogen deficiency exerted a negative influence on bone tissue around implants, while oestrogen replacement therapy and alendronate were effective against its effects. Although alendronate therapy maintained the quantity of bone around implants, studies evaluating bone turnover kinetics are warranted.

Association of haplotypes in the IL8 gene with susceptibility to chronic periodontitis in a Brazilian population.

BACKGROUND: Interleukin 8 (IL-8) is a chemokine related to the initiation and amplification of acute and chronic inflammatory processes. Polymorphisms in the IL8 gene have been associated with inflammatory diseases. We investigated whether the -845(T/C) and -738(T/A) single nucleotide polymorphisms (SNPs) in the IL8 gene, as well as the haplotypes they form together with the previously investigated -353(A/T), are associated with susceptibility to chronic periodontitis. METHODS: DNA was extracted from buccal epithelial cells of 400 Brazilian individuals (control n=182, periodontitis n=218). SNPs were genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Disease associations were analyzed by the chi(2) test, Exact Fisher test and Clump program. Haplotypes were reconstructed using the expectation-maximization algorithm and differences in haplotype distribution between the groups were analyzed to estimate genetic susceptibility for chronic periodontitis development. RESULTS: When analyzed individually, no SNPs showed different distributions between the control and chronic periodontitis groups. Although, nonsmokers carrying the TTA/CAT (OR=2.35, 95% CI=1.03-5.36) and TAT/CTA (OR=6.05, 95% CI=1.32-27.7) haplotypes were genetically susceptible to chronic periodontitis. The TTT/TAA haplotype was associated with protection against the development of periodontitis (for nonsmokers OR=0.22, 95% CI=0.10-0.46). CONCLUSION: Although none of the investigated SNPs in the IL8 gene was individually associated with periodontitis, some haplotypes showed significant association with susceptibility to, or protection against, chronic periodontitis in a Brazilian population.