Quantitation of malondialdehyde in gingival crevicular fluid by a high-performance liquid chromatography-based method

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Periodontal disease characterization in dogs with normal renal function or chronic renal failure

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Maternal periodontal disease in rats decreases insulin sensitivity and insulin signaling in adult offspring

Background: Periodontal disease during pregnancy has been recognized as one of the causes of preterm and lowbirth- weight (PLBW) babies. Several studies have demonstrated that PLBW babies are prone to developing insulin resistance as adults. Although there is controversy over the association between periodontal disease and PLBW, the phenomenon known as programming can translate any stimulus or aggression experienced during intrauterine growth into physiologic and metabolic alterations in adulthood. The purpose of the present study is to investigate whether the offspring of rats with periodontal disease develop insulin resistance in adulthood. Methods: Ten female Wistar rats were divided into periodontal disease (PED) and control (CN) groups. All rats were mated at 7 days after induction of periodontal disease. Male offspring were divided into two groups: 1) periodontal disease offspring (PEDO; n = 24); and 2) control offspring (CNO; n = 24). Offspring body weight was measured from birth until 75 days. When the offspring reached 75 days old, the following parameters were measured: 1) plasma concentrations of glucose, insulin, fructosamine, lipase, amylase, and tumor necrosis factor-α (TNF-α); 2) insulin sensitivity (IS); and 3) insulin signal transduction (IST) in insulin-sensitive tissues. Results: Low birth weight was not detected in the PEDO group. However, plasma concentrations of glucose, insulin, fructosamine, lipase, amylase, and TNF-α were increased and IS and IST were reduced (P <0.05) in the PEDO group compared with the CNO group. Conclusion: Maternal periodontal disease may induce insulin resistance and reduce IST in adult offspring, but such alterations are not attributable to low birth weight.

Efeito do celecoxib sobre o desenvolvimento de doença periodontal induzida em ratos

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Caracterização das alterações teciduais em dois modelos de indução de doença periodontal experimental em camundongos

Pós-graduação em Odontologia - FOAR

Localized periodontal disease induced by bacterial plaque and palatal radicular groove: treatment and considerations

The palatal radicular groove is a morphological tooth defect, which act as local predisposing risk factor favoring accumulation of the bacterial plaque, permitting microbial invasion via root groove way, directly into periodontal structures. A patient diagnosed with palatal radicular groove and a localized periodontal disease was treated by procedures to control bacterial action and procedures to eliminate local predisposing risk factor. To treat the periodontal bone defect a sequelae of periodontal disease, a guided tissue regeneration technique was applied by using allograft and xenograft materials associated with a resorbable demineralized bovine cortical bone membrane. The objective of surgical regenerative procedure was to recover the periodontal tissues nearly as they were before periodontal disease destruction.

Quantitation of malondialdehyde in gingival crevicular fluid by a high-performance liquid chromatography-based method

Lipid peroxidation (LPO) has been associated with periodontal disease, and the evaluation of malondialdehyde (MDA) in the gingival crevicular fluid (GCF), an inflammatory exudate from the surrounding tissue of the periodontium, may be useful to clarify the role of LPO in the pathogenesis of periodontal disease. We describe the validation of a method to measure MDA in the GCF using high-performance liquid chromatography. MDA calibration curves were prepared with phosphate-buffered solution spiked with increasing known concentrations of MDA. Healthy and diseased GCF samples were collected from the same patient to avoid interindividual variability. MDA response was linear in the range measured, and excellent agreement was observed between added and detected concentrations of MDA. Samples' intra- and interday coefficients of variation were below 6.3% and 12.4%, respectively. The limit of quantitation (signal/noise = 5) was 0.03 mu M. When the validated method was applied to the GCF, excellent agreement was observed in the MDA quantitation from healthy and diseased sites, and diseased sites presented more MDA than healthy sites (P < 0.05). In this study, a validated method for MDA quantitation in GCF was established with satisfactory sensitivity, precision, and accuracy. (C) 2012 Elsevier Inc. All rights reserved.

Persistent Periodontal Disease Hampers Anti-Tumor Necrosis Factor Treatment Response in Rheumatoid Arthritis

Objective: This study aimed to evaluate prospectively the influence and the evolution of periodontal disease (PD) in rheumatoid arthritis (RA) patients submitted to anti-tumor necrosis factor (TNF) therapy. Methods: Eighteen patients with RA (according to the American College of Rheumatology criteria) were assessed for PD before (BL) and after 6 months (6M) of anti-TNF treatment: 15 infliximab, 2 adalimumab, and 1 etanercept. Periodontal assessment included plaque and gingival bleeding indices, probing pocket depth, cementoenamel junction, and clinical attachment level. Rheumatologic evaluation was performed blinded to the dentist's assessment: demographic data, clinical manifestations, and disease activity (Disease Activity Score using 28 joints [DAS28], erythrocyte sedimentation rate [ESR], and C-reactive protein [CRP]). Results: The median age and disease duration of patients with RA were 50 years (25-71 y) and 94% were female. Periodontal disease was diagnosed in 8 patients (44.4%). Comparing BL to 6M, periodontal parameters in the entire group remained stable (P > 0.05) throughout the study (plaque and gingival bleeding indices, probing pocket depth, cementoenamel junction, and clinical attachment level), whereas an improvement in most analyzed RA parameters was observed in the same period: DAS28 (5.5 vs. 3.9, P = 0.02), ESR (21 vs. 12.5 mm/first hour, P = 0.07), and CRP (7.8 vs. 2.8 mg/dL, P = 0.25). Further analysis revealed that this improvement was restricted to the group of patients without PD (DAS28 [5.5 vs. 3.6, P = 0.04], ESR [23.0 vs. 11.5 mm/first hour, P = 0.008], and CRP [7.4 vs. 2.1, P = 0.01]). In contrast, patients with PD had lack of response, with no significant differences in disease activity parameters between BL and 6M: DAS28 (5.2 vs. 4.4, P = 0.11), ESR (17.0 vs. 21.0, P = 0.56), and CRP (9.0 vs. 8.8, P = 0.55). Conclusions: This study supports the notion that PD may affect TNF blocker efficacy in patients with RA. The possibility that a sustained gingival inflammatory state may hamper treatment response in this disease has high clinical interest because this is a treatable condition.

Periodontal disease progression in subjects with orofacial clefts over a 25-year follow-up period

AIMS: To assess rates of periodontal disease progression in subjects with cleft lip, alveolus and palate (CLAP) over a 25-year period without regular maintenance care in a specialist setting and to compare those with those of subjects without alveolar clefts, i.e. cleft lip (CL) or cleft palate (CP). MATERIAL AND METHODS: Ten subjects with CLAP and 10 subjects with CL/CP were examined in 1979, 1987, 1993 and 2004. Probing pocket depth (PPD), clinical attachment level (CAL), bleeding on probing (BoP) and plaque control record (PCR) scores were recorded in all 20 subjects. RESULTS: High plaque and BoP scores were recorded at all examinations in both groups. Over 25 years, a statistically significant loss of mean full-mouth CAL of 1.52 +/- 0.12 mm (SD) and 1.66 +/- 0.15 mm occurred in the CLAP and CL/CP group respectively (p<0.05). A statistically significant increase (p<0.05) in mean full-mouth PPD of 0.35 +/- 0.12 mm was observed in the CL/CP group, whereas only a trend for a mean full-mouth increase in PPD of 0.09 +/- 0.11 mm was observed in the CLAP group. In subjects with CLAP, a statistically significant increase (p<0.05) in PPD of 0.92 +/- 1.13 mm at cleft sites was observed compared with that of 0.17 +/- 0.76 mm at control sites. With respect to CAL, the loss at the corresponding sites amounted to 2.71 +/- 1.46 and to 2.27 +/- 1.62 mm, respectively (p=0.36). CONCLUSIONS: When stringent and well-defined supportive periodontal therapy was not provided, subjects with orofacial clefts were at high risk for periodontal disease progression. Over 25 years, alveolar cleft sites tended to have more periodontal tissue destruction compared with control sites.

IMMUNOGLOBULINS IN PERIODONTAL DISEASE

Periodontal disease is the major cause of tooth loss in man. The initial histological picture of the inflamed gingiva is characteristic of local inflammatory reaction involving polymorphonuclear leukocytes, vasculitis and localized tissue loss. Subsequent clinical stages of periodontal disease (mild gingivitis) show histological evidence of the involvement of the immune response with initial accumulation of macrophages, and lymphocytes devoid of surface staining immunoglobulins (presumably T cells). As the disease progresses, a predominance of surface and cytoplasmic staining lymphocytes and plasma cells are seen (severe gingivitis and periodontitis). Whether the occurrence of the immunoglobulin positive lymphocytes and the concurrent loss of collagen and resorption of alveolar bone seen in periodontitis is indicative of a direct cause and effect relationship has been a controversy.^ The majority of investigations in the periodontal field have involved the use of peripheral blood lymphocytes or serum. Blastogenic responses of peripheral blood lymphocytes and serum antibody titers from periodontal patients to a variety of oral bacteria have not shown any correlation between response and the severity of disease. The need to study the local immune response in inflamed gingiva is apparent. Since there are no baseline studies on the functional capabilities of the lymphoid cells present in gingiva from periodontitis patients, an in depth study involving the role of the immunoglobulin positive lymphocytes was investigated.^ Inflamed gingiva from four clinically defined periodontal disease states (mild gingivitis, severe gingivitis, periodontitis and severe periodontitis) were placed in gingival organ cultures. Class specific immunoglobulins were quantitated in gingival organ culture supernatants using an indirect sandwich technique. A significant difference in mean levels of IgA and IgG was seen between mild gingivitis and periodontitis (P < .00l, P = .001), as well as in IgG levels between periodontitis and severe periodontitis (P = .001). The predominance of IgG in gingival organ culture supernatants and the statistically significant findings that the overall mean levels of IgG between mild gingivitis and periodontitis (P = .014) and between severe periodontitis and periodontitis (P = .001) suggested a possible indicator of periodontal disease. The presence of IgG in gingival organ culture supernatants was shown to be a product of actively secreting plasma cells. The incorporation of radiolabelled amino acids into IgG was noted over a seven-day period with a peak response at day 4-5. The inhibition of IgG synthesis by cyclohexamide confirmed the contention that IgG was a product of de novo synthesis and not serum derived.^ The specificity of immunoglobulins derived from gingival organ cultures were studied using a whole bacterial agglutination test. Oral bacteria frequently cultured from periodontal patients were assessed for their ability to be agglutinated by gingival organ culture supernatants. A positive correlation of antibody titer and severity of disease was seen with five strains of Actinomyces viscosus, two of Actinomyces naeslundii and one Actinomyces israelii. The agglutination of bacteria was shown to be due to the specific interaction of immunoglobulin and cell-wall antigen. ^

Crevicular fluid biomarkers and periodontal disease progression.

AIM Assess the ability of a panel of gingival crevicular fluid (GCF) biomarkers as predictors of periodontal disease progression (PDP). MATERIALS AND METHODS In this study, 100 individuals participated in a 12-month longitudinal investigation and were categorized into four groups according to their periodontal status. GCF, clinical parameters and saliva were collected bi-monthly. Subgingival plaque and serum were collected bi-annually. For 6 months, no periodontal treatment was provided. At 6 months, patients received periodontal therapy and continued participation from 6 to 12 months. GCF samples were analysed by ELISA for MMP-8, MMP-9, Osteoprotegerin, C-reactive Protein and IL-1β. Differences in median levels of GCF biomarkers were compared between stable and progressing participants using Wilcoxon Rank Sum test (p = 0.05). Clustering algorithm was used to evaluate the ability of oral biomarkers to classify patients as either stable or progressing. RESULTS Eighty-three individuals completed the 6-month monitoring phase. With the exception of GCF C-reactive protein, all biomarkers were significantly higher in the PDP group compared to stable patients. Clustering analysis showed highest sensitivity levels when biofilm pathogens and GCF biomarkers were combined with clinical measures, 74% (95% CI = 61, 86). CONCLUSIONS Signature of GCF fluid-derived biomarkers combined with pathogens and clinical measures provides a sensitive measure for discrimination of PDP (ClinicalTrials.gov NCT00277745).

Demographic and social factors which influence periodontal disease using the National Health and Nutritional Examination Survey (NHANES)

Periodontal diseases include the various forms of gingivitis and periodontitis. Scientific literature submits 80% of the population suffers from some form of periodontal disease. The comparison of studies measuring periodontal disease is difficult because researchers use various parameters and indexes to define disease severity. The purposes of this paper were to examine the associations of gingival bleeding and 3 or more millimeters periodontal attachment loss, and age, sex, income, race/ethnicity, current tobacco use, dental visits, health insurance, stroke, heart attack, and diabetes using the periodontal examination population from the National Health and Nutritional Examination Survey (NHANES) 1999-2004. ^ When all risk factors were analyzed in the model as a whole sex, race/ethnicity, poverty, and education were statistically significant for bleeding on probing. When all risk factors were analyzed in the model as a whole sex, age, and education were statistically significant for loss of attachment. ^

Effect of periodontal treatment on the C-reactive protein and proinflammatory cytokine levels in Japanese periodontitis patients

Background: Recent epidemiological studies have shown that individuals with periodontitis have a significantly increased risk of developing coronary heart disease. In addition to conventional risk factors, chronic infection and subsequent production of systemic inflammatory markers may be associated with this increased risk. Objectives: The aim of the present study was to determine whether the presence of chronic periodontitis and subsequent periodontal treatment could influence the serum levels of C-reactive protein (CRP), interleukin-6 and tumor necrosis factor-alpha (TNF-alpha) in a Japanese population. Methods: Sera were obtained from 24 patients with moderate to advanced periodontitis at the baseline examination and at reassessment after completion of treatment. As a control, sera were also obtained from 21 subjects without periodontitis. High-sensitivity CRP (hs-CRP) was measured using nephelometry with a latex particle-enhanced immunoassay and interleukin-6 and TNF-alpha were determined by sensitive enzyme-linked immunosorbent assay. Results: The levels of hs-CRP and interleukin-6 in the sera of this Japanese population seemed to be much lower than those reported in other populations. TNF-alpha on the other hand, demonstrated similar levels between this Japanese and other populations. Periodontal status demonstrated a significant improvement in all patients following treatment. There was a trend toward higher hs-CRP levels in patients at baseline compared with control subjects. Hs-CRP level tended to decrease with improvement of the periodontal condition following treatment and approached that of control subjects, although this decline was not statistically significant. interleukin-6 and TNF-alpha levels did not change following periodontal treatment. Furthermore, there was no difference in the serum levels of these inflammatory cytokines between patients either at baseline or at reassessment and control subjects. Conclusions: In this pilot study, we were unable to show that periodontal disease significantly affects the serum levels of systemic inflammatory markers. However, this does not necessarily mean that periodontitis does not contribute to the total burden of inflammation as there was a tendency for hs-CRP to decrease following successful periodontal treatment. Large-scale studies are clearly needed to determine the impact of periodontal disease on systemic inflammation.

Managing periodontal disease: the clinician's role and the patient's responsibility

This manuscript highlights the roles and responsibilities of the clinician and patient in the successful management of periodontal disease. Clinical relevance: This article highlights the variety of factors that need to be addressed for periodontal diseases to be successfully managed. Learning objective: The reader should understand the broad range of issues that require consideration for patients to be successfully managed for their periodontal problems.

Etiologia da doença periodontal

A doença periodontal é caracterizada como um conjunto de condições inflamatórias, de carater crônico ou agudo, e de origem bacteriana, que começa por afetar o tecido gengival e pode levar, com o tempo, à perda dos tecidos de suporte dos dentes. As reações inflamatórias e imunológicas à placa bacteriana representam as características predominantes da gengivite e da periodontite. A reação inflamatória é visível, microscópica e clinicamente, no periodonto afetado e representa a reação do hospedeiro à microbiota da placa e seus produtos. O processo de infecção no sulco periodontal leva, inicialmente, a formação de uma mucosite periodontal, que pode ser definida como uma inflamação dos tecidos moles periodontáis, sem ocasionar perda óssea, sendo reversível, se o seu diagnóstico for atempado. Os processos inflamatórios e imunológicos atuam nos tecidos gengivais para proteger contra o agressãoes microbianas, impedindo os microrganismos de se disseminarem ou invadirem os tecidos. Em alguns casos, essas reações de defesa do hospedeiro podem ser prejudiciais porque também são passíveis de danificar as células e estruturas vizinhas do tecido conjuntivo. Além disso, as reações inflamatórias e imunológicas cuja extensão alcança níveis mais profundos do tecido conjuntivo, além da base do sulco, podem envolver o osso alveolar nesse processo destrutivo. Assim, tais processos defensivos podem, paradoxalmente, ser os responsáveis pela maior parte da lesão tecidual observada na gengivite e na periodontite. O objectivo desse trabalho é fazer uma revisão de literatura específica sobre a etiologia da doença periodontal respectivamente. Serão descritos os principais agentes microbianos que estão relacionados com a doença periodontal e a forma como influenciam o desenvolvimento da doença, procurando desta forma contribuir para a procura de tratamentos mais eficientes.