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AIM: Periodontitis is an inflammatory disease driven by opportunistic bacteria including Porphyromonas gingivalis and Fusobacterium nucleatum, where T-cell and NKT-cell responses to these bacteria in patients with periodontitis grade B or C are not fully elucidated. The objective is to determine if exaggerated proinflammatory Th-cell responses to periodontitis-associated bacteria, but not commensal bacteria, is a characteristic of increased periodontitis grade. METHODS: Mononuclear cells from patients with periodontitis grade C (n = 26) or grade B (n = 33) and healthy controls (HCs; n = 26) were stimulated with P. gingivalis, F. nucleatum or the commensal bacteria, Staphylococcus epidermidis and Cutibacterium acnes. Cytokine production by different T-cell populations and FOXP3-expression by regulatory T cells were assessed by flow cytometry. RESULTS: Compared to HCs, grade C patients had decreased frequencies of interleukin (IL)-10-producing CD4+ T cells before stimulation (p = .02) and increased frequencies of IFN-y-producing CD4+ T cells after stimulation with P. gingivalis (p = .0019). Grade B patients had decreased frequencies of FOXP3+ CD4+ T cells before (p = .030) before and after stimulation with anti-CD2/anti-CD3/anti-CD28-loaded beads (p = .047), P. gingivalis (p = .013) and S. epidermidis (p = .018). Clinical attachment loss correlated with the frequencies of IFN-y-producing Th1 cells in P. gingivalis- and F. nucleatum-stimulated cultures in grade B patients (p = .023 and p = .048, respectively) and with the frequencies of Th17 cells in P. gingivalis-stimulated cultures (p = .0062) in grade C patients. Patients with periodontitis grade C or grade B showed lower frequencies of IL-10-producing NKT cells than HCs in unstimulated cultures (p = .0043 and p = .027 respectively). CONCLUSIONS: Both periodontitis groups showed decreased frequencies of immunoregulatory T-cell and NKT cell subsets at baseline. Clinical attachment loss correlated with P. gingivalis-induced Th17-responses in grade C patients and with Th1-responses in grade B patients when cells were stimulated with P. gingivalis, supporting that dysregulated pro-inflammatory T-cell responses to periodontitis-associated bacteria contribute to the pathogenesis of periodontitis.
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AIM: To investigate the association between previous periodontal treatment and recurrent events after first-time myocardial infarction (MI). MATERIALS AND METHODS: From the Danish nationwide registries, patients with first-time MI between 2000 and 2015 were divided into three groups according to oral health care within 1 year prior to first-time MI. A multiple logistic regression model provided adjusted odds ratios (ORs) with 95% confidence intervals (CIs) to assess the 3-year risk of major adverse cardiovascular events (MACE). RESULTS: A total of 103,949 patients were included. Patients with treated periodontitis (PD) prior to first-time MI had an adjusted 3-year risk of MACE similar to patients presumed periodontally healthy (OR 0.97 [95% CI 0.92-1.03]). Patients with no prior dental visits were significantly older, had more comorbidities and showed significantly increased adjusted 3-year risks of MACE (OR 1.47 [95% CI 1.42-1.52]), cardiovascular death (OR 1.71 [95% CI 1.64-1.78]) and heart failure (OR 1.13 [95% CI 1.07-1.20]) compared with patients presumed periodontally healthy. CONCLUSIONS: Patients with treated PD 1 year prior to first-time MI had a similar risk of recurrent cardiovascular events as patients presumed periodontally healthy. No dental visit prior to first-time MI was an independent risk factor for recurrent events.
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Infarto do Miocárdio , Periodontite , Humanos , Estudos de Coortes , Infarto do Miocárdio/complicações , Infarto do Miocárdio/epidemiologia , Fatores de Risco , Periodontite/complicações , Periodontite/epidemiologia , Periodontite/terapia , Dinamarca/epidemiologiaRESUMO
BACKGROUND: Cytokine-producing B cells play a well-established role in modifying immune responses in chronic inflammatory diseases. We characterized B-cell cytokine responses against periodontitis-associated bacteria in patients with periodontitis. METHODS: Blood and saliva samples were collected from patients with periodontitis grade B (N = 31) or grade C (N = 25), and 25 healthy controls (HCs). Mononuclear cells were stimulated with Porphyromonas gingivalis, Fusobacterium nucleatum, Staphylococcus epidermidis, or Cutibacterium acnes, and B-cell production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, interferon (IFN)-γ, IL-10 and transforming growth factor (TGF)-ß by B cells was assessed by flow cytometry. RESULTS: HCs had higher baseline frequencies of B cells producing IFN-γ or TNF-α than grade B patients, but only B cells from grade B patients showed significant differentiation into IFN-γ-, TNF-α-, TGF-ß-, or IL-10-producing cells after challenge with P. gingivalis and into IFN-γ-, TGF-ß-, or IL-10-producing cells after challenge F. nucleatum. Notably, the baseline frequency of IL-10-producing B cells from grade C patients correlated inversely with clinical attachment loss (AL). The major proportion of the IFN-γ- and TGF-ß-producing B cells were CD27+ memory cells, while the IL-10-producing B cells were mainly CD27- CD5- . CONCLUSIONS: B cells from grade B patients, particularly those harboring P. gingivalis, showed proinflammatory B-cell responses to P. gingivalis. Moreover, the baseline frequency of IL-10-producing B cells in the grade C group correlated inversely with AL, suggesting a diminished immunoregulatory capacity of IL-10-producing B cells in these patients.
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Citocinas , Periodontite , Humanos , Citocinas/metabolismo , Interleucina-10/metabolismo , Porphyromonas gingivalis/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Periodontite/metabolismo , Interleucina-6/metabolismo , Fator de Crescimento Transformador betaRESUMO
Periodontitis is a chronic inflammatory disease of the tooth-supporting connective tissue and alveolar bone that is initiated by a bacterial biofilm in periodontal pockets. It affects about half of adults in the Western world, and is associated with a range of systemic comorbidities, e.g., cardiovascular disease (CVD), diabetes and rheumatoid arthritis, and these diseases share overlapping systemic and target tissue inflammatory mechanisms. Indeed, mounting evidence has indicated that their association is causal and built on the presence of systemic low-grade inflammation (LGI). Prior research linking periodontitis to CVD has mainly been derived from experimental studies, observational data, and small interventional trials with surrogate markers of CVD, e.g., endothelial dysfunction. However, recent data from randomised studies have demonstrated that intensive treatment of periodontitis can reduce blood pressure in patients with hypertension in conjunction with reduction of systemic inflammatory markers. Furthermore, targeted anti-inflammatory therapy has been shown to reduce recurrent events in patients with established CVD and LGI. Along this line, the concept of residual inflammatory risk has emerged as an independent new risk factor for atherothrombotic CVD. The present review summarizes translational evidence indicating that periodontitis is a risk factor for CVD dependent on LGI, and we conclude that treatment of periodontitis is likely to contribute importantly to reduction of residual inflammatory risk.
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Doenças Cardiovasculares , Diabetes Mellitus , Periodontite , Adulto , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/etiologia , Humanos , Inflamação/complicações , Periodontite/complicações , Fatores de RiscoRESUMO
BACKGROUND: Periodontitis (PD) is classified by Grades A through C according to the risk of further progression, PD Grade C (PD-C) being the most severe progressing form. It is a matter of controversy, whether the disease activity observed in PD-C is due to impaired immune reactivity toward bacteria embedded in biofilms or a hyper-reactive immune response causing tissue damage as a bystander phenomenon. Little is known about the role of complement in this respect. METHODS: Plasma and unstimulated saliva samples were collected from patients with PD-B (n = 34) or -C (n = 27) and healthy controls (HCs) (n = 28). Salivary and plasma levels of total C3, C3c, and C3dg were quantified using sandwich enzyme-linked immunosorbent assay (ELISA). RESULTS: Salivary levels of total C3 and C3dg were elevated in PD-B and PD-C patients compared to HCs (both P < 0.05), while the levels of C3c were elevated in PD-C compared to HCs. Plasma levels of C3c were higher in PD-B patients than in HCs (P < 0.05). CONCLUSION: PD-B and PD-C patients show increased complement activation compared to HCs, but no difference was found between the two disease grades. PD-B, but not PD-C, is associated with increased systemic complement activation as assessed by C3c in plasma.
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Complemento C3 , Periodontite , Complemento C3/análise , Complemento C3c , Ensaio de Imunoadsorção Enzimática/métodos , Humanos , Saliva/químicaRESUMO
BACKGROUND: The facultative bacterium Aggregatibacter actinomycetemcomitans (Aa) is strongly associated with periodontitis and is occasionally found in periodontally healthy subjects. We aimed to determine the prevalence of salivary Aa among patients with either periodontitis Grade B (periodontitis-B) or Grade C (periodontitis-C), periodontally healthy controls (HCs), and to determine if systemic antibodies against Aa or its virulence factor leukotoxin A (LtxA) may serve as biomarkers that reveal the oral presence of the bacterium and discriminate subjects with periodontitis-C, periodontitis-B, or no periodontitis from each other. METHODS: Serum and unstimulated saliva samples were collected from patients with periodontitis-C (n = 27), patients with periodontitis-B (n = 34), and HCs (n = 28). Serum level of immunoglobulin G antibodies to fragmented whole Aa and to LtxA were quantified using a bead-based assay. Aa was identified in saliva using quantitative polymerase chain reaction (qPCR). All analyses were adjusted for age, sex, and current smoking status. RESULTS: Aa was present in saliva from 11% of HCs, in 32% of patients with periodontitis-B (P = 0.04 versus HCs), and in 37% of patients with periodontitis-C (P = 0.02 versus HCs). Serum antibodies to fragments of Aa associated significantly with periodontitis-C (P = 0.03), while serum anti-LtxA antibodies associated with both periodontitis-B and periodontitis-C (P = 0.002 and P = 9×10-4 , respectively). Moreover, a significant association between serum anti-LtxA antibodies and Aa count in saliva was observed (P = 0.001). On the basis of serum anti-LtxA antibody levels, patients with periodontitis could be discriminated from HCs (AUC = 0.74 in ROC curve-analysis, P = 0.0003), and carriers of Aa could be discriminated from non-carriers (AUC = 0.78, P <0.0001). CONCLUSIONS: Aa is highly prevalent in saliva of patients with periodontitis-B or periodontitis-C. Systemic immunoglobulin G antibodies against LtxA distinguish patients with periodontitis, regardless of grade, from HCs, while their quantity reflects the concurrent bacterial burden in the oral cavity.
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Aggregatibacter actinomycetemcomitans , Periodontite , Anticorpos Antibacterianos , Biomarcadores , Exotoxinas , HumanosRESUMO
BACKGROUND AND AIM: The aims of this study were to describe the prevalence of various oral diseases and to examine the association of the oral diseases with complications and mortality of cirrhosis. METHODS: A total of 184 cirrhosis patients were enrolled and were followed up for 2 years. They underwent oral clinical and radiographic examination. At study entry, the associations between oral diseases with nutrition, inflammation, and cirrhosis complication status were examined. Then, the associations of oral diseases with all-cause and cirrhosis-related mortality were examined using Cox regression to adjust for confounding by age, gender, smoking, alcohol use, alcoholic cirrhosis, cirrhosis complications, comorbidity, Child-Pugh, and Model of End-Stage Liver Disease (MELD) score. RESULTS: At entry, 26% of the patients had gross caries, 46% periapical lesions, 27% oral mucosal lesions, and 68% periodontitis. Having one or more oral diseases was associated with a higher prevalence of cirrhosis complications (46.7 vs 20.5%), higher C-reactive protein (28.5 mg/L vs 10.4 mg/L), and higher nutritional risk score (4 vs 3). Two-thirds of the patients died during follow-up. The patients with more than one oral disease had an increasingly higher all-cause mortality (two diseases: hazard ratio [HR] 1.55, 95% confidence interval [CI] 1.02-1.98; three and four diseases: HR 1.75, 95% CI 1.05-3.24) and even higher cirrhosis-related mortality (two diseases: HR 1.60, 95% CI 1.01-2.40; three and four diseases: HR 2.04, 95% CI 1.05-8.83) compared to those with no oral disease. CONCLUSION: In cirrhosis, having more than one oral disease was associated with more complications and with higher mortality.
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BACKGROUND: The aim of the study was to determine if periodontitis, which often causes transient bacteraemia, associates with viable bacteria in standard blood donations. MATERIALS AND METHODS: This was a cross-sectional study of 60 self-reported medically healthy blood donors aged over 50 years. According to standard procedures, whole blood was separated by fractionation into plasma, buffy-coat, and red blood cell (RBC)-fractions. The buffy-coat was screened for bacterial contamination using BacT/ALERT. Samples from plasma and RBC-fractions were incubated anaerobically and aerobically at 37°C for 7 days on trypticase soy blood agar (TSA). For identification, colony polymerase chain reaction was performed using primers targeting 16S rDNA. RESULTS: From 62% of the donors with periodontitis, bacterial growth was observed on at least 1 out of 4 plates inoculated with plasma or RBCs, whereas only 13% of plates inoculated with plasma or RBCs from periodontally healthy controls yielded bacterial growth (relative risk 6.4, 95% CI: 2.1; 19.5; p=0.0011). None of the donors tested positive for bacterial contamination using BacT/ALERT. Cutibacterium acnes was found in 31% of the donations from donors with periodontitis and in 10% of the donations from periodontally healthy donors. In addition, Staphylococcus species, Bacillus mycoides, Aggregatibacter aphrophilus, and Corynebacterium kroppenstedtii were detected. DISCUSSION: Periodontitis increased the risk of bacterial contamination of blood products. Contaminating bacteria are often associated with the RBC-fraction. As the BacT/ALERT test is generally performed on platelet products, routine screening fails to detect many occurrences of viable bacteria in the RBC-fraction.
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Doadores de Sangue , Periodontite , Idoso , Bactérias , Plaquetas , Estudos Transversais , Eritrócitos , HumanosRESUMO
BACKGROUND AND OBJECTIVE: The complement system is engaged in inflammatory reactions both in the periodontal pockets and in the periodontium itself, where it can mediate tissue destruction. The aim of this study was, first, to compare salivary levels of the total complement system protein C3 and its split product, fluid-phase C3c in patients with periodontitis and periodontally healthy controls. Next, to determine if C3 and C3c levels had biomarker potential in diagnosing and monitoring periodontitis and its treatment. We hypothesized that salivary levels of total C3 and the split product C3c associated with the severity of periodontitis and reflected decreased inflammatory activity after periodontal treatment. METHODS: At baseline, stimulated saliva samples were collected from patients with periodontitis (n = 18) and periodontally healthy controls (n = 15). Subsequently, non-surgical periodontal treatment was performed in the patients, and saliva sampling from patients was repeated two-, six-, and twelve weeks post-treatment (NCT02913248 at clinicaltrials.gov). The patients were grouped as good and poor responders to treatment according to the achieved reduction in bleeding on probing (BOP). Salivary levels of C3 and C3c were quantified using sandwich ELISA. RESULTS: Patients with periodontitis had higher baseline levels of both total C3 and the split product C3c in saliva than did periodontally healthy controls (P < .0001). Receiver operating curve (ROC) analyses discriminated patients with periodontitis from controls based on both C3 (AUC (area under curve) = 0.91, P < .001) and C3c levels (AUC = 0.84, P < .001) in saliva. Periodontal treatment improved all clinical parameters (P < .01). Good responders (n = 10) had lower baseline levels of C3c than poor responders (n = 8), (P < .05), and baseline levels of C3c discriminated between good and poor responders (AUC = 0.80, P < .05). CONCLUSION: In conclusion, patients with periodontitis had higher salivary levels of C3c, and the C3c levels were predictive of reductions in BOP, that is, the poor responders. This suggests that salivary C3c levels possess potential to serve as a biomarker predicting the clinical response to non-surgical periodontal treatment.
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Periodontite Crônica , Periodontite , Biomarcadores , Humanos , Índice Periodontal , Bolsa Periodontal , Periodontite/terapia , SalivaRESUMO
INTRODUCTION: Age assessment based on dental development is often requested in order to assess whether an individual is older or younger than 18 years of age. There are several statistical approaches to estimate age based upon third molar development. The aim of this study was to apply the principles of transition analysis (TA) to a Danish reference material and to evaluate whether it was indicated to include a model that allows for logistic non-linearity as opposed to applying a model only allowing for logistic linearity. For this we chose to use the generalized additive model (gam) and the generalized linear model (glm), respectively. MATERIAL AND METHOD: A cross-sectional sample comprising 1302 panoramic radiographs of Danish subjects in the chronological age range of 13-25 years was included. All present third molars had been scored according to the 10-stage method of Gleiser and Hunt. Each transition from one stage to the subsequent stage was analyzed according to the statistical approach of TA and fitted with both the generalized linear model (glm) and the generalized additive model (gam). In order to assess whether gam or glm was more parsimonious for each transition individually, the Akaikon information criterion (AIC) was applied. RESULTS: The results emphasized the importance of applying a statistical model that sufficiently captures the spread of the age estimate. The AIC values showed that some transitions were sufficiently described by glm whereas for others the gam curves fitted significantly better. CONCLUSION: We recommend that for an age assessment tool based on TA, both a fitting allowing for non-linearity and one allowing only for linearity should be included.
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Determinação da Idade pelos Dentes/métodos , Modelos Estatísticos , Dente Serotino/crescimento & desenvolvimento , Adolescente , Adulto , Dinamarca , Feminino , Humanos , Masculino , Dente Serotino/diagnóstico por imagem , Radiografia Panorâmica , Adulto JovemRESUMO
Background: During periodontal inflammation, bacteria induces chemokine expression and migration of various inflammatory cells. The aim of the study was to learn if periodontal treatment alters salivary concentrations of macrophage activation-related chemokines and if such alterations correlate with abundance of periodontitis-associated bacteria. Methods: Twenty-five patients with periodontitis completed the study (NCT02913248 at clinicaltrials.gov). Periodontal parameters and stimulated saliva samples were obtained at baseline and 2, 6 and 12 weeks after non-surgical periodontal treatment. Salivary concentrations of monocyte chemoattractant proteins (MCP-1-4), macrophage-derived chemokine (MDC), macrophage migration inhibitory factor (MIF), monokine induced by interferon-gamma (MIG), macrophage inflammatory protein (MIP-1α) and interferon-inducible protein (IP-10) were quantified using the Luminex® xMAP™ technique and abundance of bacteria was quantified using next-generation sequencing. Results: The treatment improved all periodontal parameters and caused an increase in the concentrations of MCP-2, MDC and MIP-1α at week 12 compared to baseline, week 2 and week 6, respectively. Salivary concentrations of MCP-1-2, MDC, MIG, MIP-1α and IP-10 correlated with the abundance of specific periodontitis-associated bacteria. Conclusions: Periodontal treatment impacts salivary concentrations of MCP-2, MDC and MIP-1α, which correlate with the abundance of specific periodontitis-associated bacteria. This indicates that these chemokines reflect periodontal status and possess potential in illustrating a response to treatment.
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Objective: To characterize the salivary microbiota of patients with aggressive periodontitis, patients with chronica periodontitis and orally healthy individuals. Methods: A total of 81 unstimulated saliva samples from aggressive periodontitis patients (n = 31), chronic periodontitis patients (n = 25), and orally healthy controls (n = 25) were examined. The V1-V3 region of the 16S rDNA gene was sequenced with Illumina® MiSeqTM, and sequences were annotated to the expanded Human Oral Microbiome Database (eHOMD). Results: A mean percentage of 97.6 (range: 89.8-99.7) of sequences could be identified at species level. Seven bacterial species, including Porphyromonas gingivalis, were identified with significantly higher relative abundance in saliva from aggressive periodontitis patients than in saliva from orally healthy controls. Salivary abundance of P. gingivalis could discriminate aggressive (AUC: 0.80, p = 0.0001) and chronic periodontitis (AUC: 0.72, p = 0.006) from healthy controls. Likewise, salivary presence of P. gingivalis was significantly associated with aggressive (p < 0.0001, RR: 8.1 (95% CI 2.1-31.2)) and chronic periodontitis (p = 0.002, RR: 6.5 (95% CI: 1.6-25.9)). Conclusion: Salivary presence and relative abundance of P. gingivalis associate with aggressive and chronic periodontitis, but do not discriminate between aggressive and chronic periodontitis.
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Periodontitis is a highly prevalent chronic inflammatory disease, which is associated with a range of comorbid conditions, for which chronic low-grade inflammation is a common pathogenetic denominator. This review provides a summary of the current evidence on comorbitidy of periodontitis and highlights some of the potential clinical implications.
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Periodontite , Doença Crônica , Comorbidade , Humanos , Inflamação , Periodontite/complicaçõesRESUMO
Liver cirrhosis is a severe disease with major impact on the overall health of the patient including poor oral health. Lately, there has been increasing focus on oral diseases as cirrhosis-related complications due to the potential impact on systemic health and ultimately mortality. Periodontitis is one of the most common oral diseases in cirrhosis patients. However, no studies have investigated the composition of the subgingival microbiome in patients suffering from periodontitis and liver cirrhosis. We analysed the subgingival microbiome in 21 patients with periodontitis and cirrhosis using long-reads Illumina sequencing. The subgingival microbiota was dominated by bacteria belonging to the Firmicutes phylum and to a lesser extend the Actinobacteria and Bacteroidetes phyla. Bacteria usually considered periodontal pathogens, like Porhyromonas ginigivalis, Tannerella forsythia, Treponema denticola, generally showed low abundancy. Comparing the microbiota in our patients with that of periodontitis patients and healthy controls of three other studies revealed that the periodontitis-associated subgingival microbiota in cirrhosis patients is composed of a unique microbiota of bacteria not normally associated with periodontitis. We hypothesise that periodontitis in cirrhosis patients is a consequence of dysbiosis due to a compromised immune system that renders commensal bacteria pathogenic.
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Bactérias/patogenicidade , Disbiose/microbiologia , Cirrose Hepática/imunologia , Microbiota/imunologia , Periodontite/microbiologia , Idoso , Bactérias/genética , Bactérias/imunologia , Bactérias/isolamento & purificação , Estudos de Coortes , DNA Bacteriano/isolamento & purificação , Disbiose/imunologia , Feminino , Gengiva/imunologia , Gengiva/microbiologia , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Cirrose Hepática/complicações , Cirrose Hepática/microbiologia , Masculino , Microbiota/genética , Pessoa de Meia-Idade , Periodontite/imunologia , RNA Ribossômico 16S/genética , Simbiose/imunologiaRESUMO
While plaque-induced gingivitis is one of the most common human inflammatory diseases, several non-plaque-induced gingival diseases are less common but often of major significance for patients. The non-plaque-induced gingival lesions are often manifestations of systemic conditions, but they may also represent pathologic changes limited to gingival tissues. A classification is proposed, based on the etiology of the lesions and includes: Genetic/Developmental disorders; Specific infections; Inflammatory and immune conditions and lesions; Reactive processes; Neoplasms; Endocrine, Nutritional and metabolic diseases; Traumatic lesions; and Gingival pigmentation.
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Doenças da Gengiva , Gengivite , Gengiva , HumanosRESUMO
Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non-periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non-dental plaque biofilm-induced gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque-induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque-induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient-centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.
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Placa Dentária , Gengivite , Periodontite , Consenso , Humanos , PeriodontoRESUMO
Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non-periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non-dental plaque biofilm-induced gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque-induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque-induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient-centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.
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Gengivite , Peri-Implantite , Periodontite , Consenso , Humanos , PeriodontoRESUMO
While plaque-induced gingivitis is one of the most common human inflammatory diseases, several non-plaque-induced gingival diseases are less common but often of major significance for patients. The non-plaque-induced gingival lesions are often manifestations of systemic conditions, but they may also represent pathologic changes limited to gingival tissues. A classification is proposed, based on the etiology of the lesions and includes: Genetic/Developmental disorders; Specific infections; Inflammatory and immune conditions and lesions; Reactive processes; Neoplasms; Endocrine, Nutritional and metabolic diseases; Traumatic lesions; and Gingival pigmentation.
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Doenças da Gengiva , Gengivite , Gengiva , HumanosRESUMO
We present a reference database for third molar development based on a contemporary Danish population. A total of 1302 digital panoramic images were evaluated. The images were taken at a known chronological age, ranging from 13 to 25years. Third molar development was scored according to the Köhler modification of the 10-stage method of Gleiser and Hunt. We found that third molar development was generally advanced in the maxilla compared to the mandible and in males compared to females; in addition, the mandibular third molar mesial roots were generally more advanced in development than were the distal roots. There was no difference in third molar development between the left and right side of the jaws. Establishing global and robust databases on dental development is crucial for further development of forensic methods to evaluate age.