Application of 2017 New Classification of Periodontal Diseases and Conditions to Localized Aggressive Periodontitis: Case Series.

INTRODUCTION: This case series illustrates the use of the new classification system of periodontal diseases and conditions. This case series highlights how the assessment of the rate of progression of periodontal disease, that is, grading, allows for the identification of individual patients, who are more likely to require active periodontal treatment intervention to prevent onset of disease, need long-term disease control, or referral to a periodontist. CASE PRESENTATION: A 17-year-old female presents with slight gingival inflammation. However, exploration into indirect evidence of disease progression, that is, family history of periodontal disease, leads to the discovery of advanced disease in the mother. The patient was diagnosed with generalized Stage I Grade C periodontitis. The patient was managed with initial periodontal therapy, consisting of scaling and root planing with systemic antibiotic therapy. Special consideration was taken to mitigate the potential for rapid disease progression because of indirect evidence of familial history of aggressive periodontitis and indicated the need for early intervention. The case resulted in remission of the progression of periodontal disease. CONCLUSIONS: Applying the staging and grading system leads to an understanding of the need for periodontal referral and early periodontal treatment intervention. Wide adoption of staging and grading could increase early referral leading to early periodontal treatment intervention, decreased tooth loss, and have a potential effect on overall health improvement and wellness.

Diagnosis of aggressive periodontitis: A dilemma?

Periodontitis is one of the leading causes of tooth loss in the adult population. This disease can be classified into various categories, and one of the most destructive amongst them is aggressive periodontitis (AgP). The incidence of AgP is lower than other types of periodontitis. However, it affects young individuals and can cause severe destruction of tooth-supporting structures including tooth loss if left untreated. The current classification for diagnosing periodontal disease was established by the American Academy of Periodontology (AAP) in 1999. This classification provided strict guidelines to aid in AgP diagnosis. These include three main factors: systemically healthy individual, rapid loss of clinical attachment, and familial aggregation. In spite of these specific guidelines, AgP diagnosis is often missed clinically due to various reasons. There is still a vast variation in the diagnostic criteria for identifying AgP and not all practitioners utilize the AAP guidelines for their diagnosis. Furthermore, the definition of the disease might be changing in the future to better represent the current understanding of the disease. Since early diagnosis and prompt treatment is key in treating these patients, it is important to have calibration in the diagnosis process. This review aims to identify sources of variation and ambiguity in diagnosing AgP among dental practitioners. For this purpose, we have conducted an extensive literature search and outlined the various diagnostic aids for AgP patients reported in the literature. Understanding and correcting these variations can simplify the diagnostic process leading to faster treatment of patients affected with AgP. This review also emphasizes the importance of minimizing the bias in identifying patients with AgP and highlights the best tools for this purpose.

Support vector machine-based differentiation between aggressive and chronic periodontitis using microbial profiles.

BACKGROUND: The existence of specific microbial profiles for different periodontal conditions is still a matter of debate. The aim of this study was to test the hypothesis that 40 bacterial species could be used to classify patients, utilising machine learning, into generalised chronic periodontitis (ChP), generalised aggressive periodontitis (AgP) and periodontal health (PH). METHOD: Subgingival biofilm samples were collected from patients with AgP, ChP and PH and analysed for their content of 40 bacterial species using checkerboard DNA-DNA hybridisation. Two stages of machine learning were then performed. First of all, we tested whether there was a difference between the composition of bacterial communities in PH and in disease, and then we tested whether a difference existed in the composition of bacterial communities between ChP and AgP. The data were split in each analysis to 70% train and 30% test. A support vector machine (SVM) classifier was used with a linear kernel and a Box constraint of 1. The analysis was divided into two parts. RESULTS: Overall, 435 patients (3,915 samples) were included in the analysis (PH = 53; ChP = 308; AgP = 74). The variance of the healthy samples in all principal component analysis (PCA) directions was smaller than that of the periodontally diseased samples, suggesting that PH is characterised by a uniform bacterial composition and that the bacterial composition of periodontally diseased samples is much more diverse. The relative bacterial load could distinguish between AgP and ChP. CONCLUSION: An SVC classifier using a panel of 40 bacterial species was able to distinguish between PH, AgP in young individuals and ChP.

Definition of aggressive periodontitis in periodontal research. A systematic review.

Since its introduction in 1999, the term aggressive periodontitis (AgP) has been the topic of many investigations. Articles supporting the International Workshop for a Classification of Periodontal Diseases list several disease features, but do not offer operational criteria for identifying cases. Consequently, considerable variation in the understanding of AgP can be anticipated. AIM: To systematically assess the definitions of AgP reported in original periodontal research. METHODS: A systematic review of original research on AgP published in English. RESULTS: The electronic search yielded 833 abstracts. Of these, 472 publications fulfilled the inclusion criteria and were appraised. In 26.5% of the publications, no information on AgP operationalization is presented, but reference is made to another article. In 12.7% of the publications, no information is provided as to how the cases were defined. Many combinations of criteria for case definition were found. CONCLUSIONS: This study revealed significant heterogeneity in the understanding and use of the term AgP in original research and poor documentation of the identification of cases. The direction and magnitude of the influence of misclassification and selection bias are unknown, but ought to be considered by the critical reader, professionals and patients using this term.

Disease Staging Index for Aggressive Periodontitis.

Major advances in the knowledge about the aetiopathogenesis of aggressive periodontitis (AgP) have been achieved. An ever increasing number of scientific articles related to AgP are published every year contributing significantly to the knowledge of this unique and complex disease. AgP has been classified into localised and generalised forms based on their extent and disease progression with distinct clinical and radiological features. A classification of AgP based on severity (mild, moderate and severe) exists; however, it is not easily applicable. Therefore, studies on AgP do not categorise the disease based on severity. A disease staging index for AgP is proposed based on clinical and radiological features, as well as risk factors. Based on the presence or absence of risk factors confirmed by longitudinal studies, cases of AgP can be divided into low risk, medium risk and high risk profiles for disease progression. Clinicians can devise a broad treatment plan for their AgP cases based on this staging. More frequent recall intervals are proposed for patients at medium and high risk for disease progression. Ten cases of AgP with 10-year follow-up were used to validate the staging index by retrospectively assigning prognosis and associating it with tooth loss. The use of this staging by researchers would increase external validity of research on AgP. Long-term analysis of AgP cases are needed to validate this staging index longitudinally.

What exactly distinguishes aggressive from chronic periodontitis: is it mainly a difference in the degree of bacterial invasiveness?

At the International Workshop for Classification of Periodontal Diseases and Conditions in 1999, the classification of aggressive and chronic periodontitis that is presently used was introduced. A literature review of papers published in 2015 and having aggressive periodontitis in the title revealed that most studies use this terminology but it is questionable whether all established criteria were really applied correctly. Review of the literature showed no qualitative differences between aggressive and chronic periodontitis regarding bacterial and viral aspects. It is also unlikely that that there are major immunologic differences between aggressive and chronic periodontitis. Neutrophil function can be compromised in both conditions but may be more genetically related in aggressive periodontitis and be associated more with lifestyle factors in chronic periodontitis. In general, genetics plays a more important role in aggressive periodontitis than in chronic periodontitis. It is likely that periodontitis progresses by recurrent acute episodes during which invasion of bacteria into the connective tissue may occur. Two cases are presented for which invasive periodontitis is treated with systemic antibiotics, showing remarkable periodontal healing in terms of probing attachment gain, as well as radiographic bone gain. Periodontitis in an active state with bacterial invasion is probably accompanied with a significant increase in subgingival temperature. It is hypothesized that elevated subgingival temperature may help to distinguish between bacterial and nonbacterial invasive periodontitis. Scaling and root planing during a burst of disease activity may result in removal of connective tissue fiber attachment and down-growth of epithelium, thereby preventing the reattachment of connective tissue. Because the burst of disease is accompanied by an increase of temperature, assessment of the temperature may help in deciding whether or not to prescribe systemic antibiotics. When the use of systemic antibiotics is indicated, the antibiotic therapy may help to maintain the connective tissue attachment at the most possible coronal level. The above implies that the ability to diagnose bacterial invasive periodontitis is quite important, and future research is needed to determine if assessment of subgingival temperature may help in diagnosing invasive periodontitis. In addition, it is suggested that future classification systems of periodontitis include the item of bacterial invasive periodontitis.

Evaluation of salivary procalcitonin levels in different periodontal diseases.

BACKGROUND: The present study aims to investigate the levels of salivary procalcitonin (ProCT) in patients with different periodontal diseases. METHODS: Seventy-two non-smokers are included in this study: 21 individuals with chronic periodontitis (CP), 14 individuals with generalized aggressive periodontitis (GAgP), 18 individuals with gingivitis (G), and 19 periodontally healthy (H) participants. Clinical periodontal parameters, including probing depth (PD), clinical attachment level (CAL), plaque index, and gingival index (GI), were assessed in all participants. Saliva samples were collected and examined for evaluating ProCT levels. RESULTS: It was found that the median (interquartile range) salivary ProCT level was lowest in the H group: 0.00 (0.09) ng/mL; followed by the G group: 0.09 (0.11) ng/mL; the CP group: 0.15 (0.29) ng/mL; and highest in the GAgP group 0.28 (0.68) ng/mL. These differences were statistically significant between the H group and the other groups (P <0.05). There were positive correlations between the mean salivary ProCT level and GI, CAL, and PD. CONCLUSION: According to the present results, ProCT might play a role during periodontal inflammation, and an elevated salivary ProCT level is suggested as a potential biomarker for periodontal diseases.

Análise clínica e de citocinas no fluido gengival de pacientes com periodontite agressiva - estudo longitudinal / Clinical and cytokines analyzes on the gingival fluid of patients with aggressive periodontitis - longitudinal study

O objetivo deste estudo foi avaliar os parâmetros clínicos periodontais: profundidade clínica de sondagem, nível clínico de inserção e sangramento a sondagem e os níveis de IL-17, M-CSF, GM-CSF, MCP-1, ICAM-1 IL-8, IL-10, IL-1?, TNF-?, IL-4 no fluido gengival de pacientes portadores de periodontite agressiva, comparando esses valores aos dados obtidos de sujeitos periodontalmente saudáveis, além de comparar os dados clínicos e imunológicos iniciais aos obtidos após um ano de tratamento nos pacientes com periodontite agressiva. Foram selecionados 37 pacientes portadores de periodontite agressiva e oito pacientes periodontalmente saudáveis, utilizados como grupo controle. Após a realização do exame clínico periodontal em todos os dentes, foi escolhido um sítio profundo de cada paciente com paeriodontite e um sítio raso dos pacientes saudáveis para coleta do fluido gengival. Todos os pacientes receberam tratamento periodontal que consistiu de orientação de higiene bucal, raspagens, remoção de fatores de retenção do biofilme bacteriano, polimento e uso de antibióticos. As amostras obtidas foram processadas e analisadas com um painel de 10 citocinas através de um ensaio multiplex. As análises estatísticas mostraram que não houve diferença estatisticamente significante entre os doentes e os saudáveis em relação a GM-CSF, IL-4, IL-8 e MCP-1.

Quando foi feita a comparação longitudinal dos pacientes com periodontite agressiva, houve aumento após o tratamento para GM-CSF, ICAM-1, IL-4, IL-10, IL-17, MCP-1 e TNF-?. Com isso, pode-se concluir que mesmo após o tratamento periodontal com consultas trimestrais de manutenção e melhora dos parâmetros clínicos nos pacientes com PA que tinham um baseline mais inflamado, foi observado que alguns biomarcadores continuaram elevados, o que pode significar que esses pacientes continuam a apresentar atividade de doença ou que alguns desses biomarcadores não têm significância clínica para esses pacientes.

The aim of this study was to evaluate the periodontal clinical parameters: clinical probing depth, clinical attachment level and bleeding on probing and the IL-17, M-CSF, GM-CSF, MCP-1, ICAM-1, IL-8, IL-10, IL-1?, TNF-? and IL-4 levels in gingival crevicular fluid of aggressive periodontitis subjects, comparing these values with some data obtained from periodontal healthy patients, and also comparing clinic and immunologic initial data with the obtained after one year of treatment of aggressive periodontitis. The sample had 37 patients with aggressive periodontitis and 8 subjects clinically healthy, as control group. After the full periodontal examination, each patient with periodontitis had a deep site chosen, and a shallow site of the healthy ones, for collecting gingival fluid. All patients received periodontal treatment with oral hygiene, scaling, removal of retention factors, polishing and antibiotics. The obtained samples were processed and analyzed with a panel of 10 cytokines through a multiplex test. The statistical analyzes showed that there was no significant statistical difference between subjects with PA and healthy subjects with regard to GM-CSF, IL-4, IL-8 and MCP-1 levels.When longitudinal comparison of the subjects was made, it was noted some increase for GM-CSF, ICAM-1, IL-4, IL-10, IL-17, MCP-1 and TNF-?. Then, it can be concluded that, even after the periodontal treatment with trimestral maintenance and improvement on the clinical parameters, some biomarkers are still elevated, what can mean one of those possibilities: or the patients are still presenting some activity of the disease, or that some of these biomarkers don't have any clinical significance for this patients.

IgG sera levels against a subset of periodontopathogens and severity of disease in aggressive periodontitis patients: a cross-sectional study of selected pocket sites.

AIMS: To evaluate the association among serum immunoglobulin G (IgG) responses to Aggregatibacter actinomycetemcomitans (Aa) serotypes a, b and c, Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf) and clinical parameters in Aggressive Periodontitis (AP) subjects. Associations between periodontal pathogens and clinical and immunological parameters were also evaluated. METHODS: Thirty-eight subjects diagnosed with generalized AP (GAP) and localized AP (LAP) were included. Ten healthy controls were also evaluated. Clinical parameters were assessed and percentages of subgingival levels of Aa, Pg and Tf (beyond bacterial load), were determined by quantitative real-time polymerase chain reaction. Serum IgG antibody levels against Aa, Pg and Tf were evaluated by enzyme-linked immunosorbent assay. RESULTS: Percentages of Aa, Pg and Tf were significantly higher in AP than in controls. The response to Aa serotype c was higher in LAP subjects than in controls. There were no differences in microbial composition or antibodies responses between GAP and LAP, except for IgG response to Tf. Pg levels were correlated with probing depth (PD), BoP and CAL in GAP but not in LAP subjects. Tf levels correlated with PD and CAL in GAP subjects. In GAP, the infection levels of Aa and Pg correlated with the corresponding IgG levels to Aa serotype c and Pg. CONCLUSION: Given the evidences that IgG response in AP patients correlated with bacterial infection level in GAP, but not in LAP, and that LAP patients lack a response to Tf, despite harbouring this species, our data suggest a difference in host immune defence between these two forms of aggressive periodontitis.

Is gingival bleeding a symptom of patients with type 1 von Willebrand disease? A case-control study.

BACKGROUND: Von Willebrand disease (VWD) is the most common inherent bleeding disorder resulting in prolonged bleeding time. Gingival bleeding is a frequently reported symptom of VWD. However, gingival bleeding is also known as a leading symptom of plaque-induced gingivitis and untreated periodontal disease. Gingival bleeding in VWD patients (VWD) may be triggered by gingival inflammation and not a genuine symptom. Thus, this study evaluated whether type 1 VWD determines an increased susceptibility to gingival bleeding in response to the oral biofilm. METHODS: Fifty cases and 40 controls were examined haematologically (VWF antigen, VWF Ristocetin cofactor, factor VIII activity) and periodontally [Gingival Bleeding Index (GBI), bleeding on probing (BOP), Plaque Control Record (PCR), periodontal inflamed surface area (PISA), vertical probing attachment level]. RESULTS: GBI was significantly higher in controls (12.2%) than in VWD (10%). The study failed to find a significant difference regarding BOP between VWD (17%) and controls (17.2%). Multiple regressions identified PCR and PISA to be associated with GBI and BOP. VWD was negatively associated with GBI. Smoking and number of remaining teeth was negatively associated with BOP. CONCLUSION: VWD is not associated with a more pronounced inflammatory response to the oral biofilm in terms of GBI and BOP.

Aggressive periodontitis: case definition and diagnostic criteria.

Aggressive periodontitis is a destructive disease characterized by the following: the involvement of multiple teeth with a distinctive pattern of periodontal tissue loss; a high rate of disease progression; an early age of onset; and the absence of systemic diseases. In some patients periodontal tissue loss may commence before puberty, whereas in most patients the age of onset is during or somewhat after the circumpubertal period. Besides infection with specific microorganisms, a host predisposition seems to play a key role in the pathogenesis of aggressive periodontitis, as evidenced by the familial aggregation of the disease. In this article we review the historical background of the diagnostic criteria of aggressive periodontitis, present a contemporary case definition and describe the clinical parameters of the disease. At present, the diagnosis of aggressive periodontitis is achieved using case history, clinical examination and radiographic evaluation. The data gathered using these methods are prone to relatively high measurement errors. Besides, this diagnostic approach measures past disease history and may not reliably measure existing disease activity or accurately predict future tissue loss. A diagnosis is often made years after the onset of the disease, partly because current assessment methods detect established disease more readily and reliably than they detect incipient or initial lesions where the tissue loss is minimal and usually below the detection threshold of present examination methods. Future advancements in understanding the pathogenesis of this disease may contribute to an earlier diagnosis. Insofar, future case definitions may involve the identification of key etiologic and risk factors, combined with high-precision methodologies that enable the early detection of initial lesions. This may significantly enhance the predictive value of these tests and detect cases of aggressive periodontitis before significant tissue loss develops.

Lipid peroxidation levels and total oxidant/antioxidant status in serum and saliva from patients with chronic and aggressive periodontitis. Oxidative stress index: a new biomarker for periodontal disease?

BACKGROUND: In this study, levels of malondialdehyde (MDA), which is a significant product of lipid peroxidation (LPO), total oxidant status (TOS), total antioxidant capacity (TAOC), and the oxidative stress index (OSI), a novel value as a marker of periodontal disease activity, are investigated in serum and saliva from patients with chronic (CP) and generalized aggressive (GAgP) periodontitis. METHODS: A total of 98 patients (33 with CP, 35 patients with GAgP, and 30 periodontally healthy controls) enrolled in the study. After clinical measurements and sample collection, the MDA level, TOS, and TAOC were measured by high-performance liquid chromatography and a novel automatic colorimetric method. The OSI was calculated as [(TOS/TAOC) × 100]. RESULTS: Although the salivary MDA levels and serum and salivary TOS and OSI values were significantly higher in the periodontitis groups than in the control group (P <0.05), the serum and salivary TAOC levels were significantly lower, and no significant difference in serum MDA levels was found (P >0.05). Furthermore, oxidative stress parameters were higher in the GAgP group than in the CP group (except the serum and salivary MDA levels and serum TAOC). Significant positive and negative correlations were observed between periodontal parameters and the MDA levels and TOS, TAOC, and OSI values (except serum MDA) (P <0.05). CONCLUSIONS: The present findings suggest that an increased TOS and decreased TAOC, rather than LPO, play important roles in the pathology of periodontitis and are closely associated with clinical periodontal status. Furthermore, the OSI may be a useful and practical parameter for evaluating periodontal disease activity.

Detection of eight periodontal microorganisms and distribution of Porphyromonas gingivalis fimA genotypes in Chinese patients with aggressive periodontitis.

BACKGROUND: The microbiologic feature of aggressive periodontitis (AgP) in Chinese patients has not yet been determined. This study aims to investigate the prevalence of eight periodontal microorganisms and the distribution of the Porphyromonas gingivalis fimA genotype in a cohort of Chinese patients with AgP. METHODS: Saliva and pooled subgingival plaque samples were collected from 81 patients with AgP (25 with incisor-first molar type and 56 with generalized type [GAgP]) and 34 periodontally healthy controls. Eight periodontal microorganisms, including Aggregatibacter actinomycetemcomitans, P. gingivalis, Tannerella forsythia, Treponema denticola, Campylobacter rectus, Prevotella intermedia, Prevotella nigrescens, and Fusobacterium nucleatum were detected in these samples by the polymerase chain reaction (PCR). In addition, the distribution of fimA genotypes was assessed in P. gingivalis-positive individuals by PCR. RESULTS: The prevalence of P. gingivalis, T. forsythia, T. denticola, C. rectus, P. intermedia, F. nucleatum, and A. actinomycetemcomitans in patients with AgP was significantly higher than that in healthy controls. The prevalence of A. actinomycetemcomitans in patients with GAgP was relatively low (30.4%) compared with other pathogens. Results of logistic regression analysis showed that younger patients were more likely to harbor A. actinomycetemcomitans (odds ratio = 2.85). Type II was the most prevalent fimA genotype of P. gingivalis in patients with AgP. CONCLUSIONS: P. gingivalis, T. forsythia, T. denticola, C. rectus, P. intermedia, and F. nucleatum were the predominant periodontal pathogens of patients with GAgP in China. Type II of fimA was the most prevalent genotype of P. gingivalis in patients with AgP. The prevalence of A. actinomycetemcomitans in patients with GAgP was relatively low.

Association of aggressive periodontitis with reduced erythrocyte counts and reduced hemoglobin levels.

BACKGROUND AND OBJECTIVE: Studies have shown that erythrocyte counts and hemoglobin levels are reduced in patients with chronic periodontitis, suggesting that this condition may be associated with anemia of chronic disease. Although increased leukocyte counts have been reported in aggressive periodontitis, very little is known about the effects of aggressive periodontitis on erythrocyte counts. The present study was undertaken to determine whether generalized aggressive periodontitis is associated with reduced erythrocyte counts and reduced hemoglobin levels. MATERIAL AND METHODS: The present study was conducted as a case-control study in which 64 patients with generalized aggressive periodontitis were categorized as cases and 58 periodontally healthy individuals were categorized as controls. Erythrocyte parameters (such as erythrocyte count, hemoglobin concentration, and hematocrit and erythrocyte indices) and clinical parameters (such as gingival index, plaque index, probing depth, clinical attachment level and percentage of severe sites) were recorded. RESULTS: Significant differences were observed between cases and controls in mean erythrocyte count (4.45 ± 0.6 × 10(6) erythrocytes/µL and 4.78 ± 0.56 × 10(6) erythrocytes/µL respectively, p = 0.002) and hemoglobin level (12.43 ± 1.83 g/dL and 13.53 ± 1.64 g/dL, respectively, p = 0.001). Other erythrocyte parameters, such as hematocrit, mean corpuscular volume and mean corpuscular hemoglobin, were also significantly lower among cases compared with controls. Logistic regression analyses showed that generalized aggressive periodontitis was significantly associated with lower erythrocyte counts ( p = 0.032) and a lower hemoglobin concentration ( p = 0.017). CONCLUSION: The findings of the present study suggest that patients with generalized aggressive periodontitis tend to have lower erythrocyte counts and lower hemoglobin levels compared with periodontally healthy controls. This suggests that generalized aggressive periodontitis, like chronic periodontitis, may be associated with a risk for anemia of chronic disease.

An investigation of blood hemogram and estimation of serum iron and protein levels in aggressive periodontitis patients: a clinic biochemical study.

AIM: The aim of this study is to investigate the blood hemogram and estimation of serum iron and proteins level in aggressive periodontitis patients. MATERIALS AND METHODS: A total of 85 patients were selected and divided into two groups, 45 patients are with aggressive periodontitis and 40 patients are healthy. Periodontal parameters such as gingival infammation oral hygiene index, Russell's periodontal index and radiograph were taken. Total 10 ml blood was collected and sent for estimation of blood hemogram protein estimation and serum electrophoresis. RESULTS: There was statistical signifcant difference observed in relation to gingival infammation oral hygiene hemoglobin and total iron binding capacity level between both the groups. CONCLUSION: It has been concluded that periodontitis does not induce anemia like state, as the hematological and biochemical parameters were almost equally affected in periodontally healthy and periodontally diseased individuals, but some parameters showed statistical significant difference between the both groups. CLINICAL SIGNIFICANCE: In the present study, the clinical periodontal parameters, red blood cell parameters and serum iron and ferritin levels were compared among control and test groups. It was found that the values of gingival infammation, oral hygiene and periodontal index, hemoglobulin level and total iron binding protein were statistically signifcant between the groups. However, the values of erythrocyte count, white blood cell count, serum iron and serum proteins, serum electrophoresis did not show any signifcant correlation.

Gingival enlargement and mesiodens associated with generalized aggressive periodontitis: a case report.

UNLABELLED: This case report describes the management of an 18-year-old female who presented with generalized aggressive periodontitis, gingival enlargement and a mesiodens. Diagnosis for aggressive periodontitis was determined based on history, clinical findings and radiographic examination. Treatment included oral prophylaxis, extraction of the mesiodens and elimination of infectious microorganisms, using a combination of surgical intervention and antimicrobial therapy with long-term maintenance. CLINICAL RELEVANCE: Presence of gingival enlargement in cases of aggressive periodontitis may be clinically confusing; hence, the diagnosis should always be based on the patient's history as well as the clinical and radiographic findings.

C-reactive protein as a marker of periodontal disease.

Periodontal subgingival pathogens affect local and systemic immune and inflammatory response and cause the release of cytokines; this results in periodontal destruction and initiation of an acute phase systemic inflammatory response characterized by the release of C-reactive proteins (CRP). This study set out to evaluate the serum concentration of CRP that can be used as a marker of periodontal disease as well as a risk indicator for cardiovascular disease. Based on their periodontal status, 45 patients were divided into three groups. The following clinical parameters were recorded: plaque index, gingival index, bleeding index, probing pocket depth, and clinical attachment levels. Scoring was done on six tooth surfaces for all teeth. For the CRP assessment, blood samples were collected from subjects at the time of clinical examination. The results indicated an increase in serum CRP levels in patients with generalized aggressive periodontitis and chronic periodontitis as compared to controls.

Microbial profile of patients with periodontitis compared with healthy subjects.

OBJECTIVE: To define and compare the microbiologic profile of subgingival plaque in German patients with periodontitis (including aggressive and advanced chronic periodontitis) and healthy subjects and to determine significant association between isolates and clinical status. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythia are major periodontal pathogens, though it is recognized that other species may also contribute to the pathogenesis of periodontal disease. METHOD AND MATERIALS: Thirty-three patients with clinical and radiologic proof of aggressive and advanced chronic periodontitis and 20 healthy subjects were enrolled in this study. Clinical indices were recorded as six-point measurements on each tooth. Samples of the subgingival plaque were taken with paper points from four teeth of each individual. The samples were divided into two parts. One part was immediately cultivated, while the other one was stored at -20°C until analyzed by real-time polymerase chain reaction. RESULTS: A total of 284 anaerobic isolates (224 isolates from patients and 60 isolates from healthy controls) were identified. Forty different anaerobic species were isolated, with a mean of 6.78 species per patient and 3 species per healthy control subject. Significant differences in prevalence (after adjusting for multiple comparisons, P < .001) were found for Prevotella intermedia and nigrescens, Fusobacterium nucleatum, T forsythia, Treponema denticola, and Veillonella parvula. The first four species were associated with the aggressive periodontitis group and V parvula with healthy subjects. CONCLUSION: When compared with healthy controls, the microbial profile of subgingival plaque from periodontitis was found to contain known periodontal pathogens with a different prevalence to that described in earlier studies. P intermedia/nigrescens, F nucleatum, T forsythia, and T denticola have been found in lower proportions and small quantities in healthy subjects.