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PubMed2000

Peptostreptococcus micros smooth and rough genotypes in periodontitis and gingivitis.

BACKGROUND: Two genotypes can be distinguished within the species Peptostreptococcus micros: a smooth (Sm) and a rough (Rg) type. To date no systematic study has been performed on the prevalence and proportion of both types in untreated periodontitis patients and subjects without destructive periodontal disease. Therefore, the present study was performed to investigate: 1) the relative importance of the Sm and the Rg genotype of P micros in periodontitis and gingivitis; 2) the correlation between smoking and the 2 genotypes of P micros; and 3) the systemic antibody response against the 2 genotypes in relation to the periodontal condition and smoking. METHODS: A total of 104 untreated periodontitis patients and 41 individuals with gingivitis underwent clinical examination and microbiological sampling. Pocket samples were cultured anaerobically on blood agar plates to determine the prevalence and proportion of the Sm and Rg types of P micros. Serum antibody titers against both types of P micros were determined in all subjects by enzyme-linked immunosorbent assay (ELISA) using whole bacterial cells as antigen. Additionally, in a representative group of subjects, the antigen specificity of the serum antibodies was assessed by immunoblotting experiments. RESULTS: The prevalence of the Sm genotype was higher in subjects with periodontitis (94%) compared to subjects with gingivitis (59%), whereas the prevalence of the Rg type was not significantly different (38% versus 29%). Similar analyses were performed for subgroups of smokers and non-smokers; within the periodontitis group, the prevalence of the Sm type was not different between smokers and non-smokers (96% and 92%, respectively), whereas the prevalence of the Rg type was higher in smokers (48%) compared to non-smokers (19%). No difference in prevalence of both types was observed between smokers and non-smokers within the gingivitis group. The titers and specificity of P micros-specific immunoglobulins in periodontitis patients were not different from those in gingivitis subjects, nor were they related to smoking status or culture-positivity. CONCLUSIONS: The results of this study suggest that both the Sm and the Rg genotypes of P micros are part of the normal oral microbiota. However, the elevated prevalence of the Sm genotype in periodontitis and the elevated prevalence of the Rg type in periodontitis patients who smoke implies that both types can behave as opportunistic pathogens in destructive periodontal disease.

Adult↗
PubMed2001

Localized aggressive periodontitis in a patient with type 1 diabetes mellitus: a case report.

BACKGROUND: Poor metabolic control of diabetes mellitus (DM) has often been associated with the severity of periodontal disease. The aim of this report is to present a 9-year-old female with localized aggressive periodontitis who had a history of type 1 DM and the outcome of her treatment. METHODS: The patient had received medical, clinical, and radiographic periodontal examinations. Peripheral blood analysis was done as well. She had non-surgical periodontal treatment, and medical management of her diabetes was performed at the same time. She was followed longitudinally for 5 years. RESULTS: Medical examination revealed no pathological findings except for growth retardation. Laboratory tests showed that she had poor metabolic control, with 497 mg/dl fasting blood glucose and 15.6% HbA1c. The random migration and neutrophil chemotaxis were significantly reduced. Periodontal treatment and metabolic control of her diabetes resulted in significant improvement in her periodontal condition. No incipient periodontal breakdown was observed around the teeth after 5 years from baseline. CONCLUSIONS: This report proves the efficiency of periodontal therapy in the prevention of future periodontal breakdown in a systemically compromised patient. It seems that in certain individuals who are predisposed to the aggressive forms of periodontitis, clinical and medical examinations and intervention to the systemic condition, in combination with periodontal treatment, are important in the management of these individuals.

Aggressive Periodontitis↗
PubMed2002

Specific fibronectin fragments as markers of periodontal disease status.

BACKGROUND: The diagnosis of progressing periodontal disease typically relies on retrospective methods that detect changes in the amount of periodontal breakdown. Fibronectin (FN) fragments are found in vivo in association with periodontal disease, and specific FN fragments compromise periodontal ligament cell functions in vitro. The overall goal of this cross-sectional study was to determine whether specific FN fragments are present in gingival crevicular fluid (GCF) and can be used as markers for periodontal disease status. The eventual goal is to test these FN fragments in a longitudinal study as potential markers of disease activity. METHODS: GCF was collected from 94 subjects with untreated periodontitis from clinically healthy, mild/moderate periodontitis, and severe periodontitis sites. Sites were defined on the basis of clinical criteria, including gingival bleeding index, probing depth, and clinical attachment level. Western immunoblotting was used to detect FN fragments in GCF using antibodies to specific FN domains, including the collagen/gelatin-, central cell-, and carboxyl terminal heparin-binding domains, plus the CS-1 site on the alternatively spliced V region and the EIIIA region. FN fragments identified by immunoblotting and analyzed by NIH image software were scored based on pixel intensity and an ordinal grade scale. RESULTS: We identified several fragments highly associated with severe periodontitis sites, including 40-kDa, 120-kDa, and 68-kDa fragments. CONCLUSIONS: This study demonstrates that specific FN fragments are markers for periodontal disease status and supports the role of FN fragments as potential components in the pathogenesis of periodontal disease.

Adult↗
PubMed2003

Subgingival microflora in Turkish patients with periodontitis.

BACKGROUND: No information exists on periodontitis-associated subgingival microbiota from Turkey. We determined the occurrence, interspecies relationships, and clonal characteristics for a group of periodontal bacteria in a Turkish study population. METHODS: Subgingival microbial samples were obtained from patients with localized (LAgP, N = 18) or generalized (GAgP, N = 17) types of aggressive periodontitis, generalized chronic periodontitis (GCP, N = 14), and non-periodontitis subjects (N = 20). Culture methods were used to recover 6 periodontal bacterial species and yeasts, and a polymerase chain reaction technique was used to detect Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Intraspecies characterization of A. actinomycetemcomitans was carried out by serotyping and genotyping. RESULTS: All species, except for Micromonas micros (formerly Peptostreptococcus micros) occurred more frequently (P < 0.05) in periodontitis than non-periodontitis subjects. Detection frequencies for Tannerella forsythensis (formerly Bacteroides forsythus) and Campylobacter rectus differed among the periodontitis subgroups; the lowest frequency occurred in LAgP. The mean proportions of A. actinomycetemcomitans, P. gingivalis, and C. rectus were higher (P < 0.008) in GAgP than in non-periodontitis subjects. Significant positive associations were seen between 7 of the 22 possible combinations (P < 0.05). A. actinomycetemcomitans serotype c (34%) and non-serotypeable isolates (34%) were the most common antigenic types among the 305 strains analyzed. Eleven arbitrarily primed (AP)-PCR genotypes were distinguished among 273 isolates from 29 subjects. Yeasts were found in 23% of the 69 subjects. CONCLUSIONS: The results on the Turkish study population were generally in line with earlier reports on the occurrence and interspecies relationships of certain bacteria in periodontitis. However, A. actinomycetemcomitans was not overrepresented in LAgP, and the serotype distribution resembled that reported from the East. The high frequency of non-serotypeable isolates suggests local characteristics of the species.

Adolescent↗
PubMed2004

Vascular endothelial growth factor in gingival tissues and crevicular fluids of diabetic and healthy periodontal patients.

BACKGROUND: Periodontal disease is one of the major oral problems encountered in patients with diabetes mellitus (DM). Vascular changes, neutrophil dysfunction, altered collagen synthesis, and genetic predisposition observed in DM may contribute to periodontitis; and the vascular alterations observed in such patients may depend on vascular endothelial growth factor (VEGF) actions. Few reports are available about the mechanism of neovascularization and the angiogenic factors that contribute to the periodontal pathology and the role of VEGF in periodontal diseases. The aim of this study is to compare VEGF expression in healthy and periodontally diseased tissues with gingival crevice fluid (GCF) of healthy persons and diabetic patients. METHODS: Gingival tissue and GCF samples were collected from sites of periodontitis in 10 healthy subjects and in 10 type 2 diabetic patients, and from the sites of healthy gingiva within the same groups. Therefore, each patient became his/her own control. Additionally, 10 people without any systemic or periodontal diseases were enrolled, forming a negative control group. Thus, a total of 50 tissue and 50 GCF samples were provided. RESULTS: No VEGF staining was observed in the negative control group or in the systemically healthy people's healthy tissue samples, whereas four samples of diabetic patients showed positive staining (P < 0.05). However, VEGF was revealed in two tissue samples of periodontal sites of systemically healthy people and in six samples of the diabetic patients (P > 0.05). In all test groups, GCF VEGF levels were higher in periodontal sites (P < 0.05) than in healthy sites. CONCLUSION: The results of this study showed that VEGF is increased in all periodontal tissues of both groups and in the healthy sites of diabetic patients. Additionally, GCF VEGF values increased in periodontal sites of all test groups.

Case-Control Studies↗
PubMed2005

Risk indicators of periodontal disease in older Thai adults.

BACKGROUND: The aim of this study was to identify risk indicators for periodontitis using cross-sectional data from a group of older Thai adults. METHODS: The study group consisted of 2,005 individuals, aged 50 to 73 years old. They received detailed medical examinations and periodontal examinations including plaque score, probing depth, and clinical attachment level. These individuals were categorized into mild, moderate, or severe periodontitis if mean clinical attachment level was <2.5 mm, 2.5 to 3.9 mm, or > or = 4.0 mm, respectively. The degree of association between the severity of periodontitis and various independent variables was investigated using multinomial logistic regression analysis. RESULTS: The percentage of subjects classified as mild, moderate, and severe periodontitis was 30.5, 53.6, and 15.9, respectively. The prevalence of severe periodontitis was higher in males and increased with age. In univariate analysis, older subjects, males, less educated persons, persons with lower income, persons with higher plaque score, smokers, drinkers, and diabetics were more likely to have both moderate and severe periodontitis. In multivariate analysis, males, less educated persons, persons with higher plaque score, and current smokers were more likely to have moderate periodontitis. Three additional factors including older age, former smokers, and diabetes significantly increased the odds for having severe periodontitis. Income, alcohol consumption, body mass index, and waist circumference had no significant effects on periodontal disease severity in the multivariate model. CONCLUSIONS: Our data suggest that age, gender, education, oral hygiene status, smoking, and diabetes are significantly associated with periodontal disease severity in this study group. Longitudinal studies will establish whether these variables are true risk factors.

Age Factors↗
PubMed2006

C-reactive protein levels in patients with aggressive periodontitis.

BACKGROUND: Sera from patients with periodontal infections contain elevated levels of C-reactive protein (CRP) compared to periodontally healthy individuals. Most studies to date have included patients with chronic periodontitis, and few investigators have studied CRP levels in subjects with aggressive periodontitis (AgP). The purpose of this study was to determine the relative levels of serum CRP in AgP patients and periodontally healthy subjects and to examine patients' characteristics that might account for intergroup differences. METHODS: Serum samples were collected from 93 patients with generalized AgP (GAgP), from 97 patients with localized AgP (LAgP), and from 91 healthy controls (non-periodontitis [NP]). Periodontal examination consisted of plaque index, gingival index, probing depth, bleeding index, and attachment loss measurements. Current smoking was assessed by determination of serum cotinine levels by enzyme-linked immunosorbent assay (ELISA), and serum CRP levels were determined using a high-sensitivity ELISA assay. RESULTS: The three groups were significantly different from one another (P <0.0001). The 95% confidence interval for serum CRP concentrations were as follows: NP, 0.65919 (0.4901 to 0.8869); LAgP, 1.10138 (0.8265 to 1.468); and GAgP, 2.05318 (1.5313 to 2.7538) mg/l. CRP levels in both LAgP and GAgP subjects were significantly greater than those in NP subjects, and levels in GAgP were significantly greater than those in LAgP. Following adjustment of the data for periodontal and demographic variables and current smoking, both mean probing depth and periodontal diagnosis remained correlated with CRP levels. CONCLUSIONS: Patients with AgP have statistically significant elevations in serum CRP levels compared to subjects without periodontitis. Elevated CRP in these subjects might represent a contribution of periodontal infections to systemic inflammation in relatively young individuals.

Adult↗
PubMed2006

Diabetes mellitus and periodontal diseases.

BACKGROUND: The purpose of this review is to provide the reader with practical knowledge concerning the relationship between diabetes mellitus and periodontal diseases. Over 200 articles have been published in the English literature over the past 50 years examining the relationship between these two chronic diseases. Data interpretation is often confounded by varying definitions of diabetes and periodontitis and different clinical criteria applied to prevalence, extent, and severity of periodontal diseases, levels of glycemic control, and complications associated with diabetes. METHODS: This article provides a broad overview of the predominant findings from research published in English over the past 20 years, with reference to certain "classic" articles published prior to that time. RESULTS: This article describes current diagnostic and classification criteria for diabetes and answers the following questions: 1) Does diabetes affect the risk of periodontitis, and does the level of metabolic control of diabetes have an impact on this relationship? 2) Do periodontal diseases affect the pathophysiology of diabetes mellitus or the metabolic control of diabetes? 3) What are the mechanisms by which these two diseases interrelate? and 4) How do people with diabetes and periodontal disease respond to periodontal treatment? CONCLUSIONS: Diabetes increases the risk of periodontal diseases, and biologically plausible mechanisms have been demonstrated in abundance. Less clear is the impact of periodontal diseases on glycemic control of diabetes and the mechanisms through which this occurs. Inflammatory periodontal diseases may increase insulin resistance in a way similar to obesity, thereby aggravating glycemic control. Further research is needed to clarify this aspect of the relationship between periodontal diseases and diabetes.

Cytokines↗
PubMed2006

Gingival crevicular fluid matrix metalloproteinase (MMP)-7, extracellular MMP inducer, and tissue inhibitor of MMP-1 levels in periodontal disease.

BACKGROUND: During periodontal inflammation, matrix metalloproteinases (MMPs) are under the control of several regulatory mechanisms including the upregulation of expression by inducers and downregulation by inhibitors. Our study aimed to examine the levels and molecular forms of MMP-7, tissue inhibitor of MMP (TIMP)-1, and extracellular matrix metalloproteinase inducer (EMMPRIN) in gingival crevicular fluid (GCF) from patients with different periodontal diseases. METHODS: A total of 80 subjects (20 patients with generalized aggressive periodontitis [GAgP], 20 with chronic periodontitis [CP], 20 with gingivitis, and 20 periodontally healthy subjects) were included in this study. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing, and plaque. GCF MMP-7, TIMP-1, and EMMPRIN levels and molecular forms were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western immunoblot techniques using specific antibodies. RESULTS: Total amounts of GCF MMP-7 were found to be similar between the study groups. GAgP, CP, and gingivitis groups had significantly higher total amounts of GCF EMMPRIN compared to healthy subjects (P <0.008). Among the patient groups, the GAgP group had the highest total amount of GCF EMMPRIN relative to the gingivitis group (P = 0.0004). Soluble EMMPRIN existed in GCF in multiple molecular-weight species especially in periodontitis-affected GCF under non-reducing conditions, i.e., 30-, 55-, 100-, 180-, and 200-kDa species. All patient groups had significantly elevated total amounts of GCF TIMP-1 relative to the healthy group (P <0.0001). GAgP and CP groups also had a higher total amount of GCF TIMP-1 compared to the gingivitis group (P <0.0001 and P <0.0001, respectively). The GAgP group had higher GCF TIMP-1 and EMMPRIN levels compared to the CP group, but this elevation did not reach statistical significance. CONCLUSIONS: Our data indicate that MMP-7 is associated with the innate host defense in periodontal tissues. Increased EMMPRIN and TIMP-1 levels in GCF are associated with the enhanced severity of periodontal inflammation, indicating that these molecules can participate in the regulation of progression of periodontal diseases. To our knowledge, the present study demonstrated the presence of soluble forms of EMMPRIN in GCF of patients with different periodontal diseases for the first time.

Adolescent↗
PubMed1989

[Phagocytosis, intracellular killing and interleukin 1 production of polymorphonuclear leukocytes in human periodontal diseases].

The role of the polymorphonuclear leukocyte (PMNL) as a primary protective cell in periodontal diseases has been well recognized. Functional abnormalities of PMNL chemotaxis have been implicated in the pathogenesis of some types of periodontitis. However, no consistent correlation with other PMNL functions has been reported. In the present study, phagocytosis and intracellular killing (oxidative product formation) of the PMNL from the patients with various forms of periodontal disease were evaluated by flow cytometry. Moreover, interleukin 1 (IL-1) production by the PMNL was determined by means of the enzyme-linked immunosorbent assay (ELISA) with monoclonal antibodies against rIL-1 alpha and rIL-1 beta. In order to examine these functions of peripheral (p-PMNL) and/or gingival crevicular PMNL (g-PMNL), 15 patients with localized juvenile periodontitis (LJP), 13 patients with generalized juvenile periodontitis (GJP) and 52 patients with adult periodontitis (AP) served as subjects. About 50% of the patients in LJP and GJP group exhibited depressed p-PMNL phagocytosis. While only a minimal number of the AP patients and no healthy subjects showed any reduction of p-PMNL phagocytosis. The reduction of phagocytosis was not related to the clinical periodontal status, and no detectable improvement of p-PMNL phagocytosis could be observed after periodontal therapy. In addition, it was suggested that complement receptors on the p-PMNL might be closely related with the reduction. Compared to p-PMNL, g-PMNL from the same individual have a lower phagocytic capacity in all subjects. However, no significant difference in g-PMNL phagocytosis could be demonstrated among three patient groups. Incremental oxidative responses in p-PMNL were observed in LJP, GJP and AP patients without any significant difference being found among these three groups. The increased rate of oxidative product formation was related to the clinical periodontal status, and it followed that periodontal therapy had significant effect on the improvement of this p-PMNL function. In IL-1 production assay of PMNL, a significant amount of IL-1, especially IL-1 beta, was observed in g-PMNL, but not in p-PMNL. The g-PMNL of the patients was found to produce greater amounts of IL-1 alpha and IL-1 beta than did the healthy controls. In addition, IL-1 production of p-PMNL was induced by the stimulation with some pathogenic bacteria including Bacteroides gingivalis. These results suggest that impaired PMNL phagocytosis may contribute to the early onset of periodontal deterioration in some young patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗
PubMed1989

[Study of cytokine production in inflamed human gingival tissues in periodontitis. Interleukin-1 (IL-1 alpha, beta) and tumor necrosis factor (TNF alpha)].

It seems to be generally agreed that periodontal disease is a local manifestation of a systemic immune response. Interleukin-1 (IL-1), which has multiple biologic activities, is detected in the gingival sulcus fluid of periodontitis sites. Recent investigations have revealed that IL-1 and tumor necrosis factor (TNF) are analogous to osteoclast activating factor and promote bone resorption. These findings have suggested the possibility that IL-1 and TNF may play a significant role in the initiation and development of periodontal disease. However, it remains to be determined whether these cytokines influence periodontal tissue breakdown in periodontitis. To elucidate the mechanisms of tissue breakdown in periodontitis, we examined cytokine production by human periodontitis gingival tissue. Twelve periodontitis patients were included in this study. Control subjects with healthy periodontium consisted of nine individuals. Gingival samples were biopsied from inflamed or healthy gingival tissues. Biopsy specimens were dissected into fragments 3 mm in diameter and plated onto 24 well culture plates with RPMI 1640 medium. IL-1 activity was measured by a growth inhibition assay using melanoma cell line A 375. An enzyme-linked immunosorbent assay (ELIZA) was used for measuring levels of human IL-1 alpha, IL-1 beta. TNF alpha activity was measured by a growth inhibition assay using cell line LM2D6. IL-1 activity was detected in significantly (p less than 0.001) higher levels in culture supernatants from gingival tissues in periodontitis (48.0 +/- 23.3 units/ml) than in control tissues (2.3 +/- 0.6 units/ml), however, levels of IL-1 activity were not associated with periodontal pocket depth or extent of alveolar bone resorption in periodontitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Resorption↗
PubMed1990

Periodontal disease and NIDDM in Pima Indians.

The goal of this study was to determine the prevalence and incidence of periodontal disease and its relationship with non-insulin-dependent diabetes mellitus (NIDDM). Two thousand two hundred seventy-three Pima Indians (949 men, 1324 women) aged greater than or equal to 15 yr from the Gila River Indian Community in Arizona were examined between 1983 and 1989. Periodontal disease was diagnosed by tooth loss and by percentage of interproximal crestal alveolar bone loss ascertained from panoramic radiography. Subjects with little or no evidence of periodontal disease were classified as nondiseased. Thus, the incidence of advanced periodontal disease was determined. The age- and sex-adjusted prevalence of periodontal disease at first dental examination was 60% in subjects with NIDDM and 36% in those without. Twenty-two new cases developed in a subset of 701 subjects (272 men, 429 women) aged 15-54 yr who initially had little or no evidence of periodontal disease and had at least one additional dental examination. The incidence of periodontal disease in this group was similar in men and women (incidence-rate ratio 1.0, 95% confidence interval [Cl] 0.5-1.9, controlled for age and diabetes). Higher age predicted a greater incidence of periodontal disease (chi 2 = 30.6, df = 3, P less than 0.001, controlled for sex and diabetes). The rate of periodontal disease in subjects with diabetes was 2.6 times (95% Cl 1.0-6.6, controlled for age and sex) that observed in those without. Although periodontal disease was common in nondiabetic Pima Indians, in whom most of the incident cases occurred, diabetes clearly conferred a substantially increased risk. Thus, periodontal disease should be considered a nonspecific complication of NIDDM.

Adolescent↗
PubMed2001

[Interleukin-6 levels in the gingival crevicular fluid before and after periodontal treatment].

OBJECTIVE: The aim of this study therefore is to determine if periodontal scaling and root planning could affect the IL-6 level in the GCF of teeth with periodontitis. METHODS: 12 teeth from 12 patients with severe periodontitis were clinically examined and sampled before therapy. 2 weeks after the periodontal scaling and root planning, the same 12 teeth were examined and sampled again. The IL-6 levels in GCF were detected using ELISA method. There are some evidences that the interleukin-6 (IL-6) levels in the periodontal tissue and gingival crevicular fluid (GCF) of periodontitis sites are significantly higher than that of healthy periodontal sites. RESULTS: The IL-6 levels in GCF from the teeth declined and the periodontal clinical indices of these teeth also apparently dropped down. CONCLUSION: Periodontal treatment, including periodontal scaling and root planning could affect the IL-6 levels in GCF of teeth with periodontitis.

Adult↗
PubMed2000

Negative effects of chronic inflammatory periodontal disease on diabetes mellitus.

Periodontal disease is the result of a complex interplay of bacterial infection and host responses, and is often modified by various systemic diseases such as diabetes mellitus. Such diseases are capable of affecting the periodontium and/or the treatment of periodontal disease. However, recent research has changed our concept of how periodontal disease should be treated. Here we present several concerns directed towards the periodontal therapy of patients with diabetes mellitus based on our studies. When treating periodontitis patients who have diabetes mellitus it is important to consider the type of diabetes. Patients with non-insulin dependent diabetes mellitus can be further classified according to the degree of insulin resistance, since recent epidemiological studies have suggested that successful anti-microbial therapy might result in improved insulin resistance in highly insulin resistant patients. Because the major contributing factor for insulin resistance is currently considered to be the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and because periodontal surgery may cause transient bacteremia which may up-regulate the serum TNF-alpha level, which in turn suppresses insulin action, patients should be strictly treated non-surgically and their serum TNF-alpha levels should be periodically monitored. On the other hand, diabetic patients positive for serum anti-glutamate decarboxylase auto-antibody should be examined for the source of this antibody, since 1) gingival and periodontal ligament fibroblasts were found to express glutamate decarboxylase, and 2) some otherwise healthy periodontitis patients develop anti-glutamate decarboxylase antibody. Thus, chronic periodontitis may influence the level of this antibody which is widely used as a predictive marker for slowly progressive insulin dependent diabetes mellitus. Not only is periodontal disease thereby affected by systemic diseases, but carefully managed periodontal therapy may also have a positive effect on the general health of patients with systemic diseases.

Anti-Bacterial Agents↗
PubMed2004

Herpesviruses, the missing link between gingivitis and periodontitis?

Herpesviruses appear to assume a major etiopathogenic role in various types of destructive periodontal disease. Human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) and HCMV-EBV co-infection are closely associated with disease-active periodontitis in juveniles and adults, with acute necrotizing ulcerative gingivitis in children, and with periodontal abscesses. In particular, HCMV reactivation in periodontitis lesions seems to be linked to advancing disease. HCMV infects periodontal monocytes/macrophages and T-lymphocytes, and EBV infects periodontal B-lymphocytes. Herpesvirus-infected inflammatory cells generate a great variety of pro-inflammatory cytokines and may possess diminished ability to defend against bacterial challenge. Herpesvirus-associated periodontal sites tend to harbor elevated levels of periodontopathic bacteria, including Dialister pneumosintes, Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Prevotella nigrescens, Treponema denticola, Campylobacter rectus and Actinobacillus actinomycetemcomitans. In summary, the available data suggest that periodontitis occurs more frequently and progresses more rapidly in herpesvirus-infected than in non-infected periodontal sites. An infectious disease model based on herpesvirus-bacteria-host immune response interactions is presented to explain how a gingivitis lesion or a stable periodontal site with increased probing depth may convert into a tissue-destroying periodontitis lesion.

Adolescent↗
PubMed2005

[Teeth electroexcitability in periodontitis].

Electroodontometric study of 756 intact teeth in 209 patients 18-65 years of age with normal periodontium and different stages of periodontal disease (periodontitis) showed that 96.8% of teeth in patients with mild periodontitis retained normal sensitivity, 68.4% -- with moderate periodontitis and 55% -- with severe periodontitis. Decreased pain threshold was detected in 3.2% of teeth of patients with mild periodontitis, 22.6% -- with moderate periodontitis and 12% -- with severe periodontitis. Increased pain threshold was not detected in teeth of patients with mild periodontitis, but in 9% with moderate periodontitis and in 29% with severe periodontitis it was obvious.

Adolescent↗
PubMed2005

[Periodontal diseases, tobacco and pregnancy].

This review summarizes the impact of tobacco on the periodontium of pregnant women and the effects of periodontal diseases combined with tobacco on the pregnancy. Periodontal diseases (gingivitis and periodontitis) are gram-negative anaerobic infections. Smokers are 2-7 times more likely to develop periodontal disease than non-smokers. Tobacco, an environmental factor, undermines the host response and may facilitate the development and progression of periodontal disease. Recent epidemiological studies suggest that maternal periodontal diseases would be a risk factor of pre-term deliveries or pre-term low birth weight (PLBW). Cigarette smoking during pregnancy leads to peri-natal morbidity and mortality and it is associated with reduced birth-weight. Tobacco during pregnancy also amplifies the risk of PLBW directly and via periodontal diseases. This article highlights the etio-pathogenic interrelations between periodontal diseases and tobacco as risk factors of PLBW. The blood dissemination of periodontal bacteria and the effects of cytokines like TNF-alpha, Il-1, produced during periodontal infections could explain these obstetrical adverse events. The concept of diagnosing and treating a periodontal disease in a pregnant woman to minimizes the deleterious effects of this infection on systemic conditions represents an unprecedented challenge. Moreover, periodontist have the opportunity to take part in smoking cessation program for pregnant women.

Female↗
PubMed2005

Secretory function of neutrophilic leukocytes of the patients with periodontal diseases.

Aim of study was to examine periodontal status among 20 44 year old patients and to study the secretory function of peripheral venous blood neutrophilic leukocytes (NL) exposed to various antigens and alkaline phosphatase (AP) activity in gingival crevicular fluid (GCF) in patients suffering from gingivitis and periodontitis. Clinically were determined Russell's periodontal index (PI). Secretory function of NL affected by opsonized zymosane, non-opsonized E. coli was examined in 77 patients with gingivitis and periodontitis, and in 35 donors, free of internal diseases, by means of beta-glucuronidase (beta-GD), lysozyme (LZ). NL secreted higher levels of beta-GD in incubation medium in patients with periodontitis (p < or = 0.001) subject to degree of periodontal lesion. NL affected by various antigens secreted higher levels of LZ into non-cellular matrix in patients with gingivitis and periodontitis comparing to control environment in analogous groups. Data obtained from this study suggest that in patients with periodontitis response of NL to bacterial stimuli is specific and subject to the degree of periodontal lesion. Our study showed a significant difference of AP activity in GCF subject to pocket depth and degree of periodontal lesion. Once NL are exposed to corpuscules prone to phagocytosis, an increase in secretion of beta-GD and LZ can be explained by overall increase in secretion of NL lysosomic enzymes, thus disclosing the mechanism of inflammatory periodontal tissue damage.

Adolescent↗