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PubMed2005

Association of T CD4 lymphocyte levels and chronic periodontitis in HIV-infected brazilian patients undergoing highly active anti-retroviral therapy: clinical results.

BACKGROUND: Controversial data regarding the association between immunosuppression and prevalence/ severity of periodontal diseases in HIV infection have been reported. Thus, the aim of this study was to test the hypothesis that lower T CD4 lymphocyte levels are not related to a higher prevalence of chronic periodontitis in HIV-infected Brazilians undergoing highly active anti-retroviral therapy (HAART). METHODS: Sixty-four HIV-infected patients under HAART were classified as having chronic periodontitis; i.e., > or = three sites with probing depth (PD) and/or clinical attachment level (CAL) > or = 5 mm or periodontal healthy (no sites with PD > 3 mm and/or CAL > 4 mm). All subjects received conventional periodontal therapy. Bleeding on probing, plaque accumulation, PD, and CAL were registered at six sites/tooth at baseline and 4 months after therapy. Epidemiological features and levels of T CD4 lymphocytes were obtained from medical records. Significance of differences in periodontal clinical parameters within and between groups were determined using Wilcoxon signed-rank and Mann-Whitney or independent sample t tests. Associations between T CD4 levels and clinical parameters were determined using the chi square test. RESULTS: Sixty-one percent of the HIV-infected patients represented AIDS cases, although 69% of them were periodontally healthy. The overall T CD4 lymphocyte mean levels was 333 +/- 254 cells/mm3 and viral load was 12,815 +/- 24,607 copies/mm3. Yet the prevalence of chronic periodontitis was relatively low (36%). In addition, patients with periodontitis presented a moderate disease (mean PD = 2.2 +/- 0.10; mean CAL = 2.6 +/- 0.13) and responded successfully to periodontal therapy. These subjects showed higher levels of T CD4 cells, but lower counts of neutrophils than periodontally healthy patients. Among periodontally healthy and chronic periodontitis patients, 41.7% and 22.9%, respectively, had low levels of T CD4 lymphocytes. No significant differences between periodontal status and epidemiological and immunological parameters were observed. CONCLUSION: Based on these results, the hypothesis that lower T CD4 lymphocyte levels are not associated with higher prevalence of chronic periodontitis in HIV-infected Brazilians under HAART cannot be rejected.

Adult↗
PubMed1980

Juvenile periodontitis. Some microbiological, histopathological and clinical characteristics.

The microflora of periodontal pockets and some histopathological characteristics of adjacent tissues from individuals with clinical signs of juvenile periodontitis were studied. Adult individuals with ordinary, rapidly advancing periodontitis served as controls. All of the patients had been referred for specialist treatment. Using criteria defined by Baer (19z1), the patients were assigned to one juvenile periodontitis (eight patients), one post-juvenile periodontitis (seven patients) and one adult periodontitis group (seven patients). Only lesions around the first molars and central incisors were studied. Bacterial samples were obtained from each site and were examined by darkfield microscopy and different morphological forms identified. The soft tissue of the diseased sites was excised. The biopsies were placed in a fixative, cut in 1-mm-thick blocks and embedded in Epon. In semithin sections the infiltrated connective tissue (ICT) was identified and the ICT portion further processed for electron microscopy. The numeric and volumetric densities of different cells and structures of the ICT were determined using a morphometric point-counting procedure. The results showed that juvenile periodontitis lesions are associated with a subgingival microflora, the composition of which is different from that of adult periodontitis. Thus, in patients belonging to the adult periodontitis and post-juvenile periodontitis groups, motile microorganisms dominated the subgingival plaque samples, whereas deep pockets in juvenile periodontitis lesions contained a flora dominated by coccoid cells and straight non-motile rods. The most pronounced difference in the composition of ICT between the juvenile on one hand and the post-juvenile and adult periodontitis lesions on the other, was related to the amount of extracellular structures. Thus, in post-juvenile and adult periodontitis lesions, collagen and residual tissue made up around 50% of the infiltrate. In the juvenile periodontitis lesions, however, extracellular structures occupied only around 20% of the volume. In the ICT of the juvenile periodontitis sites, around 70% of the volume was occupied by plasma cells and blast cells. The corresponding figures for the post-juvenile and adult periodontitis sites were 50 and 30%.

Adolescent↗
PubMed1991

Microbiological and immunological aspects of experimental periodontal disease in rats: a review article.

Animal models in which microbiological and immunological aspects of periodontal disease can be studied prospectively seem well warranted. The rat bears much resemblance to man with respect to periodontal anatomy, development and composition of dental plaque, histopathology of periodontal lesions, and basic immunobiology. Furthermore, reproducible methods are available for assessment of periodontal disease in rats, and detectable periodontal destruction can be induced in a few weeks in these animals without traumatizing periodontal tissues with ligatures. Experimental periodontitis studies in germ-free rats have confirmed the pathogenicity of several suspected periodontal pathogens (Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Capnocytophaga sputigena, Eikenella corrodens, and Fusobacterium nucleatum). The studies also suggest that the number of periodontal pathogens may be higher than generally believed, since species like Streptococcus sobrinus and Actinomyces viscosus are associated with periodontal bone loss in rats. Studies in rats with congenital or induced immune defects indicate that generalized or selective immunosuppression at the time of infection with periodontal pathogens may aggravate periodontal disease. Studies in immunized rats indicate that periodontal disease can be prevented by immunization against periodontal pathogens. However, it is also possible by immunization to induce periodontal destruction; i.e., the immune system has a destructive potential which should not be overlooked. In the future, the rat model may prove valuable for initial screening of antigen preparations and immunization regimens in the search for a periodontitis vaccine.

Animals↗
PubMed2000

Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutrition Examination Survey.

BACKGROUND: The principal objectives of this study were to examine the relationship between cigarette smoking and periodontitis and to estimate the proportion of periodontitis in the United States adult population that is attributable to cigarette smoking. METHODS: Data were derived from the Third National Health and Nutrition Examination Survey, a nationally representative multipurpose health survey conducted in 1988 to 1994. Participants were interviewed about tobacco use and examined by dentists trained to use standardized clinical criteria. Analysis was limited to dentate persons aged > or =18 years with complete clinical periodontal data and information on tobacco use and important covariates (n = 12,329). Data were weighted to provide U.S. national estimates, and analyses accounted for the complex sample design. We defined periodontitis as the presence of > or =1 site with clinical periodontal attachment level > or =4 mm apical to the cemento-enamel junction and probing depth > or =4 mm. Current cigarette smokers were those who had smoked > or =100 cigarettes over their lifetime and smoked at the time of the interview; former smokers had smoked > or =100 cigarettes but did not currently smoke; and never smokers had not smoked > or =100 cigarettes in their lifetime. RESULTS: We found that 27.9% (95% confidence interval [CI]: +/-1.8%) of dentate adults were current smokers and 23.3% (95% CI: +/-1.2%) were former smokers. Overall, 9.2% (95% CI: +/-1.4%) of dentate adults met our case definition for periodontitis, which projects to about 15 million cases of periodontitis among U.S. adults. Modeling with multiple logistic regression revealed that current smokers were about 4 times as likely as persons who had never smoked to have periodontitis (prevalence odds ratio [ORp] = 3.97; 95% CI, 3.20-4.93), after adjusting for age, gender, race/ethnicity, education, and income:poverty ratio. Former smokers were more likely than persons who had never smoked to have periodontitis (ORp = 1.68; 95% CI, 1.31-2.17). Among current smokers, there was a dose-response relationship between cigarettes smoked per day and the odds of periodontitis (P <0.000001), ranging from ORp = 2.79 (95% CI, 1.90-4.10) for < or =9 cigarettes per day to ORp = 5.88 (95% CI, 4.03-8.58) for > or =31 cigarettes per day. Among former smokers, the odds of periodontitis declined with the number of years since quitting, from ORp = 3.22 (95% CI, 2.18-4.76) for 0 to 2 years to ORp = 1.15 (95% CI, 0.83-1.60) for > or =11 years. Applying standard epidemiologic formulas for the attributable fraction for the population, we calculated that 41.9% of periodontitis cases (6.4 million cases) in the U.S. adult population were attributable to current cigarette smoking and 10.9% (1.7 million cases) to former smoking. Among current smokers, 74.8% of their periodontitis was attributable to smoking. CONCLUSIONS: Based on findings from this study and numerous other reports, we conclude that smoking is a major risk factor for periodontitis and may be responsible for more than half of periodontitis cases among adults in the United States. A large proportion of adult periodontitis may be preventable through prevention and cessation of cigarette smoking.

Adolescent↗
PubMed1999

[The effect of smoking on the spread and frequency of periodontal disease].

In recent years substantial data accumulated in the literature supporting the direct detrimental effect of tobacco smoking on periodontal health. The significantly inferior periodontal condition of smokers cannot be solely attributed to poor oral hygiene, increased calculus formation and altered subgingival microflora. Smoking imposes a direct threat to the periodontal tissues. Smokers with excellent oral hygiene show significantly less periodontal bone height and attachment level than matches non-smokers. Smoking entails a 2.5 to 3.5 risk ratio for severe periodontal attachment loss. Smoking also interferes with the outcome of nonsurgical and surgical periodontal treatment and impairs periodontal regeneration. The pathomechanism of the tobacco smoking related periodontal destruction is just partly understood. Tobacco products can alter normal host responses to neutralize infections and can also stimulate pathologic mechanisms to destroy the surrounding tissues. Tobacco products can directly impair polymorphonuclear leukocyte functions. Smokers have less salivary IgA and decreased serum IgG concentration as well as depressed number of helper T lymphocytes. Consequently smoking today is considered as one of the major risk factors for destructive periodontitis. Periodontitis is also considered as a decisive risk factor for systemic diseases especially for cardiovascular disorders. A strong association has been shown between periodontal disease and coronary heart diseases, as well as between periodontal disease and cerebrovascular diseases (stroke). The subgingival microflora and the continuous latent bacteremia and endotoxemia originated from the periodontal pockets might be responsible for the damage of the vascular endothelial integrity, platelet functions and blood coagulation. Modern periodontal epidemiology rediscovered the old ide of "focal infections" and indicated that the general health has a crucial impact on the periodontal health and periodontal disease has also a major impact on the general health status of the patient.

Coronary Disease↗
PubMed1985

Microbiological and clinical effects of surgical treatment of localized juvenile periodontitis.

Since Actinobacillus actinomycetemcomitans appears to be a key etiologic agent in localized juvenile periodontitis, this study determined the effectiveness of different treatment modalities in suppressing A. actinomycetemcomitans in localized juvenile periodontitis lesions. A total of 25 deep periodontal lesions from 7 patients with localized juvenile periodontitis were included in the study. The test periodontal lesions either received scaling and root planing alone, scaling and root planing together with soft tissue curettage, or modified Widman flap surgery. Subgingival A. actinomycetemcomitans were enumerated using selective culturing. Clinical measurements included changes in probing periodontal attachment level, probing periodontal pocket depth, gingival index, plaque index, and digital subtraction of standardized serial radiographs. The microbiological and clinical effects of treatment were monitored over a period of 16 weeks. All periodontal lesions studied demonstrated high numbers of A. actinomycetemcomitans prior to treatment. Scaling and root planing alone did not markedly change the subgingival A. actinomycetemcomitans counts, nor any of the clinical parameters studied. In contrast, soft tissue curettage as well as modified Widman flap surgery suppressed A. actinomycetemcomitans to undetectable levels immediately after therapy in more than 80% of the lesions studied. A total of 5 periodontal lesions exhibited gain of probing periodontal attachment after subgingival curettage or Widman flap treatment; 3 of these sites revealed no detectable A. actinomycetemcomitans, and the remaining 2 sites harbored only low levels of A. actinomycetemcomitans. 5 periodontal lesions which lost probing attachment after treatment all demonstrated high numbers of subgingival A. actinomycetemcomitans. Changes in alveolar bone, assessed by digital subtraction of serial radiographs, correlated with changes in probing periodontal attachment level, confirming the clinical results. The present study revealed a close relationship between post-treatment A. actinomycetemcomitans levels and the clinical response to treatment, which supports the concept that A. actinomycetemcomitans is an important organism in the etiology of localized juvenile periodontitis. This study also showed that a substantial suppression of subgingival A. actinomycetemcomitans cannot be achieved by periodontal scaling and root planing alone, but can be accomplished by surgical removal of periodontal tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus↗
PubMed1998

Changes in the prevalence of residual pockets and tooth loss in treated periodontal patients during a supportive maintenance care program.

Bleeding on probing and the presence of deep periodontal pockets are considered to be the best site-specific indicators for periodontal disease progression during the maintenance phase of periodontal therapy. A major emphasis of supportive periodontal care (SPC) programs, therefore, has been the control of bleeding pockets. This investigation retrospectively evaluated the changes in the prevalence of bleeding on probing, periodontal pockets, bleeding periodontal pockets and the prevalence of tooth loss in a random sample of 273 periodontal patients participating in a supportive maintenance care program at a University Clinic. During an observation period of 67+/-46 months (range 5 months to 23 years), the overall incidence of all causes of tooth mortality was 0.23+/-0.49 teeth per patient per year of observation. 56% of subjects, however, did not experience any tooth loss, while less than 10% of patients lost more than 3 teeth. Thus, participation in the SPC program was effective in preventing tooth loss in the majority of patients. During the SPC period, however, a significant increase in the prevalence of periodontal pockets, and of bleeding on probing positive periodontal pockets, in particular, was observed. At completion of active periodontal therapy, 56.4% of patients were free from bleeding pockets. This decreased to a mere 13.6% at the latest SPC evaluation. The observed increases in the number of bleeding pockets was significantly associated with: longer times since completion of active periodontal therapy, more advanced periodontal diagnosis, higher %s of bleeding sites in the dentition, cigarette smoking, lack of inclusion of periodontal surgery in the active treatment phase, tooth loss, and the response to the active phase of periodontal treatment. The data presented in the paper indicate that the observed increase in the prevalence of bleeding pockets and tooth loss was not homogeneously distributed in the studied SPC population. Rather, high risk groups of individuals could be identified. It is suggested that better knowledge of risk indicators may lead to improved and more efficient risk management efforts during periodontal maintenance care.

Adolescent↗
PubMed2003

Healing in transplanted teeth with periodontal ligament cultured in vitro.

Regeneration of connective tissue attachment is the ultimate goal of periodontal therapy. It has been suggested that periodontal ligament cells possess the potential to create new connective tissue attachment. However, as cells from gingiva and alveolar bone occupy the root surface during initial wound healing, population by periodontal ligament cells is limited in vivo. We have been developing a new periodontal regeneration technique using in vitro tissue culture of periodontal ligament remaining on a periodontally involved root. The purpose of this study was to examine the periodontal healing after transplantation of teeth with reduced periodontal ligament that had been cultured in vitro. Twenty-five incisors from four beagles were used. After the teeth were extracted, the periodontal ligament and cementum were removed from coronal part of the roots and the roots were planed. The periodontal ligament of the apical part was retained. Fourteen teeth of the experimental group were transplanted following culture for 6 weeks. Eleven teeth of the control group were similarly prepared and immediately transplanted without tissue culture. Four weeks after transplantation, the specimens were prepared for histological analysis. Downgrowth of junctional epithelium on the root of experimental group was significantly less than control. Most of the root planed surfaces of experimental group were covered with periodontal ligament fibers oriented parallel or inclined to the root surfaces and limited new cementum formation was observed near the apical end of the planed root. There was no significant difference between groups in observations on the root surface with remaining periodontal ligament. From the above results, it was concluded that periodontal tissue culture of teeth with root planed surface and remaining periodontal ligament could reduce the extent of epithelium downgrowth and increase connective tissue adhesion on the root planed surface, as well as minimize damage to remaining periodontal ligament, after transplantation of teeth.

Animals↗
PubMed1994

Clinical implications of cellular biologic advances in periodontal regeneration.

It is known that periodontal tissues retain the ability to regenerate; however, current therapies fail in achieving predictable and consistent regeneration. Cell and molecular biology research in periodontal regeneration hold great promise in providing improved understanding of this complex phenomenon and direct us towards new possibilities of future clinical application. This paper reviews both the cells and extracellular matrix of the periodontal ligament in addition to the cell-to-matrix and cell-to-cell interaction involved in periodontal regeneration. Results of recent studies have suggested that periodontal regeneration recapitulates the process of morphogenesis, histogenesis, and cytodifferentiation, as well as cell field migration that occurs during development of the periodontium. A small population of purported periodontal stem cells is believed to be responsible for maintaining homeostasis in the periodontal ligament. This cell, which may have its origin in late periodontal mesenchyme of the dental papilla, is advocated as a tripotential cell capable of differentiating into cementoblast, osteoblast, and periodontal fibroblast. The clinical implication of advances made in cell and molecular biology research in periodontal regeneration may include future use of biomolecules in periodontal regeneration may include future use of biomolecules to improve the regenerative healing process and use of bioactive degradable membrane barriers in guided tissue regeneration as well as seeding of periodontal stem cells into periodontal defects. If the current trend continues, clinicians can look forward to seeing periodontal wound healing being substantially enhanced to achieve predictable periodontal regeneration.

Cell Communication↗
PubMed1998

Changing concepts. The effects of occlusion on periodontitis.

Despite volumes of publications on the theory of occlusion, occlusal design, and equilibration techniques, there have been few well-designed human studies directed at answering the question does occlusal trauma modify the progression of attachment loss in periodontitis. The articles reviewed indicate that occlusal forces can cause changes in the alveolar bone and periodontal connective tissue both in the presence and in the absence of periodontitis. These changes can affect tooth mobility and clinical probing depth. Although occlusal forces do not initiate periodontitis, results are inconclusive as to if or how these forces affect attachment loss owing to plaque-induced inflammatory periodontal disease. Although some studies reported a relationship between increased attachment loss and tooth mobility, others found no relationship between attachment loss and abnormal occlusal contacts. Tooth mobility results from a variety of factors, including alveolar bone loss, attachment loss, disruption of the periodontal tissues by inflammation, widening of the PDL in response to occlusal forces (physiologic adaptation), PDL atrophy from disuse, and other processes that effect the periodontium. Therefore, any relationship found between tooth mobility and progressing periodontitis does not necessarily implicate or defend occlusion as a cofactor in the progression of inflammatory periodontal disease. Periodontitis can be treated and periodontal health maintained without occlusal adjustment and in the presence of traumatic occlusal forces. Statistically greater gains in clinical periodontal attachment level have been reported, however, when occlusal adjustment was included as a component of periodontal therapy. The extent to which this is clinically meaningful is unclear. Once periodontal health is established, occlusal therapy can be used to reduce mobility, to regain bone lost owing to traumatic occlusal forces, and to treat a variety of clinical problems related to occlusal instability and restorative needs. The clinician's decision whether or not to use occlusal adjustment as a component of periodontal therapy should be related to an evaluation of clinical factors involving the patient's comfort and function and not based on the assumption that occlusal adjustment is necessary to stop the progression of periodontitis.

Adaptation, Physiological↗
PubMed1993

Identification and characterization of afferent periodontal A delta fibres in the cat.

1. The presence and responsiveness of afferent periodontal A delta fibres was studied in pentobarbitone-anaesthetized adult cats. 2. Extracellular single fibre recordings were made from fine nerve filaments split from the proximally cut end of the inferior alveolar nerve. Periodontal nerve fibres were identified by constant current stimulus pulses applied via platinum wire electrodes inserted into the periodontal space of the lower canine tooth. 3. Of a total of 252 periodontal nerve fibres, 97 (37%) were classified as A delta fibres according to their conduction velocities (CV) (> 2.5 m s-1, < 30 m s-1) as determined by electrical stimulation of the periodontal ligament. The mean (+/- S.D.) conduction velocity was 11.0 +/- 7.7 m s-1 (n = 97; range: 2.6-28.2 m s-1). 4. A good exponential correlation (r = 0.85) was found between the electrical thresholds of the A delta fibres and their conduction velocities. 5. For four A delta fibres a complete stimulus-duration curve was determined. It followed rather well the I = I0/(1-et/tau) law, where I represents the stimulus amplitude, t the stimulus duration, I0 the rheobasic current and tau the time constant. 6. In the intact tooth none of the identified periodontal A delta fibres showed any ongoing activity in the absence of intentional stimulation. 7. The responses of sixteen electrically identified periodontal A delta fibres were tested by mechanical, thermal and chemical stimuli applied to the periodontal space. Seven of nine periodontal A delta fibres tested responded to mechanical forces applied to the tooth from different directions of which none could be activated by slight touch. A rudimentary directional sensitivity was seen. When a human tooth was stimulated by a mechanical stimulus of similar strength the sensation evoked was described as a dull, poorly localized pain. 8. Six periodontal A delta fibres were activated by heat and/or cold and/or chemical stimulation. Two of eight periodontal A delta fibres tested responded to heat and four of six A delta fibres tested responded to cold stimuli applied to the alveolar bone overlying the periodontal ligament; none of them responded to both types of thermal stimuli. Two of seven periodontal A delta fibres tested were activated by a saturated solution of potassium chloride applied locally to the periodontal ligament; two of these responded also to cold. 9. The response behaviour of periodontal afferent A delta fibres observed in this study suggests that they may play a role in periodontal nociception.

Afferent Pathways↗
PubMed2002

Effects of smoking on periodontal tissues.

BACKGROUND/AIMS: Most studies about the association between tobacco and periodontal disease have shown that tobacco negatively affects periodontal tissues, although some authors have failed to demonstrate such association. Very few studies have tried to find out whether the effect of tobacco on periodontal tissues was similar for women and men. The aims of this investigation were to confirm the possible relationship between tobacco consumption and periodontitis, to study the correlation between intensity of smoking and disease severity, and to investigate any differences between genders related to the effects of tobacco consumption in periodontal health. MATERIAL AND METHODS: In this case-control study, 240 dental patients were selected according to previously defined criteria and were divided in two groups according to their periodontal status. Patients with established periodontitis constituted the case group. The remaining patients constituted the control group. Smoking status, probing depth, gingival recession, clinical attachment level, tooth mobility, periodontal bleeding index and plaque index were determined for each participant. Generated data were processed for statistical analysis using multiple comparisons, covariance analysis and logistic regression analysis. RESULTS: Logistic regression analysis showed that smokers had 2.7 times and former smokers 2.3 times greater probabilities to have established periodontal disease than non-smokers, independent of age, sex and plaque index. Among cases, probing depth, gingival recession and clinical attachment level were greater in smokers than in former smokers or non-smokers, whereas plaque index did not show differences. Bleeding on probing was less evident in smokers than in non-smokers. There was a dose-effect relationship between cigarette consumption and the probability of having advanced periodontal disease. The association between tobacco smoking and periodontal disease was more evident after 10 years of smoking, independent of age, gender and plaque index. Finally, it was observed that tobacco affected periodontal tissues more severely in men than in women. CONCLUSIONS: Smoking is a risk factor strongly associated with periodontitis. The effects of smoking on periodontal tissues depend on the number of cigarettes smoked daily and the duration of the habit. The effect of tobacco on periodontal tissues seems to be more pronounced in men than in women.

Adult↗
PubMed1997

CD29 expression on CD4+ gingival lymphocytes supports migration of activated memory T lymphocytes to diseased periodontal tissue.

The cell surface phenotypes of CD+ cells extracted from inflammatory periodontal disease tissues were analyzed using two- and three-color immunofluorescence and flow cytometry. Cells extracted from both adult periodontal and localized juvenile periodontitis lesions showed a depressed CD4/CD8 ratio (1.0 +/- 0.1 adult periodontitis and 1.1 +/- 0.1 localized juvenile periodontitis) compared with cells recovered from normal/marginal gingivitis tissue (1.8 +/- 0.2) or with normal peripheral blood cells (2.1 +/- 0.1) or periodontal disease blood cells (2.1 +/- 0.1 and 1.7 +/- 0.1 for adult periodontitis and juvenile periodontitis, respectively). The monoclonal antibodies anti-2H4 and anti-4B4 were used to identify the CD45RA and CD29 antigens respectively on CD4+ T cells from the periodontal disease lesions. In peripheral blood. CD29+ cells accounted for 66-77% of the CD4+ population, and CD45RA+ cells accounted for 22-27% of the CD4+ subset. No differences in expression were found between peripheral blood lymphocytes from normal subjects and from periodontal disease patients. Two-color analyses of lymphocytes from periodontal diseased tissues showed that 87-89% of the CD4+ population were CD29+ and that 70-79% of the CD4+ cells were CD45RA+. Normal tissues contained significantly fewer CD4+CD29+ cells (56 +/- 4%) and CD4+CD45RA+ cells (40 +/- 4%) on average, and few, if any double-labelled cells could be accounted for. These data implied that a significant percentage of the CD4+ cells from the diseased tissues were both CD29+ and CD45RA+ and that these populations are found in quite different proportions in diseased periodontal tissue than in peripheral blood or nondiseased tissue. In further analyses using three-color cytometry the mean percentage of CD4+ CD29+ CD45RA+ lymphocytes extracted from periodontal disease lesions was 43 +/- 9% of the CD4+ population. These results suggest that CD4+ T lymphocytes in periodontal disease not only demonstrate varying levels of maturity but also that the accumulation of CD4+ T cells within the periodontal tissues may be a result of increased adhesion and transendothelial migration.

Adult↗
PubMed1996

Efficacy of CPITN sextant scores for detection of periodontitis disease activity.

The relationship between CPITN sextant scores and periodontitis recurrence at individual tooth sites was evaluated in a longitudinal study in 83 treated adult periodontitis patients receiving systematic 3-month maintenance care. At baseline and semi-annual examinations over 36 months, CPITN scores were assigned to each dentition sextant using probing depths and gingival index scores, and relative periodontal attachment level was assessed at individual tooth sites using an occlusal reference stent. Periodontitis recurrence was defined as any periodontal site exhibiting either a probing depth increase of > or = 3 mm from baseline, or a probing depth increase of > or = 1 mm from baseline together with a loss of relative periodontal attachment of > or = 2 mm from baseline. 49 (59.0%) subjects developed periodontitis recurrence in 147 (29.8%) sextants at 181 (2.2%) individual periodontal sites during the 36-month study period. Baseline CPITN scores of 4 were more common in disease-active subjects than clinically-stable subjects (p = 0.003, t-test), and were associated with a statistically significant 1.66 relative risk of periodontitis recurrence within 36 months. CPITN sextant scores of 3 or 4 showed low specificity and low positive predictive values as indicators of periodontitis recurrence at > or = 1 individual sites within the affected sextant. In comparison, low CPITN sextant scores (0-2) provided high specificity (96.2-100%), high positive predictive values (99.5-100%), and a summary odds ratio of 24.2 as an indicator of clinical stability at all periodontal sites within a given dentition sextant. Changes in sextant scores for CPITN over 6-month periods showed no relationship with periodontitis recurrence at individual periodontal sites. This study suggests that while CPITN is inadequate for detection of periodontitis recurrence, low CPITN scores provide rapid presumptive identification of clinically-stable sextants in adult periodontitis patients on maintenance care.

Adult↗
PubMed2003

Periodontal regeneration with a combination of enamel matrix proteins and autogenous bone grafting.

BACKGROUND: Attempts to stimulate periodontal regeneration in the past have focused on either filling the defect with some type of material or providing a space for host cells to repopulate the site and elicit new tissue. In some cases, these approaches have been combined with the assumption that the filler material will help maintain the space necessary for the host cells to invade the area. Growth stimulating substances such as growth factors and other proteins have also been used to encourage periodontal tissue regeneration and histological evaluation supports the use of these substances. Thus, the role for and the necessity of a certain amount of space maintenance for periodontal regeneration is not exactly understood. In addition, it is not known if there is some critical size required for space maintenance or for exactly how long the space must be maintained in order for the host cells to stimulate new cementum, periodontal ligament, and bone. The goal of this study was to evaluate periodontal regeneration in intrabony defects of various sizes treated with a combination of enamel matrix proteins and autogenous bone graft. METHODS: Periodontal defects ranging in size from 1 to 6 mm were randomized and created bilaterally beside three teeth in the mandibles of baboons. Plaque was allowed to accumulate around wire ligatures placed into the defects. After 2 months, the wire ligatures were removed, the teeth and roots scaled and root planed, and a notch was placed with a chisel at the base of the defect. On one side of the mandible, neutral ethylene diamine tetracetic acid and enamel matrix derivative (EMD) were first used to treat the defect. Autogenous bone taken from the same surgical site was treated with enamel matrix derivative in a dampen dish and then added to the EMD-treated defects. The other side of the mandible served as control with neutral ethylene diamine tetracetic acid and scaling and root planing. Flaps were sutured and the animals were allowed to heal without oral hygiene procedures. After 5 months, the animals were sacrificed and the teeth were processed for histological evaluation. RESULTS: The results revealed new cementum, periodontal ligament with Sharpey's fibers, and new bone tissue similar to native periodontal tissues. Remnants of the autogenous bone chips were still present at this 5-month post-healing period. Thus periodontal regeneration occurred in all sizes of the periodontal defects. In general, EMD plus autogenous graft treatment resulted in greater tissue formation than controls. In fact, in many cases, very dramatic tissue formation occurred far coronal to the base of the defects in the EMD plus autogenous graft-treated lesions. In addition, horizontal bone fill occurred in the defects and was prominent in the 4 or 6 mm wide lesions. When evaluating the combined 1 and 2 mm defects, the height of new cementum with EMD plus graft was 3.88 mm versus 2.03 mm in the controls, a statistically significant (P < 0.005) difference. In the wider (4 and 6 mm) lesions, this difference was not significant and was much less between treated and control lesions with 2.78 and 2.57 mm of new cementum respectively. In the case of new bone height, in the smaller lesions EMD plus graft resulted in 4.00 mm new bone versus 2.22 mm in the controls, again a statistically significant (P < 0.005) difference. In the larger lesions, EMD plus autogenous bone graft had 3.24 mm new bone height compared to 2.71 mm in the controls, a difference that was not statistically significant. Additionally, in the smaller lesions, new cementum width at the level of the notch was twice as great (statistically significant, P < 0.015) in the EMD plus graft sites compared to control. The width of the periodontal ligament at the coronal aspect of the new bone tissue was similar in the smaller lesions between treated and control sites. The results from the wider defects must be interpreted cautiously as the interproximal bone heights were remodeled adjacent to the wider defects and likely limited the potential for regeneration. CONCLUSIONS: The combination of enamel matrix derivative plus autogenous bone graft stimulated statistically significant periodontal regeneration in the more narrow 1 and 2 mm lesions. No statistically significant difference was observed in the wider 4 and 6 mm lesions. In many cases, dramatic amounts of new cementum, Sharpey's fibers, periodontal ligament, and bone tissue were formed far above the notch placed at the base of the contaminated defects. This was especially significant considering the width of some of the defects and the fact that no oral hygiene was performed over the 5-month healing period. This periodontal regeneration occurred in the absence of exogenous growth factors or barrier membranes. In summary, the combination of enamel matrix derivative and autogenous bone represents a therapeutic combination that can be highly effective in stimulating significant amounts of periodontal regeneration.

Alveolar Bone Loss↗
PubMed2000

Actinobacillus actinomycetemcomitans in destructive periodontal disease. Three-year follow-up results.

BACKGROUND: Convincing data exist that A. actinomycetemcomitans is an etiologic agent of periodontal disease. The purpose of this longitudinal study was to evaluate A. actinomycetemcomitans as a diagnostic indicator for periodontal disease in treated and periodontally maintained patients. METHODS: Following comprehensive mechanical/surgical and supportive amoxicillin plus metronidazole therapy in 13 subjects with A. actinomycetemcomitans-associated destructive periodontal disease, we monitored subgingival A. actinomycetemcomitans at 4 individual sites in each patient up to 3 years post-therapy. The periodontal status was determined, and A. actinomycetemcomitans levels were quantitatively enumerated on TSBV agar in CFU/ml. Six patients with a persistence of subgingival A. actinomycetemcomitans at each reexamination within 3 years post-therapy were selected to be at risk for minor periodontal treatment outcomes and further recurrence of periodontal disease (test group). Seven subjects with a complete suppression of A. actinomycetemcomitans at each post-therapy visit served as controls. RESULTS: The periodontal parameters decreased from overall values of 6.39 mm (probing depth, PD) and 7.64 mm (clinical attachment level, CAL) at the outset to 3.81 mm (PD) and 5.62 mm (CAL) 2 years post-therapy (Friedman, P< or =0.05). At the 3-year reexamination, the PD/CAL scores increased to 4.03/5.78 mm. Among the 6 individuals (46%) with persistence of subgingival A. actinomycetemcomitans at the final 3-year visit (test group), periodontal status yielded increased levels of 4.45 mm (PD) and 6.60 mm (CAL). The control subjects (n = 7) revealed lower values of 3.67 mm (PD) and 5.09 mm (CAL). However, on a patient level, during the 3-year observational trial, the periodontal status of the 13 individuals was not statistically affected by subgingival infection with A. actinomycetemcomitans. CONCLUSIONS: Although in advanced periodontal disease, comprehensive mechanical and antimicrobial treatment is an appropriate regimen for sustained improvement of periodontal health, long-term control of subgingival infection with A. actinomycetemcomitans could not be achieved. In the maintenance care of destructive periodontitis, the persistence of A. actinomycetemcomitans is not a diagnostic parameter for periodontal disease.

Actinobacillus Infections↗
PubMed2005

Periodontitis lesions are a source of salivary cytomegalovirus and Epstein-Barr virus.

AIM: Several herpesvirus species can be detected in periodontal pockets and saliva. This study compared human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) DNA copy counts in periodontitis sites and in whole saliva, and evaluated the potential of periodontal therapy to reduce the salivary level of the two viruses. MATERIAL AND METHODS: A total of 20 systemically healthy periodontitis patients, 21-56 years of age, participated in the study. All 20 patients were examined at baseline, and seven patients also at 3 months after periodontal therapy. Treatment included oral hygiene instruction, scaling and root planing, and surgery. Clinical parameters were evaluated using established methods. In each patient, virological samples were collected from one periodontal pocket of 6-10 mm probing depth, from the adjacent inflamed periodontal pocket wall, and from unstimulated whole saliva. Relationships between subgingival, gingival tissue and salivary herpesvirus counts were evaluated using Spearman's and Kendall's rank correlation coefficient tests. The 5'-nuclease (TaqMan) real-time polymerase chain reaction (PCR) assay was employed to quantify genomic copies of periodontal HCMV and EBV. RESULTS: At baseline, the 20 periodontitis patients showed significant positive correlations between gingival tissue and salivary counts of HCMV DNA (p=0.003) and EBV DNA (p=0.045). Periodontal pocket depth was positively correlated with salivary EBV DNA counts (p=0.002). Periodontal therapy reduced average full-mouth periodontal pocket depth from 4.6 mm to 1.4 mm, plaque index from 2.1 to 0.9, and gingival index from 2.1 to 0.4. Following treatment, HCMV DNA counts decreased 37.5 fold in subgingival sites and 64.6 fold in saliva, and EBV DNA counts decreased 5.7 fold in subgingival sites and 12.9 fold in saliva. CONCLUSIONS: The present study provides compelling evidence of a periodontitis source for salivary HCMV and EBV. The potential of periodontal therapy to decrease herpesvirus salivary counts may help diminish herpesvirus transmission from person to person and herpesvirus-related diseases in exposed individuals. Further research is warranted to determine the relationship between periodontal herpesvirus counts and the risk of viral transmission to close acquaintances.

Adult↗
PubMed2005

Differential effects of estrogen on DNA synthesis in human periodontal ligament and breast cancer cells.

BACKGROUND: It is important to clarify the biological function of the female sex hormones estrogen and progesterone in periodontal ligament cells, as these hormones may affect periodontal health. We have previously shown that human periodontal ligament cells express estrogen receptor beta (ERbeta) but not ERalpha, whereas human breast cancer cells (MCF7) express both ERalpha and ERbeta. Data on progesterone receptor (PgR) expression in human periodontal ligament cells have not been reported. OBJECTIVES: Determine PgR expression in human periodontal ligament and MCF7 cells and to investigate how estrogen affects DNA and collagen synthesis in these two cell types showing different pattern of expression for ERalpha and beta. METHODS: Periodontal ligament cells were obtained from the periodontal ligament of premolars extracted for orthodontic reasons and MCF7 cells from the American Type Culture Collection (ATCC). PgR expression was determined by immunocytochemistry. DNA and collagen synthesis was determined by [(3)H]thymidine and L-[(3)H]proline incorporation, respectively. RESULTS: PgR immunoreactivity was observed in nuclei of MCF7 but not periodontal ligament cells. Treatment with estrogen (17beta-estradiol, E(2)) at physiological concentrations for 24 h stimulated DNA synthesis by more than two times in MCF7 cells, whereas there was no effect on periodontal ligament cell DNA synthesis. The ER blocker ICI 182780 fully reversed the stimulatory effect of E(2). Not only short-term (24 h) but also long-term (5 days) treatment with E(2) lacked effect on DNA synthesis in periodontal ligament cells. Neither periodontal ligament cell viability nor collagen synthesis was affected by E(2) treatment. Identical results were observed in periodontal ligament cells from male and female subjects. CONCLUSIONS: Human MCF7 but not periodontal ligament cells express PgR, suggesting that progesterone via PgR affects MCF7 but not periodontal ligament cells. Further, estrogen stimulates breast cancer MCF7 cell proliferation, whereas it has no effect on proliferation of periodontal ligament cells, probably reflecting cell type specific ER expression pattern in these two cell types.

Adolescent↗