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The influence of diet consistence, drinking water and bedding on periodontal disease in Sprague-Dawley rats.

BACKGROUND: Although rats have been extensively used in periodontal research, pre-experimental periodontal inspection has not been given high priority in previous studies of experimental periodontal disease in rats. An inspection of 50 Sprague-Dawley rats, which were to be used in a model of experimental periodontal disease, revealed signs of periodontal disease in a considerable proportion of the animals. OBJECTIVES: The objectives of the present study were to describe disease progression, identify factors responsible for induction of periodontal disease and test a method for breeding of healthy rats. METHODS AND RESULTS: A longitudinal study revealed that 33% of rats, bred under the same conditions, showed signs of periodontal disease during, or shortly after, eruption of the molars. Regular diet caused significantly more horizontal bone loss (P = 0.0001) and significantly less periodontal bone support (P < 0.0001) than the same kind of diet with a smaller grain size. Wood chip bedding in the rats' cages significantly reduced periodontal bone support (P < 0.0001) compared to a wire mesh floor and a simultaneous use of regular diet and bedding decreased it even further (P = 0.0023). Finally, by using finely milled diet, a wire mesh floor and tap water, instead of conventional breeding methods of regular diet, bedding and acidic water, it was possible to breed rats with minimal signs of periodontal disease. CONCLUSIONS: The results of the present study emphasize the need for pre- experimental examination of rats. They also show that diet and bedding conditions have the potential of seriously influencing outcomes of studies of periodontal disease in rats.

Alveolar Bone Loss↗

Effect of triclosan on healing following non-surgical periodontal therapy in smokers.

BACKGROUND: Tobacco smoking is an established risk factor for periodontitis, and is associated with periodontal attachment and tooth loss. Clinical studies have indicated that smoking may adversely affect and impede healing following periodontal therapy. Adjunctive antimicrobials, on the other hand, have been shown to enhance the effect of non-surgical periodontal therapy. The objective of this study was to evaluate the effect of a triclosan/copolymer/fluoride dentifrice on healing following non-surgical periodontal therapy in smokers. METHODS: Sixty smokers (aged 35-59 years; 23 females) with chronic periodontal disease volunteered to participate in a double-blind, randomized, controlled, clinical trial. The subjects were randomly assigned to use a triclosan/copolymer/fluoride (30 subjects) or a standard fluoride (30 subjects) dentifrice and received detailed information on proper techniques for self-performed plaque control. The participants then received non-surgical periodontal therapy followed by periodontal maintenance care every 6 months over 24 months. Clinical recordings included evaluation of oral hygiene standards, gingival health, and periodontal status. RESULTS: Subjects using the triclosan/copolymer/fluoride dentifrice exhibited significantly improved oral hygiene conditions, gingival health, and periodontal status compared with those using the standard fluoride dentifrice over the 24-month maintenance interval. CONCLUSIONS: The results suggest that an oral hygiene regimen including a triclosan/copolymer/fluoride dentifrice may sustain the short-term effect of non-surgical periodontal therapy in smokers.

Adult↗

The outcome of a preventive dental care programme on the prevalence of localized aggressive periodontitis in Down's syndrome individuals.

BACKGROUND: Periodontal disease in Down's syndrome (DS) individuals develops earlier and is more rapid and extensive than in age-matched normal individuals. The present study evaluated a group of DS patients, who had been participating in a 10-year preventive dental programme, for the impact of the programme on their periodontal status. METHODS: Thirty DS patients (mean age 23.3 +/- 4 years) were compared with 28 age-matched healthy controls (mean age 22.8 +/- 5 years). The hygiene level, gingival condition and periodontal status (periodontal probing depth, clinical attachment level and radiographic alveolar bone loss) were determined. RESULTS: In spite of similar oral hygiene and gingival measures, DS patients, as opposed to the control ones, had a severe periodontal disease. The prevalence, extent and severity of periodontitis in the DS group were significantly greater than in the control group. The teeth most commonly and severely affected were the lower central incisors and the upper first molars. DS patients lost significantly more teeth due to periodontitis. CONCLUSIONS: The clinical and radiographic picture found in the present DS group is characteristic of localized aggressive periodontitis. Within the limitations of this study, it seems that the preventive dental programme had no effect on periodontal destruction progression of localized aggressive periodontitis in DS individuals and that impaired oral hygiene plays a relatively minor role in the pathogenesis of this disease. Future controlled studies are needed to assess the effectiveness of different preventive dental programmes in preventing the progression of periodontitis in DS patients.

Adolescent↗

Tetracycline inhibition identifies the cellular origin of interstitial collagenases in human periodontal diseases in vivo.

Mammalian interstitial collagenases (E.C.3.4.24.7) are considered as key initiators of collagen degradation in periodontal diseases. However, the cellular sources of collagenases present in gingival crevicular fluid have not been completely clarified. Resident fibroblasts and epithelial cells as well as infiltrating neutrophils and monocyte/macrophages are potential sources of the enzymes. We have recently found significant differences in tetracycline inhibition between human neutrophil and fibroblast interstitial collagenases. To address the cellular source of collagenase present in gingival crevicular fluid in 2 distinct periodontal diseases, we studied the tetracycline inhibition of collagenase in gingival crevicular fluid of patients with localized juvenile periodontitis and adult periodontitis. Gingival crevicular fluid samples were collected from deep (greater than 5 mm) periodontal pockets and assayed for collagenase in the presence of 0-1000 microM doxycycline as well as a chemically modified tetracycline devoid of antimicrobial activity (4-de-dimethylaminotetracycline). The drug concentration required to inhibit 50% of collagenase activity (IC50) in localized juvenile periodontitis gingival crevicular fluid was 280 microM for doxycycline and 470 microM for 4-de-dimethylaminotetracycline. Significantly lower values, 10-20 microM, were obtained for collagenase in gingival crevicular fluid of patients with adult periodontitis. We propose that systemic tetracycline levels are efficient inhibitors of collagenase in gingival crevicular fluid in affected sites of patients with adult periodontitis but not of patients with localized juvenile periodontitis and that the fibroblast type interstitial collagenase is the predominant collagenase type in gingival crevicular fluid in affected sites of patients with localized juvenile periodontitis and the neutrophil collagenase in adult periodontitis gingival crevicular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

A longitudinal study of untreated periodontal disease.

1016 textile workers were examined during a baseline study in 1969/70. A follow-up examination in 1979/80 identified 82 subjects who had not been treated for periodontal disease in the intervening period. There were 39 male and 43 female subjects; the average age at the initial examination was 27.0 years. There was an average tooth loss of 2.5 (SEM 0.6) teeth per subject over the 10-year period. While periodontal disease was significantly related to oral hygiene at the outset, neither factor was significantly related to the degree of tooth loss. A detailed analysis of the dynamics of the periodontal condition was undertaken. The subsequent results are presented in the form of transition matrices and clearly illustrate both the progression of periodontal disease and the degree of tooth loss associated with each level of periodontal disease at the initial examination. The main findings are as follows. (a) Overall 6% of teeth initially free of periodontal disease (P.I.O.) were lost compared to 14% with destructive periodontal disease (P.I.6). (b) Progression of periodontal disease was slow for teeth initially free of periodontal disease and with mild gingivitis (P.I.0 and P.I.1) for all age groups. However severe gingivitis (P.I.2), resulted in more rapid deterioration of the supporting tissues in subjects over 35 years old at the final examination; 35% of such teeth changed to destructive periodontal disease (P.I.6) compared to 17% of corresponding teeth for the under 35-year age group. In contrast, a poorer prognosis was found for the teeth with destructive periodontal disease (P.I.6) in the younger age group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The microbiology of HIV-associated periodontal lesions.

2 intraoral lesions associated with human immunodeficiency virus (HIV) infection have recently been described: an atypical gingivitis and a rapidly progressive periodontitis. The microbiota associated with these gingival and periodontal lesions was investigated. Subgingival plaque samples were taken from 45 HIV-seropositive homosexual men and from 44 HIV-seronegative control subjects. Each sampled site was clinically and radiographically classified as HIV-associated gingivitis, HIV-associated periodontitis, healthy in an HIV-seropositive subject, or healthy, conventional gingivitis or classical periodontitis in a control subject. Plaque samples were examined by indirect immunofluorescence with polyclonal antisera to detect Bacteroides gingivalis, B. intermedius, Fusobacterium nucleatum, and Actinobacillus actinomycetemcomitans. Anaerobic culturing was used to detect black-pigmented Bacteroides species, Fusobacterium species, and A. actinomycetemcomitans to confirm the immunofluorescence findings. We detected B. gingivalis, B. intermedius, F. nucleatum, and A. actinomycetemcomitans in significantly more HIV-periodontitis sites (80, 65, 59 and 61% of sites, respectively) and HIV-gingivitis sites (61, 70, 52 and 52%, respectively) than in HIV-seropositive healthy and control sites (p less than 0.05). The results indicate that the microbiota found in HIV-periodontitis is similar to that of classical periodontitis. In contrast, however, the microbiota associated with HIV-gingivitis is strikingly different from that of conventional gingivitis. The similarity in the prevalence of periodontopathic organisms in both HIV-gingivitis and HIV-periodontitis suggests that the HIV-gingivitis lesion may be a precursor to the tissue destruction observed in HIV-periodontitis. Hence, early detection and treatment of the HIV-gingivitis lesion may prevent the rapid and extensive breakdown of periodontal tissues associated with HIV-periodontitis.

Actinobacillus↗

Risk of severe periodontal disease in a Swedish adult population. A cross-sectional study.

In this study, potential risk factors for severe periodontal disease were identified in a cross-sectional sample from the county of Jonkoping, Sweden. 547 adults 20-70 years of age were categorised clinically and radiographically by level of periodontal disease experience. These levels were used to divide the sample into groups--individuals without any reduction in periodontal bone level (60%) and those with severe periodontal bone loss (13%)--which were then used in univariate and multivariate logistic regression analyses as dependent variable. Demographic, socio-economic, general health, smoking habits, clinical, and dental care variables were used in the different regression analyses. In the univariate model, age (20-70 years) was found to be correlated with more severe periodontal disease experience (odds ratio: 1.13; 95% CI: 1.10-1.17). The association with periodontal disease was more pronounced for the older age groups (50, 60, and 70 years). A negative financial situation was also related to severe periodontal bone loss when regressed univariately (odds ratio 2.20 [95%: 1.04-4.68]). Moderate-heavy smoking (> or =10 cigarettes/day) appeared to be associated with severe periodontal destruction with an odds ratio of 9.78 (95% CI: 3.62-36.42). Of the clinical variables in the univariate model, higher mean levels of supragingival dental plaque and the presence of subgingival calculus were related to more severe periodontal disease with odds ratios of 1.02 (95%: 1.01-1.03) and 2.96 (95%: 1.50-5.88), respectively. When the same variables were regressed multivariately, age (continuous) (odds ratio 1.17 [95% CI: 1.12-1.22]), moderate-heavy smoking (odds ratio 11.84 [95% CI: 4.19-33.50]), and higher mean levels of plaque (odds ratio 1.02 [95% CI: 1.00-1.03]) remained significant. Light smoking (1-9 cigarettes/day) was not significantly associated with severe periodontal disease in the 2 regression models. The present study demonstrated that smoking, greater age, and higher mean levels of plaque are potential risk factors for severe periodontal disease in this specific population.

Adult↗

The accuracy of individual self-reported items to determine periodontal disease history.

The objective of this study was to evaluate the validity of self-reported periodontal disease and symptoms to predict periodontal disease history in a German population. We analysed data from 246 patients who answered a self-administered questionnaire on self-perceived periodontal disease and self-reported symptoms of periodontal disease. Actual periodontal status was assessed from panoramic radiographs and periodontal disease was defined as > or = 3 teeth with radiographic alveolar bone loss (ABL) > 5 mm (prevalence 39%). Sensitivity (SN) and specificity (SP) of self-reported items for diagnosis of periodontal disease history were calculated. The diagnostic accuracy of any individual item was generally low. For example, self-perceived periodontal disease had SN of 49% and SP of 67%. All self-reported items had low sensitivity, while self-reported professionally diagnosed bone loss, tooth loss caused by periodontal disease and mobility had SP > 90%. In conclusion, we did not identify a single individual question that can assess periodontal disease from self-reporting with satisfactory validity. Future studies will evaluate whether multivariate prediction rules using information from several self-reported variables are a valid means to ascertain periodontal disease history.

Adult↗

Genes and gene polymorphisms associated with periodontal disease.

The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.

Aggressive Periodontitis↗

Population studies of microbial ecology in periodontal health and disease.

It has been established that the bacterial diversity in any given environment is severely underestimated when assessed by means of culture-based techniques. Yet, almost all currently available knowledge related to the periodontal microbiota in health and disease has been generated either by culture-based surveys or by methods that require prior species identification by culture. A handful of recent studies using culture-independent molecular methods providing 16S rRNA sequences for both cultivable and not yet cultivated species of human periodontal bacteria demonstrated a high bacterial diversity in the oral cavity. It has been estimated that approximately 500 species may colonize the human oral cavity, half of which have been cultivated to date. A review of the available epidemiological data on the prevalence of certain periodontal microbiota on a population level reveals considerable variation in estimates with respect to 1) sampling strategy, 2) mode of bacterial identification, and 3) race/ethnicity of the studied population. Nevertheless, specific bacterial profiles appear to confer high odds ratios for pathological periodontal conditions and/or progressive periodontal disease. However, the currently recognized periodontal pathogens are commonly recovered from periodontally healthy children, and their carrier rate in adults is substantial. Virulent clones, such as a highly leukotoxic strain of Actinobacillus actinomycetemcomitans, have been found to be closely associated with aggressive forms of periodontitis. In conclusion, while the majority of the periodontal microbiota are commensals, a subset of likely opportunistic pathogens fulfills the epidemiologic requirements needed in order to be ascribed as risk/causative factors. Given the large proportion of the periodontal microbial habitat that is currently insufficiently explored, and assuming that the hitherto uncultivated segment of the bacterial community will include similar levels of pathogenic species, the list of periodontal pathogens should be expected to expand.

Asia↗

Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. I. Light, immunofluorescence and electron microscopic studies.

Invasion of periodontal tissues by different bacterial morphotypes has been reported in human periodontitis; however, limited information is available as to prevalence, localization and the bacterial species involved. The present study determined prevalence and gingival localization of Actinobacillus (Haemophilus) actinomycetemcomitans in periodontal lesions of juvenile periodontitis patients. Thirty-five gingival biopsies were obtained from 12 juvenile periodontitis patients at the time of periodontal therapy. One additional control biopsy was obtained from each of two adult periodontally healthy subjects, one adult periodontitis patient and one periodontally healthy monkey (Macaca fosibolius). The biopsies were carefully processed to avoid mechanical introduction of bacteria into the tissues and were examined using light and electron microscopy. Rabbit antisera specific for the three A. actinomycetemcomitans serotypes were used for immunofluorescence microscopic localization of A. actinomycetemcomitans antigens in the gingival sections. Immunofluorescence microscopy showed A. actinomycetemcomitans specific antigens in the gingival tissues of 11 of the 12 juvenile patients examined. None of the control specimens showed evidence of A. actinomycetemcomitans antigens in the gingival connective tissue. One specimen from a periodontally healthy subject and the monkey biopsy, however, showed A. actinomycetemcomitans antigens in bacterial plaque on the surface of the crevicular epithelium. Transmission electron microscopic examination showed microcolonies of small gram-negative rods in the connective tissue, as well as single bacterial cells between collagen fibers and in areas of cell debris. In addition to these extracellular bacterial cells, evidence of bacterial cells was also found within gingival connective tissue phagocytic cells. The data from the present study suggest that the gingival tissue in juvenile periodontitis lesions harbors A. actinomycetemcomitans.

Actinobacillus↗

Longitudinal study of dental implants in a periodontally compromised population.

BACKGROUND: The purpose of this longitudinal study was to determine the clinical status and the composition of the subgingival microbiota of dental implants and natural teeth in patients with a history of periodontitis. METHODS: Twenty-five partially edentulous patients treated for moderate to advanced adult periodontitis and having a total of 42 implants participated in this 3-year study. The assessment of clinical status was done 1, 2, and 3 years after prosthetic loading (T1, T2, and T3, respectively). Clinical parameters evaluated included probing depth (PD), clinical attachment level (CAL), gingival index (GI), and plaque index (PI). The subgingival microbiota at peri-implant and periodontal sites were analyzed at T1 and T2. RESULTS: No significant difference in clinical parameters between implants and teeth and within the 2 groups between different time points was observed through the study. PD and CAL measurements of sampled periodontal and peri-implant sites did not show any statistically significant difference through the study and between the 2 groups. PI of sampled periodontal sites showed a statistically significant improvement during the study. From the morphological observation of the subgingival microbiota, a significant difference in the composition of motile rods between implants and teeth was found at T1. There were no differences detected in the subgingival microbiota, culturally identified at peri-implant and periodontal sites for the duration of the study. CONCLUSIONS: In conclusion, implants were colonized by the indigenous periodontal microbiota and were well maintained in patients with a history of periodontitis. No significant association between progressing or non-progressing periodontal or peri-implant sampled sites in terms of loss of attachment and infection with at least one of the searched periodontal pathogens was found, suggesting that the presence of putative periodontopathogens at peri-implant and periodontal sites may not be associated with future attachment loss or implant failure.

Adult↗

Influence of estrogen and osteopenia/osteoporosis on clinical periodontitis in postmenopausal women.

BACKGROUND: In Western societies, more than one-third of the female population above age 65 suffers from signs and symptoms of osteoporosis, a disorder characterized by low bone mass. Estrogen deficiency is the dominant pathogenic factor for osteoporosis in women. The impact of estrogen deficiency and osteopenia/osteoporosis on periodontitis is unclear, partially due to the lack of longitudinal studies evaluating clinical signs of gingival inflammation and periodontitis progression. The purpose of this investigation was to analyze prospectively the influence of serum estradiol levels and osteopenia/osteoporosis on common clinical measurements of periodontal disease over a 2-year period. METHODS: Fifty-nine moderate/advanced adult periodontitis patients and 16 non-periodontitis subjects, all within 5 years after menopause at baseline, completed the study. Serum estradiol levels (E2) were measured yearly by 125I radioimmunoassay, and osteopenia/osteoporosis was determined by dual energy x-ray absorptiometry of the lumbar spine. Posterior interproximal clinical measurements were obtained every 6 months for the periodontitis patients, including explorer-detectable supragingival plaque, bleeding on probing (BOP) and relative clinical attachment level (RCAL). Baseline probing depths, smoking history, and demographic data also were collected. RESULTS: Data indicated that baseline demographic measurements and bone mineral density (BMD) of the lumbar spine were not different between E2-deficient and E2-sufficient subjects. Smoking activity (packs smoked/day, years smoked) was higher in periodontitis patients (P=0.0001). E2-sufficient periodontitis subjects had a higher frequency of supragingival plaque without increasing gingival inflammation. E2 status did not influence the percentage of sites losing RCAL for either periodontitis or non-periodontitis groups, but when non-smoking osteopenic/osteoporotic periodontitis patients were evaluated, E2-deficient subjects had more BOP (43.8% versus 24.4%, P<0.04) and a trend toward a higher frequency of > or =2.0 mm RCAL loss (3.8% versus 1.2%, P<0.1) than E2-sufficient subjects. CONCLUSIONS: These data suggest that E2 supplementation (serum E2>40 pg/ml) is associated with reduced gingival inflammation and a reduced frequency of clinical attachment loss in osteopenic/osteoporotic women in early menopause.

Analysis of Variance↗

The association between osteopenia and periodontal attachment loss in older women.

BACKGROUND: Recent research suggests that osteopenia may be a predisposing factor for periodontal tissue destruction. If so, then a relationship should exist between measures of systemic bone mineral density and periodontal tissue destruction. The purpose of the present cross-sectional study was to evaluate the association between systemic bone mineral density and the clinical signs of periodontal tissue destruction in a large population of elderly dentate women. METHODS: A total of 292 dentate women (average age 75.5 years) were randomly selected for a cross-sectional periodontal substudy from participants at the Pittsburgh Field Center of the Study of Osteoporotic Fractures (SOF), a prospective study of a cohort of elderly women (age > or =65 years at baseline) to determine risk factors for fractures. Bone mineral density (BMD) was measured using single photon absorptiometry (radius, calcaneus) and dual energy x-ray absorptiometry (hip, spine). Oral health examinations, including periodontal probings and an assessment of bleeding on probing, were made using an NIDR probe at 3 buccal sites of all teeth. Multiple regression models were used to assess the association between bone mineral density and measures of periodontal disease status while controlling for potential confounders. Periodontal status variables examined included: average loss of periodontal attachment (LOA); number of sites with at least 4 mm LOA; number of sites with at least 6 mm LOA; number of sites with bleeding on probing; and deepest probing depth per person. RESULTS: This study found no statistically significant association between the 5 indicators of periodontal disease and measures of systemic BMD at 8 anatomic sites after controlling for age, smoking, and number of remaining natural teeth. Some suggestive findings support a weak association between generalized osteopenia and periodontal disease. CONCLUSIONS: Systemic osteopenia is, at best, only a weak risk factor for periodontal disease in older non-black women.

Absorptiometry, Photon↗

Herpesviruses and periodontopathic bacteria in Trisomy 21 periodontitis.

BACKGROUND: Little is known about the etiology and pathogenesis of periodontal disease in Trisomy 21 patients. This study determined the occurrence of herpesviruses and putative periodontopathic bacteria in Trisomy 21 periodontitis. METHODS: Nineteen Trisomy 21 patients (17 to 37 years of age) contributed subgingival samples from molar and bicuspid teeth presenting interproximal periodontitis lesions (probing depths, 5 to 8 mm) and from shallow periodontal sites (probing depths, 1 to 3 mm). Samples were obtained at baseline, and at 1 and 4 weeks after subgingival debridement by means of hand instruments and ultrasonic scalers. Epstein-Barr virus type 1 and 2 (EBV-1 and EBV-2), human cytomegalovirus (HCMV), and herpes simplex virus (HSV) were identified by sensitive and specific nested polymerase chain reaction. Putative periodontopathic bacteria were identified by means of non-selective and selective culture. RESULTS: Of 19 Trisomy 21 periodontitis lesions, 6 (32%) were positive for EBV-1, 5 (26%) were positive for HCMV, 3 (16%) were positive for HSV, and 2 (11%) showed viral co-infection. Of 19 shallow periodontal sites, only one revealed HCMV. Prevotella intermedia, Bacteroides forsythus, and Capnocytophaga species were detected in higher proportions in deep than in shallow periodontal pockets (P = 0.02). Subgingival debridement did not reduce genomic herpesvirus presence but caused a decrease in proportions of Porphyromonas gingivalis and Capnocytophaga species. CONCLUSIONS: Periodontal herpesvirus-bacteria coinfections may play important roles in the pathogenesis of destructive periodontal disease in Trisomy 21 patients. Herpesviruses may reduce the periodontal defense and promote growth of subgingival bacteria capable of causing periodontal breakdown.

Adolescent↗

Eikenella corrodens in subgingival plaque: relationship to age and periodontal condition.

BACKGROUND: The purpose of this study was to determine the prevalence and distribution of Eikenella corrodens (E. corrodens) in subgingival plaque in different age and periodontitis groups and to examine whether its presence is related to periodontal diseases. METHODS: A total of 273 subgingival plaque samples from 213 periodontitis patients and 60 healthy subjects were assessed. Smears from each plaque sample were made and E. corrodens was detected by means of indirect immunofluorescent technique. Mean percentage of E. corrodens per total bacteria (distribution) was calculated in each sample. The prevalence (% of positive samples) and distribution of E. corrodens were statistically analyzed based on age or diagnosis by means of Fisher's exact test and analysis of variance (ANOVA). RESULTS: Prevalence of E. corrodens decreased by age in the healthy control group; however, prevalence did not change in periodontitis groups. Distribution of E. corrodens was highest in juvenile periodontitis (JP) (2.3 +/- 1.5%) followed by post-JP (1.7 +/- 2.1%), prepubertal periodontitis (1.4 +/- 1.1%), rapidly progressive periodontitis (0.8 +/- 0.7%), adult periodontitis (0.7 +/- 0.6%), and healthy subjects (0.3 +/- 0.3%) (ANOVA, P<0.0001). The <20-year-old age group with periodontitis showed the highest distribution of E. corrodens (2.2 +/- 1.6%) compared to the older age groups who were either healthy or had periodontitis (ANOVA, P<0.0001). CONCLUSIONS: Since the distribution of E. corrodens is significantly higher in JP, post-JP, and PP, E. corrodens might play an important role in the occurrence or progression of periodontitis in young patients.

Adult↗

Clinical and microbiologic study of periodontitis associated with Kindler syndrome.

BACKGROUND: Little is known about the onset and prevalence of periodontal disease in patients with the rare Kindler syndrome, a genodermatological disorder. This study investigated the level of clinical periodontal attachment in relation to age and presence of putative periodontopathogenic bacteria in individuals with Kindler syndrome. METHODS: Eighteen individuals diagnosed with Kindler syndrome and 13 control subjects, aged 4 to 37 years, from rural Panama received a limited clinical periodontal examination. Subgingival samples were collected for identification of putative periodontal pathogens by polymerase chain reaction. RESULTS: Mild to severe gingivitis was a common finding in all adults of the study population. Seventy-two percent (13/18) of the Kindler patients and 46% (6/13) of the control subjects showed mild to severe periodontal disease (P = 0.001, chi-square test). The onset of periodontitis was earlier and the progression occurred at a faster rate in the Kindler group. There was a strong correlation (r = 0.83) between the level of attachment loss and age in the Kindler group and a weaker correlation (r = 0.66) in the control group. The appearance of gingival tissues suggested atypical periodontitis with spontaneous bleeding and fragile, often desquamative, gingiva. In periodontitis patients, Porphyromonas gingivallis and Diallster pneumosintes tended to occur more frequently in control individuals compared to those with Kindler syndrome. CONCLUSIONS: In the Kindler group, periodontitis had an onset in early teenage years and progressed more rapidly compared to non-Kindler individuals of the same geographic and ethnic group. Clinical and microbiological findings suggest atypical periodontitis in Kindler patients. We propose to include Kindler syndrome in the category of medical disorders predisposing to destructive periodontal disease.

Adolescent↗

Periodontal referral patterns, 1980 versus 2000: a preliminary study.

BACKGROUND: A review of the periodontal literature offers little information concerning trends in referral patterns of patients for periodontal therapy. Over the last 2 decades, there has been a significant increase in the knowledge base concerning inflammatory periodontal disease. It might be assumed that the collective advances in knowledge have impacted periodontal referral patterns. Thus, the purpose of this study was to examine the differences in periodontal referral patterns in the same offices separated by a 20-year interval (i.e., 1980 and 2000). METHODS: A retrospective chart analysis was conducted on a total of 782 patient charts from three conveniently selected periodontal practices. Charts were randomly selected from two time periods: 1980-1981 and 2000-2001. The following information was obtained from each patient record: gender, age at time of initial examination, tobacco smoking status at time of initial examination, periodontal case type, number of missing teeth at initial examination (not including third molars), and number of teeth scheduled for extraction per periodontal treatment plan. Descriptive data were analyzed using frequency distributions, measures of central tendency, and measures of dispersion. Non-parametric statistics were used to examine the relationship of disease severity as a function of site, time period, and patient age. RESULTS: The following trends were noted: 1) an increase in the average age of patients at the time of the initial examination; 2) a decrease in the percentage of patients using tobacco at the time of the initial interview; 3) an increase in the percentage of periodontal Case Type IV patients with a concomitant decrease in the number of periodontal Case Type II patients; 4) an increase in the average number of missing teeth per patient at the initial examination; and 5) an increase in the average number of teeth scheduled for extraction per periodontal treatment plan. CONCLUSIONS: Characteristics of patients referred in 1980 compared to those referred in the year 2000 indicate that, although fewer patients used tobacco, there were several noteworthy trends. At referral, patients exhibited a greater loss of teeth, had more severe disease, and required extraction of a greater number of teeth in 2000 compared to 1980. Possible reasons for these trends are discussed.

Adult↗