Association of a Common Genetic Factor,PTGER3, With Outcome of Periodontal Therapy and Preterm Birth

Background: Clinical evidence suggests an association between preterm birth and periodontal disease. This study explores whether specific genetic polymorphisms are associated with success of periodontal therapy in pregnant women with periodontal disease and, further, whether any of these same polymorphisms are also associated with spontaneous preterm birth (sPTB). Methods: One hundred sixty high‐risk pregnant women (6 to 20 weeks of gestation) with periodontal disease (≥3 sites with attachment loss ≥4 mm) were studied. All women received scaling and root planing plus oral hygiene instruction. Periodontal examinations were performed before treatment and 20 weeks later. Participants were classified according to two study outcomes: 1) success or failure of periodontal treatment; and 2) presence or absence of sPTB. Maternal DNA samples from mucosal swabs were characterized using a 1536‐SNP (single‐nucleotide polymorphism) custom polymerase chain reaction chip. A probabilistic model of each dichotomous outcome, derived using a stepwise Bayesian procedure, was compared to respective null hypotheses on the basis of Monte Carlo simulations and significance estimates obtained using three measures (z‐test, Welch t‐test, and probability convolution). The models were further confirmed by logistic regression analyses. Results: The models revealed a significant relation between a specific polymorphism of prostaglandin E receptor 3 (a gene associated with inflammatory response) and both periodontal treatment failure (odds ratio 11.09, P <0.0002) and sPTB (odds ratio 6.89, P <0.0032). Conclusions: These results demonstrate that the risk of unsuccessful periodontal treatment is associated with tag SNPs in specific genes that regulate the inflammatory response, one of which is also associated with sPTB.     

Specific infections as the etiology of destructive periodontal disease: a systematic review

Destructive periodontal disease has been primarily defined and investigated as an infectious disease. The aim of this study was to systematically search for cohort studies where microbiological diagnoses were performed before the onset of destructive periodontal disease and where statistically significant associations were identified. A search was executed in PubMed. The results showed that three studies published after 2005 supported the infection hypothesis for one putative periodontal pathogen: Aggregatibacter actinomycetemcomitans. These three studies were conducted in predominantly non‐Caucasian pediatric populations living in geographic areas with an elevated child‐mortality rate. These studies did not obtain physical or laboratory markers of health, making it possible that A. actinomycetemcomitans was not a cause but a marker for poor environmental or systemic health. No cohort studies were identified supporting the infection hypothesis in adults, Caucasians or in a population residing in areas with child‐mortality rates reflective of healthy population goals. While the possibility cannot be excluded that A. actinomycetemcomitans has an etiological role in certain specific pediatric populations, there are no cohort studies supporting an infectious etiology of destructive periodontal disease in adults.     

Correlation between periodontal disease, inflammatory alterations and pre-eclampsia

Politano GT, Passini R, Nomura ML, Velloso L, Morari J, Couto E. Correlation between periodontal disease, inflammatory alterations and pre‐eclampsia. J Periodont Res 2011; 46: 505–511. © 2011 John Wiley & Sons A/S Background and Objective: Several studies have hypothesized that periodontal disease may increase the risk of pre‐eclampsia. The correlation between the two diseases would probably be based on hypertension‐related cytokine release in the local periodontal environment. The aim of this study was to evaluate the association between periodontal disease and pre‐eclampsia, and the correlation of the two conditions with interleukin‐6 (IL‐6) and tumor necrosis factor‐α(TNFα) mRNA expression. Material and Methods: A case–control analysis of 116 pregnant women, 58 with pre‐eclampsia (cases) and 58 normotensive pregnant women (controls) was performed. In addition to collection of socio‐demographic data and periodontal evaluation, peripheral blood samples were collected for laboratory analysis of IL‐6 and TNFα mRNA expression by real‐time PCR. Results: There was an association between periodontitis and pre‐eclampsia (adjusted odds ratio 3.73; 95% confidence interval 1.32–10.58). Increased TNFα mRNA expression was observed in pre‐eclamptic women; however, there was no correlation between periodontitis and systemic cytokine expression. In the case group, systemic cytokine mRNA levels were similar in pregnant women with and without periodontitis (means ± SD): 0.73 ± 0.24 vs. 0.82 ± 0.38 for TNFα and 1.31 ± 1.49 vs. 1.09 ± 0.74 for IL‐6, respectively. Conclusion: Periodontitis was clinically related to pre‐eclampsia; however, the supposed mechanism that correlates the two diseases, i.e. a systemic inflammatory process involving cytokines TNFα and IL‐6 in the presence of periodontal disease, could not be confirmed in this study.     

Prevalence and distribution of principal periodontal pathogens worldwide

Background: Detailed genetic analysis of bacteria has demonstrated an unanticipated genetic diversity within species, which often reveals evolutionary lineages that are disproportionately associated with infection. There is evidence that some evolutionary lineages of bacteria have adapted to particular ethnic groups.
Aim: This review analyzes to what extent observed differences in periodontal disease prevalence among ethnically or geographically distinct populations may be explained by restricted host adaptation of clones of principal periodontal pathogens.
Results: Carriage rates of several putative periodontal pathogens and particular subsets of these species vary between ethnic groups. Few of these differences can, with the limited information available, be directly related to differences in periodontal disease prevalence. Asian populations are regularly colonized with Actinobacillus actinomycetemcomitans serotype c with questionable pathogenic potential. Conversely, the JP2 clone of A. actinomycetemcomitans has enhanced virulence and causes significantly higher prevalence of aggressive periodontitis in adolescents whose descent can be traced back to the Mediterranean and Western parts of Africa. Some genetically distinct types of Porphyromonas gingivalis are more associated with disease than others, but additional work is required to relate this to clinical differences.
Conclusions: Studies that take into account differences linked to the genetics of both patients and potential pathogens are likely to give better insight into the aetiology of periodontal diseases.     

Immunohistochemical localization of elastin, fibrillins and microfibril-associated glycoprotein-1 in the developing periodontal ligament of the rat molar

Sugawara Y, Sawada T, Inoue S, Shibayama K, Yanagisawa T. Immunohistochemical localization of elastin, fibrillins and microfibril‐associated glycoprotein‐1 in the developing periodontal ligament of the rat molar. J Periodont Res 2009; doi: 10.1111/j.1600‐0765.2008.01196.x. © 2009 John Wiley & Sons A/S Background and Objective: Elastic system fibers are a major component of the periodontal ligament, but little information is available about their detailed composition or the mechanism of elastogenesis in the developing periodontal ligament. The purpose of this study was to investigate immunolocalization of elastin, fibrillins and microfibril‐associated glycoprotein‐1 (MAGP‐1) in the developing periodontal ligament of the rat molar. Material and Methods: Frozen sections of demineralized as well as non‐demineralized periodontal ligament of Wistar rats of various ages from 19 days to 7 weeks were incubated with anti‐elastin, anti‐fibrillin‐1 and ‐2 and anti‐MAGP‐1 antibodies followed by peroxidase‐conjugated secondary antibodies. After incubation with diaminobenzidine solution, immunoreaction products were observed with a light microscope. Results: In the developing periodontal ligament of 19‐day‐old rats, fibers immunopositive to elastin were not present, but fibers positively stained for fibrillin‐2 and MAGP‐1 were widely distributed throughout the ligament. The latter fibers were arranged in the apico‐occlusal direction along with blood vessels. In 3‐week‐old rats, fibers stained for elastin were observed for the first time in the apical region of the ligament. The number and distribution pattern of these elastin‐positive fibers was basically the same as those in rats aged 5 and 7 weeks. In contrast, fibrillin‐2‐ and MAGP‐1‐positive fibers were more extensively distributed in the ligament, and their pattern of distribution was comparable to that of reported oxytalan fibers. Fibrillin‐1 was, however, not detected either in demineralized sections or in non‐demineralized sections, indicating its absence in periodontal ligament. Conclusion: Elastin expressed in the periodontal ligament assembled into elaunin fibers in the vicinity of blood vessels. Both fibrillin‐2 and MAGP‐1 are structural components not only of the elastin‐associated microfibrils but also of elastin‐free microfibrils, with possible roles in elastogenesis and in periodontal ligament homeostasis.     

Expression of periodontal interleukin‐6 protein is increased across patients with neither periodontal disease nor diabetes,patients with periodontal disease alone and patients with both diseases

Ross JH, Hardy DC, Schuyler CA, Slate EH, Mize TW, Huang Y. Expression of periodontal interleukin‐6 protein is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases. J Periodont Res 2010; 45: 688–694. © 2010 John Wiley & Sons A/S Background and Objective: Epidemiological studies have established that patients with diabetes have an increased prevalence and severity of periodontal disease. Interleukin (IL)‐6, a multifunctional cytokine, plays a role in the tissue inflammation that characterizes periodontal disease. Our recent study has shown a trend of increase in periodontal IL‐6 expression at the mRNA level across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases. However, the periodontal IL‐6 expression at the protein level in these patients has not been investigated. Material and Methods: Periodontal tissue specimens were collected from eight patients without periodontal disease and diabetes (group 1), from 17 patients with periodontal disease alone (group 2) and from 10 patients with both periodontal disease and diabetes (group 3). The frozen sections were prepared from these tissue specimens and IL‐6 protein expression was detected and quantified. Results: The nonparametric Kruskal–Wallis test showed that the difference in IL‐6 protein levels among the three groups was statistically significant (p = 0.035). Nonparametric analysis using the Jonckheere–Terpstra test showed a tendency of increase in periodontal IL‐6 protein levels across group 1 to group 2 to group 3 (p = 0.006). Parametric analysis of variance (ANOVA) on IL‐6 protein levels showed that neither age nor gender significantly affected the difference of IL‐6 levels among the groups. Conclusion: Periodontal IL‐6 expression at the protein level is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases.     

A trend of increase in periodontal interleukin-6 expression across patients with neither diabetes nor periodontal disease, patients with periodontal disease alone, and patients with both diseases

Background and Objective: Epidemiological studies have established that patients with diabetes have increased prevalence and severity of periodontal disease. However, the periodontal expression of inflammatory cytokines and matrix metalloproteinases (MMPs) in diabetic patients has not been well characterized. The objective of this study was to determine the difference in the periodontal expression of MMP‐1, MMP‐8, interleukin‐6, tumor necrosis factor‐α and interleukin‐1β between diabetic and nondiabetic patients. Material and Methods: Periodontal tissue specimens were collected from nine nondiabetic patients without periodontal disease (group 1), from 11 nondiabetic patients with periodontal disease (group 2) and from seven diabetic patients with periodontal disease (group 3). The expression of MMP‐1, MMP‐8, interleukin‐6, tumor necrosis factor‐α and interleukin‐1β was quantified using real‐time polymerase chain reaction. Results: The nonparametric Kruskal–Wallis test showed that the difference in interleukin‐6 expression among the groups was statistically significant (p = 0.04). Furthermore, the generalized Kruskal–Wallis nonparametric linear‐by‐linear association test showed a statistically significant trend of increase in the expression of interleukin‐6 from group 1 to group 2 to group 3 (p = 0.02) and a suggestion of such a trend for MMP‐1 (p = 0.05). No increase in MMP‐8 expression was observed in patients in group 3 compared to patients in groups 1 and 2. Although the average expression levels of MMP‐1, interleukin‐1β and tumor necrosis factor‐α were increased from group 1 to group 3, the differences were not statistically significant. Conclusion: A trend of increased interleukin‐6 expression in periodontal tissues was observed across patients with neither diabetes nor periodontal disease, patients with periodontal disease alone, and patients with both diseases.     

Effects of surgical removal of mandibular third molar on the periodontium of the second molar

Abstract: Objective: The effects on periodontal tissues of adjacent second molars after semi‐impacted mandibular third molar surgery were evaluated. The influence of flap design was studied. Methods: Twenty volunteers randomly underwent the three‐cornered flap technique (group A) or the distal wedge flap technique (group B). The periodontal probing depth was measured by using a ‘Williams’‐type probe just prior to surgery and three months post‐operatively. Six sites, mesio‐buccal, buccal, disto‐buccal, disto‐lingual, lingual and mesio‐lingual, around the second molar were selected for measurement. Kruskal–Wallis test and Dunn test (post hoc) were used. Significance level was set at 5%. Results: There were no complications (oedema, alveolitis, etc.) in any of the patients of the study. The results showed that both methods caused shallow pocket depth (P > 0.05) and there were no statistically significant differences between the flap techniques (P > 0.05). Flap design was not an important factor affecting the periodontal status of the second molar. Conclusion: The decision to use any of the various flap designs for access to mandibular third molars should be based on operator preference rather than on the assumption that periodontal health of the adjacent second molar will be improved.     

Treatment of experimental periodontal disease by photodynamic therapy in immunosuppressed rats

Background and Objective: The aim of this study was to compare photodynamic therapy (PDT) as an adjunctive treatment of induced periodontitis with scaling and root planing (SRP) in dexamethasone‐inhibited rats. Material and Methods: The animals were divided into two groups: ND (n=90), saline solution treatment; D (n=90), dexamethasone treatment. In the ND and D Groups, periodontal disease was ligature‐induced at the first mandibular molar. After 7 days, the ligature was removed and all animals received SRP and were divided according to the following treatments: SRP, saline solution; Toluidine Blue‐O (TBO), phenothiazinium dye; and PDT, TBO and laser irradiation. Ten animals in each treatment were killed at 7, 15 and 30 days. The radiographic and histometric values were statistically analysed. Results: In the ND and D Groups, radiographic analysis showed less bone loss in animals treated by PDT in all the experimental periods than SRP and TBO at 15 days (p<0.05). After a histometric analysis was carried out in the ND and D groups, the animals treated by PDT showed less bone loss in all periods than SRP and TBO after 15 days (p<0.05). Conclusions: The PDT was an effective adjunctive treatment of induced periodontitis compared with SRP in dexamethasone‐inhibited rats.     

Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar rats

Background: Inability to mount a suitable brain‐neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. Objective: The present study was designed to determine the effects of glutamate administration to new‐born Wistar rats on the development and progression of naturally occurring and ligature‐induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. Method: New‐born rats were treated 1× daily subcutaniously with 2 mg/g of monosodium‐L‐glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature‐induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. Results: The results revealed that the glutamate‐lesioned rats developed significantly more periodontal tissue destruction compared to sham‐lesioned control rats in both the ligated and non‐ligated teeth. Conclusions: This study supports our resent findings indicating that inappropriate brain‐neuroendocrine‐immune regulation may play a rôle in periodontal disease susceptibility and progression.     

Serum IgG antibody response to periodontal pathogens in minority populations: relationship to periodontal disease status and progression

Differences in periodontal disease prevalence, severity, subgingival microflora and host immune response have been reported for various ethnic/racial groups, which implies that risk factors for destructive periodontal disease progression may also vary in these populations. As it is possible that these differences may be due to confounding variables other than ethnicity/race, we have measured serum IgG antibody response to six periodontal pathogens, and compared these data with microbiological, clinical and demographic parameters in three urban minority populations. The study population consisted of 23 Asiatic, 48 African-American and 37 Hispanic subjects, who were resident in the greater New York region. Clinical indices that were recorded included pocket depth, attachment level, gingival erythema, bleeding upon probing, suppuration and supragingival plaque. Attachment level measurements were taken twice at each visit, and the difference between the means of pairs of measurements taken at baseline and two months later was used to determine disease progression. Subgingival microbiological species were identified and enumerated using DNA-DNA checkerboard hybridization. Serum IgG antibody levels to Actinobacillus actinomycetemcomitans serotyopes a and b, Bacteroides forsythus, Campylobacter rectus, Porphyromonas gingivalis and Prevotella intermedia were measured by enzyme-linked immunosorbant assay (ELISA). Mean serum IgG antibody to P. gingivalis was found to be higher in the African-American group, while IgG antibody to B. forsythus was lower in the Hispanic group. However, the African-American group also had greater mean probing depth, attachment loss, number of missing teeth and numbers of individuals within the unskilled occupational group. When the data were analyzed by occupational status, mean serum IgG antibody to P. gingivalis increased from professional to skilled to unskilled groups. For the entire study population, prior disease and subsequent attachment loss were associated with elevated serum IgG antibody to P. gingivalis. Increasing pocket depth, attachment level, gingival erythema and age were also positively correlated with serum IgG antibody to P. gingivalis, but not with serum IgG antibody to the other five subgingival species. No correlation was found between whole-mouth bacterial levels and homologous serum IgG antibody levels. These results suggest that elevated serum IgG antibody to P. gingivalis reflects destructive periodontal disease status, and may be considered a risk factor for disease progression in these ethnic/racial populations. In addition, although differences in serum IgG antibody profiles to subgingival species were found among the three ethnic/racial groups, environmental and socioeconomic variables may have a greater influence on serum IgG antibody levels in these populations.     

Step‐wise treatment of two periodontal‐endodontic lesions in a heavy smoker

Aim To report a clinical case of two advanced periodontal‐endodontic lesions with a focus on treatment issues related to tobacco use. Summary A 53‐year‐old Caucasian male was referred to the School of Dentistry, Basel, Switzerland, for periodontal treatment. The major diagnoses were chronic (smoker) periodontitis and advanced combined periodontal‐endodontic lesions on the mandibular left lateral incisor and right incisor. Conventional root canal treatment was performed, and subsequently led to reduced radiolucencies around the affected roots after 14 months. The remaining osseous defect was augmented by guided tissue regeneration using bovine bone substitute and resorbable membrane. The follow‐up revealed a stable situation from clinical (probing depth 2–4 mm) and radiological points of view 32 months after initiation of treatment. Treatment considerations related to tobacco use are discussed. Key learning points ? After conventional root canal treatment, osseous healing should occur before further complementary therapy is taken into account. ? Issues related to tobacco use have to be considered before treatment is initiated.     

Validity of self‐reported periodontal measures,demographic characteristics,and systemic medical conditions

1 Background

The objective of the present study was to assess self‐reported periodontal screening questions, demographic characteristics, systemic medical conditions, and tobacco use for predicting periodontal disease among individuals seeking dental therapy in a university dental clinic.

2 Methods

In this retrospective study, a total of 4,890 randomly selected dental charts were evaluated from among patients who had attended the University of Minnesota School of Dentistry clinics for treatment. Radiographic bone loss measurements were used to assess the severity of periodontal disease. Demographic characteristics as well as medical history of the patients were also recorded. Five self‐reported periodontal screening questions were included, with answers limited to Yes/No. Generalized logit models were used to assess the association between bone loss and the predictors.

3 Results

The sample's mean age was 54.1 years and included 52.6% males and 14.9% smokers, with a mean of 3.5 missing teeth. Self‐reported tooth mobility, history of “gum treatment,” and the importance of retaining teeth as well as age, tobacco use, and cancer were statistically significant predictors (P < 0.05) of a radiographic diagnosis of moderate and severe periodontal disease. With respect to severe periodontal disease, significant associations (P < 0.05) were also found with “bleeding while brushing,” gender, diabetes, anxiety, and arthritis.

4 Conclusions

Self‐reported periodontal screening questions as well as demographic characteristics, smoking, and systemic medical conditions were significant predictors of periodontal disease, and they could be used as valid, economic, and practical measures.     

The association of psychosocial factors and smoking with periodontal health in a community population

Chiou L‐J, Yang Y‐H, Hung H‐C, Tsai C‐C, Shieh T‐Y, Wu Y‐M, Wang W‐C, Hsu T‐C. The association of psychosocial factors and smoking with periodontal health in a community population. J Periodont Res 2009; doi: 10.1111/j.1600‐0765.2008.01194.x. © 2009 John Wiley & Sons A/S Background and Objective: The association between psychosocial factors and periodontal disease has been widely reported and might be modified by smoking status. This study investigated the association of periodontal status with psychosocial factors and smoking in a community population. Material and Methods: A structured questionnaire was administered to a total of 1764 civilian noninstitutional (general population excluding from nursing homes, sanitariums and hospitals) Taiwanese individuals to assess the presence and severity of psychosocial factors [using the 12‐item Chinese health questionnaire (CHQ‐12)], smoking habits and other related factors. Periodontal status was established using the community periodontal index and by measuring clinical loss of attachment. Results: Psychological factors and smoking were significantly associated with loss of attachment (odds ratio = 1.69, 95% confidence interval = 1.01–2.77, comparing the CHQ‐12 score of ≥ 6 with the CHQ‐12 score of 0–2 and p = 0.032 for linear trend; odds ratio = 2.21, 95% confidence interval = 1.45–3.37, comparing smokers with nonsmokers) but not with community periodontal index. The association was found to be stronger among smokers than among nonsmokers. Smokers with a CHQ‐12 score of ≥ 6 had a higher odds ratio of loss of attachment (odds ratio = 2.49, 95% confidence interval = 0.91–6.49) than nonsmokers (odds ratio = 1.43, 95% confidence interval = 0.76–2.58). For periodontal health measured using the community periodontal index, married and divorced/widowed subjects tended to have poorer periodontal health (odds ratio = 3.38, 95% confidence interval = 1.26–10.81 and odds ratio = 3.83, 95% confidence interval = 1.21–13.83, respectively) than single subjects among nonsmokers but not among smokers. Conclusion: Poor mental health had a stronger association with periodontal disease among smokers than among nonsmokers, especially in accumulative attachment loss. Our findings suggest that mental health and smoking might have a synergistic effect on the risk of developing periodontal disease.     

Frequency of 530‐bp deletion in Actinobacillus actinomycetemcomitans leukotoxin promoter region

Actinobacillus actinomycetemcomitans strains showing a 530‐bp deletion in the promoter region of the leukotoxin gene operon elaborate high amounts of leukotoxin that may play a role in the pathogenesis of periodontal disease. This study used polymerase chain reaction detection to determine the occurrence of the 530‐bp deletion in 94 A. actinomycetemcomitans strains from individuals of various ethnic backgrounds. Eleven blacks and one Hispanic subject but no Caucasian or Asian subjects showed the 530‐bp deletion in the leukotoxin promoter region, suggesting that the deletion is mainly a characteristic of individuals of African descent. A. actinomycetemcomitans strains exhibiting a deletion in the leukotoxin promotor region occurred both in individuals having severe periodontitis and in adolescents revealing no evidence of destructive periodontal disease.     

Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline

Abstract. Since recent studies have implicated Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis, this investigation determined the effectiveness of subgingival debridement, topical Betadine Solution®, and systemic tetiacycline in suppressing subgingival A. actinomycetemcomitans and other microorganisms. A total of 20 deep periodontal pockets and 10 normal periodontal sites of 6 localized juvenile periodontitis patients was included in the study. Each patient was treated in 3 stages over a period of 22 weeks, and the result of treatment was monitored for an additional 38 weeks. The first stage of treatment included plaque control, as well as thorough scaling and root planing, composed of at least 6 h of debridement. No concomitant periodontal surgery was performed. In the second stage, Betadine saturated cotton gauze was inserted into the periodontal pockets for 10 min. Stage 3 involved systemic tetracycline therapy (1 g/day) for J4 days. The subgingival microflora was determined at frequent intervals by selective culturing of A. actinomycetemcomitans and Capnocytophaga and by direct microscopic examination. The clinical effect was assessed by measuring changes in probing periodontal attachment level, probing periodontal pocket depth, radiographic alveolar bone mass, and other relevant clinical parameters. Scaling and root planing reduced the total subgingival bacterial counts and the proportions of certain Gram-negative bacteria, but no periodontal pocket became free of A actinomycetemcomitans. Betadine application had little or no effect on the subgingival microflora. In contrast, tetracycline administered via the systemic route suppressed. A actinomycetemcomitans, Capnocytophaga, and spirochetes to low or undetectable levels in all test periodontal pockets. A, actinomycetemcomitans reappeared in 9 of the deep periodontal pockets after the administration of tetracycline. Most of these 9 pockets became free of detectable A. actinomycetemcomitans during the second week of tetracycline administration, whereas pockets which yielded no A. actinomycetemcomitans after tetracycline therapy became free of the organisms during the first week of tetracycline treatment. This data suggests that systemic tetracycline therapy of localized juvenile periodontitis should, as a practical rate, be continued for 3 weeks. Periodontal destruction continued in 4 deep pockets which all showed high posttetracycline A, actinomycetemcomitans counts. All 6 pockets which demonstrated a marked gain in periodontal attachment yielded no cultivable A. actinomycetemcomitans. No association was found between periodontal disease status and subgingival Capnocytophaga, spirochetes or motile rods. The present study indicates that A. actinomycetemcomitans is an important etiologic agent in localized juvenile periodontitis. Also, this study demonstrates that the effectiveness of therapy can be monitored by subgingival A. actinomycetemcomitans counts, and that periodontal A, actinomycetemcomitans infections cannot be resolved by root surface debridement alone but can be cured by systemic tetracycline therapy.     

Plasma vitamin D and cytokines in periodontal disease and postmenopausal osteoporosis

Jabbar S, Drury J, Fordham J, Datta HK, Francis RM, Tuck SP. Plasma vitamin D and cytokines in periodontal disease and postmenopausal osteoporosis. J Periodont Res 2011; 46: 97–104. © 2010 John Wiley & Sons A/S Background and Objective: Osteoporosis and periodontal disease are chronic diseases, in the pathogenesis of which plasma osteoprotogerin (OPG) and RANKL are important. The study aimed to investigate the relationship between periodontal disease and plasma cytokines, vitamin D and bone mineral density in postmenopausal women with and without osteoporosis. Material and Methods: One hundred and eighty‐five postmenopausal women with osteoporosis and 185 age‐ and sex‐matched control subjects were recruited. Periodontal disease was subdivided into active or past periodontal disease. Osteoprotegerin, RANKL, 25‐hydroxyvitamin D₃ (25OHD), biochemical markers of bone turnover (serum C‐terminal telopeptide, CTX), anthropometry and bone mineral density were measured. Results: A significantly higher proportion of the women with osteoporosis had active or past periodontal disease or both compared with control subjects (87.6 vs. 37.8%, p < 0.001). Plasma 25OHD was significantly lower (p < 0.001) and RANKL and OPG significantly higher in the women with osteoporosis than in control subjects (p < 0.0001). RANKL, OPG and CTX were significantly higher in women with active periodontal disease than in those without (p < 0.001), as were OPG and CTX in past periodontal disease (p < 0.001). In active and past periodontal disease, 25OHD was significantly lower (p < 0.001). Multiple logistic regression analysis showed that periodontal disease was best predicted by RANKL, 25OHD, C‐terminal telopeptide and weight, r² = 10.4%. Conclusion: Periodontal disease is more common in women with osteoporosis and is associated with lower vitamin D and higher concentrations of RANKL and OPG. Raised cytokines may provide the underlying mechanism that links these two conditions.     

Income inequality and periodontal diseases in rich countries: an ecological cross-sectional study

There are adverse effects of income inequality on morbidity and mortality. This relationship has not been adequately examined in relation to oral health. Aims : To examine the relationship between income inequality and periodontal disease in rich countries. Participants : Adults aged 35–44 years in 17 rich countries with populations of more than 2 million. Methods : National level data on periodontal disease, income inequality and absolute national income were collected from 17 rich countries with populations of more than 2m. Pearson and partial correlations were used to examine the relationship between income inequality and percentage of 35–44‐year‐old adults with periodontal pockets ≥4mm and ≥6mm deep, adjusting for absolute national income. Results : Higher levels of income inequality were significantly associated with higher levels of periodontal disease, independently of absolute national income. Absolute income was not associated with levels of periodontal disease in these 17 rich countries. Conclusion : Income inequality appears to be an important contextual determinant of periodontal disease. The results emphasise the importance of relative income rather than absolute income in relation to periodontal disease in rich countries.