bluuebunny/crossref_metadata_2025_split huggingface dataset:
Subgingival microbiota of chronic periodontitis subjects from different geographic locations
Authors: Haffajee A. D. , Bogren A. , Hasturk H. , Feres M. , Lopez N. J. , Socransky S. S. 
Published: October 2004

AbstractBackground: Most clinical studies assume that the subgingival microbiota is similar from one geographic location to another. The purpose of the present investigation was to examine the composition of the subgingival microbiota in chronic periodontitis subjects from four countries.Method: Subjects with chronic periodontitis (N, Sweden=101; USA=115; Brazil=58; Chile=26) were recruited. Subjects were measured at baseline for plaque, gingivitis, bleeding on probing (BOP), suppuration, pocket depth (PD) and attachment level (AL) at six sites per tooth. Subgingival plaque samples taken from the mesial aspect of each tooth at baseline were individually analyzed for their content of 40 bacterial species using checkerboard DNA–DNA hybridization (total samples=6036). % DNA probe counts comprised by each species was determined for each site and averaged across sites in each subject. Significance of differences in proportions of each species among countries was determined using ancova adjusting for age, mean pocket depth, gender and smoking status. p‐Values were adjusted for multiple comparisons.Results: On average, all species were detected in samples from subjects in the four countries. Thirteen species differed significantly in adjusted mean proportions among countries even after adjusting for multiple comparisons. Porphyromonas gingivalis, one species that differed in proportions among countries, comprised adjusted means of 7.5, 11.9, 1.6 and 6.6% of the microbiota in subjects from Brazil, Chile, Sweden and USA (p<0.001), while mean proportions of Treponema denticola were 6.7, 4.2, 0.8 and 2.3, respectively (p<0.001). In contrast, a key periodontal pathogen, Tannerella forsythensis, exhibited mean proportions ranging from 6.2–8.5% and did not differ significantly among countries. Besides these species, prominent species in Brazil were Actinomyces naeslundii genospecies 1 and 2 (8.4%, 7.2%) and Prevotella intermedia (6.5%); in Chile, Prevotella melaninogenica (6.4%) and Neisseria mucosa (5.3%); in Sweden A. naeslundii genospecies 2 (8.4%), Capnocytophaga gingivalis (7.1%) and Peptostreptococcus micros (5.0%); in USA A. naeslundii genospecies 2 (7.5%), P. intermedia (6.8%) and C. gingivalis (6.1%).Conclusions: The microbial profiles of subgingival plaque samples from chronic periodontitis subjects in four countries showed surprisingly marked differences. These differences persisted after adjusting for age, mean pocket depth, gender and smoking status.
Longitudinal stability of serum immunoglobulin G responses to periodontal bacteria
Authors: Papapanou P. N. , Neiderud A. M. , Disick E. , Lalla E. , Miller G. C. , Dahlén G. 
Published: October 2004

AbstractBackground: The value of seroepidemiology in the study of periodontal infections has not been adequately explored. This study examined serum immunoglobulin (IgG) responses to periodontal bacteria in patients with periodontitis and periodontitis‐free individuals over a 30‐month period.Methods: Eighty‐nine patients with chronic periodontitis and 42 control subjects with no deep periodontal pockets and no or minimal attachment loss (30–72 years old, 43% men) were included. Patients were examined at baseline, after completed periodontal therapy 4 months post‐baseline, and at 30 months, and controls, at baseline and 30 months. IgG antibodies to 19 periodontal species were determined by checkerboard immunoblotting.Results: On average, patients displayed at baseline up to 800‐fold higher titers than controls to all but three species. Over the 30‐month period, titers remained stable at low levels in controls. In patients, periodontal conditions improved from a baseline mean probing depth of 3.6 mm, bleeding on probing of 62% and an average of 21.5 pockets of=6 mm/person, to 2.5 mm mean pocket depth, 30% bleeding on probing, and 1.2 deep pockets, at 30 months. Over time, antibody titers showed a modest decline in patients, but remained significantly elevated at 30 months in comparison with controls. Antibody‐level changes over time were not significantly different between subjects that did and did not receive adjunctive systemic antibiotics.Conclusions: Conspicuous differences in IgG titers to periodontal bacteria exist between periodontitis patients and periodontally healthy controls. Despite successful periodontal therapy, titers remained elevated over a 30‐month period, suggesting that serology may mark the history of past periodontal infection.
The CD14 −159C‐to‐T promoter polymorphism in periodontal disease
Authors: Folwaczny Matthias , Glas Jürgen , Török Helga‐Paula , Fricke Kathinka , Folwaczny Christian 
Published: October 2004

AbstractBackground: A single‐nucleotide promoter polymorphism in the CD14 gene was associated with various inflammatory conditions. The present study sought to determine the frequency of the CD14 −159C‐to‐T polymorphism among subjects with periodontitis and healthy control individuals.Methods: A total of 70 patients with periodontal disease and 75 healthy controls were genotyped for the CD14 −159C‐to‐T polymorphism. Genotyping was performed by polymerase chain reaction and restriction fragment length polymorphism analysis. The allele frequencies and distribution of genotypes within both study groups were compared using Fisher's exact test at a level of significance of 5% (p<0.05).Results: Overall, the frequency for the CD14 −159T allele in patients with periodontitis was 39.3% (55/140) and 48.0% (72/150) for the controls (p=0.135). The CD14 −159C allele was significantly more prevalent (p=0.013) among females with periodontitis (33.3%; 24/72) as compared with healthy control subjects (55.6%; 30/54). In contrast, the distribution of the CD14 −159C‐to‐T polymorphism showed no significant difference among males with and without periodontitis (p=0.816).Conclusion: Herein, the C −159T promoter polymorphism of the CD14 gene was associated in female but not in male patients with periodontal disease.
Significant influence of scaler tip design on root substance loss resulting from ultrasonic scaling: a laserprofilometric in vitro study
Authors: Jepsen Søren , Ayna Mustafa , Hedderich Jürgen , Eberhard Jörg 
Published: October 2004

AbstractObjectives: Ultrasonic scalers have become increasingly popular for subgingival debridement. The aim of the present study was to investigate the influence of different working tip designs (narrow versus wide) on root substance loss caused by either magnetostrictive or piezoelectric ultrasonic devices.Methods: In this in vitro study, a magnetostrictive ultrasonic system with either Slimline or TFI‐10 inserts and a piezoelectric ultrasonic system with either Perioprobe or Type‐A inserts were compared at different application forces. Loss of root dentin was determined by defect width, defect depth and defect volume resulting from standardized instrumentation using laser profilometry.Results: There were consistent and statistically significant differences between all groups. The mean observed dentin alterations for the magnetostrictive ultrasonic device operating a Slimline insert at a lateral force of 0.3 N were 254.4 μm, 6.3 μm and 22.5 μm3 and for the TFI‐10 tip 759.0 μm, 23.5 μm and 160.2 μm3 for the parameters defect width, depth and volume, respectively. For the piezoelectric ultrasonic system operating a Perioprobe insert, the corresponding mean values were 352.0 μm/12.1 μm/56.4 μm3 and for the universal Type‐A insert they were 402.4 μm/14.0 μm/133.4 μm3. With application forces of 0.7 N, root substance removal increased up to twofold.Conclusion: The present investigation could demonstrate that the aggressiveness of magnetostrictive and piezoelectric ultrasonic devices to root substance was significantly influenced by the scaler tip designs, increasing for wider scaler tips as compared with narrow, probe‐shaped inserts.
Effects of post‐surgical cleansing protocols on early plaque control in periodontal and/or periimplant wound healing
Authors: Heitz F. , Heitz‐Mayfield L. J. A. , Lang N. P. 
Published: October 2004

AbstractObjective:The aim of this RCT was to evaluate early wound healing following specific post‐surgical care protocols.Material and Methods:Following periodontal flap surgery, 60 patients were randomly assigned to follow one of two post‐surgical protocols. Subjects smoking >20 cigarettes per day were excluded. Patients following the control protocol rinsed twice daily for 1 min with 0.1% of chlorhexidine (CHX) for 4 weeks. In addition to CHX rinsing, patients assigned to the test protocol applied CHX locally using a special very soft surgical toothbrush (Chirugia®) from days 3 to 14, and a soft toothbrush (Ultrasuave®) from days 14 to 28, twice daily. Baseline measurements included gingival crevicular fluid (GCF) flow rate, probing depth, probing attachment level, presence of bleeding on probing and full‐mouth plaque score. Measurements were repeated at 1, 2 and 4 weeks after surgery.Results:Both post‐surgical protocols resulted in successful wound healing and optimal wound closure at 4 weeks. There were no statistical differences in the GCF flow rate between test and control protocols. There was a lower incidence of recession of 2 mm following the test protocol.Conclusion:The use of specific post‐surgical cleansing protocols including the introduction of mechanical cleansing at day 3, using local application of CHX in addition to daily rinsing with CHX may be recommended.
The involvement of platelet‐derived growth factor receptors and insulin‐like growth factor‐I receptors signaling during mineralized nodule formation by human periodontal ligament cells
Authors: Nemoto Eiji , Shimonishi Mitsuru , Nitta Yasutaka , Shimauchi Hidetoshi 
Published: October 2004

Background and objective:  Periodontal ligament cells are regarded to have the capacity to differentiate into cementoblasts or osteoblasts, and are capable of forming a mineralized nodule in vitro. However, the precise mechanisms are unclear. Here we evaluated the possible involvement of growth factor receptors, such as the platelet‐derived growth factor receptor (PDGFR), insulin‐like growth factor‐I receptor (IGF‐IR), and epidermal growth factor receptor (EGFR) on periodontal ligament cells and their ligands during periodontal ligament cells differentiation in vitro.Methods:  Human periodontal ligament cells were differentiated via culturing in the presence of dexamethasone, ascorbic acid, and β‐glycerophosphate for mineralized nodule formation, characterized by von Kossa staining. Expressions of receptors and their ligands were analyzed by flow cytometry/reverse transcription‐polymerase chain reaction.Results:  During the differentiation, PDGFR‐α was held at a lower level compared with the control. PDGFR‐β, however, was maintained at a slightly higher level that was reversed to the control level when mineralized nodules formed. In contrast, IGF‐IR and EGFR were not substantially different from the control. The mineralized nodule formation was strongly inhibited by a PDGFR kinase blocker (AG1295 and AG1296), partially inhibited by an IGF‐IR kinase blocker (I‐Ome‐AG538 and AG1024), and not inhibited by an EGFR kinase blocker (AG99). PDGF‐A, PDGF‐C, PDGF‐D, IGF‐I, and IGF‐II, but not PDGF‐B, were expressed on the control as well as dexamethasone/ascorbic acid‐treated periodontal ligament cells during mineralized nodule formation; however, the pattern of their expressions was quite different.Conclusion:  These findings suggest that a pathway of PDGFs/PDGFR and IGFs/IGF‐IR on periodontal ligament cells are involved during mineralized nodule formation, and that PDGFs and IGFs expressed by periodontal ligament cells may contribute to the formation.
Epidermal growth factor stimulates urokinase‐type plasminogen activator expression in human gingival fibroblasts. Possible modulation by genistein and curcumin
Authors: Smith Patricio C. , Santibañez Juan F. , Morales Juan P. , Martinez Jorge 
Published: October 2004

Background:  Regulation of the extracellular matrix turnover is a crucial process in wound healing and the progress of periodontal disease. It has been proposed that urokinase‐type plasminogen activator (uPA), under the control of growth factors or cytokines, provides the proteolytic potential to the accomplishment of these cellular events. Epidermal growth factor (EGF) is one of the growth factors that has been shown to be active in uPA regulation.Methods:  In this study, we have assessed the effect of EGF on uPA expression in primary cultures of human gingival fibroblasts. We also studied the signaling pathways involved in this process and the role of the dietary phytoestrogens curcumin and genistein as potential modulators of this response.Results:  Human gingival fibroblasts expressed a basal uPA activity, which was inhibited by genistein, but not by curcumin. After treatment with 10 ng/ml EGF, uPA production was strongly stimulated. Exposure to genistein and curcumin inhibited EGF‐stimulated urokinase production, although only genistein showed a statistically significant inhibitory response. Using more specific inhibitors, we found that the mitogen‐activated extracellular kinase and c‐Jun N‐terminal kinase (JNK) inhibitors PD98059 and SP600125 also blocked the EGF‐dependent stimulatory effect. On the other hand, SB203580, inhibitor of the p38 member of mitogen‐activated protein kinase family, did not alter this response. In accordance to these findings, EGF stimulated a potent activation of JNK and a mild activation of extracellular signal‐regulated kinases 1/2. Finally, EGF stimulated the phosphorylation of its receptor and tyrphostin (AG1478), curcumin and genistein were able to inhibit this stimulatory effect.Conclusions:  These results indicate that EGF constitutes a strong stimuli on uPA expression in human gingival fibroblasts. Our data also shows that EGF‐stimulated uPA production involves the activation of the extracellular signal‐regulated kinases 1/2 and JNK signaling pathways and might be modulated by the natural phytoestrogens curcumin and genistein.
Effects of alendronate on restoration of biomechanical properties of periodontium in replanted rat molars
Authors: Shibata T. , Komatsu K. , Shimada A. , Shimoda S. , Oida S. , Kawasaki K. , Chiba M. 
Published: October 2004

Objective:  We examined the effect of the pretreatment of roots with alendronate on the restoration of the support function of the healing periodontal ligament in replanted rat molars.Methods:  The left maxillary first molars were extracted, placed in 0.9% NaCl containing 1 mm alendronate (alendronate group) or 0.9% NaCl (control group) for 5 min, and were replanted into their sockets. Groups of animals were killed at 7, 14, and 21 days after replantation. Normal control rats were also killed on the same days. The force required to extract the replanted or normal tooth from its socket was measured, and a load–deformation curve was developed and analyzed. Micro‐computed tomography and histologic analyses were also made.Results:  The mechanical properties of the healing periodontal ligament in the alendronate group were gradually restored from 7 to 21 days. However, fractures of the roots and bones during mechanical testing occurred in most of the replanted teeth in the control group at 21 days. The rates of restoration of the mechanical strength, extensibility, stiffness, and toughness for the alendronate group at 21 days were 67, 98, 74, and 68% of the normal controls, respectively. Micro‐computed tomography and histologic observations revealed that bone‐like structures within the pulp and ankylosis between the roots and socket bones occurred commonly in the control group, but were uncommon in the alendronate group.Conclusions:  Our findings suggest that the pretreatment with alendronate inhibits the formation of abnormal mineralized tissues and results in better restoration of the support function of the healing periodontal ligament in replanted teeth.
Prevotella intermedia lipopolysaccharide stimulates release of nitric oxide by inducing expression of inducible nitric oxide synthase
Authors: Kim Sung‐Jo , Ha Mi‐Suk , Choi Eun‐Young , Choi Jeom‐Il , Choi In‐Soon 
Published: October 2004

Objectives:  The purpose of this study was to examine the effects of lipopolysaccharide from Prevotella intermedia, a major cause of inflammatory periodontal disease, on the production of nitric oxide (NO) and expression of inducible nitric oxide synthase (iNOS) in the murine macrophage cell line RAW264.7. We also attempted to throw light on the signaling mechanisms involved in P. intermedia lipopolysaccharide‐induced NO production.Material and methods:  Lipopolysaccharide from P. intermedia ATCC 25611 was prepared by the standard hot phenol–water method. NO production was assayed by measuring the accumulation of nitrite in culture supernatants. Western blot analysis of iNOS and analysis of reverse transcription‐polymerase chain reaction (RT‐PCR) products were carried out.Results:  We found that P. intermedia lipopolysaccharide can induce iNOS expression and stimulate the release of NO without additional stimuli and demonstrated an important role of the transcription factor nuclear factor‐κB (NF‐κB) and microtubule polymerization in NO production. The production of NO required l‐arginine but not activation of protein kinase C or protein tyrosine kinase.Conclusions:  The present study clearly shows that P. intermedia lipopolysaccharide fully induced iNOS expression and NO production in RAW264.7 cells in the absence of other stimuli. The ability of P. intermedia lipopolysaccharide to promote the production of NO may be important in the pathogenesis of inflammatory periodontal disease.
The interleukin‐10 knockout mouse is highly susceptible to Porphyromonas gingivalis‐induced alveolar bone loss
Authors: Sasaki Hajime , Okamatsu Yoshimasa , Kawai Toshihisa , Kent Ralph , Taubman Martin , Stashenko Philip 
Published: October 2004

Objective:  Interleukin‐10 is an anti‐inflammatory cytokine that reduces periapical bone loss, but its role in periodontal bone loss is unclear. In the present study, we tested the hypothesis that endogenous interleukin‐10 is a potent suppressor of Porphyromonas gingivalis‐induced alveolar bone loss in vivo.Methods:  Interleukin‐10 knockout (–/–) and wild‐type mice were inoculated intraorally with P. gingivalis. Non‐infected animals served as negative controls. Alveolar bone loss, gingival cytokine levels, and gingival gene expression were assessed using morphometric analysis, enzyme‐linked immunosorbent assay (ELISA), and semiquantitative reverse transcription polymerase chain reaction (RT–PCR), respectively.Results:  P. gingivalis‐infected interleukin‐10–/– mice exhibited severe alveolar bone loss compared to non‐infected interleukin‐10–/– and wild‐type mice by day 42. Surprisingly, bone resorptive cytokines interleukin‐1α and tumor necrosis factor alpha (TNF‐α) were not up‐regulated in gingival tissues by P. gingivalis‐infection. Although interleukin‐1β was marginally increased, blockade of both interleukin‐1 isoforms or interleukin‐1 receptor type I with neutralizing antisera failed to reduce alveolar bone loss in interleukin‐10–/– mice, indicating the operation of an interleukin‐1‐independent mechanism. No strong correlations between bone loss and other cytokines was observed, although interferon gamma (IFNγ), interleukin‐6, interleukin‐4, and prostaglandin E2 were modestly up‐regulated in infected interleukin‐10–/– mice. P. gingivalis infection reduced the expression of cell markers in gingival tissue on days 7 and 14 in both interleukin‐10–/– and wild‐type animals, suggestive of bacteria‐induced cytotoxicity or apoptosis. This was followed by up‐regulated expression of receptor activator of nuclear factor kappa B ligand (RANKL) and CD40 ligand (CD40L on days 28 and 70 in infected interleukin‐10–/– mice only.Conclusion:  The interleukin‐10–/– mouse is highly susceptible to bone loss induced by the periodontal pathogen P. gingivalis, which is mediated via an interleukin‐1‐independent pathway.
Periodontal pathogens in atheromatous plaques. A controlled clinical and laboratory trial
Authors: Cairo F. , Gaeta C. , Dorigo W. , Oggioni M. R. , Pratesi C. , Pini Prato G. P. , Pozzi G. 
Published: October 2004

Objective:  A possible relationship between periodontitis and cardiovascular disease has been suggested. The aims of this controlled clinical study were: (i) to ascertain the presence of periodontal bacteria DNA [Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythensis (formerly Bacteroides forsythus)] in carotid atheromatous plaques and (ii) to assess the concomitant presence of the same periodontal bacteria DNA, if any, in periodontal pockets and in carotid atheroma in the same patient.Methods:  A total of 52 patients scheduled for carotid endarderectomy were enrolled in this study. The test group consisted of 26 dentate patients; the control group included 26 edentulous patients. A complete periodontal examination, including radiographic orthopanoramic and subgingival plaque sample, was performed in the test population. Oral and X‐ray examinations were performed in the control group. Atheromatous plaques were harvested during surgical procedure for each dentate and edentulous patient and then sent to the microbiological laboratory. Subgingival plaque samples and carotid specimens were examined using the polymerase chain reaction (PCR) technique by means of specific primers for periodontal bacteria. Amplification of extracted DNA was tested using human beta‐globin specific‐primers.Results:  Out of 52 endarterectomy samples, 12 (seven dentate, five edentulous patients) were excluded as negative to DNA amplification. In subgingival plaque samples of 19 test patients, T. forsythensis (79%), F. nucleatum (63%), P. intermedia (53%), P. gingivalis (37%) and A. actinomycetemcomitans (5%) were found. No periodontal bacteria DNA was detected by PCR in any of the carotid samples in either patient group.Conclusion:  The presence of periodontal bacteria DNA in atheromatous plaques could not be confirmed by this study and thus no correlation could be established between species associated with periodontal disease and putative bacteria contributing to atheromatous plaques.
Chronic Immune Activation Associated with Chronic Helminthic and Human Immunodeficiency Virus Infections: Role of Hyporesponsiveness and Anergy
Authors: Borkow Gadi , Bentwich Zvi 
Published: October 2004

SUMMARYChronic immune activation is one of the hallmarks of human immunodeficiency virus (HIV) infection. It is present also, with very similar characteristics, in very large human populations infested with helminthic infections. We have tried to review the studies addressing the changes in the immune profiles and responses of hosts infected with either one of these two chronic infections. Not surprisingly, several of the immune derangements and impairments seen in HIV infection, and considered by many to be the “specific” effects of HIV, can be found in helminth-infected but HIV-noninfected individuals and can thus be accounted for by the chronic immune activation itself. A less appreciated element in chronic immune activation is the immune suppression and anergy which it may generate. Both HIV and helminth infections represent this aspect in a very wide and illustrative way. Different degrees of anergy and immune hyporesponsiveness are present in these infections and probably have far-reaching effects on the ability of the host to cope with these and other infections. Furthermore, they may have important practical implications, especially with regard to protective vaccinations against AIDS, for populations chronically infected with helminths and therefore widely anergic. The current knowledge of the mechanisms responsible for the generation of anergy by chronic immune activation is thoroughly reviewed.