bluuebunny/crossref_metadata_2025 huggingface dataset:
Combining Schwann Cell Bridges and Olfactory-Ensheathing Glia Grafts with Chondroitinase Promotes Locomotor Recovery after Complete Transection of the Spinal Cord
Authors: Fouad Karim , Schnell Lisa , Bunge Mary B. , Schwab Martin E. , Liebscher Thomas , Pearse Damien D.
Published: February 2005

Numerous obstacles to successful regeneration of injured axons in the adult mammalian spinal cord exist. Consequently, a treatment strategy inducing axonal regeneration and significant functional recovery after spinal cord injury has to overcome these obstacles. The current study attempted to address multiple impediments to regeneration by using a combinatory strategy after complete spinal cord transection in adult rats: (1) to reduce inhibitory cues in the glial scar (chondroitinase ABC), (2) to provide a growth-supportive substrate for axonal regeneration [Schwann cells (SCs)], and (3) to enable regenerated axons to exit the bridge to re-enter the spinal cord (olfactory ensheathing glia). The combination of SC bridge, olfactory ensheathing glia, and chondroitinase ABC provided significant benefit compared with grafts only or the untreated group. Significant improvements were observed in the Basso, Beattie, and Bresnahan score and in forelimb/hindlimb coupling. This recovery was accompanied by increased numbers of both myelinated axons in the SC bridge and serotonergic fibers that grew through the bridge and into the caudal spinal cord. Although prominent descending tracts such as the corticospinal and reticulospinal tracts did not successfully regenerate through the bridge, it appeared that other populations of regenerated fibers were the driving force for the observed recovery; there was a significant correlation between numbers of myelinated fibers in the bridge and improved coupling of forelimb and hindlimb as well as open-field locomotion. Our study tests how proven experimental treatments interact in a well-established animal model, thus providing needed direction for the development of future combinatory treatment regimens.
Rapid Activity-Driven SNARE-Dependent Trafficking of Nicotinic Receptors on Somatic Spines
Authors: Liu Zhaoping , Tearle Adam W. , Nai Qiang , Berg Darwin K.
Published: February 2005

Rapid trafficking of glutamate receptors contributes importantly to synaptic plasticity, but whether similar trafficking extends to other ionotropic receptors is unknown. Nicotinic acetylcholine receptors containing α7 subunits are widely expressed in the nervous system and allow calcium influx. Because of this, α7-containing receptors regulate diverse events, depending on the signaling pathways available. We find that the receptors codistribute with target solubleN-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) postsynaptically and that nicotinic stimulation rapidly induces SNARE-dependent vesicular endocytosis accompanied by receptor internalization. At the same time, a SNARE-dependent process recruits receptors to the cell surface from internal pools. Overall, the trafficking does not markedly change the number of surface receptors or their combined whole-cell response to nicotine. SNARE-dependent trafficking is needed, however, for the receptors to remain capable of activating the transcription factor cAMP response element-binding protein and attendant gene expression when repeatedly challenged. Thus, trafficking appears to be essential for maintaining functional coupling between α7-receptor responses and downstream signaling.
Ceruloplasmin Oxidase Activity as a Biomarker of Lead Exposure
Authors: Leelakunakorn Warin , Sriworawit Rosawan , Soontaros Suganya
Published: February 2005

Ceruloplasmin Oxidase Activity as a Biomarker of Lead Exposure: Warin Leelakunakorn, et al. Department of Pathology, Faculty of Medicine, Mahidol University, Thailand—The most sensitive method used in monitoring the blood lead‐level is atomic absorption spectrophotometry. Its limitation due to its high cost has made delta‐aminolaevulinic acid dehydratase (δ‐ALAD) inhibition more popular. This work demonstrates that ceruloplasmin (Cp), the blue‐colored copper containing alpha‐2 globulin (α 2 globulin) glycoprotein in serum, can serve as a high‐potential biomarker for lead exposure. Sephadex G‐200 column chromatography demonstrated that lead‐intoxicated patient serum transferrin and ceruloplasmin are bound to lead. The ceruloplasmin's oxidase and δ‐ALAD activities are reduced when the blood‐lead level increases (thresholds of 10.0 and 12.5 µg/100 mL respectively), with a correlation coefficient of –0.8643 and –0.6785 which accurately estimate a blood lead level of 74.7% and 46.0%, respectively. When the blood‐lead level was less than 20 µ g/100 mL, correlation coefficients of –0.5785 and –0.6963 suggested that Cp may serve as a good biomarker. Other advantages in using Cp in monitoring the bloodlead level were its stability: the enzyme was more stable at –20°C, for more than 2 wk, and its practical and rapid determination procedure.
Anti‐Caspase‐8 Autoantibody Response in Silicosis Patients is Associated with HLA‐DRB1, DQB1 and DPB1 Alleles
Authors: Ueki Ayako , Isozaki Yumika , Kusaka Masayasu
Published: February 2005

Anti‐Caspase‐8 Autoantibody Response in Silicosis Patients is Associated with HLA‐DRB1, DQB1 and DPB1 Alleles: Ayako Ueki, et al. Kawasaki University of Medical Welfare—We reported previously the autoantibodies directed to caspase‐8 among patients with silicosis, systemic sclerosis (SSc) and systemic lupus erythematosus (SLE), and in healthy individuals. In this study, we analyzed the correlation between anti‐caspase‐8 autoantibody responses and HLA class II alleles in silicosis patients. The frequencies of HLA‐DRB1∗0406 were significantly higher in antibody positive patients (16.67%) than in control individuals (3.03%, p=0.0006). The lysine (K) at position 71 as in DRB1∗0406 has been reported to be associated with rheumatoid arthritis (RA) and insulin dependent diabetes mellitus (IDDM). The haplotype HLA‐DR4; DQB1∗0302 was detected in 4 of 12 antibody positive patients. RA, IDDM, or pemphygus vulgaris link to the haplotype. The frequencies of DQB1∗0401 were significantly lower in antibody positive patients (0%) than that in controls (13.33%, p=0.0390). The aspartic acid at position 57 in the DQB1 molecule as in DQB1∗0401 is reported to play a role in the resistance to IDDM. The frequency of DPB1∗0601 in antibody positive patients (5.88%) was significantly higher than that in controls (0.56%, p=0.0003). DPB1∗0601 is reported to be a risk factor among RA patients, and glutamate at position 69 of the DPB1 molecule may be involved. Repeated and continuous screening of autoantibodies seems to be necessary among workers in contact with Si‐related substances for the detection of immunological disorders in the early stage.
Occlusal Trauma: Effect and Impact on the Periodontium
Authors: Hallmon William W.
Published: February 2005

This focused review is limited to a number of investigations in an attempt to specifically address the histological and clinical effects of excessive occlusal forces on the teeth and periodontium and to provide a basis of classification for this interaction. This review does not include the effects of occlusal forces on dental implants or dental prostheses/appliances. Ann Periodontol 1999;4:102‐107.
Tooth‐Related Issues
Authors: Blieden Timothy M.
Published: February 2005

Several conditions exist around teeth that may predispose the periodontium to disease. These situations may occur as a result of the condition or position of teeth or as a result of tooth treatment. In certain cases these tooth‐related factors may contribute to the initiation of periodontal disease. While the etiology of periodontal disease is bacterial, factors that enhance bacterial accumulation or allow the ingress of bacteria into the periodontium should be considered in the classification and diagnosis of periodontal diseases. This is because many times these tooth‐related issues can cause site‐specific problems that require treatment in an otherwise intact periodontium. Several factors related to tooth/root anatomy, restorative, and endodontic considerations have been associated with gingival inflammation, attachment loss, and bone loss. These factors will be reviewed as they relate to their potential to promote damage to the periodontium. Ann Periodontol 1999;4:91‐96.
Three‐Year Post‐Placement Survival of Implants Mobile at Placement
Authors: Orenstein Ira H. , Tarnow Dennis P. , Morris Harold F. , Ochi Shigeru
Published: February 2005

Background: Although rigid fixation of endosseous implants at the time of placement is generally thought to be a prerequisite for successful osseointegration, the Dental Implant Clinical Research Group (DICRG) of the Department of Veterans Affairs has reported on implants that integrated despite being mobile at placement. The present study examines the frequency of osseointegration and the 36‐month post‐placement survival of implants mobile at placement in a prospective, multicenter, longitudinal clinical study of more than 3,000 implants conducted by the DICRG.

Methods: A total of 3,111 implants of 6 different designs were placed in all jaw regions in more than 800 patients at 32 study centers. At the time of this report, 2,770 of these implants had been followed for 36 months post‐placement. They included 89 implants that were mobile at placement. Data for demographic variables, implant coating, bone quality, incision type, bone augmentation, and antibiotic usage were recorded. An electronic hand‐held probe was used to measure mobility at uncovering and at regular follow‐up intervals.

Results: Eighty‐nine of 2,770 inserted implants were mobile at placement. Results are reported for two periods: from placement to 36 months and from prosthetic loading to 36 months. The latter method eliminated early failures and resulted in substantially higher scores for both mobile implants at placement (95.9% survival from prosthetic loading to 36 months post‐placement versus 79.8% from placement to 36 months) and implants not mobile at placement (98.4% versus 93.4%). Mobility at placement was significant to 3‐year survival (P <0.001). Hydroxyapatite (HA) coating improved the performance of implants mobile at placement (91.8% for HA‐coated versus 53.6% for non‐HA) and those not mobile at placement (97.2% for HAcoated versus 87.4% for non‐HA). Radiographic findings suggested that crestal bone response around implants which were mobile versus immobile at placement was similar.

Conclusions: Although implant stability at the time of placement is clearly desirable as seen in the superior 3‐year survival of stable implants, it may not be an absolute prerequisite to osseointegration or to longterm survival. Several factors may influence the decision to remove or replace a mobile implant. HA‐coating significantly improved the performance of both mobile and immobile implants at placement to 3 years post‐placement (P <0.001). Ann Periodontol 2000;5:32‐41.
Periodontitis and Diabetes Interrelationships: Role of Inflammation
Authors: Iacopino Anthony M.
Published: February 2005

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifi‐cally immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes‐induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes‐induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis‐induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin‐1 beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic β cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes‐induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes. Ann Periodontol 2001;6:125‐137.
The Relationship Between Skeletal and Oral Bone Mineral Density: An Overview
Authors: Chesnut Charles H.
Published: February 2005

Is oral osteopenia (bone loss of the jaws) a component of systemic osteopenia/osteoporosis (systemic bone loss, with or without fracture) or only an accompanying manifestation of periodontal disease? Put other ways: 1) is systemic osteopenia a risk factor for periodontitis; 2) is systemic osteopenia a risk factor for oral osteopenia independent of periodontal disease; or 3) is periodontal disease the primary (exclusive) risk factor for oral osteopenia? Despite 2 decades of scientific inquiry into these questions, the answers remain elusive. Ann Periodontol 2001;6: 193‐196.
Genes of Periodontopathogens Expressed During Human Disease
Authors: Song Yo‐Han , Kozarov Emil V. , Walters Sheila M. , Cao Sam Linsen , Handfield Martin , Hillman Jeffrey D. , Progulske‐Fox Ann
Published: February 2005

Background: Since many bacterial genes are environmentally regulated, the screening for virulence‐associated factors using classical genetic and molecular biology approaches can be biased under laboratory growth conditions of a given pathogen, because the required conditions for expression of many virulence factors may not occur during in vitro growth. Thus, technologies have been developed during the past several years to identify genes that are expressed during disease using animal models of human disease. However, animal models are not always truly representative of human disease, and with many pathogens, there is no appropriate animal model.

Methods: A new technology, in vivo‐induced antigen technology (IVIAT) was thus engineered and tested in our laboratory to screen for genes of pathogenic organisms induced specifically in humans, without the use of animal or artificial models of infection. This technology uses pooled sera from patients to probe for genes expressed exclusively in vivo (or ivi, in vivo‐induced genes). IVIAT was originally designed for the study of Actinobacillus actinomycetemcomitans pathogenesis, but we have now extended it to other oral pathogens including Porphyromonas gingivalis.

Results: One hundred seventy‐one thousand (171,000) clones from P. gingivalis strain W83 were screened and 144 were con‐ firmed positive. Over 300,000 A. actinomycetemcomitans clones were probed, and 116 were confirmed positive using a quantitative blot assay.

Conclusion: IVIAT has proven useful in identifying previously unknown in vivo‐induced genes that are likely involved in virulence and are thus excellent candidates for use in diagnostic and therapeutic strategies, including vaccine design. Ann Periodontol 2002;7:38‐42.
Immune Processes in Periodontal Disease: A Review
Authors: Kinane Denis F. , Lappin David F.
Published: February 2005

The inflammatory and immune processes in periodontitis are complex and, although a great deal of information is available, many questions remain. Variation in human susceptibility to periodontitis has long been accepted, but the pathological basis of this is poorly understood. Similarly, we know little of the differences, if any, between the pathology of chronic and aggressive periodontitis. Genetics and environmental influences play a role in the susceptibility process, but if and how that translates through the immune and inflammatory processes to produce the plasma cell‐dominated lesions seen in periodontitis remain to be elucidated. This review will focus on immunological aspects of the inflammatory changes seen in gingivitis and periodontitis, addressing both humoral and cellular responses to the microbial insult from dental plaque. A tendency for an individual or site to form an extensive plasma cell infiltrate may indicate an inability to defend against periodontopathogens and thus a predisposition to periodontitis. The issues to be considered include: 1) homing of immune and inflammatory cells to target tissues; 2) their local proliferation and synthetic activity; 3) the cytokine profile of the leukocytes; 4) the immunoglobulin subclasses of locally produced antibodies; 5) mucosal and systemic immune characteristics of the response; 6) the humoral immune response in periodontal health and disease states; and 7) the antigenic target of the immune response in periodontal lesions. Ann Periodontol 2002;7:62‐71.
Periodontal Disease Increases the Risk of Preterm Delivery Among Preeclamptic Women
Authors: Riché Estelle L. , Boggess Kim A. , Lieff Susi , Murtha Amy P. , Auten Richard L. , Beck James D. , Offenbacher Steven
Published: February 2005

Background: Preterm births are a major cause of neonatal morbidity and mortality, and represent an important public health issue. About 30% of preterm births are due to medical conditions of the mother or the fetus, among which preeclampsia plays a major role. We have previously reported that maternal periodontal disease enhances the risk for preterm delivery and preeclampsia. Our current objective was to determine whether maternal periodontal disease increases the risk for preterm delivery among preeclamptic women.

Methods: Women were enrolled prior to their twenty‐sixth week of gestation. Periodontal status was assessed at baseline and defined as healthy, mild, or moderate/severe. Repeat examinations were performed at delivery to assess changes in periodontal status.

Results: A cohort of 1,020 women was studied, 47 of whom had preeclampsia. A strong association between periodontal disease status at enrollment and rate of premature delivery was observed among preeclamptic women after adjusting for the major risk factors for preterm delivery, including maternal race; age; marital status; WIC (women, infants, children program) or food stamps; insurance; previous preterm delivery; and chorioamnionitis. Among preeclamptic women, 49.3% with mild periodontal disease and 82.6% with moderate to severe disease delivered preterm (hazard ratios [HR] 4.11 and 11.0, respectively). Periodontal disease worsening during pregnancy in preeclamptic women was also associated with an increased risk of preterm births (HR 8.44).

Conclusion: These results suggest that mothers with preeclampsia may be at greater risk for preterm delivery if periodontal disease is present early in pregnancy or progresses during pregnancy. Ann Periodontol 2002;7:95‐101.
Periodontal Disease as a Risk Factor for Adverse Pregnancy Outcomes. A Systematic Review
Authors: Scannapieco Frank A. , Bush Renee B. , Paju Susanna
Published: February 2005

Background: Recent studies have implicated a variety of infections, including periodontal diseases, as risk factors for adverse pregnancy outcomes such as prematurity and low birth weight.

Rationale: A number of studies have shown that bacterial vaginosis is related to preterm and/or low birth weight (PT/LBW), which continues to be a significant cause of infant morbidity and mortality. It is also possible that other infectious processes, including periodontal diseases, contribute to PT/LBW. This systematic review examines the literature to determine the possible relationship between PT/LBW and periodontal diseases.

Focused Question: Does prevention/control of periodontal disease as compared to controls have an impact on the initiation/progression of adverse pregnancy outcomes?

Search Protocol: MEDLINE, pre‐MEDLINE, MEDLINE Daily Update, and the Cochrane Oral Controlled Trials Register were searched to identify published studies that related variables associated with PT/LBW and periodontal disease. Searches were performed for articles published through October 2002.

Inclusion criteria: Randomized controlled clinical trials (RCTs), case‐control, and cohort studies were included. Study populations included mothers, with or without periodontal disease, who gave birth to preterm and/or mature infants. The interventions considered included all forms of periodontal therapy.

Exclusion criteria: Only studies on humans were included.

Data Collection and Analysis: Due to study heterogeneity, meta‐analysis was not possible.

Main Results

Of the over 660 studies identified, 12 (6 case‐control, 3 cross‐sectional and longitudinal, and 3 intervention) met inclusion and exclusion criteria and were included in the analysis.

While several studies implicated periodontal disease as a risk factor for PT/LBW, few assessed the impact of the prevention and treatment of periodontal disease on outcomes.

Several epidemiologic studies did not support periodontal disease as a risk factor for PT/LBW

Reviewers' Conclusions

Periodontal disease may be a risk factor for PT/LBW

Additional longitudinal, epidemiologic, and interventional studies are needed to validate this association and to determine whether it is causal.

It is not yet clear whether periodontal diseases play a causal role in adverse pregnancy outcomes.

Preliminary evidence to date suggests that periodontal intervention may reduce adverse pregnancy outcomes.

Ann Periodontol 2003;8:70‐78
The Informativeness of Attachment Loss on Tooth Mortality
Authors: Hujoel P.P. , Löe H. , Anerud A. , Boysen H. , Leroux B.G.
Published: February 2005

Background: In periodontal clinical trials, clinical attachment level measurements are commonly used as surrogates for tooth loss. Conclusions regarding treatment efficacy in these trials are valid if: 1) the surrogate is informative on tooth loss, and 2) the surrogate captures the effect of treatment on tooth loss. The goal of this study was to evaluate the first criterion: Are serial clinical attachment loss measurements informative on overall tooth mortality?

Methods: Young Norwegian men (aged 17 to 35) were first examined in 1969 (n=565) and followed for 26 years with examinations in 1971 (n=381), 1973 (n=292), 1975 (n=245), 1981 (n=228), 1988 (n=202), and 1995 (n=223). Several aspects of the serial attachment loss measurements were related to tooth mortality risk using statistical models that take into account the time‐dependent changes of the clinical attachment loss measurements.

Results: The results provided evidence that moderate attachment losses were informative on tooth mortality. Both the lifetime cumulative attachment loss, as well as attachment loss since young adulthood, of ≥2 mm or ≥3 mm was informative on tooth mortality. Tooth mortality risk increased as the attachment loss increased; loss ≥3 mm at the buccal or mesial site increased tooth mortality risk, by 91% (relative risk, 1.91; 95% confidence interval, 1.01‐3.60) and 270% (RR, 3.70; 95% CI, 1.83‐7.49), respectively.

Conclusions: We concluded that clinical attachment loss was moderately informative on overall tooth mortality in this Norwegian population. Since this finding has now been demonstrated in 3 different populations, the focus of further research should be on evaluating whether the second criterion for a valid surrogate is satisfied: Does clinical attachment loss capture the effect of periodontal treatments on tooth loss? J Periodontol 1999;70: 44‐48.
Relationship of the Subgingival Microbiota to a Chairside Test for Aspartate Aminotransferase in Gingival Crevicular Fluid
Authors: Wong Man‐Ying , Lu Chia‐Lin , Liu Cheing‐Meei , Hou Lein‐Tuan , Chang Wen‐Kuei
Published: February 2005

Background: The aim of the present study was to evaluate the association between the occurrence of certain specific periodontal pathogens and aspartate aminotransferase (AST) levels in gingival crevicular fluid (GCF).

Methods: Thirty systemically healthy subjects with moderate to advanced periodontitis were selected. Within each subject, the AST contents of GCF from sites with probing depth between 5 mm and 7 mm were measured using a chairside colorimetric test. AST‐positive site refers to one that had an AST level ≥800 μIU. Subgingival plaque samples from one AST‐positive and one negative site were collected for microbiological examination. One site with probing depth ≤3 mm and no gingival inflammation was selected as a healthy control. Clinical parameters of the chosen sites, including the plaque index and gingival index scores, probing depth, and clinical attachment level were measured. Culture and immunofluorescence (IF) were used for detecting common periodontal pathogens, including Actinobacillus actinomycetemcomitans, Peptostreptococcus micros, Campylobacter rectus, Eikenella corrodens, Fusobacterium nucleatum, Capnocytophaga species, Prevotella intermedia, Prevotella melaninogenica, and Porphyromonas gingivalis. Logistic regression was used to analyze the correlation between the AST test and certain specific pathogens.

Results: The GCF scores and total cultivable bacterial counts were higher in AST‐positive sites than either AST‐negative or healthy sites. The prevalence and proportions of specific periodontal pathogens such as C. rectus, E. corrodens, F. nucleatum, Capnocytophaga species, P. intermedia, and P. gingivalis were significantly higher in positive than in negative sites. In analyzing the correlation of the proportion of 6 pathogens with the AST test by logistic regression, only P. gingivalis showed a significant positive correlation. The odds ratio of having a high proportion of P. gingivalis in the presence of a positive AST test was 1.21.

Conclusions: The present study showed that at AST‐positive sites, there is a higher prevalence and higher proportion of certain periodontal pathogens. Although only the correlation of P. gingivalis and AST values was statistically significant, the results imply that certain periodontal pathogens may be associated with elevation of AST levels in GCF. J Periodontol 1999;70: 57‐62.
Periodontal and Computer Tomography Scanning Evaluation of Endosseous Implants in Conjunction With Sinus Lift Procedure. A 6‐Case Series
Authors: Murakami Kei , Itoh Takami , Watanabe Satoshi , Itoh Takatoshi , Naito Toru , Yokota Makoto
Published: February 2005

The aim of the present study was to evaluate endosseous implants in conjunction with the sinus lift procedure using periodontal parameters and computed tomography (CT) scanning. In 6 patients, 8 sinus lift procedures were performed to the atrophic posterior maxilla. Fourteen endosseous implants were placed. The condition of the peri‐implant mucosa was assessed postoperatively at an average of 31 months using periodontal parameters such as plaque index, probing depth, clinical attachment level, and bleeding on probing. All the implants were maintained in a clinically healthy condition throughout the observation period. CT images revealed the difference in the morphology of the sinus floor between the locations of the block‐shaped bone and the small pieces of bone which were both grafted. The results indicated that endosseous implants in conjunction with the sinus lift procedure could be maintained by monitoring the periodontal parameters. J Periodontol 1999;70:1254‐1259.
A Novel Insertion Sequence Increases the Expression of Leukotoxicity in Actinobacillus actinomycetemcomitans Clinical Isolates
Authors: He Tao , Nishihara Tatsuji , Demuth Donald R. , Ishikawa Isao
Published: February 2005

Background: The expression of leukotoxin varies among Actinobacillus actinomycetemcomitans strains and is dependent in part on the structure of the ltx promoter region. Highly leukotoxic strains, characterized by a 530 base pair (bp) deletion within the ltx promoter, have been associated with juvenile periodontitis in the United States and Europe. In the present study, we analyzed the ltx promoter structure to elucidate whether A. actinomycetemcomitans from Japanese periodontitis patients exhibits the highly toxic phenotype.

Methods: Forty‐five A. actinomycetemcomitans strains, including 43 clinical isolates, the highly leukotoxic strain JP2, and a minimally leukotoxic strain 652 were used in the study. The ltx promoter structure was analyzed by polymerase chain reaction (PCR), with oligonucleotide primers focusing the ltx promoter region, and nucleotide sequencing. Leukotoxic activity was determined by trypan blue exclusion. Western blotting assay was performed to detect the level of leukotoxin polypeptide.

Results: A 495 bp PCR product was amplified from JP2, a 1025 bp product from 652 and 41 of the clinical isolates, and a 1926 bp product from the remaining two clinical isolates (Aa IS1, Aa IS2). Sequencing of the 1926 bp PCR fragment showed that it was similar to that of strain 652 but contained an 886 bp region that was identified as an insertion sequence (IS). Both AaIS strains expressed high levels of leukotoxicity, similar to strain JP2. In addition, a mutant (Aa IS–) that had lost the IS element expressed a significantly lower level of leukotoxicity compared with AaIS strains. Furthermore, the levels of leukotoxin polypeptide expressed by these strains were consistent with their whole cell leukotoxicity.

Conclusions: A. actinomycetemcomitans clinical strains which were isolated from Japanese periodontitis patients do not possess the 530 bp ltx promoter deletion. The results of this study suggest that a high level of leukotoxin expression correlates with the insertion of the transposable DNA element. J Periodontol 1999;70:1261‐1268.
Possible Potentiation of Toxins From Prevotella intermedia, Prevotella nigrescens, and Porphyromonas gingivalis by Cotinine
Authors: Sayers Nicola M , James Jacqueline A. , Drucker David B. , Blinkhorn Anthony S.
Published: February 2005

Background: Smoking is a recognized risk factor for the initiation and progression of periodontitis. However, the mechanism by which smoking induces its negative effects on the periodontium is not clear. This study aimed to test the hypothesis that synergy may occur between cotinine and bacterial products isolated from 3 putative periodontopathogens.

Methods: A chick embryo toxin assay was used to investigate bacterial toxins (cell‐free extracellular toxins and cellfree cell lysates) from 5 species with and without cotinine. A total of 9 putative periodontopathogens (3 species) and 2 non‐oral controls (2 species) were studied. The periodontal species were: Prevotella intermedia (n = 4), Prevotella nigrescens (n = 4), and Porphyromonas gingivalis (n = 1). The control species tested were: Staphylococcus aureus (n = 1) and Escherichia coli (n = 1).

Results: The toxicity kill was significantly greater than expected by simple addition alone (P <0.05, Fisher's exact test) between cotinine (800 ng/ml) and 1) the cell‐free extracellular toxins of P. nigrescens MH1 and 2) the cellfree cell lysates of P. intermedia MH2. Synergy occurred with cotinine plus the cell‐free extracellular toxins in all but 3 periodontal isolates, and the cell‐free cell lysates in all but 2 periodontal isolates. Cotinine significantly (P<0.05, Fisher's exact test) enhanced the effects of cell‐free extracellular toxins and cell lysates from one control species (E. coli), but not the other (S. aureus).

Conclusions: These findings indicate that synergy in an in vitro assay can occur between cotinine and toxins from putative periodontopathogens. This may be one important mechanism by which smoking increases the severity of periodontitis. J Periodontol 1999;70:1269‐1275.
Bacterial Adhesion of Actinobacillus actinomycetemcomitans Serotypes to Titanium Implants: SEM Evaluation.A Preliminary Report
Authors: Ökte Emel , Sultan Nedim , Doğan Başak , Asikainen Sirkka
Published: February 2005

Background: In this study, the adherence ability of Actinobacillus actinomycetemcomitans serotypes to titanium implant surfaces was evaluated to demonstrate if any selective adherence occurs according to the serotypes of the microorganism.

Methods: The study material included 3 reference strains of A. actinomycetemcomitans serotypes a, b, and c (ATCC 29523, ATCC 43718, ATCC 33384) and 2 clinical isolates of A. actinomycetemcomitans serotypes and e (IDH 781, IDH 1705), together with commercially available titanium blade implants. For each strain, bacterial suspensions with identical concentrations (5 × 107 cells/ml) were prepared and 0.5 ml of each was added on to the implant surfaces, which had been precoated with glycine‐bovine serum albumin (BSA). After incubation at 37°C for 60 minutes in 5% CO2 in air, the implants with attached bacteria were prepared for scanning electron microscopic (SEM) observations. Bacterial adhesion was quantified on the textured body surfaces of the implants, and results were statistically analyzed with analysis of variance followed by Duncan's test. The surface ultrastructure of the bacterial cells was also evaluated descriptively.

Results: The tested strains adhered to implant surfaces in different quantities. Serotype a (ATCC 29523) showed the highest adherence affinity (statistically significant, P<0.01). When compared with each other, serotypes b, c, and d (ATCC 43718, ATCC 33384, and IDH 781) attached equally well, whereas serotype (IDH 1705) had a statistically significant low adherence capability.

Conclusions: It is suggested that in vitro A. actinomycetemcomitans adhesion to implant surfaces is strain dependent. J Periodontol 1999;70:1376‐1382
Povidone‐Iodine's Effects and Role in the Management of Periodontal Diseases: A Review
Authors: Greenstein Gary
Published: February 2005

This review article addresses the effects of povidone‐iodine (PVP‐I) and its utility in the treatment of periodontal diseases. There are data to support the following statements: PVP‐I is a potent antiseptic and, when used as a component in a rinse with H2O2, the rinse can decrease the level of gingivitis. With regards to patients with adult periodontitis, there is some evidence to indicate that PVP‐I delivered via an ultrasonic device achieves better results in deep pockets than ultrasonic debridement when water is the irrigant. The benefits of PVP‐I in the treatment of refractory periodontitis are unclear. Subgingival irrigation with PVP‐I may reduce the incidence of bacteremia if it is employed as a pre‐procedural intrasulcular irrigant; however, this technique is not recommended for high‐risk patients. PVP‐I is a safe antiseptic and does not appear to impede wound healing or induce resistant bacteria. It is an approved drug whose intraoral use is an unlabeled indication. In conclusion, the literature suggests that utilization of PVP‐I is potentially beneficial in the management of some periodontal diseases. However, additional clinical trials are needed to verify this assessment, since it is based upon a limited number of studies J Periodontol 1999; 70:1397‐1405.
Assessment of Familial Patterns of Microbial Infection in Periodontitis
Authors: Irfan Uma M. , Dawson Deborah V. , Bissada Nabil F.
Published: February 2005

The purpose of this article is to review approaches to the assessment of familial patterns of microbial infection and disease in periodontitis, and to identify statistical methods appropriate to such considerations of family data. Previous studies have provided evidence for the presence of familial aggregation of periodontal pathogens and periodontitis and have alluded to possible transmissibility of these organisms within families. Modern statistical techniques permit the appropriate analysis of the correlated data inherent in families, properly allowing for these statistical dependencies while including the possibility of adjustment for risk factors which may also aggregate in families. Such approaches as multiple linear regression, multivariate logistic regression, and regressive modeling provide the necessary tools to assess the familial aggregation of risk factors and disease in periodontitis. In particular, regressive models permit the analysis of familiality (membership to family) as a risk factor without reference to a specific underlying biologic mechanism, and also permit the possibility of adjustment for covariates, such as age and access to dental care. They also allow consideration of specific mechanisms, e.g., susceptibility genes of major effect. Using such techniques, it is possible to more completely explore and describe familial patterns of periodontal infection and other aspects of periodontal disease. J Periodontol 1999; 70:1406‐1418.
Position Paper: Tobacco Use and the Periodontal Patient
Authors:   The Research, Science and Therapy Committee of The American Academy of Periodontology
Published: February 2005

This paper was prepared by the Research, Science and Therapy Committee of The American Academy of Periodontology and is intended for the information of the dental profession. The purpose of the paper is to provide the reader with a general overview of the relationship of tobacco use and periodontal diseases. This paper will review the epidemiological and clinical findings that have led to our understanding of the role of tobacco use in relation to periodontal diseases and their treatment. In addition, this paper will review the possible underlying mechanisms for these effects from tobacco use. The practitioner can use this information in treatment decisions and in giving advice to the patients who use tobacco products. J Periodontol 1999;70:1419‐1427.
Role of Interactions Between Integrins and Extracellular Matrix Components in Healthy Epithelial Tissue and Establishment of a Long Junctional Epithelium During Periodontal Wound Healing: A Review
Authors: Gräber Hans‐Georg , Conrads Georg , Wilharm Jens , Lampert Friedrich
Published: February 2005

Following the surgical treatment of adult periodontitis, the epithelial regeneration of the periodontal attachment is non‐physiological and thus unsatisfactory, if membranes or artificial bone material are not used. Re‐epithelialization is based on the proliferation, migration, and differentiation of basal epithelial cells which are in contact with a wound matrix and whose molecular makeup differs from the extracellular matrix of intact regions. Interactions between basal epithelial cells and the extracellular matrix are mediated by special receptors on the cell surface which are known as integrins and belong to the family of cellular adhesion molecules (CAM). Various studies indicate that integrin‐mediated interaction plays a decisive role in regulating the proliferation, migration, and differentiation of the epithelial cells. This review provides an overview of the in vivo and in vitro expression of integrins by epithelial cells and the interaction between integrins and extracellular matrix (ECM) in the case of a stationary epithelium and during wound healing. The regulation of these cell‐cell and cell‐matrix interactions may represent a method for inhibiting non‐physiological epithelial regeneration on the molecular level. J Periodontol 1999;70:1511‐1522.
Relationship Between Herpesviruses and Adult Periodontitis and Periodontopathic Bacteria
Authors: Contreras A. , Umeda M. , Chen C. , Bakker I. , Morrison J.L. , Slots J.
Published: February 2005

Background: Various mammalian viruses and specific bacteria seem to play important roles in the pathogenesis of human periodontitis. This study examined the relationship between subgingival herpesviruses and periodontal disease and potential periodontopathic bacteria in 140 adults exhibiting either periodontitis or gingivitis.

Methods: A nested‐polymerase chain reaction (PCR) method determined the presence of Epstein‐Barr virus type 1 and type 2 (EBV‐1, EBV‐2), human cytomegalovirus (HCMV), and herpes simplex virus (HSV) and a 16S rRNA PCR detection method identified Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Prevotella intermedia, Prevotella nigrescens, and Treponema denticola.

Results: Using a logistic analysis, EBV‐1 showed significant positive association with P. gingivalis (odds ratio [OR] 3.37), and with coinfections of P. gingivalis and P. intermedia (OR 4.03); P. gingivalis and B. forsythus (OR 3.84); P. gingivalis and T. denticola (OR 4.17); P. gingivalis, B. forsythus, and T. denticola (OR 4.06); and P. gingivalis, P. nigrescens, and T. denticola (OR 3.29). EBV‐1 also showed positive association with severe periodontitis (OR 5.09), with increasing age (OR 1.03), and with periodontal probing depth at the sample sites (OR 1.77). HCMV was positively associated with coinfections of P. gingivalis and P. nigrescens (OR 3.23); P. gingivalis, B. forsythus, and P. nigrescens (OR 3.23); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.59); with severe periodontitis (OR 4.65); and with age (OR 1.03). Patients with mixed viral infections revealed significant associations with P. gingivalis (OR 2.27), and with coinfections of P. gingivalis and B. forsythus (OR 2.06); P. gingivalis and P. nigrescens (OR 2.91); P. gingivalis, B. forsythus, and P. nigrescens (OR 2.91); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.70) with the clinical diagnosis of slight (OR 3.73), moderate (OR 3.82), or severe periodontitis (OR 4.36), and with probing depth at the sample sites (OR 1.39). HSV and EBV‐2 showed no significant associations with any of the variables tested.

Conclusions: The results indicate that subgingival EBV‐1, HCMV, and viral coinfections are associated with the subgingival presence of some periodontal pathogens and periodontitis. Herpesviruses may exert periodontopathic potential by decreasing the host resistance against subgingival colonization and multiplication of periodontal pathogens. J Periodontol 1999;70:478‐484.
One Stage Full‐ Versus Partial‐Mouth Disinfection in the Treatment of Chronic Adult or Generalized Early‐Onset Periodontitis. I. Long‐Term Clinical Observations
Authors: Mongardini Claudio , van Steenberghe Daniel , Dekeyser Christel , Quirynen Marc
Published: February 2005

Background: A standard treatment strategy for periodontal infections often consists of 4 consecutive sessions of scaling and root planing (per quadrant, at 1‐ to 2‐week intervals), without proper disinfection of the remaining intra‐oral niches for periodontopathogens. This could theoretically lead to a reinfection of previously disinfected pockets by bacteria from an untreated region/niche. This study aimed to investigate, over an 8‐month period, the clinical benefits of a one stage full‐mouth disinfection in the control of severe periodontitis.

Methods: Sixteen patients with early‐onset periodontitis and 24 patients with severe adult periodontitis were randomly assigned to test and control groups. The control group was scaled and root planed, per quadrant, at 2‐week intervals and given standard oral hygiene instructions. A one stage full‐mouth disinfection (test group) was sought by scaling and root planing the 4 quadrants within 24 hours in combination with the application of chlorhexidine to all intra‐oral niches for periodontopathogens. Besides oral hygiene, the test group also rinsed twice daily with a 0.2% chlorhexidine solution and sprayed the tonsils with a 0.2% chlorhexidine spray, for 2 months. The plaque index, gingival index, probing depth, bleeding on probing, gingival recession, and clinical attachment level were recorded at baseline and at 1, 2, 4, and 8 months afterwards.

Results: The one stage full‐mouth disinfection resulted, in comparison to the standard therapy, in a significant (P <0.001) additional probing depth reduction and gain in attachment up to 8 months. For initial pockets ≥7 mm, the “additional” probing depth reduction at the 8 month follow‐up was 1.2 mm for single‐rooted and 0.9 mm for multi‐rooted teeth, with corresponding additional gains in attachment of 1.0 mm and 0.8 mm, respectively. The additional improvements were observed for all subgroups (adult periodontitis, generalized early‐onset cases, smokers), with the largest differences in the non‐smoking adult periodontitis patients.

Conclusions: These findings suggest that a one stage full‐mouth disinfection results in an improved clinical outcome for the treatment of chronic adult or early‐onset periodontitis as compared to scaling and root planing per quadrant at 2‐week intervals. J Periodontol 1999;70:632‐645.
A 15‐Month Evaluation of the Effects of Repeated Subgingival Minocycline in Chronic Adult Periodontitis
Authors: Van Steenberghe D. , Rosling B. , Söder P.Ö , Landry R.G. , van der Velden U. , Timmerman M.F.T. , McCarthy E.F. , Vandenhoven G. , Wouters C. , Wilson M. , Matthews J. , Newman H.N.
Published: February 2005

Background: A double‐blind, randomized, parallel, comparative study was designed to evaluate the long‐term safety and efficacy of subgingivally administered minocycline ointment versus a vehicle control.

Methods: One hundred four patients (104) with moderate to severe adult periodontitis (34 to 64 years of age; mean 46 years) were enrolled in the study. Following scaling and root planing, patients were randomized to receive either 2% minocycline ointment or a matched vehicle control. Study medication was administered directly into the periodontal pocket with a specially designed, graduated, disposable applicator at baseline; week 2; and at months 1, 3, 6, 9, and 12. Scaling and root planing was repeated at months 6 and 12. Standard clinical variables including probing depth and attachment level) were evaluated at baseline and at months 1, 3, 6, 9, 12, and 15. Microbiological sampling using DNA probes was done at baseline; at week 2; and at months 1, 3, 6, 9, 12, and 15.

Results: Both treatment groups showed significant and clinically relevant reductions in the numbers of each of the 7 microorganisms measured during the entire 15‐month study period. When differences were detected, sites treated with minocycline ointment always produced statistically significantly greater reductions than sites which received the vehicle control. For initial pockets ≥5 mm, a mean reduction in probing depth of 1.9 mm was seen in the test sites, versus 1.2 mm in the control sites. Sites with a baseline probing depth ≥7 mm and bleeding index >2 showed an average of 2.5 mm reduction with minocycline versus 1.5 mm with the vehicle. Gains in attachment (0.9 mm and 1.1 mm) were observed in minocycline‐treated sites, with baseline probing depth ≥5 mm and ≥ 7 mm, respectively, compared with 0.5 mm and 0.7 mm gain at control sites. Subgingival administration of minocycline ointment was well tolerated.

Conclusions: Overall, the results demonstrate that repeated subgingival administration of minocycline ointment in the treatment of adult periodontitis is safe and leads to significant adjunctive improvement after subgingival instrumentation in both clinical and microbiologic variables over a 15‐month period.J Periodontol 1999;70:657‐667.