bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dose‐Effect Relation of Smoking and the Interleukin‐1 Gene Polymorphism in Periodontal Disease
Authors: Meisel P. , Schwahn C. , Gesch D. , Bernhardt O. , John U. , Kocher T. 
Published: February 2005

Background: Periodontitis is a bacterial inflammatory disease leading to attachment loss with the consequence of tooth loss. There exists a multifactorial risk pattern including bacterial challenge, smoking, age, gender, diabetes, and socioeconomic and genetic factors. Smoking has the highest impact on the course of the disease modulated by all the other factors. Here, we report the relationship between smoking and the genetic polymorphism of interleukin‐1 (IL‐1).Methods: In a randomly selected population‐based study, we genotyped 1,085 test persons for the IL‐1 genotype, examined their periodontal status, and assessed their smoking behavior including present and past quality and quantity of smoking.Results: There was a significant dose‐effect relationship between the exposure to tobacco smoke and the extent of periodontal disease assessed as attachment loss and tooth loss. Moreover, there was a gene‐environmental interaction. Subjects bearing at least one copy of the variant allele 2 at positions IL‐1A –889 and IL‐1B +3954 (genotype positive) had an enhanced smoking‐associated periodontitis risk as compared to their IL‐1 genotype‐negative counterparts. With genotype‐negative non‐smokers as a reference, logistic regression resulted in odds ratios of 0.98 (95% confi‐ dence interval: 0.83 to 1.14), 2.37 (1.96 to 2.87), and 4.50 (2.30 to 8.82) for genotype‐positive non‐smokers, genotype‐negative smokers, and genotype‐positive smokers, respectively.Conclusions: There is a gene‐environmental interaction between smoking and the IL‐1 genetic polymorphism. Smokers bearing the genotype‐positive IL‐1 allele combination have an increased risk of periodontitis. The IL‐1 genotype has no influence in non‐smokers. J Periodontol 2004;75:236‐242.
Regulatory Effects of Interleukin‐1β and Prostaglandin E2 on Expression of Receptor Activator of Nuclear Factor‐κB Ligand in Human Periodontal Ligament Cells
Authors: Nukaga Jun , Kobayashi Makoto , Shinki Toshimasa , Song Hong , Takada Takatora , Takiguchi Takashi , Kamijo Ryutarou , Hasegawa Kohji 
Published: February 2005

Background: Receptor activator of nuclear factor‐κB ligand (RANKL), which is expressed on the cell membrane of osteoblasts/ stromal cells, stimulates osteoclastogenesis. We investigated the regulatory effects of interleukin‐1β (IL‐1β) and prostaglandin E2 (PGE2) on expression of RANKL in human periodontal ligament (HPDL) cells and the mechanisms involved in the PGE2 effect.Methods: The HPDL cells were treated with IL‐1β, alone or in combination with indomethacin (INDO) or NS398, a cyclooxygenase‐ 2 (COX‐2) inhibitor. The HPDL cells were also pretreated with H89, a protein kinase A (PKA) inhibitor or GF109203X, a protein kinase C (PKC) inhibitor and subsequently treated with PGE2, PGE receptor (EP)2 agonist, EP4 agonist, forskolin, dibutyryl cAMP (db‐cAMP), or 3‐(isobutyl)‐1‐methylxantine (IBMX). After each treatment, expression of EP2, EP4, or RANKL mRNA was analyzed by reverse transcription‐polymerase chain reaction and Southern hybridization. Expression of RANKL protein was detected by Western blotting, and cAMP accumulation was determined using a cAMP enzyme immunoassay kit.Results: IL‐1β stimulated the expression of RANKL at messenger RNA (mRNA) and protein levels in HPDL cells. Endogenous PGE2 partially mediated the IL‐1β–induced RANKL mRNA expression. Exogenously added PGE2 also stimulated RANKL expression at mRNA and protein levels in the cells. The PGE2‐ stimulated RANKL expression was mediated by EP2/4 and cAMP‐dependent PKA, while PKC was possibly involved in the PGE2 action.Conclusion: Human periodontal ligament cells activated with inflammatory factors such as IL‐1β and PGE2 may directly stimulate osteoclastogenesis through RANKL, which is stimulated to express by these factors. J Periodontol 2004;75:249‐259.
Nicotine Effects on Alveolar Bone Changes Induced by Occlusal Trauma: A Histometric Study in Rats
Authors: Nogueira‐Filho Getúlio R. , Neto Edgard B. Fróes , Casati Marcio Zaffalon , Reis Silvia R.A. , Tunes Roberto S. , Tunes Urbino R. , Sallum Enilson Antonio , Nociti Francisco H. , Sallum Antonio W. 
Published: February 2005

Background: The aim of the present study was to verify nicotine effects on alveolar bone changes induced by occlusal trauma during a periodontitis experimental model in rats.Methods: Thirty adult male rats were used. The animals were randomly assigned to one of three groups receiving daily intraperitoneal injections: A, nicotine solution (0.44 mg/ml) and occlusal overload; B, saline solution and occlusal overload; or C, saline solution. Rats from groups A and B underwent bilateral amputation of the second and third molar cusps to simulate an occlusal overload. The first molars were then randomly assigned to receive a cotton ligature in the sulcular area, while the contralateral tooth was left unligated. The animals were sacrificed 30 days later. The resected mandibles were processed, and histomorphometric measurements were performed in the alveolar bone adjacent to the furcation area of the first molars.Results: Nicotine enhanced the bone loss induced by occlusal trauma (P <0.001) on the ligated teeth of group A (12.27 ± 4.4 mm2), when compared to groups B (8.43 ± 3.51 mm2) and C (4.43 ± 2.17 mm2). Alveolar bone loss (P <0.01) was also observed in the contralateral teeth of groups A (nicotine + trauma) and B (saline + trauma), when compared to group C (saline only).Conclusion: Within the limits of the study, it is concluded that nicotine may influence the alveolar bone changes induced by occlusal trauma by enhancing bone loss. J Periodontol 2004;75:348‐352.
Role of the c‐myc Proto‐Oncogene in the Proliferation of Hereditary Gingival Fibromatosis Fibroblasts
Authors: Tipton David A. , Woodard Ernest S. , Baber Mark A. , Dabbous Mustafa Kh. 
Published: February 2005

Background: Hereditary gingival fibromatosis (HGF) is a fibrotic gingival enlargement. In previous work, HGF fibroblasts grew faster and produced more collagen and fibronectin (FN) than normal gingival (GN) fibroblasts. HGF FN and collagen production, but not proliferation, were under autocrine transforming growth factor (TGF)‐β control, suggesting other means of activation of HGF proliferation. Elevated/prolonged expression of the protooncogene c‐myc is implicated in disregulation of cell growth. The objectives of this study were to: 1) determine if c‐myc expression is abnormal in quiescent and serum‐stimulated HGF and GN fibroblasts and 2) determine the relationship between c‐myc expression and fibroblast proliferation using a c‐myc antisense oligonucleotide (ODN).Methods: Proliferation was determined by enzyme‐linked immunosorbent assay (ELISA), measuring incorporation of bromodeoxyuridine into DNA. Expression of c‐myc was determined by quantitative polymerase chain reaction (PCR), using incorporation of fluorescent dCTP and detection via electrophoresis.Results: Proliferation was minimal until 24 hours or more after serum stimulation, when HGF proliferation was greater than GN (P ≤0.02). All cells expressed c‐myc mRNA at quiescence and ≥1 hour after serum stimulation. Expression of c‐myc in quiescent HGF fibroblasts was elevated, and it peaked and remained higher after serum stimulation than in GN cells. Proliferation of an HGF cell line was inhibited by 4 μM c‐myc antisense ODN (14% decrease; P ≤0.006) and 8 μM c‐myc antisense ODN (~80% decrease; P ≤0.0001), but generally not by c‐myc sense ODN. This effect was reversed by hybridizing the c‐myc antisense and sense ODNs (P = 0.007).Conclusion: Data suggest that elevated proliferation of an HGF fibroblast cell line is related to elevated c‐myc expression. J Periodontol 2004;75:360‐369.
Root Coverage Using the Coronally Positioned Flap With or Without a Subepithelial Connective Tissue Graft
Authors: Silva Robert Carvalho Da , Joly Julio César , de Lima Antonio Fernando Martorelli , Tatakis Dimitris N. 
Published: February 2005

Background: Various surgical techniques have been proposed for treating gingival recession. This randomized clinical trial compared the coronally positioned flap (CPF) alone or in conjunction with a subepithelial connective tissue graft (SCTG) the treatment of gingival recession.Methods: Eleven non‐smoking subjects with bilateral and comparable Miller Class I recession defects were selected. The defects, at least 3.0 mm deep, were randomly assigned to the test (CPF + SCTG) or control group (CPF alone). Recession depth (RD), probing depth (PD), clinical attachment level (CAL), width of keratinized tissue (KT), and gingival/mucosal thickness (GT) were assessed at baseline and 6 months postoperatively.Results: Recession depth was significantly reduced 6 months postoperatively (P <0.05) for both groups. Mean root coverage was 75% and 69% in the test and control groups, respectively. There were no significant differences between the two groups in RD, PD, or CAL, either at baseline or at 6 months postoperatively. However, at 6 months postoperatively, the test group showed a statistically significant increase in KT and GT compared to the control group (P <0.05).Conclusions: The results indicate that both surgical approaches are effective in addressing root coverage. However, when an increase in gingival dimensions (keratinized tissue width, gingival/ mucosal thickness) is a desired outcome, then the combined technique (CPF + SCTG) should be used. J Periodontol 2004;75: 413‐419.
Periodontitis and Coronary Artery Calcification: The Atherosclerosis Risk in Communities (ARIC) Study
Authors: Nakib Sarah A. , Pankow James S. , Beck James D. , Offenbacher Steven , Evans Gregory W. , Desvarieux Moise , Folsom Aaron R. 
Published: February 2005

Background: Periodontitis has been linked to coronary heart disease (CHD) risk, possibly through providing a systemic inflammatory burden. Few studies have evaluated periodontitis and subclinical measures of atherosclerosis. Coronary artery calcification (CAC) is an emerging marker for atherosclerosis, and past studies suggest that it predicts incident CHD in asymptomatic populations.Methods: In 1996‐1998, dental examinations were performed on 6,931 participants in the Atherosclerosis Risk in Communities (ARIC) cohort. Extent of periodontitis was measured by the percent of sites with attachment level (AL) ≥3 mm. In 1999‐2000, CAC was measured by cardiac gated mechanical or helical computed tomography in 269 dental examinees and edentulous subjects from the Minnesota and North Carolina field centers of ARIC who were free of clinically recognized CHD. A traditional Agatston score for CAC was calculated.Results: Compared to subjects with no or mild periodontitis (<10% of sites with AL ≥3 mm), subjects with moderate or severe periodontitis (≥10% of sites with AL ≥3 mm) were more likely to have CAC ≥100, but this difference was not statistically significant (odds ratio [OR]: 1.78; 95% confidence interval [CI]: 0.65 to 4.86). This association was partially but not completely attenuated when adjusted for demographic factors and traditional CHD risk factors (OR: 1.51; 95% CI: 0.54 to 4.23).Conclusions: These results suggest that periodontitis is not strongly associated with CAC. This study offers some reference for the magnitude of the association between CAC and periodontitis and information regarding the minimal power necessary for future studies. J Periodontol 2004;75:505‐510.
Association of Fcγ Receptor IIa Genotype With Chronic Periodontitis in Caucasians
Authors: Yamamoto Kouji , Kobayashi Tetsuo , Grossi Sara , Ho Alex W. , Genco Robert J. , Yoshie Hiromasa , De Nardin Ernesto 
Published: February 2005

Background: Functional polymorphisms of immunoglobulin G (IgG) Fc receptors IIIa and IIIb (FcγRIIIa and FcγRIIIb) have been shown as risk factors for periodontitis. The aim of this study is to examine whether FcγRIIa polymorphism is associated with a disease risk as well.Methods: Baseline periodontal and general health examinations were carried out on 1,221 Caucasian adults. From these, 422 subjects with moderate to severe, or little or no periodontal disease were assigned to two groups according to their mean clinical attachment loss (CAL). Subjects with mean CAL ≥2.94 mm were diagnosed with chronic periodontitis (n = 213, 62 never‐smokers and 151 smokers). Subjects with mean CAL ≤1.77 mm were considered as having little or no periodontal disease and designated as controls (n = 209, 125 never‐smokers and 84 smokers). The FcγRIIa genotype for three bi‐allelic polymorphisms (FcγRIIa‐R/ R131, R/H131, and H/H131) was determined by means of allelespecific polymerase chain reactions.Results: The distribution of FcγRIIa genotype between the patient and control groups was significantly different, with enrichment of the high ligand‐binding genotype FcγRIIa‐H/H131 in the patients (patients versus controls: 36.6% versus 25.4%; P = 0.04). Multivariate logistic regression model demonstrated that subject age and gender, smoking, and the FcγRIIa genotype were significantly associated with severity of chronic periodontitis. For smokers, a signifi‐ cant over‐representation of FcγRIIa‐H/H131 in the patient group compared to the control group (patients versus controls: 35.1% versus 19.0%; P = 0.03). Additionally, smokers with FcγRIIa‐H/H131 exhibited significantly greater mean CAL (mean ± SE: 3.44 ± 0.16 mm) than those with FcγRIIa‐R/H131 (2.91 ± 0.14 mm) and R/R131 (2.82 ± 0.16 mm) (P = 0.04). There was no association between FcγRIIa genotype and the disease susceptibility or severity in subjects who had never smoked.Conclusions: Our results suggest that the FcγRIIa‐H/H131 genotype may be associated with chronic periodontitis risk (and disease severity) in Caucasian smokers. Further studies with families and studies of mechanisms are necessary to help establish the extent to which this is a genetic determinant of periodontal diseases. J Periodontol 2004;75:517‐522.
Inhibitory Effect of a Novel Bisphosphonate, TRK‐530, on Dental Calculus Formation in Rats
Authors: Haq Sikder M.N. , Itoh Masatoshi , Iwatsuki Naofumi , Shinoda Hisashi 
Published: February 2005

Background: A newly developed bisphosphonate, TRK‐530 (disodium dihydrogen[4‐(methylthio)phenylthio]methanebisphosphonate), has recently been reported to show anti‐inflammatory and anti‐bone‐resorbing activity. Since bisphosphonates have been shown to inhibit the formation of calcium‐phosphate crystals in vitro, TRK‐530 may inhibit the formation of dental calculus. Therefore, the present study was performed to examine whether this compound has such an effect.Methods: Three groups of Wistar rats fed a calculogenic diet (RC16) were treated with TRK‐530 in drinking water at concentrations of 0 (control group), 0.75, and 1.5 mM. Another group received a daily subcutaneous injection of TRK‐530 at a dose of 2.25 µmoles/rat, which was assumed to correspond to the maximum amount of this compound absorbed from the intestine when rats received 1.5 mM TRK‐530 in drinking water. Rat dental calculus formation was evaluated. The crystalline nature of dental calculus was studied by x‐ray diffraction analysis. Finally, the effects of TRK‐530 on the precipitation of calcium‐phosphate from solution were tested in vitro.Results: TRK‐530 in drinking water inhibited dental calculus formation dose‐dependently. However, subcutaneous injection of TRK‐530 did not have any significant effect, suggesting that the anticalculus effect of TRK‐530 in drinking water was topical, not systemic. The calculus that formed in both the control and experimental groups was primarily hydroxyapatite, a main constituent of human dental calculus. TRK‐530 inhibited the precipitation of calcium‐phosphate from solution in vitro.Conclusions: TRK‐530 inhibited the formation of dental calculus in a dose‐dependent fashion via a local effect. Inhibition of the precipitation of calcium‐phosphate from solution might be involved in the anticalculogenic mechanism of this drug. J Periodontol 2004;75:537‐545.
Soluble Cell Adhesion Molecules in Gingival Crevicular Fluid in Periodontal Health and Disease
Authors: Hannigan E. , O'Connell D.P. , Hannigan A. , Buckley L.A. 
Published: February 2005

Background: Cell adhesion molecules (CAMs) are cell surface proteins involved in the binding of cells to each other, to endothelial cells, or to the extracellular matrix. The soluble forms of CAMs (sCAMs) are thought to be produced by proteolytic cleavage from the cell surface and are shed into the gingival crevicular fluid (GCF). The aim of this study was to investigate whether sCAMs, sICAM‐1, sVCAM‐1, and sE‐Selectin were present in GCF in both periodontal health and disease and to examine their relationship with periodontal inflammation.Methods: GCF was collected from a clinically healthy, a gingivitis, and a periodontitis site in 29 subjects with chronic periodontitis and from a single clinically healthy site in 22 subjects without chronic periodontitis. The volume of GCF was measured and each sample was analyzed for sCAMs by enzyme‐linked immunosorbent assay (ELISA). The effect of treatment (oral hygiene instruction, scaling and root planing) on the levels of sCAMs in each site of the diseased group was also investigated.Results: Statistically significant differences (P <0.05) were found between the levels of sVCAM‐1 in periodontal health and disease. These results indicate that changes in the levels of sCAMs may be a sensitive indicator to differentiate healthy sites from those with periodontitis. Statistically significant changes in the levels of sICAM‐1 were recorded after treatment (P <0.05).Conclusions: Further studies are required to establish if these potential biomarkers will enable the identification of those sites most at risk for disease progression and also evaluate the response to treatment, thereby playing a preventive role in the pathogenesis of periodontal disease. J Periodontol 2004;75:546‐550.
Relationship of Actinobacillus actinomycetemcomitans Serotype b to Aggressive Periodontitis: Frequency in Pure Cultured Isolates
Authors: Yang H. W. , Asikainen S. , Doğan B. , Suda R. , Lai C. H. 
Published: February 2005

Background: To our knowledge, the association of the five serotypes of Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) to the new diagnostic classification scheme defined by the American Academy of Periodontology in 1999 has not yet been described. The goal of this study was to characterize the frequencies of the five serotypes of A. actinomycetemcomitans in A. actinomycetemcomitans isolates from various forms of periodontitis using both old and new diagnostic classifications and to determine the relationships between serotype and age and clinical diagnosis.Methods: A total of 345 A. actinomycetemcomitans isolates from 115 A. actinomycetemcomitans culture‐positive subjects (mean age 38.0 ± 18.3 years, 59% female) were collected. Based on the new classifications, 33 subjects had aggressive periodontitis and 82 chronic periodontitis. According to old classifications, there were six prepubertal periodontitis (PPP), 12 localized juvenile periodontitis (LJP), 15 post‐localized juvenile periodontitis (PLJP), 28 refractory periodontitis (Ref‐P), and 54 adult periodontitis (AP) cases. Serotypes of A. actinomycetemcomitans were determined by an indirect immunofluorescence assay using serotype‐specific polyclonal antisera to A. actinomycetemcomitans strains ATCC 29523, ATCC 43728, ATCC 33384, IDH 781 and IDH 1705 (serotype a, b, c, d, and e, respectively). Proportions of serotype b were examined between different diagnostic and age groups with a Z‐test for proportions.Results: Most subjects (n = 100, 86.96%) were infected with a single serotype (22 serotype a, 44 serotype b, 30 serotype c, 1 serotype d, and 3 serotype e). There were 11 subjects (9.57%) with two serotypes and two subjects (1.74%) with 3 serotypes. Two individuals had isolates lacking any detectable serotype antigen. Serotype b was the predominant serotype in children under 18 years of age and young adults between 19 to 35 years, although serotype b status was not significantly associated with age. Serotypes d and e were not found in patients under 35 years old. In 62 adult patients, one subject had serotype d and three had serotype e. Serotype b was the most common serotype in aggressive periodontitis (60.61%). The proportion of cases with serotype b was significantly higher in aggressive periodontitis compared to chronic periodontitis (P = 0.031). Other serotypes were not significantly associated with new diagnostic categories. Serotypes d and e were not detected in aggressive periodontitis.Conclusion: The results of this study show that proportions of serotype b of A. actinomycetemcomitans are significantly greater in culture‐positive patients with aggressive periodontitis than those with chronic periodontitis. J Periodontol 2004;75:592‐599.
Successful Treatment of Oral Lichen Planus‐Like Chronic Graft‐Versus‐Host Disease With Topical Tacrolimus: A Case Report
Authors: Sánchez Andrés R. , Sheridan Phillip J. , Rogers Roy S. 
Published: February 2005

Background: Bone marrow transplantation (BMT) is a common treatment used for deficiencies of host marrow or in the control of blood malignancies. Post‐allogeneic BMT complications include graft‐versus‐host disease (GVHD). GVHD occurs when immunologically active T lymphocytes are transplanted into an immunosuppressed recipient who is genetically disparate from the donor. In this case report we describe the occurrence of oral lichen planus‐like lesions as the first manifestation of chronic GVHD (c‐GVHD) and the subsequent management of this disease with topical tacrolimus.Methods: Diagnostic aids included routine histology and direct immunofluorescence studies to rule out immunobullous diseases and to confirm the c‐GVHD. Treatment consisted of topical application of 0.1% tacrolimus ointment three times a day.Results: Routine histology confirmed the clinical diagnosis of oral lichen planus‐like c‐GVHD. Treatment with tacrolimus ointment completely resolved the oral lesions after 2 months of therapy.Conclusions: Topical tacrolimus at low concentrations (0.1%) shows promise in the management of oral lichen planus‐like c‐GVHD. Controlled studies are necessary to assess the efficacy, the duration of therapy required for effective results, and the safety of this treatment over the long‐term. J Periodontol 2004;75:613‐619.
A Technique for Standardized Evaluation of Soft and Hard Peri‐Implant Tissues in Partially Edentulous Patients
Authors: Meijndert Leo , Meijer Henny J.A. , Raghoebar Gerry M. , Vissink Arjan 
Published: February 2005

Background: There is a growing need to evaluate the esthetics of implant‐supported crowns and bridges. An important tool for such an evaluation is standardized assessment of the soft and hard peri‐implant tissue levels.Methods: A simple acrylic device has been developed for reliable and reproducible assessment of soft and hard periimplant tissues using standardized color slides and standardized dental x‐rays. With this device, changes in both the soft and hard tissues around implant‐supported crowns can be evaluated as a function of time. The reproducibility of the technique was tested on color slides as well as on dental x‐rays in a series of implant‐supported crowns and their neighboring teeth. Results: The reproducibility of this technique was excellent. The measuring errors for repeated measurements of the soft and hard tissues were 0.14 ± 0.02 mm and 0.13 ± 0.01 mm, respectively.Conclusions: The device is a reliable tool to assess changes in both soft and hard tissues around crowns and implants over time. Likewise, it is suggested that this technique also can be used to objectively assess soft and hard tissue changes around natural teeth with or without prosthetic restorations. J Periodontol 2004;75:646‐651.