bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of Herpesviruses and Periodontal Pathogens in Subgingival Plaque of Patients With Chronic Periodontitis, Generalized Aggressive Periodontitis, or Gingivitis
Authors: Imbronito Ana Vitória , Okuda Osmar Shizuo , Maria de Freitas Nivea , Moreira Lotufo Roberto Fraga , Nunes Fabio Daumas 
Published: December 2008

Background: Herpesviruses may be related to the etiology of aggressive periodontitis (AgP) and chronic periodontitis (CP) by triggering periodontal destruction or by increasing the risk for bacterial infection. This case‐control study evaluated the presence of herpes simplex virus type I (HSV‐1), Epstein‐Barr virus type I (EBV‐1), human cytomegalovirus (HCMV), Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia (previously T. forsythensis) in patients with generalized AgP (AgP group), CP (CP group), or gingivitis (G group) and in healthy individuals (C group).Methods: Subgingival plaque samples were collected with paper points from 30 patients in each group. The nested polymerase chain reaction (PCR) method was used to detect HSV‐1, EBV‐1, and HCMV. Bacteria were identified by 16S rRNA‐based PCR.Results: HSV‐1, HCMV, and EBV‐1 were detected in 86.7%, 46.7%, and 33.3% of the AgP group, respectively; in 40.0%, 50.0%, and 46.7% of the CP group, respectively; in 53.3%, 40.0%, and 20.0% of the G group, respectively; and in 20.0%, 56.7%, and 0.0% of the C group, respectively. A. actinomycetemcomitans was detected significantly more often in the AgP group compared to the other groups (P <0.005). P. gingivalis and T. forsythia were identified more frequently in AgP and CP groups, and AgP, CP, and G groups had higher frequencies of P. intermedia compared to the C group.Conclusion: In Brazilian patients, HSV‐1 and EBV‐1, rather than HCMV, were more frequently associated with CP and AgP.
Involvement of Interleukin‐1 Genotypes in the Association of Coronary Heart Disease With Periodontitis
Authors: Geismar Karen , Enevold Christian , Sørensen Lars Korsbæk , Gyntelberg Finn , Bendtzen Klaus , Sigurd Bjarne , Holmstrup Palle 
Published: December 2008

Background: Epidemiologic studies demonstrated an association between periodontitis (PE) and coronary heart disease (CHD). The coexistence of the two disease entities could be dependent on mutual risk factors, and polymorphism of the interleukin (IL)‐1 gene cluster associated with the severity of PE might also be involved in the pathogenesis of CHD.Methods: The study consisted of 225 dentate white subjects, including 97 patients with CHD and 128 controls. Patients with confirmed diagnoses of CHD were recruited after being discharged from a cardiology department, and controls without CHD were recruited consecutively from the Copenhagen City Heart Study. Mean alveolar bone level (ABL) was measured on radiographs. ABL was stratified into ABL1 (ABL ≤2 mm), ABL2 (2 mm <ABL ≤4 mm), and ABL3 (ABL >4 mm). Genotypes were analyzed by amplifying the polymorphic regions of the IL‐1 gene cluster using polymerase chain reaction, followed by restriction digestion and gel electrophoresis.Results: In the univariate analysis, allele 2 of IL‐1B+3954 and IL‐1B−511 was associated with ABL (P = 0.040 and P = 0.039, respectively), whereas no association was found with allele 2 of IL‐1A+4845 or IL‐1RN variable number tandem repeat (VNTR) (P = 0.445 and P = 0.375, respectively). A lower ABL was associated with the occurrence of allele 2 of IL‐1B−511. The multiple logistic regression analysis also showed a significant association of allele 1 of IL‐1B−511 with high ABL (P = 0.049) and of allele 2 of IL‐1A+4845 with high ABL among individuals with CHD (P = 0.050). There was no association between any of the polymorphisms of IL‐1 and CHD in the univariate or multiple analyses. However, in a binary multiple logistic regression model, carriage of allele 1 of IL‐1RN VNTR was found to be associated with the occurrence of both CHD and ABL3 (P = 0.016).Conclusion: Allele 1 of IL‐1RN VNTR may be associated with the coexistence of CHD and PE in a multiple regression model.
Humoral Factors Released From Human Periodontal Ligament Cells Influence Calcification and Proliferation in Human Bone Marrow Mesenchymal Stem Cells
Authors: Mizuno Noriyoshi , Ozeki Yoshitaka , Shiba Hideki , Kajiya Mikihito , Nagahara Takayoshi , Takeda Katsuhiro , Kawaguchi Hiroyuki , Abiko Yoshimitsu , Kurihara Hidemi 
Published: December 2008

Background: Transplantation of bone marrow mesenchymal stem cells (MSCs) is believed to be a new modality for periodontal tissue regeneration. However, little is known about the factors that influence the functions of the transplanted MSCs. Periodontal ligament cells may be implicated in regulating MSC functions.Methods: To examine the effect of humoral factors (HFs) produced by human periodontal ligament (HPL) cells on human MSC (hMSC) gene expression, hMSCs were cocultured separately with HPL cells. The gene expression of the hMSCs was analyzed by microarray. Moreover, the effect of conditioned medium (CM) from cultures of HPL cells (CM‐HPL cells) on the proliferation and mineralizing capacity of hMSCs was examined.Results: Thirty‐five genes whose expressions were upregulated more than two‐fold and 32 genes whose expressions were downregulated more than two‐fold were identified in hMSCs cocultured separately with HPL cells. CM‐HPL cells prevented calcification in hMSCs cultured with bone morphogenetic protein‐2 but not dexamethasone. CM‐HPL cells stimulated cell proliferation in hMSCs, whereas CM from culture of human osteoblasts did not influence the proliferation.Conclusions: To the best of our knowledge, this is the first study on the global gene expression of MSCs cocultured with periodontal ligament cells. A particular humoral factor released from periodontal ligament cells is suggested to affect differentiation and proliferation in MSCs.
Association Between Involuntary Smoking and Salivary Markers Related to Periodontitis: A 2‐Year Longitudinal Study
Authors: Nishida Nobuko , Yamamoto Yumiko , Tanaka Muneo , Kataoka Kosuke , Kuboniwa Masae , Nakayama Kunio , Morimoto Kanehisa , Shizukuishi Satoshi 
Published: December 2008

Background: Insufficient data exist regarding the longitudinal influence of involuntary smoking on periodontitis progression. This study examined the relationship between involuntary smoking and periodontitis progression and the effects of involuntary smoking on salivary inflammatory and microbiologic markers related to periodontitis.Methods: Participants were recruited during annual health checkups in 2003 and 2005. In 2005, 200 of 273 (73%) Japanese employees examined at baseline underwent periodontal measurements, including clinical attachment level (CAL) and probing depth (PD). Periodontitis progression was identified when a subject displayed one or more teeth with an increase ≥2.0 mm in CAL and PD during the 2 years. Salivary marker levels, including cotinine, were determined by enzyme assay, including enzyme‐linked immunosorbent assay. The proportions of six periodontal pathogens in saliva were assessed using real‐time polymerase chain reaction methodology. Based on receiver‐operating characteristic analysis, non‐, involuntary, and active smokers were defined as subjects exhibiting salivary cotinine levels of 0, 1 to 7, and ≥8 ng/ml, respectively.Results: By simple logistic regression analysis, age, alcohol consumption, smoking, breakfast habits, and working hours were related to the risk for significant periodontitis progression. Multiple logistic regression analysis revealed significantly higher periodontitis odds ratios (OR) in involuntary (OR = 2.23; 95% confidence interval [CI]: 1.03 to 4.83) and active (OR = 2.27; 95% CI: 1.02 to 5.04) smokers relative to non‐smokers following adjustment for covariates. Levels of salivary markers, including albumin, aspartate aminotransferase, and lactoferrin, were significantly elevated in involuntary smokers relative to non‐smokers. In contrast, the percentages of periodontal pathogens did not differ between the smoking groups, with the exception of Prevotella nigrescens, which displayed significantly lower levels in involuntary smokers compared to non‐smokers.Conclusion: Involuntary smoking increased the inflammatory response and was associated with a greater risk for periodontitis progression.
Pain Perception and Anxiety During Scaling in Periodontally Healthy Subjects
Authors: Guzeldemir Esra , Toygar Hilal Uslu , Cilasun Ulkem 
Published: December 2008

Background: Dental pain, anxiety, and fear may result in avoiding dental treatment. In this study, we aimed to evaluate patients' pain perception during scaling and its relationship with dental anxiety.Methods: One hundred thirteen patients (72 women and 41 men; mean age, 35.59 ± 9.28 years) participated. Pain levels after scaling were assessed with a visual analog scale (VAS) and an anxiety questionnaire consisting of seven questions, each with five possible answers.Results: The patients were asked to indicate their pain level on a 100‐mm VAS, and the mean VAS score was 19.91 ± 17.76 mm. No age and gender differences with regard to pain perception were found. VAS scores were significantly higher in non‐smokers (P <0.001); there was a slightly significant relationship between smoking and pain (0.264; P <0.05). The anxiety score ranged from 7 to 35; the mean anxiety score was 14.00 ± 5.30 (range, 7 to 29). The anxiety score was significantly higher in women (P <0.001). The only question correlated with pain during scaling in men was, “How fearful are you of having your teeth cleaned?” (0.322; P = 0.040). Scores for patients aged 29 to 39 years were significantly higher than scores for those aged 51 to 61 years (P <0.01).Conclusions: Although most patients experienced limited pain during scaling, a significant relationship was found between pain and smoking. Women and patients aged 30 to 40 years are likely to be more anxious during scaling. The question, “How fearful are you of having your teeth cleaned?” may not adequately cover all aspects of anxiety for patients' experience of pain during scaling. Clinicians should determine individual treatment approaches to reduce patients' fear, pain, and anxiety related to scaling.
Posterior Implant Single‐Tooth Replacement and Status of Adjacent Teeth During a 10‐Year Period: A Retrospective Report
Authors: Misch Carl E. , Misch‐Dietsh Francine , Silc Jennifer , Barboza Eliane , Cianciola Louis J. , Kazor Christopher 
Published: December 2008

Background: The purpose of this case series study was to evaluate posterior single‐tooth implant survival and the long‐term conditions of the adjacent teeth.Methods: A retrospective evaluation of 1,162 consecutive patients with a single missing posterior tooth treated with 1,377 external hex implants supporting 1,365 restorations surrounded by natural teeth over a 1‐ to 10‐year period was reviewed from four private offices. Implant survival data were collected relative to stage I to stage II healing, stage II to prosthesis delivery, and prosthesis delivery to up to 10 years of follow‐up. Long‐term adjacent tooth conditions were assessed, including decay, endodontic therapy (root canal therapy [RCT]), and/or extraction during the follow‐up period.Results: Of the 1,377 implants inserted, there were 11 surgical failures from stage I to stage II healing. There was one failure from stage II healing to prosthesis delivery. There were two prosthetic‐phase failures. The surgical success rate was 99.2%, whereas the overall survival rate was 98.9% at an average of 61 months of follow‐up (range, 12 to 125 months). A total of 2,589 adjacent teeth were followed during the study. No natural adjacent tooth was lost during this period. Interproximal decay developed in 129 adjacent teeth (5%), and nine adjacent teeth required RCT (0.4%) as a result of decay or restoration.Conclusions: The use of single‐tooth implants as replacements for posterior missing teeth is a viable long‐term treatment. Adjacent natural teeth complications are minimal for as long as 10 years after implant insertion.
Antecedent Hypoglycemia Impairs Autonomic Cardiovascular Function
Authors: Adler Gail K. , Bonyhay Istvan , Failing Hannah , Waring Elizabeth , Dotson Sarah , Freeman Roy 
Published: December 2008

OBJECTIVE— Glycemic control decreases the incidence and progression of diabetic complications but increases the incidence of hypoglycemia. Hypoglycemia can impair hormonal and autonomic responses to subsequent hypoglycemia. Intensive glycemic control may increase mortality in individuals with type 2 diabetes at high risk for cardiovascular complications. We tested the hypothesis that prior exposure to hypoglycemia leads to impaired cardiovascular autonomic function.
RESEARCH DESIGN AND METHODS— Twenty healthy subjects (age 28 ± 2 years; 10 men) participated in two 3-day inpatient visits, separated by 1–3 months. Autonomic testing was performed on days 1 and 3 to measure sympathetic, parasympathetic, and baroreflex function. A 2-h hyperinsulinemic [hypoglycemic (2.8 mmol/l) or euglycemic (5.0 mmol/l)] clamp was performed in the morning and in the afternoon of day 2.
RESULTS— Comparison of the day 3 autonomic measurements demonstrated that antecedent hypoglycemia leads to 1) reduced baroreflex sensitivity (16.7 ± 1.8 vs. 13.8 ± 1.4 ms/mmHg, P = 0.03); 2) decreased muscle sympathetic nerve activity response to transient nitroprusside-induced hypotension (53.3 ± 3.7 vs. 40.1 ± 2.7 bursts/min, P &lt; 0.01); and 3) reduced (P &lt; 0.001) plasma norepinephrine response to lower body negative pressure (3.0 ± 0.3 vs. 2.0 ± 0.2 nmol/l at −40 mmHg).
CONCLUSIONS— Baroreflex sensitivity and the sympathetic response to hypotensive stress are attenuated after antecedent hypoglycemia. Because impaired autonomic function, including decreased cardiac vagal baroreflex sensitivity, may contribute directly to mortality in diabetes and cardiovascular disease, our findings raise new concerns regarding the consequences of hypoglycemia.
Anti–α8 integrin immunoliposomes in glomeruli of lupus‐susceptible mice: A novel system for delivery of therapeutic agents to the renal glomerulus in systemic lupus erythematosus
Authors: Scindia Yogesh , Deshmukh Umesh , Thimmalapura Pushpa‐Rekha , Bagavant Harini 
Published: November 2008

AbstractObjectiveGlomerular mesangial cells are active participants in the pathogenesis of lupus glomerulonephritis (GN). Thus, targeted delivery of therapeutic agents to mesangial cells would be an attractive approach to treatment. However, lack of known unique mesangial cell surface markers has hampered this process. This study was undertaken in a mouse model of lupus GN to identify mesangial markers and to develop a system for targeted drug delivery to the glomerulus.MethodsBased on previous observations, α8 integrin expressed on the surface of glomerular mesangial cells was selected as a target molecule for delivery. Two mouse strains susceptible to lupus GN, NZM2328 and (NZM2328 × NOD)F1, were studied. Glomerular expression of α8 integrin in normal and nephritic mice was confirmed by immunofluorescence and quantitative polymerase chain reaction analysis. Liposomes were formulated and conjugated with an anti–α8 integrin antibody. These immunoliposomes were loaded with DiI, a red fluorescent dye, to allow tracking in vivo, and injected into the tail vein of female mice at different ages. Specificity of targeting was studied by fluorescence microscopy and flow cytometry.ResultsExpression of α8 integrin was observed in the glomeruli of normal and nephritic mice. Anti–α8 integrin immunoliposomes were detected in the glomerulus and glomerular mesangial cells after tail vein injection in normal and nephritic mice. Delivery of DiI by anti–α8 integrin immunoliposomes was tissue specific, being observed predominantly in the glomeruli, with some nonspecific uptake by CD11b cells.ConclusionThese findings are the first demonstration of specific delivery of anti–α8 integrin immunoliposomes to the mesangium following tail vein injection in mice. Anti–α8 integrin immunoliposomes thus offer a novel approach for targeted drug therapy in lupus and other glomerular diseases.
Spliceosomal peptide P140 for immunotherapy of systemic lupus erythematosus: Results of an early phase II clinical trial
Authors: Muller Sylviane , Monneaux Fanny , Schall Nicolas , Rashkov Rasho K. , Oparanov Boycho A. , Wiesel Philippe , Geiger Jean‐Marie , Zimmer Robert 
Published: November 2008

AbstractObjectiveTo assess the safety, tolerability, and efficacy of spliceosomal peptide P140 (IPP‐201101; sequence 131–151 of the U1‐70K protein phosphorylated at Ser140), which is recognized by lupus CD4+ T cells, in the treatment of patients with systemic lupus erythematosus (SLE).MethodsAn open‐label, dose‐escalation phase II study was conducted in two centers in Bulgaria. Twenty patients (2 male and 18 female) with moderately active SLE received 3 subcutaneous (SC) administrations of a clinical batch of P140 peptide at 2‐week intervals. Clinical evaluation was performed using approved scales. A panel of autoantibodies, including antinuclear antibodies, antibodies to extractable nuclear antigens (U1 RNP, SmD1, Ro/SSA, La/SSB), and antibodies to double‐stranded DNA (anti‐dsDNA), chromatin, cardiolipin, and peptides of the U1‐70K protein, was tested by enzyme‐linked immunosorbent assay (ELISA). The plasma levels of C‐reactive protein, total Ig, IgG, IgG subclasses, IgM, IgA, and IgE, and of the cytokines interleukin‐2 and tumor necrosis factor α were measured by ELISA and nephelometry.ResultsIgG anti‐dsDNA antibody levels decreased by at least 20% in 7 of 10 patients who received 3 × 200 μg IPP‐201101 (group 1), but only in 1 patient in the group receiving 3 × 1,000 μg IPP‐201101 (group 2). Physician's global assessment of disease activity scores and scores on the SLE Disease Activity Index were significantly decreased in group 1. The changes occurred progressively in the population of responders, increased in magnitude during the treatment period, and were sustained. No clinical or biologic adverse effects were observed in the individuals, except for some local irritation at the highest concentration.ConclusionIPP‐201101 was found to be safe and well tolerated by subjects. Three SC doses of IPP‐201101 at 200 μg significantly improved the clinical and biologic status of lupus patients.
Activation of the receptor EphB4 by its specific ligand ephrin B2 in human osteoarthritic subchondral bone osteoblasts
Authors: Kwan Tat Steeve , Pelletier Jean‐Pierre , Amiable Nathalie , Boileau Christelle , Lajeunesse Daniel , Duval Nicolas , Martel‐Pelletier Johanne 
Published: November 2008

AbstractObjectiveAbnormal subchondral bone metabolism is involved in osteoarthritis (OA). It has been suggested that ephrin B2 and its specific receptor EphB4 participate in bone homeostasis. We previously reported that human OA subchondral bone osteoblasts could be classified into 2 subpopulations: low (L), having proresorption properties, and high (H), having proformation properties. The purpose of this study was to investigate the importance of the ephrin system in OA subchondral bone osteoblasts.MethodsThe presence of the EphB4 receptor was determined by immunohistochemistry, and its expression level, modulation upon treatment, and consequences of activation by ephrin B2 were determined by quantitative polymerase chain reaction. The effects of ephrin B2 activation of the EphB4 receptor on bone resorption activity were also determined. EphB4 receptor activation signaling pathways were investigated by specific enzyme‐linked immunosorbent assay.ResultsEphB4 receptors were present in subchondral bone osteoblasts and osteocytes. Compared with normal and H‐OA osteoblasts, EphB4 receptor expression levels were significantly increased in L‐OA osteoblasts, with no difference between normal and H‐OA osteoblasts. EphB4 receptor levels in L‐OA osteoblasts were significantly up‐regulated by prostaglandin E2 (PGE2) and interleukin‐17 (IL‐17). Ephrin B2, PGE2, and IL‐17 significantly inhibited bone resorption activity in these cells. EphB4 activation by ephrin B2 significantly inhibited the expression of IL‐1β, IL‐6, matrix metalloproteinase 1 (MMP‐1), MMP‐9, MMP‐13, and RANKL, but not MMP‐2 and osteoprotegerin. EphB4 receptor activation significantly inhibited the phosphatidylinositol 3‐kinase/Akt pathway.ConclusionThis study is the first to provide evidence that EphB4 receptor activation by ephrin B2 in OA subchondral bone could affect abnormal metabolism in this tissue by inhibiting resorption factors and their activities. Ephrin B2 could be targeted as a specific therapeutic approach in the development of a disease‐modifying OA drug.
Biochemical markers of bone turnover associated with calcium supplementation in children with juvenile rheumatoid arthritis: Results of a double‐blind, placebo‐controlled intervention trial
Authors: Carrasco Ruy , Lovell Daniel J. , Giannini Edward H. , Henderson Carol J. , Huang Bin , Kramer Sandy , Ranz Julie , Heubi James , Glass David 
Published: November 2008

AbstractObjectiveTo determine the effects of calcium supplementation on bone physiology in corticosteroid‐free children with juvenile rheumatoid arthritis (JRA) by measuring serum and urinary bone‐related hormones, minerals, and markers of bone formation and resorption.MethodsIn this double‐blind trial, patients were randomized to receive daily oral supplementation with 1,000 mg of calcium and 400 IU of vitamin D or with placebo and 400 IU of vitamin D for 24 months. The effect of calcium supplementation on bone physiology was determined periodically using markers of bone turnover.ResultsOne hundred ninety‐eight patients met the inclusion criteria and were followed up in the study. At baseline, there were no differences in markers of bone turnover between the groups. Patients with ≤4 joints with active disease had higher serum levels of calcium and parathyroid hormone (PTH). Calcium‐treated patients with ≤4 joints with active disease had lower levels of osteocalcin (OC). At followup, levels of 1,25‐dihydroxyvitamin D3, PTH, OC, and urine phosphorus were lower in the group receiving calcium supplementation. Hypercalciuria, as determined by the urinary calcium‐to‐creatinine ratio, was not noted in 24‐hour urine studies.ConclusionLevels of markers of bone physiology were significantly decreased in children with JRA receiving calcium supplementation. The physiologic changes were noted as early as 12 months into calcium supplementation. The hypercalciuria noted on spot testing of the urinary calcium‐to‐creatinine ratio was not demonstrated on further evaluation, nor did it lead to renal pathology. These findings suggest that the calcium supplementation met physiologic needs and caused an increased calcium loss in urine.