bluuebunny/crossref_metadata_2025_split huggingface dataset:
E‐selectin and L‐selectin polymorphisms in patients with periodontitis
Authors: Houshmand B. , Rafiei A. , Hajilooi M. , Mani‐Kashani K. , Gholami L. 
Published: October 2008

Background amd Objective:  Periodontitis is a multifactorial disease in which environmental and genetic determinant factors contribute to individual subject’s susceptibility. A DNA polymorphism in the regulating region of adhesion molecule genes is suggested to modulate the molecule’s physiological effects. The aim of this study was to investigate the genetic association between the E‐selectin Ser128Arg and L‐selectin Phe206Leu polymorphisms and periodontitis.Material and Methods:  DNA was isolated from the whole blood of 88 patients with periodontitis and 139 healthy individuals. All samples were genotyped for the E‐selectin Ser128Arg and L‐selectin Phe206Leu polymorphisms using the polymerase chain reaction with sequence specific primers.Results:  Our findings revealed a significant difference in the Ser128Arg polymorphism of E‐selectin, but not in the L‐selectin polymorphism, between periodontal patients and controls. The 128Arg allele was present more frequently in patients than in healthy individuals (31.25% vs. 12.2%, p < 0.0001). In addition, there was an association between the presence of the 128Arg allele and periodontitis (odds ratio 2.9; 95% confidence interval: 1.75–4.4, p < 0.0001). No significant association was found between the polymorphisms tested and the subgroups of periodontal disease (i.e. chronic periodontitis and aggressive periodontitis).Conclusion:  The findings of this study showed that the Ser128Arg polymorphism of E‐selectin might contribute to the susceptibility of Iranian individuals to periodontitis.
Nicotinic acetylcholine receptor activation mediates nicotine‐induced enhancement of experimental periodontitis
Authors: Breivik T. , Gundersen Y. , Gjermo P. , Von Hörsten S. , Opstad P. K. 
Published: October 2008

Background and Objective:  Smokers have an increased risk of developing periodontitis as well as showing more rapid progression and resistance to treatment of the disease, but the biological mechanisms are poorly understood. Our objective was to investigate putative biological mechanisms by which nicotine may enhance the susceptibility and thus the course of periodontitis in an animal model.Material and Methods:  Ligature‐induced periodontitis was applied in periodontitis‐susceptible Fischer 344 rats. The animals were given daily intraperiotonal (i.p.) injections of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (1 mg/kg) 45 min before subcutaneous (s.c.) injections in the neck skin with nicotine (0.8 mg/kg), or treated with the same amount of saline i.p. and nicotine s.c., or with mecamylamine and saline. Control rats received i.p. and s.c. injections of saline only. Periodontal bone loss was assessed when the ligatures had been in place for 3 weeks. Two hours before decapitation, all rats received lipopolysaccharide (LPS; 100 μg/kg, i.p.) to induce a robust immune and stress response.Results:  Compared with saline/saline‐treated control rats, saline/nicotine‐treated rats developed significantly more periodontal bone loss, and LPS provoked a significantly smaller increase in circulating levels of the cytokines tumour necrosis factor α (TNF‐α), transforming growth factor 1β (TGF‐1β) and interleukin‐10 (IL‐10). Mecamylamine pretreatment of nicotine‐treated rats abrogated the increased periodontal bone loss and the LPS‐induced TNF‐α decrease, but had no significant effects on the levels of TGF‐1β and IL‐10, or the stress hormone corticosterone.Conclusion:  The results indicate that nicotine enhances susceptibility to periodontitis via nAChRs, which may act via suppressing protective immune responses through the cholinergic anti‐inflammatory pathway.
In vivodetermination of multiple indices of periodontal inflammation by optical spectroscopy
Authors: Liu K. Z. , Xiang X. M. , Man A. , Sowa M. G. , Cholakis A. , Ghiabi E. , Singer D. L. , Scott D. A. 
Published: October 2008

Background and Objective: Visible, near‐infrared (optical) spectroscopy can be used to measure regional tissue hemodynamics and edema and therefore may represent an ideal tool with which to study periodontal inflammation in a noninvasive manner. The study objective was to evaluate the ability of optical spectroscopy to determine simultaneously multiple inflammatory indices (tissue oxygenation, total tissue hemoglobin, deoxyhemoglobin, oxygenated hemoglobin and tissue edema) in periodontal tissuesin vivo.Material and Methods: Spectra were obtained, processed and evaluated from healthy, gingivitis and periodontitis sites (n = 133) using a portable optical, near‐infrared spectrometer. A modified Beer–Lambert unmixing model that incorporates a nonparametric scattering loss function was used to determine the relative contribution of each inflammatory component to the overall spectrum.Results: Optical spectroscopy was harnessed to generate complex inflammatory profiles of periodontal tissues. Tissue oxygenation at periodontitis sites was significantly decreased (p < 0.05) compared to sites with gingivitis and healthy controls. This was largely the result of an increase in deoxyhemoglobin in the periodontitis sites compared with healthy (p < 0.01) and gingivitis (p = 0.05) sites. Tissue water contentper seshowed no significant difference between the sites, but a water index associated with tissue electrolyte levels and temperature differed significantly between periodontitis sites and both healthy and gingivitis sites (p < 0.03).Conclusion: This study established that optical spectroscopy can simultaneously determine multiple inflammatory indices directly in the periodontal tissuesin vivo. Visible, near‐infrared spectroscopy has the potential to be developed into a simple, reagent‐free, user‐friendly, chairside, site‐specific, diagnostic and prognostic test for periodontitis.
Periodontal disease in patients with familial Mediterranean fever: from inflammation to amyloidosis
Authors: Cengiz M. I. , Bagci H. , Cengiz S. , Yigit S. , Cengiz K. 
Published: October 2008

Background and Objective:  Familial Mediterranean fever stimulates a very intense acute‐phase reactants response and if left untreated eventually leads to amyloidosis. The aim of this study was to determine the prevalence of periodontal disease among patients with familial Mediterranean fever in the Black Sea region in Turkey and to evaluate whether periodontitis is related to amyloidosis in patients with familial Mediterranean fever.Material and Methods:  One‐hundred and thirty three patients with familial Mediterranean fever and 50 healthy subjects were included in this study. Periodontal health and disease were evaluated using the gingival index, papillary bleeding index, plaque index and periodontal disease index. The concentrations of serum acute‐phase reactants were measured at baseline and at 4–6 wk after completion of the nonsurgical periodontal therapy. Genetic testing for familial Mediterranean fever was performed using the familial Mediterranean fever StripAssay. Kidney biopsy was carried out on all proteinuric patients.Results:  The prevalence of moderate to severe periodontitis in familial Mediterranean fever patients with amyloidosis (80.6%) was significantly greater (p < 0.01) than in familial Mediterranean fever patients without amyloidosis (38%) and in controls (20%). Serum levels of acute‐phase reactants in familial Mediterranean fever patients were reduced significantly following nonsurgical periodontal therapy (p < 0.01).Conclusion:  Periodontal therapy seems to reduce the serum levels of acute‐phase reactants in patients with familial Mediterranean fever. Therefore, treating periodontitis might help to alleviate the disease burden in patients with familial Mediterranean fever.
Association between lactoferrin gene polymorphisms and aggressive periodontitis among Taiwanese patients
Authors: Wu Y‐M. , Juo S‐H. , Ho Y‐P. , Ho K‐Y. , Yang Y‐H. , Tsai C‐C. 
Published: October 2008

Background and Objective:  A dramatic difference in the frequencies of the Lys/Arg single nucleotide polymorphism in the lactoferrin genotype between a small population of patients with localized juvenile periodontitis and healthy subjects has been reported. As the single nucleotide polymorphism could be associated with ethnicity, the present study aimed to investigate the association between polymorphisms of the lactoferrin gene and periodontitis.Material and Methods:  Sixty‐five patients with aggressive periodontitis, 278 with chronic periodontitis and 88 healthy controls were genotyped for the Lys/Arg polymorphism of the lactoferrin gene at position 29 [reference sequence (rs) 1126478] in the N‐terminal alpha‐helical region.Results:  The frequencies of the GG genotype and the G allele were highest in the aggressive periodontitis group, followed by the chronic periodontitis group and then the healthy controls. The frequency of the G allele was significantly higher in aggressive periodontitis and chronic periodontitis groups than in healthy controls (p = 0.0037 and 0.0212). Although the difference of the GG genotype distribution between subjects with chronic periodontitis and healthy controls did not reach significance, the distribution of genotypes between aggressive periodontitis and healthy controls was significantly different. The association of the gene polymorphism and aggressive periodontitis still existed, even after adjusting for age, gender and smoking status by logistic regression analysis (GG/AG+AA: odds ratio = 2.16, 95% confidence interval = 1.09–4.35, p = 0.0287). After the study, subjects were further stratified by their smoking status; the GG genotype was still significantly associated with the risk of aggressive periodontitis in the nonsmoking group (odds ratio = 2.69, p = 0.018). However, there were no statistical differences between chronic periodontitis vs. healthy controls and aggressive periodontitis vs. healthy controls in the smoking group.Conclusion:  The present study revealed that the A/G polymorphism in the lactoferrin gene might be associated with aggressive periodontitis. The A allele might reduce the risk of development of aggressive periodontitis in a Taiwanese population. Our results also support the hypothesis that lactoferrin genetic polymorphisms could play a role in the risk for periodontitis separate from the smoking factor. The functionality of this gene’s polymorphisms has to be further elucidated.
Identifying early osteoclastic resorptive lesions in feline teeth: a model for understanding the origin of multiple idiopathic root resorption
Authors: DeLaurier A. , Boyde A. , Jackson B. , Horton M. A. , Price J. S. 
Published: October 2008

Background and Objective: Domestic cats commonly suffer from external osteoclastic tooth resorption, a disease with many similarities to human multiple idiopathic root resorption. In both diseases, it is unclear whether anatomical features of the tooth surface are associated with a predisposition for resorptive lesions. The aim of the present study was to investigate the origin and progression of early feline osteoclastic resorptive lesions in teeth exhibiting no clinical signs of disease.Material and Methods: The entire surfaces of 138 teeth from 13 adult cats were analysed using back‐scattered electron microscopy. The distribution of lesions was assessed by tooth type, location and between individuals.Results: Seventy‐three (53%) teeth showed at least one resorptive lesion. Eleven (85%) cats had lesions, and there was a significant association between increasing age and incidence of resorptive lesions. The highest frequency occurred in mandibular molars (82%). On average, there were 3.5 lesions per tooth. Fifty‐two (38%) teeth featured resorptive lesions at the cemento–enamel junction. Twenty‐three per cent of teeth with resorptive lesions showed evidence of repair of lesions that was limited to the root surface. There was no evidence of repair of resorptive lesions at the cemento–enamel junction.Conclusion: Resorption is prevalent without evidence of clinical disease, and occured at younger ages than previously reported. It can initiate anywhere on the root surface, but lack of repair of lesions at the cemento–enamel junction indicates that mechanisms of replacement are absent or compromised in this region. Whereas resorption of the root may undergo repair, resorption at the cervix may progress to clinically evident lesions.
Matrix metalloproteinase inhibitors reduce collagen gel contraction and α‐smooth muscle actin expression by periodontal ligament cells
Authors: Bildt M. M. , Bloemen M. , Kuijpers‐Jagtman A. M. , Von den Hoff J. W. 
Published: October 2008

Background and Objective:  Orthodontic tooth movement requires remodeling of the periodontal tissues. The matrix metalloproteinases (MMPs) degrade the extracellular matrix components of the periodontal ligament, while the tissue inhibitors of metalloproteinases (TIMPs) control their activity. Synthetic MMP inhibitors have been developed to inhibit MMP activity. In this study, periodontal ligament cells in contracting collagen gels served as a model for enhanced periodontal remodeling. The effect of MMP inhibitors on gel contraction and on MMP and TIMP expression was analyzed.Material and Methods:  Human periodontal ligament cells were cultured in three‐dimensional collagen gels and incubated with the MMP inhibitors BB94, CMT‐3, doxycycline and Ilomastat. Gel contraction was determined using consecutive photographs. The relative amounts of MMPs and TIMPs were analyzed using substrate zymography and mRNA expression using quantitative polyermase chain reaction.Results:  All MMP inhibitors reduced MMP activity to about 20% of the control activity. They all reduced contraction, but CMT‐3 and doxycycline had the strongest effect. These inhibitors also reduced MMP‐2, MMP‐3 and α‐smooth muscle actin mRNA expression. The expression of MMP‐1 mRNA seemed to be increased by CMT‐3. No effects were found on the amounts of MMPs and TIMPs.Conclusion:  Synthetic MMP inhibitors strongly reduced gel contraction by periodontal ligament cells. This was primarily caused by an inhibitory effect on MMP activity, which reduces matrix remodeling. In addition, α‐smooth muscle actin expression was reduced by CMT‐3 and doxycycline, which limits the contractile activity of the fibroblasts.
Gingipain enzymes from Porphyromonas gingivalis preferentially bind immobilized extracellular proteins: a mechanism favouring colonization?
Authors: McAlister A. D. , Sroka A. , Fitzpatrick R. E. , Quinsey N. S. , Travis J. , Potempa J. , Pike R. N. 
Published: October 2008

Background and Objective:  Porphyromonas gingivalis, an anaerobic bacterium associated with adult periodontal disease, employs a number of pathogenic mechanisms, including protease/adhesin complexes (gingipains), fimbriae and hemagglutinins, to maintain attachment within colonized hosts. Here we examined the binding of gingipains and whole, live P. gingivalis cells to immobilized extracellular matrix proteins in the presence of soluble forms of the same proteins, to investigate whether this may constitute a colonization mechanism in the oral environment.Material and Methods:  Binding of purified gingipain molecules and whole bacterial cells to immobilized matrix proteins was examined in the presence and absence of soluble competitors using enzyme‐linked immunosorbent assays.Results:  Purified gingipains or whole, live bacteria preferentially bound immobilized forms of matrix proteins, even in the presence of soluble forms of the same proteins. Fimbriae appeared to be redundant for adhesion to immobilized proteins in the presence of the gingipains, indicating that the protease/adhesins and hemagglutinins may be more important for adhesion under these conditions.Conclusion:  The data presented here provide evidence for a model of adhesion for P. gingivalis within the fluid environment of the oral cavity, where preferential binding of matrix‐located proteins over soluble forms facilitates colonization of the host.
Experimental periodontitis in mice selected for maximal or minimal inflammatory reactions: increased inflammatory immune responsiveness drives increased alveolar bone loss without enhancing the control of periodontal infection
Authors: Trombone A. P. F. , Ferreira Jr S. B. , Raimundo F. M. , De Moura K. C. R. , Avila‐Campos M. J. , Silva J. S. , Campanelli A. P. , De Franco M. , Garlet G. P. 
Published: October 2008

Background and Objective:  Inflammatory immune reactions that occur in response to periodontopathogens are thought to protect the host against infection, but may trigger periodontal destruction. However, the molecular and genetic mechanisms underlying host susceptibility to periodontal infection and to periodontitis development have still not been established in detail.Material and Methods:  In this study, we examined the mechanisms that modulate the outcome of Aggregatibacter (Actinobacillus) actinomycetemcomitans‐induced periodontal disease in mice mouse strains selected for maximal (AIRmax) or minimal (AIRmin) inflammatory reactions.Results:  Our results showed that AIRmax mice developed a more severe periodontitis than AIRmin mice in response to A. actinomycetemcomitans infection, and this periodontitis was characterized by increased alveolar bone loss and inflammatory cell migration to periodontal tissues. In addition, enzyme‐linked immunosorbent assays demonstrated that the levels of the cytokines interleukin‐1β, tumor necrosis factor‐α and interleukin‐17 were higher in AIRmax mice, as were the levels of matrix metalloproteinase (MMP)‐2, MMP‐13 and receptor activator of nuclear factor‐κB ligand (RANKL) mRNA levels. However, the more intense inflammatory immune reaction raised by the AIRmax strain, in spite of the higher levels of antimicrobial mediators myeloperoxidase and inducible nitric oxide synthase, did not enhance the protective immunity to A. actinomycetemcomitans infection, because both AIRmax and AIRmin strains presented similar bacterial loads in periodontal tissues. In addition, the AIRmax strain presented a trend towards higher levels of serum C‐reactive protein during the course of disease.Conclusion:  Our results demonstrate that the intensity of the inflammatory immune reaction is associated with the severity of experimental periodontitis, but not with the control of A. actinomycetemcomitans periodontal infection, suggesting that the occurrence of hyperinflammatory genotypes may not be an evolutionary advantage in the complex host–pathogen interaction observed in periodontal diseases.
Granulocyte chemotactic protein 2 (gcp‐2/cxcl6) complements interleukin‐8 in periodontal disease
Authors: Kebschull M. , Demmer R. , Behle J. H. , Pollreisz A. , Heidemann J. , Belusko P. B. , Celenti R. , Pavlidis P. , Papapanou P. N. 
Published: October 2008

Background and Objective:  Mucosal inflammatory responses are orchestrated largely by pro‐inflammatory chemokines. The chemokine granulocyte chemotactic protein 2 (CXCL6) is involved in neutrophil recruitment and migration. Previous studies have shown that granulocyte chemotactic protein 2 is up‐regulated during mucosal inflammation (e.g. in inflammatory bowel disease), similarly to the functionally and structurally related chemokine interleukin‐8. Nevertheless, unlike interleukin‐8, a role of granulocyte chemotactic protein 2 in gingival inflammation has not been yet demonstrated. In this study we aimed to evaluate the expression of the chemokine granulocyte chemotactic protein 2 in clinically healthy vs. diseased gingival tissues and to explore possible correlations with clinical and microbiological markers of periodontitis.Material and Methods:  Gene expression in 184 ‘diseased’ and 63 ‘healthy’ gingival tissue specimens from 90 patients with periodontitis was analyzed using Affymetrix U133Plus2.0 arrays. The expression of granulocyte chemotactic protein 2 was further confirmed by real‐time reverse transcription–polymerase chain reaction, western blotting and enzyme‐linked immunosorbent assay, while the localization of granulocyte chemotactic protein 2 in gingival tissues was analyzed by immunohistochemistry. Plaque samples from the adjacent periodontal pockets were collected and evaluated for 11 species of periodontal bacteria using checkerboard DNA–DNA hybridizations.Results:  Among all known chemokines, GCP‐2 expression was the most up‐regulated (3.8‐fold, p < 1.1 × 10−16), in ‘diseased’ vs. ‘healthy’ tissue as compared to a 2.6‐fold increased expression of interleukin‐8 mRNA (p < 1.2 × 10−15). Increased expression of granulocyte chemotactic protein 2 correlated with higher levels of ‘red’ and ‘orange’ complex pathogens and with increased probing depth, but not with attachment loss. Immunohistochemistry showed that granulocyte chemotactic protein 2 was expressed in gingival vascular endothelium.Conclusion:  The level of expression of granulocyte chemotactic protein 2 correlates with the severity of periodontitis and appears to act as a hitherto unrecognized functional adjunct to interleukin‐8 in diseased gingival tissues.
Surface components of Porphyromonas gingivalis
Authors: Yoshimura F. , Murakami Y. , Nishikawa K. , Hasegawa Y. , Kawaminami S. 
Published: October 2008

Background and Objective:  Research on Porphyromonas gingivalis, a periodontopathogen, has provided a tremendous amount of information over the last 20 years, which may exceed in part than that on other closely related members in terms of phylogenetic as well as proteomic criteria, including Bacteroides fragilis and B. thetaiotaomicron as major anaerobic, opportunistic pathogens in the medical field. In this minireview, we focused on recent research findings concerning surface components such as outer membrane proteins and fimbriae, of P. gingivalis.Material and Methods:  Elucidation of the surface components in P. gingivalis was especially difficult because outer membrane proteins are tightly bound to lipopolysaccharide and they are resistant to dissociation and separation from each other, even during sodium dodecyl sulfate–polyacrylamide gel electrophoresis, unless samples are appropriately heated. In addition, P. gingivalis is asaccharolytic and therefore a potent proteolytic bacterium, another factor causing difficulty in research. The study of the surface components was carefully carried out considering these unique features in P. gingivalis when compared with other gram‐negative bacteria, including Escherichia coli and Pseudomonas aeruginosa.Results:  Separation of outer membrane proteins, and characterization of OmpA‐like proteins and RagAB as major proteins, is described herein. Our recent findings on FimA and Mfa1 fimbriae, two unique appendages in this organism, and on their regulation of expression are also described briefly.Conclusion:  Surface components of P. gingivalis somehow have contact with host tissues and cells because of the outermost cell elements. Therefore, such bacterial components are potentially important in the occurrence of periodontal diseases.