bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cyclosporin A Regulates Interleukin‐1ßand Interleukin‐6 Expression in Gingiva: Implications for Gingival Overgrowth
Authors: Myrillas Theofilos T. , Linden Gerard J. , Marley John J. , Irwin Chris R. 
Published: February 2005

Background: Gingival overgrowth is a common side effect following the administration of cyclosporin A (CsA); however, the cellular mechanisms remain poorly understood. CsA's immunosuppressant properties involve the regulation of synthesis and cellular response to cytokines. A CsA‐induced alteration in the cytokine profile within gingival tissue could provide a mechanism for gingival hyperplasia. The aim of this study was to investigate the effects of CsA on the production of 2 cytokines — interleukin‐1ß(IL‐1ß) and interleukin‐6 (IL‐6) — by both gingival fibroblasts and peripheral blood mononuclear cells (PBMC).Methods: Cells were stimulated for 24 hours in the presence of CsA over a concentration range of 100 to 2,000 ng/ml and the resultant cytokine production determined by ELISA. In addition, levels of both cytokines within normal, inflamed, and overgrown gingival tissue were determined.Results: CsA inhibited IL‐6 production by gingival fibroblasts in a dose‐dependent manner. In contrast, at a concentration of 2,000 ng/ml, CsA stimulated IL‐6 production by PBMC ( P< 0.05). Fibroblasts derived from overgrown gingiva produced significantly higher levels of IL‐6 than their normal counterparts ( P <0.05). CsA inhibited IL‐1ßproduction by PBMC over the whole concentration range ( P <0.05). IL‐1ßwas not found in measurable quantities in any of the fibroblast cultures. Levels of IL‐6 extracted from overgrown gingival tissue were significantly higher than in inflamed or normal tissue. In contrast IL‐1ßlevels in overgrown tissue were not statistically significantly greater than those in inflamed tissue.Conclusions: These results show that CsA does regulate cytokine expression in gingival tissue. This effect may play an important role in the pathogenesis of CsA‐induced gingival overgrowth. J Periodontol 1999;70:294‐300.
Site‐Specific Attachment Level Change Detected by Physical Probing in Untreated Chronic Adult Periodontitis: Review of Studies 1982‐1997
Authors: Breen Harry J. , Johnson Newell W. , Rogers Pauline A. 
Published: February 2005

Background: Site‐specific attachment level change, detected from sequential physical probing measurements, is currently the most common method of determining the progression/regression or stability of disease status in subjects with chronic adult periodontitis. The sensitivity and accuracy of detection is dependent on the type of probe used, the recording method, the measurement error, and the method of data analysis. In recent years, there has been world‐wide interest in developing instruments and methods to minimize measurement error. Published data report disturbingly wide variation in the prevalences and rates of site‐specific attachment level change which are difficult to reconcile with biological likelihood. The present paper aims to summarize the salient points from the key studies and to compare the results.Methods: The literature between 1982 and 1997 was reviewed for studies in which site‐specific attachment level change was detected by physical probing methods in patients with chronic adult periodontitis. Results: The review documents 23 studies by probe generation, to the thresholds and probe type used. The 23 studies used an array of probe types from the 3 probe generations. compares methods and results and summarizes the results accordingResults: The review documents 23 studies by probe generation, to the thresholds and probe type used. The 23 studies used an array of probe types from the 3 probe generations. compares methods and results and summarizes the results accordingConclusions: From this review, we conclude that: 1) There are surprisingly few papers which have addressed the question of site‐specific attachment level change in untreated chronic adult periodontitis. 2) There are considerable differences in the probes used, in the thresholds achieved, in the number of measurements taken, in the number of subjects and sites studied, and in the duration of the studies. Valid comparisons between studies are, therefore, rarely possible. 3) Only out of 23 papers from 1982 to 1997 have adequate data. Most papers report only losing sites and therefore ignore many of the measurements recorded. Only one paper describes losing sites, gaining sites, and sites showing exacerbation/remission patterns of change. 4) The range of changes described show such variation that it has to be concluded that we cannot reliably detect site‐specific attachment level change by physical probing and thus, at the end of the 20th century, we have no clear idea of the natural history of this disease. J Periodontol 1999;70:312‐328.
Bacteriostatic Effects of Hyaluronic Acid
Authors: Pirnazar Payman , Wolinsky Larry , Nachnani Sushma , Haake Susan , Pilloni Andrea , Bernard George W. 
Published: February 2005

Background: This investigation is one of a series of projects seeking to ascertain whether hyaluronic acid (HA) is therapeutically effective in tissue regeneration procedures. The rationale for these investigations is to test the hypothesis that HA can serve as a bioabsorbable carrier for other substrates as well as itself actively promote the regeneration of tissue.Methods: In this paper, we report on the bacteriostatic and bactericidal properties of 3 molecular weight formulations of recombinant HA (low, 141 kD; medium, 757 kD; and high, 1,300 kD) on selected oral and non‐oral microorganisms in the planktonic phase. Three concentrations of each HA formulation were screened, 0.5, 1.0, and 2.0 mg/ml, using a standard broth culture assay.Results: Recombinant HA exerted varied bacteriostatic effects on all the bacterial strains tested depending on its molecular weight (MW) and concentration. The high concentrations of the medium MW HA had the greatest bacteriostatic effect, particularly on the Actinobacillus actinomycetemcomitans, Prevotella oris, Staphylococcus aureus, and Propionibacterium acnes strains. The 1.0 mg/ml concentration of high MW HA had the greatest overall bacteriostatic effect, inhibiting the growth of all 6 bacterial strains tested. Among the bacterial strains studied, HA was found to have no bactericidal effects, regardless of concentration or molecular weight.Conclusions: The results of this study suggest that HA in the MW range of 1,300 kD may prove beneficial in minimizing bacterial contamination of surgical wounds when used in guided tissue regeneration surgery. J Periodontol 1999;70:370‐374.
A New Injectable Calcium Phosphate Biomaterial for Immediate Bone Filling of Extraction Sockets: A Preliminary Study in Dogs
Authors: Gauthier Olivier , Boix Damien , Grimandi Gaël , Aguado Eric , Bouler Jean‐Michel , Weiss Pierre , Daculsi Guy 
Published: February 2005

Background:
Many different bone substitutes, such as autografts, allografts or synthetic biomaterials have been proposed to restore alveolar bone loss and support efficient placement of dental implants. This experimental study evaluated the osteoconductive properties of an injectable bone substitute (IBS) composed of a polymeric carrier and a calcium phosphate mineral phase, used to fill mandibular and maxillary canine extraction sockets.
Methods:
The polymer was a cellulose derivative (methyl‐hydroxy‐propyl‐cellulose, MHPC), and the mineral phase consisted of granules of biphasic calcium phosphate (BCP) ceramics 200 to 500 μm in diameter. Mandibular and maxillary premolars extracted from 3 dogs (a total of extraction sites) were immediately treated with the IBS left unfilled as control sites. Animals were sacrificed months after implantation and all extraction sockets were prepared for histological evaluation.
Results:
Qualitative histological studies showed that the IBS was able to support the extensive apposition of wellmineralized newly formed lamellar bone over the entire socket surface and appeared to prevent alveolar ridge bone loss in treated extraction sites. Quantitative evaluation showed that the amount of newly formed bone was significantly higher in mandibular than maxillary extraction sockets for both treated and control sites.
Conclusions:
An injectable bone substitute composed of a polymeric carrier and calcium phosphate was effective in enhancing the bone fill of extraction sockets. This approach may prove promising for periodontal lesions. The material expressed osteoconductive capacities, and the biological properties of the mineral phase were conserved. J Periodontol 1999;70:375‐383.
Monoclonal Antibodies Against Integrin Subunits α6 and β1 Inhibit Migration of Gingival Epithelium in Organ Culture
Authors: Gräber Hans‐Georg , Wilharm Jens , Conrads Georg 
Published: February 2005

Background: The main problem in the posterior instrumental treatment of periodontitis is the re‐epithelization of the periodontal defects, leading to the formation of an unphysiological, long junctional epithelium inhibiting the regeneration of periodontal attachment. A precondition for the re‐epithelization is the interaction between epithelial cells and their extracellular matrix mediated by integrins. Integrins are cellular adhesion molecules (CAM), binding to different structures of the extracellular matrix, e.g., collagen, laminin, or fibronectin.Methods: Biopsy specimens of marginal gingiva, composed of epithelium and subepithelial connective tissue, were cultivated on microporous membranes in tissue culture plates. The culture medium was supplemented with monoclonal antibodies directed against human integrin subunits. The period of cultivation was 6 days and the medium was replaced daily. After cultivation, the tissue development was analyzed by histological and immunohistochemical methods.Results: We found that the combination of antibodies directed against the integrin subunits α6 and β1 inhibited the migration of epithelium completely in 9 out of 10 cultures, whereas control cultures containing none or only irrelevant antibodies demonstrated connective tissues completely covered by epithelium.Conclusions: Influencing the regeneration of periodontal tissue on a molecular basis by using antibodies directed against integrin subunits may be of future interest in postsurgical treatment of periodontal diseases. J Periodontol 1999;70:388‐393.
Increase of Urokinase‐Type Plasminogen Activator Receptor Expression in Human Gingival Fibroblasts by Porphyromonas gingivalis Lipopolysaccharide
Authors: Ogura Naomi , Nagura Hideaki , Abiko Yoshimitsu 
Published: February 2005

Background: Urokinase‐type plasminogen activator receptor (uPAR) presenting on the cell surface with glycosylphosphatidylinositol (GPI) anchor is a key component in the plasminogen activator (PA)‐plasmin system and plays a critical role in extracellular matrix degradation. It is believed that uPAR serves to localize and accelerate this generation system. In this study, we examined the levels of both uPA and uPAR in human gingival fibroblasts treated with Porphyromonas gingivalis lipopolysaccharide (LPS).Methods: Human gingival fibroblasts from the seventh to tenth doubling passages were plated at 5 x 104 cells per well in 24‐well plates. The confluent‐stage cells were cultured for 24 hours in α‐MEM medium containing 2% fetal calf serum, after which they were incubated with P. gingivalis LPS. PA activity was measured using plasminogen and plasmin substrate S2251.Results: PA activity in the cell lysate was increased by LPS and reached maximum at 1 μg/ml LPS after being incubated for 8 hours. PA activity released by phosphatidylinositol‐specific phospholipase C, which detaches the GPI anchor, was also increased by LPS. The activity was inhibited by amiloride, which is a specific inhibitor for uPA. LPS increased the protein and mRNA levels of both uPA and uPAR in gingival fibroblasts.Conclusions: These findings suggest that increase of the uPAR level by LPS may play an important role in the progression of periodontal diseases through pericellular proteolysis. J Periodontol 1999;70:402‐408.
Persistence of Oral Colonization by the Same Actinobacillus actinomycetemcomitans Strain(s)
Authors: Saarela Maria H. , Doğan Başak , Alaluusua Satu , Asikainen Sirkka 
Published: February 2005

Background: The Gram‐negative facultatively anaerobic coccobacillus Actinobacillus actinomycetemcomitans is the major pathogen in localized juvenile periodontitis (LJP) and some forms of adult periodontitis (AP). A. actinomycetemcomitans can be grouped into 5 serotypes (a through e) based on differences in the carbohydrate moiety of cell surface lipopolysaccharide. The A. actinomycetemcomitans population is genetically heterogeneous. Since the studies on A. actinomycetemcomitans colonization have mostly applied only culture techniques, the clonality of the follow‐up isolates has not been established. Thus, it is possible that, although A. actinomycetemcomitans could be repeatedly isolated from an individual, the intitial colonizing strain was replaced by another strain. The aim of the study was to determine whether oral A. actinomycetemcomitans strains change spontaneously over time or after periodontal treatment.Methods: A total of 922 A. actinomycetemcomitans isolates were recovered from 115 subjects. From each subject A. actinomycetemcomitans isolates were obtained from 2 to 9 follow‐up samples 0.5 to 11.5 years apart. After the first sampling occasion, 99 subjects were treated for either LJP or AP, whereas the 16 non‐periodontitis subjects received no treatment. All A. actinomycetemcomitans isolates were serotyped and 235 isolates from 52 subjects genotyped with AP‐PCR and/or with ribotyping.Results: Isolates of only one serotype, or non‐serotypeable isolates alone, were repeatedly found in 104 subjects; serotype a occurred in 25%, b in 33%, c in 23%, d in 5%, e in 7%, and non‐serotypeable isolates in 8% of these subjects. Two serotypes (or serotypeable isolates together with non‐serotypeable isolates) occurred simultaneously in 9 subjects and in each of these subjects at least one of the serotypes was detected at each sampling occasion. In one subject the initial serotype reappeared although a different serotype was once seen alone, whereas in another subject the initial serotype could not be recovered later. Identical genotypes of A. actinomycetemcomitans were repeatedly detected in each of 52 subjects with follow‐up isolates of the same serotype.Conclusions: The results showed that spontaneous or treatmentinduced change in the oral A. actinomycetemcomitans strain(s) is extremely rare and that colonization with the same strain(s) seems to be remarkably persistent. J Periodontol 1999;70:504‐509.
Effects of Tobacco Products on the Attachment and Growth of Periodontal Ligament Fibroblasts
Authors: James Jacqueline A. , Sayers Nicola M. , Drucker David B. , Hull Peter S. 
Published: February 2005

Background: Cigarette smoking is one of the most significant risk factors in the development and further advancement of inflammatory periodontal disease, however, the role of either nicotine or its primary metabolite cotinine in the progression of periodontitis is unclear. This study aimed to investigate the effects of nicotine and cotinine on the attachment and growth of fibroblasts derived from human periodontal ligament (PDL).Methods: Primary cultures were prepared from the roots of extracted premolar teeth. Cells were used at both low (P3 to P5) and high (P11 to P13) passage. Cell numbers were determined over 14 days using either the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyl tetrazolium bromide (MTT) assay or with a Coulter counter. Cultures were exposed to culture medium supplemented with 1) 15% fetal calf serum (FCS) only; 2) 1% FCS only; 3) 1% FCS and nicotine (concentration range 5 ng/ml to 10 mg/ml); or 4) 1% FCS and cotinine (concentration range 0.5 ng/ml to 10 µg/ml).Results: Nicotine significantly (P <0.05, by ANOVA) inhibits attachment and growth of low passage cells at concentrations >1 mg/ml and high passage PDL fibroblasts at concentrations >0.5 mg/ml. Cotinine, at the highest concentration used (10 µg/ml), appeared to inhibit attachment and growth of both low and high passage fibroblasts but this was not statistically significant (P >0.05, by ANOVA).Conclusions: Tobacco products inhibit attachment and growth of human PDL fibroblasts. This may partly explain the role of these substances in the progression of periodontitis. J Periodontol 1999;70:518‐525.
Expression of p53 Protein and Ki‐67 Antigen in Gingival Hyperplasia Induced by Nifedipine and Phenytoin
Authors: Saito Keiichi , Mori Shiro , Tanda Naoko , Sakamoto Seizaburo 
Published: February 2005

Background: Although it has been thought that drug‐induced gingival hyperplasia is not related to tumorigenesis, recent case reports have shown that squamous cell carcinomas may arise in gingival hyperplasia induced by cyclosporin and phenytoin. The possible implications between the pathogenesis of this disease and tumorigenesis have not been elucidated and remain to be studied.Methods: We immunohistochemically examined the expression of tumor‐related markers such as p53 protein and Ki‐67 antigen in 11 hyperplastic gingival tissues induced by nifedipine and phenytoin, as well as 5 control tissues using an avidin‐biotin‐peroxidase complex method.Results: Two specimens out of 4 nifedipine‐induced and 4 out of 7 phenytoin‐induced hyperplastic gingival tissues revealed the expression of p53protein in the nuclei of epithelial cells, while no expression of p53 protein was observed in the epithelia of the 5 non‐hyperplastic control tissues. The immunoreactions against p53 protein showed sporadic distribution in the suprabasal layers of hyperplastic epithelia. The mean percentage of epithelial cells expressing Ki‐67 antigen in the hyperplastic gingival tissues was more than 10% higher than that in the controls. The expression of Ki‐67 antigen was suppressed in the typical rete pegs deeply elongated into lamina propria of hyperplastic gingival tissues. Intense immunostaining of Ki‐67 antigen was found in fibroblasts of hyperplastic gingival tissues, while that of the control tissues was negligible.Conclusions: The expression of p53 protein in gingival hyperplasia suggests that the pathogenesis of this disease is involved with impaired DNA, while the growth arrest observed in the hyperplastic epithelia with typically elongated rete pegs as expressed with Ki‐67 antigen may prevent the invasive expansion of epithelial cells undergoing DNA damage within gingival tissues and may consequently suppress tumorigenic progression. J Periodontol 1999;70:581‐586.
In Vitro Stimulation of Human Gingival Epithelial Cell Attachment to Dentin by Surface Conditioning
Authors: Vanheusden Alain J. , Goffinet Gérhard , Zahedi Sharam , Nusgens Betty , Lapiére Charles M. , Rompen Eric H. 
Published: February 2005

Background: Chemical root conditioning is widely used to improve the outcome of regenerative periodontal therapies by favoring the attachment of the regenerated periodontal structures. Although the effect of root conditioning on periodontal mesenchymal cells is well documented, very little is known about its potential effect on the re‐formation of the junctional epithelium, a crucial event for the protection of the wound. The goal of the present study was to test in vitro the consequences of dentin conditioning with citric acid or minocycline on the attachment kinetics and morphology of human gingival keratinocytes (HGK).Methods: The attachment kinetics of HGK to samples of powdered human dentin (particle size 44 to 76 µm) were examined by use of 3H‐labeled cells. The morphology of attached epithelial cells was then determined by scanning electron microscopy (SEM).Results: When the initial adhesion kinetics of cells on untreated dentin were tested, the percentage of attached HGK proved to be dependent on the number of plated cells and the time of incubation from 0 to 12 hours). Conditioning the dentin by 3% citric acid or by minocycline‐HCl (at 0.01, 0.1, or 2.5%) significantly increased (P <0.005) keratinocyte attachment beyond 6 hours, without notable differences between the 2 substances at any concentration. The attachment kinetics of HGK preincubated for 24 hours by 10 µg/ml minocyline‐HCl on untreated dentin was found to be similar to that observed for non‐preincubated cells. These results are in agreement with the SEM observations: indeed, the surface conditioning of dentin significantly modified the morphology of attached HGK, whereas the preincubation of these cells with minocyline‐HCl did not.Conclusions: These results suggest that minocycline‐HCl does not exert a direct effect on human gingival epithelial cells. In contrast, conditioning the dentin by citric acid or by minocycline stimulates the attachment of HGK, which could lead to a rapid periodontal healing by favoring the re‐formation of a junctional epithelium. J Periodontol 1999;70:594‐603.
Androgens Modulate Interleukin‐6 Production by Gingival Fibroblasts In Vitro
Authors: Gornstein Russell A. , Lapp Carol A. , Bustos‐Valdes Sergio M. , Zamorano Pedro 
Published: February 2005

Background: Pregnancy and puberty gingivitis have been attributed to increased concentrations of circulating sex hormones. This inflammatory gingival condition is accompanied by the local production of cytokines. The aims of this in vitro study were to assess, in the presence or absence of testosterone (T) or dihydrotestosterone (DHT), the production of interleukin‐6 (IL‐6) by human gingival fibroblasts (hGF), and to evaluate the effects of flutamide (a common anti‐androgen) in this system.Methods: The effects of the androgens, T and DHT, on IL‐6 production were measured in vitro in serum‐free, phenol red‐free medium. Cells were incubated with or without androgens for 72 hours; the concentration of IL‐6 secreted into the medium after an additional 24‐hour challenge with IL‐1β plus hormones was estimated by radioimmunoassay. The reverse transcription polymerase chain reaction was used to examine hGF and periodontal ligament cells (PDL) for the presence of androgen receptor.Results: In serum‐free medium, T and DHT at concentrations of 5 x 10‐8 to 10‐7M significantly (P <0.05) inhibited IL‐6 production by hGF. Flutamide, up to concentrations of 2 x 10‐5M, did not reverse this inhibition. The androgen receptor was identified in both hGF and PDL.Conclusions: We concluded that elevated levels of androgens, specifically testosterone and dihydrotestosterone, could affect the stromal cell response to an inflammatory challenge by downregulation of IL‐6 production. This in vitro study lends support to the hypothesis that increased hormones during pregnancy or puberty could modulate the development of localized inflammation. J Periodontol 1999;70:604‐609