bluuebunny/crossref_metadata_2025_split huggingface dataset:
Smoking Influences Decision Making in Periodontal Therapy: A Retrospective Clinical Study
Authors: Papantonopoulos George H. 
Published: February 2005

Background: Mechanical periodontal therapy consists of a non‐surgical course, followed by surgical treatment to eliminate or reduce remaining pathological pockets. Only if diligent mechanical therapy fails are additional measures considered. It has been documented that smoking interferes with the host defense mechanisms. This study addresses the question is meticulous non‐surgical periodontal therapy equally successful in smokers and non‐smokers? If not, is a thorough and cumbersome non‐surgical approach in smokers worth undertaking?Methods: Thirty‐five smokers and 35 non‐smokers were selected retrospectively from a pool of 306 patients treated in a private practice over a 17‐month period. All had at least 14 teeth present with 8 presenting with gingival pockets ≥6 mm. Non‐surgical treatment was performed in 6 to 10 appointments and results were evaluated 6 to 12 weeks after therapy. Bleeding on probing sites with probing depths ≥5 mm were then considered for surgical treatment.Results: Before treatment smokers had statistically significantly higher mean percent of pockets 4 to 5 mm and ≥6 mm (40.36 ± 10.65 and 26.51 ± 11.95, respectively, compared to 30.38 ± 7.57 and 20.42 ± 10.03 for nonsmokers) and showed significantly lower proportional reduction of these parameters with treatment (50.80 ± 33.76 and 81.36 ± 19.82 for pocket 4 to 5 mm and 6 mm, compared to 68.43 ± 21.23 and 91.7 ± 8.92 for nonsmokers). A multivariate analysis gave smoking, plaque control, and initial percent of sites ≥6 mm to be significant predictors of the percent of teeth in need of further therapy. In non‐smokers, treatment was apparently successful in all tooth types with the exception of upper first and second molars (28.5% failure) and lower second molar (20% failure). In smokers, rates of further treatment needs were particularly high in the premolar‐molar area in both jaws, ranging from 31.4% to 48.5% for an individual tooth type; 42.8% of smokers and 11.5% of non‐smokers needed further treatment in 16% of their teeth (pretest probability). A decision analysis showed that for smokers with at least 1 of 5 sites ≥6 mm, one should initiate surgical treatment, rather than first treat non‐surgically. If the point of indifference that the decision is correctly set at 95%, the pretest probability should be >12%. There is a higher risk that non‐surgical therapy will fail, for instance if we lower the point of indifference to 60%, the pretest probability should be 7>31%.Conclusions: It is concluded that smoking impairs healing after nonsurgical periodontal therapy. The decision analysis of this study questions the need for a thorough course of non‐surgical treatment in smokers with advanced periodontal disease. J Periodontol 1999;70:1166‐1173.
An 18‐Year Longitudinal Study of Untreated Mucogingival Defects
Authors: Freedman Arnold L. , Green Kevan , Salkin Leslie M. , Stein Marc D. , Mellado Jose R. 
Published: February 2005

Background: A study was conducted to observe the changes in areas with untreated mucogingival defects over an 18‐year period. The results in this group after 4 and 10 years were previously published.Methods: Upon entering dental school, a group of 39 freshman dental students were assessed for plaque index, gingival index, probing depth, and width of keratinized tissue. At that time, 112 sites of inadequate keratinized gingiva were found. Seventeen of the original 39 participants with a total of 61 sites were reassessed for the same parameters after 18 years.Results: The results revealed that 19 sites showed a slight increase in keratinized tissue, 35 were unchanged (for a total of 54 stable sites), and 7 sites showed a slight decrease in keratinized tissue. The mean width of keratinized tissue at the beginning of the study was 1.74 ± 0.545 mm and 2.02 ± 0.885 mm after 18 years. This represented a small, but statistically significant increase in the width. The plaque index (PI) and gingival index (GI) of this group at baseline (PI = 0.77 ± 0.439 and GI = 0.93 ± 0.447) and at 18 years (PI = 0.36 ± 0.344 and GI = 0.65 ± 0.303) indicated a high level of oral hygiene and gingival health.Conclusions: It was concluded that in the absence of gingival inflammation, areas with small amounts of keratinized tissue may remain stable over long periods of time. J Periodontol 1999;70:1174‐1176.
Single Nucleotide Polymorphisms of the N‐Formyl Peptide Receptor in Localized Juvenile Periodontitis
Authors: Gwinn Maureen R. , Sharma Ashu , De Nardin Ernesto 
Published: February 2005

Background: Neutrophils from patients with localized juvenile periodontitis (LJP) exhibit decreased binding and responsiveness to various chemotactic agents, including N‐formyl‐lmethionyl‐l‐leucyl‐l‐phenylalanine (FMLP). This altered reaction of neutrophils is thought to account in part for the increased susceptibility of LJP patients to infections by periodontal organisms. Receptors for FMLP are involved in the activation and the subsequent response to certain chemotactic stimuli.Methods: In order to determine if this decreased response is due to a genetic variation in the receptor, we directly compared DNA encoding the FMLP receptor from controls matched for gender and race and LJP patients by single strand conformation polymorphism analysis (SSCP).Results: Using this technique, we observed a characteristic SSCP pattern in 29 out of 30 patient samples in the FMLP receptor DNA. This pattern differed from those obtained from the 20 control subjects as well as 31 patients with adult periodontitis. DNA sequencing of 30 patients indicated single nucleotide polymorphisms (SNPs) in the FMLP receptor DNA from the LJP patients when compared to 20 controls (P = 0.0005). Two single nucleotide base alterations were consistently seen: either a thymine to cytosine substitution at base 329 in 17 LJP patients or a cytosine to guanine substitution at base 378 in 5 LJP patients. A combination of both alterations were seen in 7 LJP patients. Both alterations resulted in amino acid changes in the second intracellular loop of the receptor, specifically phenylalanine to serine at residue 110 and cysteine to tryptophan at residue 126. This region of the FMLP receptor has recently been shown to play a role in ligand binding and Gprotein activation.Conclusions: This study suggests that a molecular alteration in the second intracellular loop of the FMLP receptor molecules in LJP patients may play a role in the decreased chemotactic activity reported for some LJP patients. J Periodontol 1999;70:1194‐1201.
Changes in Gingival Crevicular Fluid Levels of Immunoglobulin A Following Therapy: Association With Attachment Loss
Authors: Grbic John T. , Lamster Ira B. , Fine James B. , Lam Kei S. , Celenti Romanita S. , Herrera‐Abreu Miriam , Singer Robert E. 
Published: February 2005

Background: In previous studies, we demonstrated that increased levels of immunoglobulin A (IgA) in gingival crevicular fluid (GCF) may be “protective,” while increased levels of the polymorphonuclear lysosomal enzyme, β‐glucuronidase, in GCF were associated with increased risk of disease activity. In this study, we examined the effect of scaling and root planing (SRP) on the levels of β‐glucuronidase, IgG, and IgA in GCF over a 24‐week period and compared these to clinical attachment loss (CAL).Methods: Twenty‐nine patients with periodontal disease were examined for attachment level, probing depth, plaque, and bleeding on probing at 6 sites per tooth. GCF was collected from the mesial aspect of all teeth excluding third molars and analyzed for β‐glucuronidase, IgG, and IgA. After baseline data were collected, each patient received SRP, and GCF was collected again at 2, 4, 6, 8, 12, and 24 weeks post‐SRP while clinical data were obtained at 4, 8, 12, and 24 weeks. In addition, we analyzed whether the magnitude of the IgA response to SRP would affect the rate of periodontal disease progression by examining GCF IgA levels at 2 time intervals: 2 to 4 weeks post‐SRP and 6 to 12 weeks post‐SRP.Results: Seventeen patients (58.6%) exhibited at least 1 site losing ≥2.5 mm of CAL during the 24‐week study. β‐glucuronidase in GCF was significantly decreased at 2 weeks following SRP and then demonstrated a gradual increase throughout the study period. Levels of IgA in GCF significantly increased following SRP, reaching a peak at 6 weeks and then gradually decreasing throughout the study. Furthermore, we found an inverse relationship between GCF IgA levels at 6 to 12 weeks post‐SRP and the occurrence of CAL.Conclusions: These results support the hypothesis that maintenance of high levels of IgA in GCF may be “protective” against periodontal attachment loss. Furthermore, levels of β‐glucuronidase appear to be a more sensitive indicator of gingival inflammation than clinical measures. J Periodontol 1999;70:1221‐1227.
Morphological Study of Root Surfaces in Teeth With Adult Periodontitis
Authors: Abelleira Antonio Crespo , Cobos María Ángeles Rodríguez , Boquete Isaac Manuel Fuentes , Oreja María Teresa Castaño , Barreiro Francisco Javier Jorge , Pato Raquel Beatríz Rodríguez 
Published: February 2005

Background: Our study correlates the histological alterations in the cementum (especially resorption areas) of teeth with the different stages of adult periodontitis. Methods: Sixty‐seven teeth affected by adult periodontitis and 7 healthy teeth extracted from patients over 40 years old were used. The teeth were divided into 3 groups according to radiographic data: group 1: five teeth with bone loss less than one‐third of the normal alveolar height; group 2: thirty‐one teeth with bone loss between one and two thirds; and group 3: thirty‐one teeth with bone loss greater than two thirds. The samples were prepared for light and scanning electron microscopy, considering the gingival, middle, and apical thirds in each root.Results: Two control teeth, 4 teeth in group 1, and all teeth in groups 2 and 3 showed resorption areas. Regarding the gingival third, the control teeth did not show any resorption, while 25% of affected teeth in group 1, 38.7% of teeth in group 2, and 35.5% of teeth in group 3 exhibited resorption. Regarding the middle third, 50% of affected teeth belonging to the control group and group 1; 67.7% of teeth in group 2; and 87.1% of teeth in group 3 showed resorption. Regarding the apical third, all teeth belonging to the control group and group 1 showed resorption, while 93.5% and 87.1% of teeth in groups 2 and 3, respectively, exhibited resorption. Most of the resorptions did not extend beyond the cementum. However, in 29.0% of teeth in group 2 and 38.7% of teeth in group 3, resorption had spread as far as the dentin. All the lesions in the control group and group 1 were practically repaired, while only 71.0% of teeth in group 2 and 61.3% of teeth in group 3 showed some sign of reparation. However, in groups 2 and 3, practically all lesions affecting dentin were repaired.Conclusions: These data suggest that the spread of root resorption is associated with inflammation. This study also suggests that the capacity for repair of root resorption is diminished with greater severity of periodontitis. J Periodontol 1999;70:1283‐1291.
In Situ Localization and Characterization of Active Proteases in Chronically Inflamed and Healthy Human Gingival Tissues
Authors: Sarment David P. , Korostoff Jonathan , D'Angelo Marina , Polson Alan M. , Feldman Roy S. , Billings Paul C. 
Published: February 2005

Background: Studies have indicated an important role for host‐derived proteases in the pathogenesis of periodontal disease. The objectives of this study were: 1) to develop an assay measuring protease activity in situ and 2) to localize and characterize the enzymatic activity in intact inflamed and healthy gingiva.Methods: Gingival specimens were prepared and overlaid with a quenched fluorescent substrate. Protease activity was visualized by fluorescence microscopy and correlated with histologic features.Results: In inflamed tissues, enzymatic activity was detected mainly in the connective tissue (predominantly matrix metalloproteases) and, to some extent, in the epithelium (predominantly serine proteases). In contrast, clinically healthy tissues failed to exhibit significant amounts of protease activity. Quantitative and qualitative characteristics of protease activity in intact tissues were found to be pH dependent.Conclusions: The method described here enabled assessment of active proteases in intact tissues where cell‐cell and cell‐matrix interactions had been maintained. Our results indicate that there are substantial differences in the distribution of specific proteases between clinically healthy and inflamed periodontal tissues. J Periodontol 1999;70:1303‐1312.
Longitudinal Study of Dental Implants in a Periodontally Compromised Population
Authors: Sbordone Ludovico , Barone Antonio , Ciaglia Renato Nicodemo , Ramaglia Luca , Iacono Vincent J. 
Published: February 2005

Background: The purpose of this longitudinal study was to determine the clinical status and the composition of the subgingival microbiota of dental implants and natural teeth in patients with a history of periodontitis. Methods: Twenty‐five partially edentulous patients treated for moderate to advanced adult periodontitis and having a total of 42 implants participated in this 3‐year study. The assessment of clinical status was done 1, 2, and 3 years after prosthetic loading (T1, T2, and T3, respectively). Clinical parameters evaluated included probing depth (PD), clinical attachment level (CAL), gingival index (GI), and plaque index (PI). The subgingival microbiota at peri‐implant and periodontal sites were analyzed at T1 and T2.Results: No significant difference in clinical parameters between implants and teeth and within the 2 groups between different time points was observed through the study. PD and CAL measurements of sampled periodontal and peri‐implant sites did not show any statistically significant difference through the study and between the 2 groups. PI of sampled periodontal sites showed a statistically significant improvement during the study. From the morphological observation of the subgingival microbiota, a significant difference in the composition of motile rods between implants and teeth was found at T1. There were no differences detected in the subgingival microbiota, culturally identified at peri‐implant and periodontal sites for the duration of the study.Conclusions: In conclusion, implants were colonized by the indigenous periodontal microbiota and were well maintained in patients with a history of periodontitis. No significant association between progressing or non‐progressing periodontal or peri‐implant sampled sites in terms of loss of attachment and infection with at least one of the searched periodontal pathogens was found, suggesting that the presence of putative periodontopathogens at peri‐implant and periodontal sites may not be associated with future attachment loss or implant failure. J Periodontol 1999;70:1322‐1329
Microvascular Changes After Placement of Titanium Implants: Scanning Electron Microscopy Observations of Machined and Titanium Plasma‐Sprayed Implants in Dogs
Authors: Matsuo Masato , Nakamura Takatsuna , Kishi Yoshiaki , Takahashi Kazuto 
Published: February 2005

Background: The purpose of this study was to clarify the osseointegration process of titanium implants through study of the vascular architecture and bone apposition. The smooth machined‐surface implant is tightly fixed to the bone by its threads. The rough titanium plasma‐sprayed (TPS) coated implants give a scaffold for new bone. Methods: Twelve beagle dogs were used, and 2 surface types of implants were inserted in the mandible. Vascular injection was given 14, 30, and 120 days after surgery. The soft tissue was digested by proteinase solution, and specimens were examined by scanning electron microscope (SEM).Results: Fourteen days after placement of machined implants, new vessels could be seen branching out from the vascular network of the bone marrow. In TPS implants, a vascular network was seen between the bone‐implant interface. At 30 days, the vessels were arranged in a groove corresponding to the machined fixture. With TPS implants, new bone was visible along the surface of the fixture, and the vascular network was buried in the bone. At 120 days after placement of machined implants, bone had formed a smooth surface. A few blood vessels were arranged along the bone surface. With TPS implants, a rough bone surface and flat vessels were observed on its surface.Conclusions: Implants become osseointegrated in different ways, depending on their structures and the characteristics of their surfaces. From the microcirculation point of view, the vessels are an important factor for the remodeling of bone. J Periodontol 1999;70:1330‐1338.
Effect of Periodontitis and Smoking on Blood Leukocytes and Acute‐Phase Proteins
Authors: Fredriksson Margareta I. , Figueredo Carlos M.S. , Gustafsson Anders , Bergström Kurt G. , Åsman Björn E. 
Published: February 2005

Background: We have previously found hyperreactive neutrophils, intrinsic or induced, in periodontitis patients by in vitro quantitation of free oxygen radicals. The effects of periodontitis and cigarette smoking on blood parameters have generally been described separately. Our aim was to compare these systemic effects of periodontitis and cigarette smoking, separately and in combination, in order to study the hyperreactivity in peripheral neutrophils.Methods: Blood cells and acute‐phase proteins were studied in 40 periodontitis patients and 43 healthy controls. The generation of free oxygen radicals from neutrophils was measured as luminolenhanced chemiluminescence (CL) after activation of their Fcγ receptors with opsonized Staphylococcus aureus.Results: An increase in CL in peripheral neutrophils from periodontitis patients was confirmed. Smoking had no significant effect on CL. The periodontitis patients had higher concentrations of C‐reactive protein (CRP) than the controls. ANOVA analysis showed that the increase in neutrophil count, haptoglobin, and α‐1 antitrypsin levels was significantly influenced by cigarette smoking. IgG2 was lower in patients than in controls (P <0.017, ANOVA), and there was an interaction between periodontitis and smoking (P <0.047, ANOVA). The lower concentration of IgG2 in patients who smoke may impair neutrophil function and be a mechanism by which smoking aggravates periodontitis.Conclusions: In general, the combination of periodontitis and cigarette smoking alters the parameters studied. The effects of periodontitis on CRP and IgG2 means that periodontal lesions may also leak agents, priming the peripheral neutrophils to increased CL. J Periodontol 1999;70:1355‐1360.
Chlorhexidine‐Induced Changes to Human Gingival Fibroblast Collagen and Non‐Collagen Protein Production
Authors: Mariotti Angelo J. , Rumpf Deborah A.H. 
Published: February 2005

Background: Chlorhexidine (CHX) has been used extensively as an adjunctive therapy in the treatment of periodontal disease. It is well known that chlorhexidine is toxic to bacteria, but recent evidence has suggested that chlorhexidine may also have deleterious effects on gingival fibroblast proliferation as well as collagen and non‐collagen protein production in cell culture. The purpose of this study was to examine the effects of chlorhexidine on gingival fibroblast proliferation as well as collagen and non‐collagen protein production in cell culture.Methods: Human gingival fibroblasts were incubated in MEM containing chlorhexidine concentrations ranging from 1 µM to 1300 µM at 37°C for 1, 5, or 15 minutes. Control cells received an equal volume of MEM without chlorhexidine for similar times at 37°C. Following incubation, the media were removed, cells washed twice with MEM supplemented with 10% FBS, and fibroblasts in treatment and control groups were allowed to recover in the same media for 24 hours.Results: In all strains, cellular proliferation was dependent on the concentration of solubilized chlorhexidine in cell culture but independent of the duration of chlorhexidine exposure. The average inhibitory concentration necessary to reduce cellular proliferation by 50% (ID50) was 222.1 µM. In regard to collagen and non‐collagen protein production, fibroblasts exposed to chlorhexidine concentrations (1 µM) well below the ID50 had a 65% reduction in collagen production and a 57% reduction in noncollagen protein production.Conclusions: These results suggest that chlorhexidine will induce a dose dependent reduction in cellular proliferation and that concentrations of chlorhexidine that have little effect on cellular proliferation can significantly reduce both collagen and noncollagen protein production of human gingival fibroblasts in vitro. Hence, the introduction of commercially available concentrations (0.12%) or diluted commercial concentrations (as low as 0.00009%) of chlorhexidine to surgical sites for short periods of time prior to wound closure can conceivably have serious toxic effects on gingival fibroblasts and may negatively affect wound healing. J Periodontol 1999;70:1443‐1448.
Regulation of Gingival Fibroblast Interleukin‐6 Secretion by Cyclosporine A
Authors: Morton Rakhi Sinha , Dongari‐Bagtzoglou Anna I. 
Published: February 2005

Background: Cyclosporine A (CsA) is a widely used immunosuppressant, with clinical applications ranging from organ transplants to chronic inflammatory diseases. One of the side effects associated with CsA treatment is the development of gingival overgrowth. Exuberant growth of connective tissue within the periodontium can result from hyperactivity of resident fibroblasts. Fibroblasts are capable of secreting interleukin‐6 (IL‐6), which has been shown to enhance proliferation as well as collagen and glycosaminoglycan synthesis by these cells. We tested the hypothesis that one of the pathogenetic mechanisms underlying CsA‐induced fibrosis is an enhanced IL‐6 secretion by gingival fibroblasts (GF) in response to this drug.Methods: The ability of CsA to upregulate GF IL‐6 secretion alone or in combination with bacterial challenge or other inflammatory cytokines was tested in an in vitro system. Fibroblast cultures were established from systemically healthy gingival tissue donors and were challenged with CsA in the absence or presence of bacteria, IL‐1β, or tumor necrosis factor (TNF) α as co‐stimulants. Nifedipine and phenytoin were also tested to further support findings with CsA. After 72 hours of incubation, culture supernatants were collected and analyzed for IL‐6 content by ELISA.Results: We have shown that GF respond to CsA with an increase in IL‐6 secretion. The magnitude of this response varies among cultures derived from different tissue donors. We have also demonstrated that GF IL‐6 responses to bacterial challenge or TNFα are downregulated by CsA. However, CsA synergizes with IL‐1β to further upregulate IL‐6 secretion, and this effect is shared by phenytoin and nifedipine.Conclusions: We conclude that one of the pathogenetic mechanisms underlying drug‐induced gingival overgrowth may be enhanced secretion of IL‐6 by GF in response to these medications. This is the first report on direct and indirect effects of gingival overgrowth‐related medications on GF IL‐6 metabolism. This work will lay the foundation for future studies directed towards the development of prevention or treatment modalities for gingival overgrowth based on blocking the fibrogenic activities of IL‐6 at the cellular level. J Periodontol 1999;70:1464‐1471.