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PubMed1992

Transamidase and collagenase activity in healthy and diseased human gingival tissues.

Transamidases are a class of calcium-dependent mammalian enzymes which cross-link proteins by catalyzing the formation of (gamma-glutamyl)-epsilon-lysine bonds. It is possible that these enzymes play an important anabolic role in tissue healing. This study was to quantitate transamidase activity in human gingival tissue and examine the relation between transmidase activity and degree of inflammation. Forty-four out of a total 120 collected human gingival specimens from healthy and diseased patients were selected based on histometric and microbiologic criteria. Specimens were minced and homogenized in 10 mM CaCl2 and then extracted for 30 min, in 50 mM tris-HCl buffer (pH 7.5) containing 100 mM CaCl2. Following low speed centrifugation at 4 degrees C, the supernatant solution was assayed for both transamidase and collagenase activities by radioactive amine incorporation, and digestion of tritiated collagen, respectively. Appreciable levels of transamidase and collagenase activities in healthy gingivae were found. These enzyme activities were significantly elevated in the diseased and healing tissues. Unlike other transamidases, calcium was required in the enzyme extraction process.

Acyltransferases↗
PubMed1978

A rapid chairside test for the severity of periodontal disease using gingival fluid.

A study was done in an attempt to develop a simple test for the severity of periodontal disease. Gingival fluid collected on filter paper was tested for protein content, and the resulting color was compared to standard color filters. Tissue was excised and prepared for histologic examination. The inflammatory cell infiltrate on each slide was graded on a scale of zero to three. Zero was least and three was the highest number of inflammatory cells. The results indicate that the white cell infiltrate graded 0 or 1 on the histologic inflammatory index has a color index of B 1/8 TO B1 whereas the tissue graded 2 or 3 HII has a range of B2 to B6 on the color scale. This test can give the dental practitioner a general idea of the severity of the inflammation.

Color↗
PubMed1994

Inhibition of crevicular fluid neutrophil elastase by alpha 1-antitrypsin in periodontal health and disease.

Gingival crevicular fluid (GCF) was collected from two healthy, two gingivitis and two periodontitis sites of two groups of individuals presenting for treatment of chronic adult periodontitis (group 1, 25 subjects; group 2, seven subjects) and from distal approximal sites of two incisors and one molar of 10 subjects with periodontal health. GCF eluates of periodontitis group 1 and controls, prepared by a technique that lysed polymorphonuclear leucocytes (PMN) in the samples, were assayed for functional neutrophil elastase (NE) and immunoreactive alpha 1-antitrypsin (alpha 1-AT) and alpha 1-antitrypsin-neutrophil elastase complex (alpha 1-AT-NE). Periodontitis group 2 GCF eluates, generated by a method that did not disrupt PMNs, were assayed for functional NE in the presence and absence of a specific NE inhibitor. A greater amount of NE (ng/5-s sample) was found in eluates of GCF from diseased sites irrespective of whether or not the eluates contained products of lysed PMNs. However, the GCF eluates prepared without disrupting PMNs contained only about one-tenth as much NE as eluates of corresponding sites that included constituents of lysed PMNs. The amount of alpha-AT in GCF was insufficient to inactivate most of the NE available for release into the gingival sulcus at either healthy or diseased sites. In addition, much of the alpha 1-AT in GCF was not complexed with NE under conditions of excess NE. More than 90% of the NE in GCF from each site category was inactivated by the NE specific inhibitor. It is concluded, because of the large quantity of NE available in PMNs compared to the amount of NE inhibitors in GCF, that at least locally transient free NE occurs, which contributes to tissue destruction in chronic adult periodontitis.

Adult↗
PubMed2000

Aetiology and pathogenesis of periodontal disease.

Gingivitis is modified by several factors including smoking, ion channel blocking drugs and hormonal changes such as those seen in puberty or pregnancy. Periodontitis is also initiated by microbial plaque which follows on from gingivitis, but occurs in only 10 to 15% of the population and is influenced by the individual's immune and inflammatory response. Studies on the humoral and cellular immune response in periodontal disease indicate that: a) homing of relevant immune cells takes place within the periodontium; b) plasma cells are among the most active secretory cells in the gingiva; c) that immunoglobulin subclasses are similar between blood and the gingival pocket fluid for IgG but not for IgA; and that d) an individual's ability to mount a specific antibody response to periodontopathogenic organisms may indicate their susceptibility to the disease and their likely response to treatment. Recent reviews of the pathology of periodontal disease suggest that a histopathological established lesion with plasma cell predominance is likely to undergo periodontal bone loss. Furthermore, susceptibility to periodontitis may be related to whether plasma cells predominate in the tissues of an individual or a site as result of the microbial challenge of dental plaque. A tendency for an individual or site to form an extensive plasma cell infiltrate may indicate an inability to defend against periodontal bacteria and thus a predisposition to periodontitis. The various susceptibility factors such as smoking, medical condition, genetics, plaque control and local factors may all interact to influence the host response and specifically the immune response.

Alveolar Bone Loss↗
PubMed1999

Pharmacokinetics and pharmacodynamics of moist snuff in humans.

INTERVENTION: Four brands of moist snuff and a non-tobacco mint snuff were tested. Subjects reported to the laboratory for five experimental sessions. After baseline measurement of dependent variables, each subject placed 2 g of one of the brands of snuff (or one Skoal Bandits pouch) between the cheek and gum for 30 minutes. The subjects remained in the experimental laboratory for an additional 60 minutes. SUBJECTS: Ten volunteers who were daily users of smokeless tobacco. MAIN OUTCOME MEASURES: Plasma nicotine concentration, cardiovascular effects, and subjective effects. RESULTS: Large amounts of nicotine were delivered rapidly to the bloodstream. The amount of nicotine absorbed and the rate of absorption were related to the pH of the snuff product in aqueous suspension. Cardiovascular and subjective effects were related to the amount of nicotine absorbed. CONCLUSIONS: Snuff products are capable of rapidly delivering high doses of nicotine, which can lead to dependence. Long-term use of snuff can lead to a number of adverse health effects including oral cancers, cardiovascular diseases, and gingival diseases. For these reasons, it is important that the public health community considers oral snuff use as a burden on public health in the same way that cigarette smoking is recognised.

Adult↗
PubMed1989

[Examination of periodontal disease with gingival crevicular fluid. Correlation between capacitance and clinical findings].

An intimate relationship between the inflammatory state of the gingiva and the amount of gingival crevicular fluid (GCF) is well known. For the measurement of the volume of GCF, filter paper has been used in the past. In the present study, an electrostatic capacity measuring apparatus with sensor that is insertable into gingival sulcus was fabricated. Capacitance of GCF was measured in patients with periodontitis and the following results were obtained. 1. The measuring apparatus was controlled by a personal computer to obtain the data every 0.1 second. As the GI increased at the site of measurement, higher values were obtained, with longer persistence of the trend of increase in the measured value. 2. In view of the stability of the measured values, the amount of GCF appeared to be best expressed as the value obtained after 10 seconds. 3. The correlation between the capacitance and the clinical findings was evaluated at 500 sites. The correlation was the highest in GI followed by P1I, GBI and PD, suggesting the utility of this method in the detection of initial gingival inflammation.

Electrolytes↗
PubMed1974

Study of CoQ10-enzymes in gingiva from patients with periodontal disease and evidence for a deficiency of coenzyme Q10.

The specific activities of both the succinate dehydrogenase-coenzyme Q(10) reductase and the DPNH-cytochrome c reductase [NADH:(acceptor)oxidoreductase, EC 1.6.99.3] were determined in mitochondria from 40 diseased gingival biopsies from patients with periodontal disease and from 24 control biopsies from nondiseased areas (clinically evaluated) of gingival tissues from the same mouths of the patients from whom the diseased gingival tissues were taken. The control tissue was taken during normal surgical procedures, such as for gingival recontouring and tuberosity removal. The diseased gingival biopsies showed a mean specific activity for the succinate dehydrogenase-coenzyme Q(10) reductase which was higher (P < 0.02) than that of the control biopsies, and which increased (P < 0.01) when the assays utilized exogenous coenzyme Q(3), and corresponded to an average deficiency of coenzyme Q(10)-enzyme activity of 35%. About 60% of the 40 diseased gingival tissues showed a deficiency of coenzyme Q(10) at its site in this succinate-coenzyme Q(10) enzyme. Of the 24 control tissues, 20% showed deficiencies of coenzyme Q(10). As a group, the control tissues showed no deficiency of coenzyme Q(10). No deficiency of coenzyme Q(10) at its site in DPNH-cytochrome c reductase was observed for either the control or diseased gingival tissues, as groups or individually.

Adolescent↗
PubMed2000

Collagen fibers and inflammatory cells in healthy and diseased human gingival tissues: a comparative and quantitative study by immunohistochemistry and automated image analysis.

BACKGROUND: Periodontal disease is histologically characterized by the degradation of extracellular matrix components associated with a gingival infiltration of inflammatory cell populations. The purpose of this in situ study was to quantify inflammatory cell subsets and the area fraction (AA%) occupied by collagen fibers in healthy and diseased upper gingival connective tissue in order to investigate the association, if any, between collagen loss and inflammatory cell infiltrate. METHODS: Paraffin gingival tissue sections from 10 healthy controls (C), 9 patients with gingivitis (G), and 10 patients with severe chronic periodontitis (P) were immunohistochemically stained by antibodies against CD45, CD3, CD8, CD20, CD68, TIA-1, and GrB molecules, and the collagen fibers were stained using sirius red F3Ba. The quantitative evaluations of inflammatory cell numbers and the AA% occupied by collagen fibers were performed by morphometric and automated image analysis. RESULTS: In group P, CD45+, CD20+, CD68+, TIA-1+, and GrB+ cell numbers were significantly increased (P<0.05) when compared to both C and G groups. The present study revealed significant differences (P <0.01) between means of AA% observed in group C (63%), group G (46%), and group P (26%), and AA% of group G and group P was inversely correlated with the numbers of TIA-1+ cells (P<0.01) and GrB+ cells (P<0.01 and P<0.05, respectively). CONCLUSIONS: This study showed great differences in the number of the distinct inflammatory cell subsets according to the severity of the periodontal disease and suggested that activated cytotoxic cells could play a pivotal role in the loss of collagen fibers observed during these pathological states. During periodontitis, collagen loss was significantly correlated with all inflammatory cell subset numbers. Finally, the quantitative evaluation of the area fraction occupied by gingival collagen fibers may reflect the clinical severity of the periodontal disease.

Adolescent↗
PubMed2002

Cathepsin-L, a key molecule in the pathogenesis of drug-induced and I-cell disease-mediated gingival overgrowth: a study with cathepsin-L-deficient mice.

Drug-induced gingival overgrowth, the chronic side effect of calcium antagonists, is frequently seen due to the increase in patients with hypertension, although the etiology of the disease is largely unknown. I-cell disease, which accompanies gingival overgrowth, is characterized by a deficiency in UDP-N-acetyl-glucosamine and is classified as one of the lysosomal storage diseases. Here, we hypothesized that a common mechanism may underlie the etiology of gingival overgrowth seen in patients treated with calcium antagonist and in patients with I-cell disease. A calcium antagonist, nifedipine, specifically suppressed cathepsin-L activity and mRNA expression, but not that of cathepsin-B in cultured gingival fibroblasts. The activity of cathepsin-L was suppressed up to 50% at 24 hours after treatment of the cells with the reagent. The selective suppression of cathepsin-L activity appeared not to be dependent on Ca(2+), since treatment of the cells with thapsigargin suppressed both cathepsin-B and -L activity. Mice deficient in the cathepsin-L gene manifested enlarged gingivae. Histological observation of the gingivae demonstrated typical features of acanthosis, a phenotype very similar to that of experimentally induced gingival overgrowth. Since cathepsin-L deficiency was reported to be associated with thickening of the skin, impaired cathepsin-L activity may play a key role in the establishment of skin and gingival abnormalities seen in I-cell disease. In addition, reduced cathepsin-L activity may play an important role in inducing drug-induced gingival overgrowth.

Animals↗
PubMed2006

B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease.

Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.

B-Lymphocytes↗
PubMedDate not supplied

Development of a classification system for periodontal diseases and conditions.

Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classification system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics. Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology. These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings, including: (1) considerable overlap in disease categories, (2) absence of a gingival disease component, (3) inappropriate emphasis on age of onset of disease and rates of progression, and (4) inadequate or unclear classification criteria. The 1993 European classification lacked the detail necessary for adequate characterization of the broad spectrum of periodontal diseases encountered in clinical practice. The need for a revised classification system for periodontal diseases was emphasized during the 1996 World Workshop in Periodontics. In 1997 the American Academy of Periodontology responded to this need and formed a committee to plan and organize an international workshop to revise the classification system for periodontal diseases. The proceedings in this volume are the result of this reclassification effort. The process involved development by the Organizing Committee of an outline for a new classification and identification of individuals to write state-of-the-science reviews for each of the items on the outline. The reviewers were encouraged to depart from the preliminary outline if there were data to support any modifications. On October 30-November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon (Figure 1). This paper summarizes how the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics. In addition, an analysis of the rationale is provided for each of the modifications and changes.

Adolescent↗