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Mitotic activity of keratinocytes in nifedipine- and immunosuppressive medication-induced gingival overgrowth.

BACKGROUND: The purpose of the study was to compare mitotic activity in the basal cell layer of normal human gingiva and in nifedipine- and immunosuppressive medication-induced gingival overgrowth. METHODS: Gingival samples were collected from 19 generally healthy individuals, 12 nifedipine-medicated cardiac patients, and 22 immunosuppression-medicated (azathioprine, prednisolone, and cyclosporin A) organ transplant recipients. The transplant recipients were divided into those not taking nifedipine and those taking nifedipine. Cryostat sections were stained with monoclonal antibody for Ki-67, using an avidin-biotin-enzyme complex method. The mitotic activities of epithelial cells were determined as percentages of Ki-67 labeled cells in relation to total numbers of epithelial cells in the basal layer of oral, oral sulcular, and sulcular epithelium. RESULTS: Mitotic activities were significantly higher in all 3 medication groups in the oral epithelium (P < or =0.003), and in the immunosuppression group in the sulcular epithelium (P= 0.032) than in the controls. In the oral sulcular epithelium, mitotic activity was fairly similar in all medication groups. In the nifedipine group a significant negative correlation was found between duration of nifedipine medication and the percentage of Ki-67 labeled cells in the oral epithelium (P= 0.025). CONCLUSIONS: The results suggest that the increased epithelial thickness observed in nifedipine- and cyclosporin A-induced gingival overgrowth is associated with increased mitotic activity, especially in the oral epithelium.

Adult↗

Heterogeneity of host immunological risk factors in patients with aggressive periodontitis.

BACKGROUND: The pathogenesis of early-onset periodontitis (EOP) can be explained by various host risk factors. Previous studies have focused on a single (among many possible) immunological risk factor and the association among the factors has not been assessed. We comprehensively investigated the associations among multiple host immunological risk factors in EOP patients to further elucidate their role in the pathogenesis of EOP. METHODS: Sixty-eight EOP patients (50 generalized EOP, 18 localized EOP), 51 EOP-suspected patients (S-EOP), 43 adult periodontitis (AP) patients, and 36 periodontally healthy subjects (HS) participated in this cross-sectional study. We examined peripheral neutrophil functions, phenotypic and functional characterization of peripheral lymphocytes (lymphocyte subsets, T-cell proliferative activity), cytokine productivity (interleukin [IL]-1, IL-2, tumor necrosis factor [TNF]-alpha, interferon [IFN]-gamma, IL-4 and IL-6), serum immunoglobulin G (IgG) antibody titers against 12 periodontal bacteria, and HLA class II genotypes. RESULTS: G-EOP, S-EOP, and AP patient groups showed significantly lower percentages of pan T cells and CD8-positive cells (P < 0.02) compared with the HS group. L-EOP patients showed depressed IL-4 and TNF-alpha productivity compared with the HS group (P < 0.02). The EOP group showed significantly elevated antibody levels against Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola, and Fusobacterium nucleatum compared with the HS group (P < 0.05). The frequency with DQB1*0503 was significantly higher in the EOP patient group than the HS group (P = 0.045) due to the higher frequency in L-EOP patients than the HS group (P = 0.035). There were wide interindividual variations in each of the tests among patient and HS groups; however, EOP patients showed wider intradiagnostic group variations in certain host defensive cell functions than the other groups. There were some EOP patients who showed extremely low or high values in some tests; the EOP patients could be further divided into subgroups according to their host defensive and immunological profiles. However, there was heterogeneity in some of the other host immunological tests even in the subgroups. CONCLUSIONS: The association of host immunological risk factors in EOP patients is widely varied and more complex than previously thought. These results indicate the difficulty of explaining the pathogenesis of EOP based on a single host risk factor and also emphasize the importance of critical assessment of not only EOP patient groups, but also individual patients.

Adult↗

Cyclooxygenase-2 is upregulated in inflamed gingival tissues.

BACKGROUND: Increased release of prostaglandins (PG) within periodontal tissues is considered to play a pathogenetic role during periodontal disease progression. The rate-limiting step in the formation of PG from arachidonic acid is catalyzed by cyclooxygenase (COX). Currently there are 2 known isoforms of the enzyme. COX-1 is constitutively expressed in various tissues whereas COX-2 is an inducible enzyme believed to be responsible for PG synthesis at sites of inflammation. The purpose of this study was to compare COX-2 expression in inflamed and healthy human gingiva and further explore some of the pathogenetic mechanisms which may lead to elevated COX-2 expression in vivo. METHODS: Thirty-two gingival biopsies were obtained during routine oral surgical procedures and were processed histologically using hematoxylin and eosin to determine the degree of inflammation. Of these biopsies, 7 with low and 7 with high histological levels of inflammation were further processed immunohistochemically in order to assess the levels of COX-2 expression in situ. To explore some potential mechanisms of COX-2 upregulation, gingival connective tissue primary cell cultures were established and challenged with periodontal bacteria or proinflammatory cytokines in vitro. The levels of COX-2 expression were analyzed by Western blot of cell lysates. COX-2 activity was assessed by quantifying prostaglandin E2 (PGE2) levels in culture supernatants by competitive EIA. RESULTS: We have shown by immunohistochemistry that COX-2 expression was significantly higher (P < 0.01) in tissues with higher levels of inflammatory infiltrates. Expression of COX-2 was detected in gingival epithelium, endothelial cells as well as cells with fibroblast morphology. In vitro studies indicated that gingival fibroblasts (GF) did not express COX-2 constitutively. However, when these cells were challenged with interleukin (IL)-1 beta or bacterial cells (A. actinomycetemcomitans JP2 or B. forsythus ATCC 43037), COX-2 expression as well as COX-2 activity were upregulated. COX-2 expression was upregulated as early as 2 hours post IL-1 beta challenge and was accompanied by a sustained PGE2 release in the culture supernatants. Cyclosporin A (CsA) did not inhibit COX-2 expression induced by bacterial challenge. In contrast, NS-398, a selective inhibitor of COX-2 activity, almost completely abolished PGE2 synthesis by these cells in response to bacterial or cytokine challenge. CONCLUSIONS: We conclude that COX-2 expression is significantly upregulated in inflamed periodontal tissues. Both inflammatory cytokines such as IL-1 beta and bacterial constituents may be responsible for the enhanced COX-2 expression and PGE2 synthesis in vivo.

Aggregatibacter actinomycetemcomitans↗

Expression of cytokines and inducible nitric oxide synthase in inflamed gingival tissue.

BACKGROUND: Periodontopathic bacteria induce inflammation of periodontal tissues. The cytokines and nitric oxide released in periodontal lesions have been reported to play a protective role in bacterial infection and to relate to the process of inflammation. To clarify the relationship between colonization of periodontopathic bacteria and cytokines, we evaluated profiles of inflammatory cytokines, chemokine, anti-inflammatory cytokines, and inducible nitric oxide synthase (iNOS) and colonization by Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, which are major pathogens of periodontitis. METHODS: mRNA expression of cytokines and iNOS in inflamed and healthy gingival tissue was determined using reverse transcription-polymerase chain reaction (RT-PCR), and the relationship between their profiles and the detection of specific bacteria was analyzed. RESULTS: The relative expression of interleukin (IL)-6 and iNOS mRNAs in periodontal lesions was significantly higher than those in healthy individuals. IL-6 mRNA expression was also significantly higher at bleeding on probing (BOP)-positive sites than at BOP-negative sites. The expressions of IL-1alpha and IL-8 increased, but IL-10 expression decreased at sites where A. actinomycetemcomitans was detected. We found no correlation between the expression of cytokine and iNOS mRNA and infection by P. gingivalis. CONCLUSIONS: The expression of IL-6 may reflect inflammation in gingival tissue, and iNOS may be involved in the inflammatory process in periodontitis. The presence of A. actinomycetemcomitans or P. gingivalis might relate to the different cytokine profiles of IL-1alpha, IL-8, and IL-10.

Actinobacillus Infections↗

Root trunk concavities as a risk factor for regenerative procedures of class II furcation lesions in dogs.

BACKGROUND: The purpose of this study was to evaluate the influence of root trunk concavities on guided tissue regeneration. METHODS: The second, third, and fourth mandibular bicuspids of 4 healthy mongrel dogs were used. Full flaps were elevated and furcation lesions (5 mm in height and 2 mm in depth) were surgically created. One mm deep concavities were prepared on the root trunks and part of the crown of all teeth. The second bicuspids remained as controls (C); the left third and fourth bicuspids received normal expanded polytetrafluoroethylene (ePTFE) membranes (NM) and the right bicuspids received modified ePTFE membranes (MM). The MM were made by removing the collar from an NM, cutting it into 2 mm segments, and suturing each of the segments to the collar of each MM. Normal and modified membranes were sutured to their corresponding teeth and the flaps sutured. After the healing period, the mandibles were removed and the teeth processed for histomorphometry. RESULTS: The results showed that the junctional epithelium measured a mean of 0.71 mm for C, 0.64 mm for NM, and 0.14 mm for MM. The differences between C and MM and between NM and MM were both statistically significant at the 5% level (Kruskal-Wallis test). Mean bone height measurements for the buccal surfaces from the furcation roofs were 2.79 mm for C, 2.60 mm for NM, and 1.06 mm for MM and for the mid-portion 1.10 mm for C, 1.23 mm for NM, and 0.30 mm for MM. Differences were statistically significant at the 1% level between C and MM and between NM and MM for the buccal measurements, and at the 5% level between NM and MM for the mid-portion measurements. CONCLUSIONS: Root trunk concavities are important risk factors for regenerative procedures. The collars of the membranes should be modified to improve results when concavities are present.

Alveolar Process↗

Effects of pretreatment clinical parameters on bioactive glass implantation in intrabony periodontal defects.

BACKGROUND: The various methods for regeneration of periodontal tissue that have been developed can be classified into guided tissue regeneration and bone implantation. Since the implantation materials have shown both deficiencies and merits, dentists have begun exploring the bioactive glass first used in plastic surgery. This paper examines the effectiveness of this new material on periodontal intrabony defects. METHODS: Clinical effects of bioactive glass implantation in intrabony periodontal defects were evaluated 6 months after surgery in 38 intrabony defects from 38 patients with chronic periodontitis. Twenty-one experimental defects received bioactive glass implantation (test group), while 17 control defects were treated with a flap procedure only (control group). The criteria for comparative observation were preoperative and postoperative probing depth (PD), clinical attachment level (CAL), bone probing depth (BPD), and gingival recession. RESULTS: Reductions in PD were observed in both groups (P<0.01). The reduction in PD was significantly greater in the test group when preoperative PD exceeded 7 mm (P<0.01). Improvements in CAL were also observed in both groups (P<0.01), with the test group showing significantly greater gains (P<0.05). In those cases where preoperative CAL was less than 7 mm, there was no statistically significant difference between the two groups. Reduction in BPD was observed in both groups, with the test group showing significantly greater reduction (P <0.01). There was no significant difference in BPD change, however, when preoperative BPD was < or =7 mm. Significantly greater reduction of BPD in the test group was observed when intrabony defect depth was >4 mm (P <0.05). Significant improvements in PD, CAL, and BPD were noted in the test group when the crestal involvement exceeded 100 degrees. Correlation test between various clinical parameters indicated that greater changes in PD and CAL in the test group were observed when preoperative CAL was large (P<0.001), and greater changes in PD (P<0.05), CAL (P<0.01), and BPD (P<0.05) were noted when preoperative BPD was large. Correlation between crestal involvement and CAL change was noted only in the control group (P<0.01). High correlations were observed between PD changes and CAL changes and between CAL changes and BPD changes in both groups. CONCLUSIONS: Use of a bone substitute in a flap operation resulted in significantly greater improvements in CAL and BPD over flap operation alone and seemed to have positive effects in postoperative PD, CAL, and BPD in those cases with more severe preoperative CAL and BPD.

Adult↗

Upregulation of keratinocyte growth factor in cyclosporin A-induced gingival overgrowth.

BACKGROUND: Drug-induced gingival overgrowth (GO) is a frequent and adverse side-effect associated principally with the administration of the immunosuppressive drug cyclosporin A (CsA) and also certain anti-epileptic and anti-hypertensive drugs. It is characterized by a marked increase in the thickness of the epithelial layer and the accumulation of excessive amounts of connective tissue. Although the mechanism by which the drugs cause GO is not yet understood, keratinocyte growth factor (KGF), which is a potent epithelial cell mitogen, has been implicated in other hyperplastic conditions, including mammary and prostatic hyperplasia, and could also be involved in the molecular pathology of GO. METHODS: Immunohistochemistry was used to examine the expression of KGF in normal gingiva (NG) and GO tissue sections. The relative level of KGF mRNA in GO tissue and cells was compared with that of NG tissue and fibroblast cells using the semi-quantitative reverse transcribed-polymerase chain reaction (RT-PCR) and DNA sequencing was carried out to confirm the identity of the PCR product. RESULTS: KGF antigen and mRNA were readily detected in the GO tissue immunohistochemically and by RT-PCR, respectively, but were not expressed in the NG tissue. Moreover, KGF transcripts were found to be approximately 2 times higher in the GO than in the NG fibroblasts in vitro, although the difference was not statistically significant. CONCLUSIONS: This study has shown, for the first time, that the level of KGF is elevated in GO and suggests that KGF may have an important role in the enhanced epithelial proliferation associated with GO.

Adolescent↗

The effect of antimicrobial periodontal treatment on circulating tumor necrosis factor-alpha and glycated hemoglobin level in patients with type 2 diabetes.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) may play an important role in insulin resistance. In this study, we hypothesized that TNF-alpha produced due to periodontal inflammation synergistically affects insulin resistance as well as TNF-alpha produced from adipose tissues in insulin-resistant type 2 diabetes patients. Therefore, to understand the effects of antimicrobial periodontal therapy on serum TNF-alpha concentration and subsequent metabolic control of diabetes, we examined the periodontal and diabetic status on 13 type-2 diabetes patients. METHODS: These patients were treated with local minocycline administration in every periodontal pocket around all existing teeth once a week for a month. Before and after treatment, the number of total bacteria in the periodontal pockets and circulating TNF-alpha concentration were measured and the HbA1c value was assessed. RESULTS: Antimicrobial therapy significantly reduced the number of microorganisms in periodontal pockets (P <0.01). After treatment, the circulating TNF-alpha level was significantly reduced (P <0.015). The HbA1c value was also reduced significantly (P <0.007). In addition, the 6 patients who were not receiving insulin therapy demonstrated decreased fasting insulin levels (P <0.03), and HOMA-R (P <0.03) indices. The average reductions in circulating TNF-alpha concentration and HbA1c value were 0.49 pg/ml and 0.8%, respectively. CONCLUSION: The results indicate that anti-infectious treatment is effective in improving metabolic control in diabetics, possibly through reduced serum TNF-alpha and improved insulin resistance.

Adult↗

Interleukin-1beta and thiobarbituric acid reactive substance (TBARS) levels after phase I periodontal therapy in patients with chronic periodontitis.

BACKGROUND: Interleukin-1beta (IL-1beta), a potent stimulator of bone resorption, has been implicated in the pathogenesis of periodontal tissue destruction. There is also a clearly defined and substantial role for free radicals or reactive oxygen species in periodontal destruction. The thiobarbituric acid reactive substances (TBARS) is a commonly applied test to measure free radical activity. The aims of this study were to investigate the amount of crevicular IL-1beta, tissue TBARS levels, and the clinical status of patients with advanced chronic periodontitis and the effect of phase I periodontal therapy on these clinical parameters and measurements. METHODS: Twenty-five chronic periodontitis and 25 healthy control (C) patients were selected for the study. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) were recorded from each sampling area. Gingival crevicular fluid (GCF) sampling and clinical index scores were recorded at the initial examination (IE) and 6 weeks after phase I periodontal therapy (APT). Assays for GCF IL-1beta were carried out by enzyme-linked immunosorbent assay (ELISA). Gingival tissue samples were obtained from sites requiring periodontal flap surgery due to unresolved pockets to determine the tissue TBARS levels. The paired-samples t test was used to compare the IL-1beta levels and clinical parameters between IE and APT. The independent-samples t test was used to determine the significance of all parameters between IE and C, and between APT and C. The correlation among the IL-1beta levels, clinical parameters, and tissue TBARS levels was analyzed using the Pearson correlation. RESULTS: The concentration of IL-1beta levels was not statistically different among IE, APT, and C groups, but the total amount of IL-1beta levels was statistically different among the 3 groups. While the levels of IL-1beta and the clinical parameters were reduced following phase I periodontal treatment, pretreatment IL-1beta, post-treatment IL-1beta, and TBARS levels were statistically higher in IE and APT groups than C specimens. Tissue TBARS levels in the APT group were statistically greater than controls. No correlations were noted between tissue TBARS levels and clinical parameters in the APT group. A positive statistical correlation was detected between the total IL-1beta and TBARS levels in the APT group. CONCLUSION: These data suggest that the levels of crevicular IL-1beta and gingival tissue TBARS are closely associated with periodontal status. This relationship may be valuable in treating and monitoring periodontal disease progression.

Adolescent↗

Thirty-six month follow-up of 25 patients treated with combination anorganic bovine-derived hydroxyapatite matrix (ABM)/cell-binding peptide (P-15) bone replacement grafts in human infrabony defects. I. Clinical findings.

BACKGROUND: Long-term evaluation of periodontal therapy is important for clinical decision making. METHODS: A synthetic cell-binding peptide (P-15) combined with anorganic bovine-derived hydroxyapatite bone matrix (ABM) was evaluated as a bone replacement graft in human periodontal osseous defects. Following initial preparation and reevaluation, flap surgery was performed. A variety of 1-, 2-, 3-wall bony defects were curetted and root surfaces subjected to mechanical debridement only. The bone defects were grafted with ABM/P-15, and the host flaps replaced or slightly coronally positioned. Weekly, then monthly deplaquing was performed until surgical reentry at 6 to 7 months. Patients were then followed on approximate 3-month recalls for 3 years. Twenty-five of the original 31 patients qualified for long-term evaluation in that their ABM/P-15 treated sites did not receive any additional therapy at the time of reentry. RESULTS: Significant clinical changes for the overall group of bony defects included improvement in mean clinical attachment level from 5.4 mm at surgery to 4.5 mm at the 6-month reentry to 3.8 mm at 3 years. There was also a decrease in mean probing depth from 5.3 mm at surgery to 3.1 mm at the 6-month reentry to 2.9 mm at 3 years. The mean gingival recession changed from +0.1 mm at surgery to 1.4 mm at the 6-month reentry to 0.9 mm at 3 years. All of these differences were at least P <0.05 from surgery to the 6-month reentry, and surgery to 3 years, but were not significant from reentry to 3 years via repeated measures analysis of variance. CONCLUSIONS: These favorable 3-year results with ABM/P-15 suggest that it may have a beneficial effect in the long-term clinical management of infrabony defects. Further long-term randomized controlled studies are needed to better assess the role of ABM/P-15 in long-term healing of periodontal osseous defects.

Adult↗

Smoking and polymorphisms of the interleukin-1 gene cluster (IL-1alpha, IL-1beta, and IL-1RN) in patients with periodontal disease.

BACKGROUND: Polymorphisms within the interleukin-1 cluster are known to be associated with adult periodontal disease. However, interactions of genetic with other risk factors, especially smoking, remain questionable. The aim of this cross-sectional study was to evaluate the genetic influence on periodontal variables in relation to environmental factors. METHODS: One-hundred fifty-four (154) Caucasian subjects were clinically and radiographically assessed for their periodontal status, their smoking history recorded, and their allelic pattern of IL-1alpha, IL-1beta, and IL-1RN polymorphisms determined by genotyping. RESULTS: In assessing periodontitis with mean probing depth, mean attachment loss, or mean bone loss, no differences were found in allele frequencies or combined allotypes between subjects with mild or moderate versus those with severe signs of periodontitis. However, the extent of attachment loss defined as percentage of sites >4 mm was significantly associated with the composite genotype of IL-1alpha/1beta in smokers (odds ratio [OR] = 4.00; 95% confidence interval [CI] 1.03 to 16.70; P= 0.02). No differences were found in genotype negative subjects irrespective of their smoking status. They had nearly identical attachment loss as genotype positive non-smokers. Similar non-significant results were found with respect to extent of bone loss. An increased risk of more extended attachment loss was observed also in individuals carrying mutations of the combined genotype IL-1alpha/IL-1RN, again showing enhanced risk only in genotype-positive and smoking subjects. CONCLUSIONS: The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.

Adult↗

Subgingival microbiota of Brazilian subjects with untreated chronic periodontitis.

BACKGROUND: Different periodontopathogenic microbiota have been associated with periodontal diseases in several populations. The present investigation determined the subgingival microbiota of untreated chronic periodontitis Brazilians using the checkerboard DNA-DNA hybridization technique. METHODS: Twenty-five periodontitis patients (mean age, 41 +/- 2; mean probing depth [PD], 3.3 +/- 0.2; mean attachment level [AL], 3.6 +/- 0.2) with no history of previous periodontal therapy and a control group of 14 healthy subjects (mean age, 34 +/- 0.6; mean PD, 1.8 +/- 0.2; mean AL, 1.7 +/- 0.1) were selected. Measurements of PD, AL, bleeding on probing, plaque accumulation, and suppuration were recorded at 6 sites/tooth. Subgingival plaque samples were obtained from 4 sites in each tooth/subject in both groups. The presence and levels of 41 subgingival species were determined in 4,032 plaque samples using whole genomic DNA probes and the checkerboard method. RESULTS: Periodontal pathogens, as well as some unusual species (E. faecalis, E. coli and Bartonella sp.), were detected significantly more often and/or in higher levels in the periodontitis group (P < 0.05). Most species were more frequently detected in interproximal sites. B. forsythus, P. gingivalis, E. nodatum, and F. nucleatum ss vincentii showed a significant positive correlation with mean PD and AL (P < 0.05). CONCLUSIONS: The subgingival microbiota of Brazilians with untreated chronic periodontitis were complex, including high proportions of periodontopathogens commonly found in other populations, as well as some unusual species.

Adult↗

Effect of estrogen deficiency on skeletal and alveolar bone density in sheep.

BACKGROUND: This study provides a longitudinal assessment of changes in alveolar and skeletal bone mineral density (BMD) in ovariectomized animals. METHODS: Following ovariectomy (OVX) (n = 6) or sham-operation (n = 6) intraoral radiographs were made at 4-month intervals and serum 17-beta-estradiol, osteocalcin, and interleukin (IL)-6, urinary deoxypyridinium, and salivary IL-6, deoxypyridinium, and osteocalcin concentrations were evaluated. Twelve months after surgery, animals were sacrificed and the mandible and radius/ulna removed. Bones were sectioned and radiographed. Mean BMD and cortical thicknesses were calculated from each region. RESULTS: OVX animals had a progressive decrease in serum 17-beta-estradiol, increased serum osteocalcin and IL-6, urinary deoxypyridinium and salivary IL-6, osteocalcin and deoxypyridinium (P < 0.001), suggesting that they were becoming osteoporotic. The BMD of the radius/ulna and mandibular alveolar bone was significantly reduced in OVX animals (P < 0.05 and P < 0.001, respectively). Reduced alveolar bone BMD became evident in OVX animals 6 months after surgery and became more severe during the subsequent 6 months. Alveolar crestal height was also significantly reduced in OVX animals (P < 0.001). These biochemical and density changes preceded a significant reduction in serum 17-beta-estradiol, which occurred between 4 and 8 months following surgery. CONCLUSIONS: Serial measurements of alveolar BMD predicts loss of skeletal BMD in OVX sheep. Changes in alveolar BMD precede estrogen deficiency, suggesting that early signs of reduced BMD may be detected in peri-menopausal women. The presence of biomarkers of bone metabolism within saliva and their correlation with reduced BMD suggests that saliva could be used as an adjunct screening method for assessment of skeletal bone density.

Alveolar Process↗

Effects of phase I periodontal treatment on gingival crevicular fluid levels of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1.

BACKGROUND: Matrix metalloproteinase-1 (MMP-1) is a member of a family of enzymes which are capable of degrading most extracellular matrix macromolecules. Extracellular control of MMPs is exerted by tissue inhibitors of metalloproteinases (TIMP) and by mechanisms of pro-MMP activation. Levels of MMPs and TIMPs change during healing, inflammation, and normal tissue turnover. The aim of this study was to evaluate the effects of phase I periodontal treatment on gingival crevicular fluid (GCF) levels of MMP-1 and TIMP-1. METHODS: Ten patients with chronic periodontitis who had sites with probing depths > or = 4 mm and 10 periodontally healthy persons (controls) were included in this study. Clinical measurements including plaque (PI) and gingival (GI) indexes, probing depths (PD), and clinical attachment loss (CAL) were recorded both at baseline (before treatment, BT) and after phase I periodontal treatment (AT). Assays for MMP-1 and TIMP-1 were performed by an enzyme-linked immunosorbent assay (ELISA) method. RESULTS: All of the clinical conditions significantly improved and GCF volume decreased AT (P<0.05). Levels of MMP-1 were higher in patients BT than in controls (C) (P<0.05). Levels of MMP-1 were reduced AT compared to BT (P<0.05). In addition, TIMP-1 levels were lower at BT than AT and in C (P<0.05). Statistically significant differences were found between levels of TIMP-1 at BT and AT (P<0.05). The ratio of MMP-1 to TIMP-1 was significantly lower in C than patients at BT; this ratio was also significantly lower at AT than BT (P<0.05). CONCLUSIONS: These results suggest that levels of MMP-1 in GCF decreased and total levels of TIMP-1 in GCF increased after phase I periodontal therapy. The ratio of MMP-1 to TIMP-1 changed after phase I periodontal therapy, becoming close to that of the controls.

Adult↗

Er:YAG laser scaling of diseased root surfaces.

BACKGROUND: The removal of calculus and plaque is an essential component of a therapeutic approach to control periodontal disease. Er:YAG laser scaling was recently introduced as an alternative to conventional scaling procedures. In this histological study, the effects of laser instrumentation of diseased root surfaces are compared to mechanical removal of plaque and calculus with ultrasonic instruments and scalers. METHODS: Areas of subgingival calculus were identified on 40 freshly extracted human teeth. Each of these areas was randomly divided into 2 equal parts. The control site was treated either with scaling and root planing or with an ultrasonic instrument. The test site was cleaned using an Er:YAG laser according to the manufacturer's instructions. The end point of debridement was the inability to mechanically or visibly detect any remaining calculus. After pre- and postsurgical photographs and impressions for scanning electronic microscopic investigation, a plastic embedding technique was used to cut the undecalcified roots into 15 microm thick sections. RESULTS: Clinically and histologically, scaling resulted in complete debridement at all samples, producing a smooth root surface. At the test sites, laser scaling was accompanied by an increased removal of tissue and roughened surfaces. CONCLUSIONS: Laser scaling results in an increased loss of cementum and dentin, which should be taken into account in clinical situations.

Aluminum Silicates↗

New biomarker evidence of oxidative DNA damage in whole saliva from clinically healthy and periodontally diseased individuals.

BACKGROUND: There is an increasing body of evidence implicating reactive oxygen species in the pathogenesis of periodontal tissue destruction. 8-Hydroxy-deoxyguanosine (8-OHdG) is one of the most commonly used markers to evaluate oxidative damage in a number of disorders including chronic inflammatory diseases. The aim of the present study was to evaluate 8-OHdG levels in whole saliva of patients with periodontitis and to assess the changes after initial treatment. METHODS: Saliva samples were collected from 78 patients with untreated periodontitis and 17 healthy control subjects. Clinical parameters and levels of 8-OHdG were assessed first to establish a baseline and again after initial periodontal treatment from 15 patients. 8-OHdG levels were determined by enzyme-linked immunosorbent assay. RESULTS: The mean value of 8-OHdG in the saliva of periodontally diseased subjects, 4.28 +/- 0.10 ng/ml, was significantly higher (P<0.01) than that of clinically healthy subjects (1.56 +/- 0.10 ng/ml). A significant decrease in salivary 8-OHdG was observed after therapy (P<0.01). CONCLUSION: In the present study, we evaluated for the first time 8-OHdG levels in whole saliva of patients with periodontitis and assessed changes after initial periodontal treatment. Our study indicated that 8-OHdG levels in saliva appear to reflect the status of periodontal health.

8-Hydroxy-2'-Deoxyguanosine↗

Immunohistochemical analysis of lymphocyte subpopulations in cyclosporin A-induced gingival overgrowth.

BACKGROUND: Cyclosporin A (CsA) is an immunosuppressive agent that is known to induce gingival overgrowth (GO). Pharmacological, genetic, immunologic, and inflammatory factors seem to be involved in the complex pathogenesis of drug-induced GO. Lymphocyte subpopulations in human gingival connective tissue have been implicated in the pathogenesis of inflammatory periodontal diseases. One purpose of this study was to quantify CD4, CD8-, CD57-, and epithelial membrane antigen (EMA)-positive cells in the gingiva of renal transplant recipients treated with CsA, and compare them to findings in healthy controls. A second aim was to correlate cell numbers with clinical findings. METHODS: The study included 19 kidney recipients who were taking CsA and had significant GO (CsAGO+), 13 recipients who were taking CsA but showed no GO (CsAGO-), and 14 systemically healthy individuals with gingivitis (C). Sections from gingival biopsies were incubated with monoclonal antibodies for CD4, CD8, EMA, and CD57, and then analyzed using the avidin-biotin complex method. In each specimen, the mononuclear cell types were quantified and their distribution was evaluated in 3 separate tissue zones: S = subepithelial connective tissue beneath the sulcular epithelium; O = subepithelial connective tissue beneath the oral epithelium; and M = middle connective tissue. RESULTS: There were no significant differences among the groups with respect to the numbers of CD4+ and CD8+ cells in each of the 3 zones (P >0.05). In zone S, the CsAGO+ group had significantly more EMA-positive cells than either the C or CsAGO- groups (P <0.05). There were significant differences among the groups regarding numbers of CD57+ (natural killer) cells in zone M, with the lowest cell numbers in the CsAGO+ patients (P<0.05). CONCLUSIONS: The results showed that low numbers of natural killer cells are important in the expression of plaque-induced inflammatory changes in CsA-associated GO. It appears that these cells may influence the drug's ability to induce proliferative activity.

Adult↗

Effects of selective cyclooxygenase-2 inhibition on gingival tissue levels of prostaglandin E2 and prostaglandin F2alpha and clinical parameters of chronic periodontitis.

BACKGROUND: The purpose of the present study was to evaluate the effect of a relatively selective cyclooxygenase (COX)-2 inhibitor (nimesulide) and non-selective COX-1/COX-2 inhibitor (naproxen) used as an adjunct to non-surgical (scaling and root planing [SRP]) periodontal therapy in chronic periodontitis patients on the gingival tissue (GT) levels of prostaglandin (PG)E2 and PGF2alpha. METHODS: Thirty patients with chronic periodontitis were divided into 3 groups of 10 each. One group received 100 mg of nimesulide; one received 275 mg of naproxen sodium; and the third group received placebo tablets in a 2 x 1 regimen for 10 days as an adjunct to SRP. GT samples were obtained before drug intake and on day 10. Plaque index (PI) and papillary bleeding index (PBI) scores were recorded at baseline, day 10, and at 3 months; probing depth (PD) and clinical attachment level (CAL) were recorded at baseline and at 3 months. The levels of PGE2 were detected using an enzyme immunoassay (EIA), and the levels of PGF2alpha were analyzed by radioimmunoassay (RIA). Differences among and within the groups were assessed using non-parametric statistical analysis. Ten periodontally healthy individuals served as controls. RESULTS: All 3 groups showed statistically significant reductions in PBI and PI on day 10 and at 3 months (P < 0.02), and in PD and CAL at 3 months (P < 0.02, P < 0.05, respectively). In the naproxen group, GT PGE2 levels exhibited a significant decrease (P < 0.05). However, the decrease of GT PGE2 levels in the nimesulide group was insignificant (P > 0.05), while a significant increase was observed in the placebo group (P < 0.05) on day 10. Both the nimesulide and naproxen groups showed a significant decrease (P<0.05) in PGF2alpha level, while the placebo group showed a significant increase (P<0.05). CONCLUSIONS: Nimesulides, relatively selective COX-2 inhibitors, may have additional inhibitory effects on GT PGF2alpha levels in the first week following non-surgical periodontal treatment. However, nimesulide has an insignificant effect on reducing PGE2 levels in gingival tissue. The determination of GT levels of COX-1 and COX-2 enzymes as well as PGE2 and PGF2alpha in long-term studies may provide further support for the adjunctive use of selective COX-2 inhibitors in treatment of chronic periodontitis.

Adult↗