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Aim: To determine whether combinations of enzymes in gingival crevicular fluid (GCF) can act as improved biomarkers compared with single enzymes for predicting the outcome of treatment and also for diagnosing the clinical status of sites., Methods: Thirty subjects with chronic periodontitis were recruited to a 12-month longitudinal pilot study. GCF samples from three representative sites: healthy (≤3 mm), deep non-bleeding (NB) (≥6 mm) and deep bleeding (DB) (≥6 mm) sites and clinical data were collected at baseline, 3 months, 6 months and 12 months following periodontal treatment. Active enzyme levels (MMP-8, cathepsin G, elastase, trypsin-like activity and sialidase) in GCF samples were assessed. The enzyme profiles and clinical data of each site were analysed for correlation and logistic regression was performed to find the predictive value of the active enzyme levels regarding the outcome of treatment., Results: Twenty-two individuals completed the study. All active enzyme levels were significantly higher in diseased sites than healthy sites. Logistic regression showed that the combination of MMP8, elastase and sialidase provided accurate predictions of treatment outcome (88% for NB and 86% for DB), which was significantly better than each enzyme alone (61%)., Conclusion: This pilot has suggested that combined active enzyme profiling could provide significant prediction of outcome of treatment., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Aim: To explore whether subjects harbouring A. actinomycetemcomitans, P. gingivalis or T. forsythia at baseline showed increased clinical benefits with the adjunctive use of systemic amoxicillin and metronidazole (AMX-MET) during non-surgical treatment of generalized aggressive periodontitis (GAgP)., Material and Methods: Forty one subjects were included in this 6-month randomized placebo-controlled clinical trial using a 7-day course of systemic AMX-MET or placebo as adjuncts to non-surgical periodontal therapy. Clinical and microbiological parameters were collected at baseline, 2 and 6 months after treatment. Microbiological cultures were processed for pooled subgingival samples and identities of isolates were determined by PCR for A. actinomycetemcomitans, P. gingivalis and T. forsythia, Results: At 6 months, the test treatment resulted in significant additional improvements in the primary outcome variable compared to placebo, and the effect of the adjunctive antimicrobials was not modified by the baseline microbiological status in the primary analysis. However, secondary exploratory subgroup analyses showed improved clinical outcomes in subjects harbouring A. actinomycetemcomitans at baseline compared to subjects who did not harbour this pathogen., Conclusions: All subjects benefited from the tested adjunctive antimicrobial regimen, although subjects who harboured A. actinomycetemcomitans at baseline may show greater clinical benefits. Larger appropriately powered studies are needed to confirm whether adjunctive AMX-MET is more beneficial for GAgP patients who harbour A. actinomycetemcomitans, along with other key periodontal pathogens., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Previously, we showed that systemic metronidazole and amoxicillin significantly improved the outcomes of non-surgical debridement in generalized aggressive periodontitis patients. This study aimed to observe whether re-treatment with adjunctive antimicrobials would give the placebo group benefits comparable with the test group., Methods: Thirty-eight of 41 subjects, from the initial 6-month trial, completed the second phase, re-treatment of sites with remaining pockets 5 mm. Subjects on placebo in phase one, received adjunctive antibiotics for 7 days. Clinical parameters were collected at 2 months posttreatment (8 months from baseline)., Results: Patients who received antibiotics at initial therapy, showed statistically significant improvement in pocket depth reduction and in the % of sites improving above clinically relevant thresholds, compared with patients who received antibiotics at re-treatment. In deep pockets (7 mm), the mean difference was 0.9 mm (p=0.003) and in moderate pockets (4-6 mm) it was 0.4 mm (p=0.036). For pockets converting from 5 to 4 mm, this was 83% compared with 67% (p=0.041) and pockets converting from 4 to 3 mm was 63% compared with 49% (p=0.297)., Conclusions: At 8 months, patients who had antibiotics at initial therapy showed statistically significant benefits compared with those who had antibiotics at re-treatment., (© 2010 John Wiley & Sons A/S.)

Aim: The aim of this analysis was to investigate the relationship between a vitamin D receptor (VDR) polymorphism and the diagnosis and progression of periodontitis., Material and Methods: Data were derived from two different studies, including 231 subjects with healthy periodontium, 224 aggressive periodontitis and 79 chronic periodontitis (CP) patients in a case-control investigation. Sixty-one of these CP patients also took part in an observational study with a 1-year follow-up, in which progression of periodontitis was determined at the subject level. All 534 subjects provided a blood sample from which genomic DNA was extracted to study VDR -1056 TaqI polymorphism., Results: The interaction between smoking and VDR polymorphism was associated with the diagnosis of periodontitis in Caucasians [p=0.001, odds ratio (OR)=1.33, 95% confidence intervals (CI)=1.12-1.57] and all subjects (p=0.033, OR=1.60, 95% CI=1.04-2.48). In the longitudinal study, subjects were divided into two clusters at 1 year according to the median number of progressing sites (Delta cumulative attachment loss >2 mm). Logistic regression analysis revealed that the interaction between VDR Taq-I polymorphism and smoking showed limited evidence of association with the "severe progression" cluster (p=0.033, OR=15.24, 95% CI=1.24-187.42)., Conclusions: Vitamin D receptor Taq-I TT polymorphism was moderately associated with both the presence and the progression of periodontitis in smokers, while no association was detected in non-smoking individuals. VDR genetic factors may interact with smoking in the pathogenesis of periodontitis.

Background: Interleukin-6 (IL-6) polymorphisms have been shown to affect IL-6 promoter activity. This study investigated the possible role of IL-6 genetic polymorphisms and haplotypes in the predisposition to aggressive periodontitis (AgP)., Material and Methods: A case-control association study on 224 AgP patients and 231 healthy controls was performed in order to detect differences in genotype distributions of five single nucleotide polymorphisms (SNPs) located in the promoter region of the IL-6 gene., Results: The IL-6 -1363 polymorphism was associated with a diagnosis of AgP in subjects of all ethnicities (p=0.006, adjusted logistic regression). The -1480 SNP was associated with LAgP in subjects of all ethnicities (p=0.003). The -1480 and -6106 polymorphisms were associated with Localized AgP in Caucasians (n=24) (p=0.007 and 0.010, respectively). Haplotypes determined by the -1363 and -1480 polymorphisms were also associated with LAgP (p=0.001) in Caucasians., Conclusions: This study supports the hypothesis of a link between IL-6 genetic factors and AgP and highlights the importance of two IL-6 polymorphisms (-1363 and -1480) in modulating disease phenotype and susceptibility.

Introduction: Neutrophils (PMN) in aggressive periodontitis (AgP) patients have been reported to be hyperactive especially with regards to superoxide production. Polymorphisms in genes influencing PMN function have been proposed as candidate risk factors for AgP. The aim of this study was to test the association of specific gene polymorphisms affecting PMN functions with AgP., Materials and Methods: Two hundred and twenty-four patients with confirmed diagnosis of AgP and 231 subjects with healthy periodontium took part in the study. A blood sample was collected from subjects and genotypes for p22phox (CYBA) NADPH oxidase, FP, Fcalpha and Fcgamma receptors were analysed in a blind fashion., Results: The C242T p22phox NADPH oxidase T allele was significantly associated with AgP in a multiple logistic regression model adjusting for confounders, and this was observed for all subjects [p = 0.002, odds ratio (OR) = 1.87, 95% confidence interval (CI) = 1.27-2.83] and Caucasians (p = 0.009, OR=2.07, 95% CI = 1.20-3.59). Concomitant presence of C242T p22phox NADPH oxidase T allele and FcgammaRIIIb NA1 homozygosity was associated with the generalized AgP phenotype in Caucasians (p = 0.001, OR = 30.35, 95% CI = 3.81-241.97)., Conclusions: C242T p22phox NADPH oxidase and FcgammaR polymorphisms may predispose to AgP through a modulation of neutrophil superoxide production.

Objectives: To assess the periodontal status of relatives of Aggressive Periodontitis (AgP) patients, and to evaluate the reliability of the family history report as provided by the proband., Material and Methods: Data from 54 AgP patients were gathered along with a family history report for each of their relatives. Only 27 patients (probands) had relatives willing to be examined. This yielded a total of 61 relatives from whom the periodontal status was obtained. The family history report for each examined relative was compared with the periodontal diagnosis made at examination to assess reliability., Results: Eight percentage of the examined relatives, aged between 12-76, were diagnosed with AgP, while chronic periodontitis was present in 39%, gingivitis in 38% and 15% were healthy. If the report provided by the proband was positive, the likelihood of finding any type of periodontitis in that relative was 85.7%, whereas if the report was negative the likelihood of the absence of periodontitis was 70.6%., Conclusion: The percentage of examined relatives who were affected with AgP (8%), although lower than percentages reported in other AgP family studies, was still higher than the prevalence of the condition in random populations. Reliability of periodontal family history was considered good and more reliable when it was positive.

Background: The objective of this study was to assess the adjunctive clinical effect of the administration of systemic amoxicillin and metronidazole in the non-surgical treatment of generalized aggressive periodontitis (GAP)., Methods: Forty-one systemically healthy subjects with GAP were included in this 6-month double-blind, placebo-controlled, randomized clinical trial. Patients received a course of full-mouth non-surgical periodontal treatment delivered over a 24 h period using machine-driven and hand instruments. Test subjects received an adjunctive course of systemic antibiotic consisting of 500 mg amoxicillin and 500 mg metronidazole three times a day for 7 days. Clinical parameters were collected at baseline, and at 2 and 6 months post-treatment., Results: In both the test and the placebo groups, all clinical parameters improved at 2 and 6 months. In deep pockets (> or =7 mm), the test treatment resulted in an additional 1.4 mm (95% confidence interval 0.8, 2.0 mm) in full-mouth probing pocket depth (PPD) reduction and 1 mm (0.7, 1.3 mm) of life cumulative attachment loss (LCAL) gain at 6 months. In moderate pockets (4-6 mm), the adjunctive benefit was smaller in magnitude: PPD reduction was 0.4 mm (0.1, 0.7 mm) and LCAL gain was 0.5 mm (0.2, 0.8 mm). In addition, the 6-month data showed LCAL gains > or =2 mm at 25% of sites in test patients compared with 16% in placebo (p=0.028). Similarly, PPD reductions of 2 mm or more were observed in 30% of sites in test and 21% of sites in placebo patients. Seventy-four percent of pockets with PPD > or =5 mm at baseline were 4 mm or shallower at 6 months in the test group. This compared with 54% in the placebo group (p=0.008). Disease progression at 6 months was observed at 1.5% of test and 3.3% of sites in test and placebo, respectively (p=0.072)., Conclusions: These data indicate that a 7-day adjunctive course of systemic metronidazole and amoxicillin significantly improved the short-term clinical outcomes of full-mouth non-surgical periodontal debridement in subjects with GAP.

Objectives: Growth factors play a major part in wound healing, including in the periodontium. However, the presence of growth factors in gingival crevicular fluid (GCF) in humans during periodontal wound healing has not yet been determined. Our hypothesis is that such factors are present in GCF and that changes in their levels might be of value as a prognostic marker of wound-healing activity and therapeutic progress following periodontal surgery. The aim of this study was therefore to measure transforming growth factor-beta1 (TGF-beta1) in GCF collected from sites that have undergone guided tissue regeneration (GTR) and conventional flap (CF) surgery and to compare these with GCF collected from unaffected healthy sites., Materials and Methods: GCF samples were collected, using filter paper strips, at baseline (pre-surgical) and then at intervals up to 26 weeks from 16 patients undergoing GTR and from 11 patients undergoing CF surgery. After elution and acid treatment, TGF-beta1 levels were measured by ELISA., Results: Treatment of periodontal defect sites significantly reduced the mean probing pocket depth (PPD) and improved the mean lifetime cumulative attachment loss (LCAL). Average GCF volumes also significantly increased at all sites at 2 weeks post-surgery and thereafter declined to baseline levels, except at the GTR test sites that were still elevated at 7 weeks. TGF-beta1 could be detected in almost all GCF samples, and 2 weeks after surgery, the average levels increased two-fold at the surgically treated but not at the control sites, which remained unchanged., Conclusion: TGF-beta1 is readily detectable in GCF and increases transiently following periodontal surgery. This suggests that changes in the levels of this growth factor in GCF might be useful for monitoring the progress of periodontal repair and regeneration.

Objectives: The aim of this study was to investigate high-frequency ultrasound imaging for periodontal assessment., Material and Methods: A newly developed ultrasonic scanner with a frequency of 20 MHz was used. Pig jaws were selected as the experimental model. Three teeth per jaw were imaged with the scanner and duplicate measurements were made of the distance from a fixed landmark on the teeth to the alveolar bone crest. These measurements were compared to transgingival and direct measurements of the same teeth following reflection of the soft tissues. One further jaw was used for histological comparison with the ultrasound image., Results: Using ultrasonography, it was possible to image the main periodontal structures. The ultrasound measurements showed better repeatability than either of the other two methods (repeatability coefficient: 0.44 mm for ultrasound, 0.93 mm for transgingival probing and 0.6 mm for direct measurements). Also, ultrasound was in better agreement with direct, open probing measurements (0.004 +/- 0.58 mm) than transgingival probing with direct measurements (0 +/- 0.7 mm)., Conclusions: Ultrasonography provides a highly accurate and repeatable technique for periodontal assessment in this model.

Aim: The aims of this study were to monitor the prevalence and progression of lifetime cumulative attachment loss (LCAL) in a group of young British male military recruits over a 3-year period, and to determine the relationship between signs of LCAL and selected periodontal variables., Methods: 100 subjects, aged 16-20 years (mean 17 years) at baseline, were examined at 0 (baseline), 12 and 30 months. LCAL, probing depth, plaque, bleeding on probing, gingival colour and supra- and subgingival calculus were assessed on the mesio-buccal, disto-buccal, mesio-lingual and disto-lingual surfaces of all teeth present, excluding third molars. Data were analysed cross-sectionally at each examination., Results: Over the period of the study, the prevalence of LCAL > or =1 and 2 mm ranged from 95-100%, whereas LCAL > or =3 mm ranged from 40-47%. The extent of LCAL > or =1 mm ranged from 76-86%. However, the extent of LCAL > or =2 mm was dramatically lower (10.5-12.7%), and LCAL > or =3 mm was uncommon (0.5-0.9%). Examining the number of subjects according to the number of sites affected above a threshold, showed that a small number of subjects have a large number of sites above threshold. Using Pearson's rank correlation coefficient a significant correlation (p<0.05) was found between LCAL and the periodontal variables of gingival bleeding and supra- and subgingival calculus., Conclusions: These data suggest that the onset and progression of chronic periodontitis can be seen in young adults, and in this group gingival bleeding and supra- and subgingival calculus are the variables most strongly associated with early periodontitis.

Aim: In the present 6-month multicentre trial, the outcome of 2 different approaches to non-surgical treatment of chronic periodontitis, both involving the use of a locally delivered controlled-release doxycycline, was evaluated., Material and Methods: 105 adult patients with moderately advanced chronic periodontitis from 3 centres participated in the trial. Each patient had to present with at least 8 periodontal sites in 2 jaw quadrants with a probing pocket depth (PPD) of > or =5 mm and bleeding following pocket probing (BoP), out of which at least 2 sites had to be > or =7 mm and a further 2 sites > or =6 mm. Following a baseline examination, including assessments of plaque, PPD, clinical attachment level (CAL) and BoP, careful instruction in oral hygiene was given. The patients were then randomly assigned to one of two treatment groups: scaling/root planing (SRP) with local analgesia or debridement (supra- and subgingival ultrasonic instrumentation without analgesia). The "SRP" group received a single episode of full-mouth supra-/subgingival scaling and root planing under local analgesia. In addition, at a 3-month recall visit, a full-mouth supra-/subgingival debridement using ultrasonic instrumentation was provided. This was followed by subgingival application of an 8.5% w/w doxycycline polymer at sites with a remaining PPD of > or =5 mm. The patients of the "debridement" group were initially subjected to a 45-minute full-mouth debridement with the use of an ultrasonic instrument and without administration of local analgesia, and followed by application of doxycycline in sites with a PPD of > or =5 mm. At month 3, sites with a remaining PPD of > or =5 mm were subjected to scaling and root planing. Clinical re-examinations were performed at 3 and 6 months., Results: At 3 months, the proportion of sites showing PPD of < or =4 mm was significantly higher in the "debridement" group than in the "SRP" group (58% versus 50%; p<0.05). The CAL gain at 3 months amounted to 0.8 mm in the "debridement" group and 0.5 mm in the "SRP" group (p=0.064). The proportion of sites demonstrating a clinically significant CAL gain (> or =2 mm) was higher in the "debridement" group than in the "SRP" group (38% versus 30%; p<0.05). At the 6-month examination, no statistically significant differences in PPD or CAL were found between the two treatment groups. BoP was significantly lower for the "debridement" group than for the "SRP" group (p<0.001) both at 3- and 6 months. The mean total treatment time (baseline and 3-month) for the "SRP" patients was 3:11 h, compared to 2:00 h for the patients in the "debridement" group (p<0.001)., Conclusion: The results indicate that simplified subgingival instrumentation combined with local application of doxycycline in deep periodontal sites can be considered as a justified approach for non-surgical treatment of chronic periodontitis.

Background, Aims: Conventional treatment of chronic periodontitis involves mechanical debridement of periodontal pockets. Recently, subgingival antimicrobials have been used adjunctively following such debridement. This 2-centre study compared the clinical effects of subgingival scaling (SRP) with SRP plus subgingival application of 25% metronidazole gel, Elyzol (SRP+gel), in patients with chronic adult periodontitis., Method: Voluntary informed written consent was obtained from 45 subjects at the Eastman (mean age 46, range 34-63) and 43 subjects at RAF Halton (mean age 47, range 34-71) who participated in this blind, randomised split-mouth design study. All had at least 2 sites in each quadrant with probing pocket depth (PPD) > or = 5 mm. PPD, bleeding on probing (BOP), and clinical probing attachment levels (CAL) measured using a stent, were recorded at baseline and at 1, 3, 6 and 9 months post-therapy. After subgingival scaling of all quadrants, 2 quadrants were randomly selected to be treated with metronidazole gel., Results: A paired t-test on baseline values showed no bias between groups. Both treatments effectively reduced the signs of periodontitis. At each follow-up visit, reduction in PPD, CAL and BOP after the combined treatment was greater than for SRP alone. Paired t-tests showed that the improvement in the SRP+gel group was statistically significantly better (p<0.001) than for SRP alone (mean 0.5 +/- 0.6 mm. 95% CI 0.4-0.6 mm.) Similarly, the % of sites which improved to a final pocket depth of < or = 3 mm and the % of sites which improved over the 9 months of the study by as much as > or = 2 mm were greater for SRP+gel than for SRP alone., Conclusions: At the end of the study, the mean reductions for PPD were 1.0 mm (SRP) compared to 1.5 mm (SRP+gel), and for CAL they were 0.4 mm (SRP) compared to 0.8 mm (SRP+gel), with mean difference for CAL between treatments of 0.4 +/- 0.6 mm (95% confidence intervals of 0.3-0.6 mm). The combination therapy of SRP+gel was superior to the conventional treatment of SRP alone, and these differences were maintained for 9 months.

Osteocalcin (Oc) and the collagen cross-links pyridinoline (Pyr) and deoxypyridinoline (dPyr) are used as markers of bone turnover in metabolic bone diseases. The aims of this study were: 1) to establish if Oc, Pyr and dPyr can be detected in GCF and 2) using the orthodontic tooth movement model of alveolar bone resorption to evaluate GCF levels of osteocalcin and these collagen cross-links as markers of bone breakdown. Plaque, colour and bleeding indices, probing measurements and GCF samples were collected at two sites in each of 20 adolescents, during 4 stages of fixed appliance therapy: (1) prior to appliance fit, (2) post appliance fit, (3) during active retraction of the maxillary canines, (4) during retention. GCF was collected onto filter paper strips and the volume determined by weighing. An ELISA kit was used for the detection of osteocalcin, whereas Pyr and dPyr were assayed using high performance liquid chromotography (HPLC). Wilcoxon signed ranks test and Bonferroni correction revealed statistically significant increases in plaque (p= 0.012), GCF volume (p=0.024) and osteocalcin concentration (p=0.012), between stages 1 and 2. There were no statistically significant differences between the other variables at this stage or between any of the variables at stages 2 and 3, or between stages 3 and 4. All but 3 of the GCF samples yielded detectable osteocalcin, with large site and subject variation. The median values of osteocalcin and osteocalcin concentration of all the samples were 87.5 pg and 66 pg/microl, with a range of 0-1,248 pg, 0-1,572 pg/microl. The detection of osteocalcin in GCF during every stage, the wide variation between subjects, and the lack of a consistent pattern related to stages of orthodontic treatment, suggests that osteocalcin may merely be a constituent of GCF associated with the developing dentition, which would reduce its potential as a marker of bone turnover in this group. None of the 16 GCF samples analysed for Pyr and dPyr gave a positive result. This study confirms that fitting an orthodontic appliance results in plaque accumulation and increased gingival inflammation, and that GCF volume is the most sensitive indicator of that inflammation. Osteocalcin was detected in GCF collected from adolescents, whereas Pyr and dPyr could not be detected. Further work is required to establish whether GCF osteocalcin levels can be used as a marker of bone turnover, and whether improvements in the sensitivity of detecting Pyr & dPyr make further study of these promising bone markers worthwhile.

The present clinical trial was designed to evaluate the effects of a bioactive glass, Perioglas, in the treatment of periodontal intrabony defects. 20 patients, 23-55 years of age (44 sites), with intrabony defects completed the 1-year study. Teeth with furcation involvement were excluded. After completion of initial therapy, defects were randomly assigned to either a test or control procedure. Following flap reflection, root planing and removal of chronic inflammatory tissue in both groups, the test defects were restored with the bioactive glass particulate material. Mucoperiosteal flaps were replaced, sutured and a periodontal dressing was used. All the patients received postoperative antibiotics and analgesics and were seen at 1 week for suture removal. Follow-up was then carried out weekly and at 3 months, 6 months, 9 months and 1 year post-surgery. Plaque score, bleeding score, probing pocket depth (PPD), probing attachment level (PAL) and gingival recession were recorded at baseline, 3 months and 1 year. Standardised radiographs for computer-assisted densitometric image analysis (CADIA) were taken at baseline, immediately post-operatively and at 1 year. The CADIA data showed a significant increase (F-ratio: 15.67, p < 0.001) in radiographic density and volume between the defects treated with the Perioglas when compared to those treated with surgical debridement only. PPD and PAL showed significant improvements in both experimental and control sites, with a greater trend to improvement in the experimental sites. It was concluded that this bioactive glass is effective as an adjunct to conventional surgery in the treatment of intrabony defects.

The aim of this study was to investigate the accuracy and reproducibility of experienced and inexperienced examiners using 3 automated periodontal probes (Florida Pocket Probe, Florida Disk Probe, Peri Probe) in comparison with 3 conventional periodontal probes (Marquis, Williams and EN-15 probes). Test blocks of aluminium had 30 holes of diameter 1.10 mm and depths ranging from 2.75 to 10.0 mm. machined with a tolerance of +/- 0.01 mm. 8 experienced examiners and 8 inexperienced examiners were selected to perform duplicate measurements on the blocks over 6 visits using each of the 6 probes. 1 automated and 1 conventional probe were used at each examination. The % accuracy and reproducibility for each of the duplicate measurements was calculated and analysed using Friedman 2-way analysis of variance and the Wilcoxon matched pairs test. On average, all probes showed high reproducibility, with the Florida Disk Probe, the Florida Pocket Probe and the Williams probe ranked best and the other 3 probes were less reproducible. On average, all probes showed a high degree of accuracy, automated probes were ranked best and were significantly better than conventional probes. Experience had little effect on reproducibility, with only the Peri Probe showing significant differences at the 5% level between the groups. Experience appeared to be more important for accuracy, as experienced examiners were more accurate than inexperienced examiners, with significant differences at the 5% level for the EN-15, Florida Disk Probe and Peri Probe. However, inexperienced examiners were significantly more accurate using the Williams probe. This in vitro study has shown that automated probes offer increased accuracy over conventional probes and the Florida Pocket and disk probes compare well with conventional probes for reproducibility.

Perioscan requires a plaque sample to detect the presence of enzymes capable of degrading N-benzoyl-DL-arginine-2-naphthylamide (BANA) from relatively few anaerobic periodontal pathogens. Periocheck assays the presence of neutral proteases in crevicular fluid. The aim of this study was to compare these test kits with traditional clinical methods of detecting periodontal disease and to monitor the ability of the kits to reflect the response to initial therapy. 19 patients with moderately severe chronic periodontitis were seen before and after a course of oral hygiene and root instrumentation consisting of 4 appointments. Clinical measurements and test assays were collected at 5 diseased sites and 2 healthy sites in each subject. Complete data from 125 sites were available for statistical analysis. At baseline Periocheck had a sensitivity of 88% and a specificity of 61% whereas Perioscan had a sensitivity of 99% and a specificity of 55%, when related to the clinical diagnosis. A composite clinical assessment, based on improvement or deterioration of one whole unit change of the subjective clinical indices and 2 mm changes or greater in probing depth or probing attachment level, revealed 75 sites which improved following treatment, whereas 45 sites did not change and 5 sites deteriorated. The probability that the tests agreed with the clinical outcome after treatment, was calculated as 50.4% for Periocheck and 52% for Perioscan. The diagnostic kits did not reliably reflect the clinical assessment of periodontal disease in the cross sectional study, or the outcome following treatment.

2 periodontal dressings, Coe-pak and RD8 (a product under development), were assessed following periodontal surgery, using a double-blind study of randomised split-mouth design, with each patient acting as their own control. Matched sites were selected for periodontal flap surgery under local analgesia. Sites were randomly allocated to each group. The dressings were applied by a single operator and both patients and clinical assessors were blind as to the dressing employed. The dressings were assessed as to their handling properties, in addition to a 7-day post-operative assessment of the surgical sites and a subjective patient report. Maximum pain levels were relatively low (4 in a scale 0-10); subjects reported more pain and analgesics required with RD8 than with Coe-pak. This was reflected in the results of the patient assessment which indicated that 50% preferred Coe-pak, compared to 25% who preferred the RD8 dressing. The results showed RD8 to be an acceptable periodontal dressing when compared to Coe-pak. There were no statistically significant differences between treated sites in both groups with regard to post-operative plaque scores, bleeding scores or tissue healing.

Gingival crevicular fluid (GCF) sampling was performed on 2 occasions separated by 1 year, at 2 sites in the mouths of 102 male adolescents, mean age 17.85 years. Samples were collected onto 5 filter paper strips which were sequentially applied to the mouth of the crevice over a 9-min collection period. Volume and flow rates of GCF were determined for each site and were compared with clinical measurements of plaque, gingival colour, bleeding, gingival index (GI) and pocket depth, using a general linear models (GLM) procedure. While the initial volume of GCF showed no association with any clinical measurement, there was an association between flow rate of GCF and gingival colour. The volume of GCF collected in the final, 5th sample was associated with the GI. The sample site strongly influenced all measures of GCF volume. It is proposed that the flow rate of GCF may be a better indicator of gingival inflammation than the more imprecise clinical assessments of inflammation, since GCF flow rates more precisely reflect changes in tissue permeability. The association between the final sample, collected after 9 min, and clinical measurements, was probably a reflection of the association between clinically-detectable inflammation and the susceptibility of the site to mild irritation.

We have estimated the levels of Interleukin-1 beta (IL-1 beta) by ELISA in gingival crevicular fluid (GCF) at 58 sites from 37 patients with adult periodontitis. GCF was collected for 5 s on filter papers and a 2nd sample was collected for 30 s 1 min later. 68/116 strips yielded detectable levels of IL-1 beta. IL-1 beta was present in both the 1st and 2nd samples at 28 sites, in the 1st only at 4 sites and in the 2nd only at 8 sites; 18 sites were below the level of detection for the assay. When the concentrations of IL-1 beta were calculated in the original volume of GCF on each strip, the mean value for positive strips was 34.16 +/- 29.45 (SD) pg/microliters with a range from 1.75 to 97.13 pg/microliters. There were no statistically significant correlations with the plaque index, bleeding index or probable crevice depth (pocket depth). The results indicate that IL-1 is present in the GCF from a proportion of sites with evidence of previous periodontal destruction.

We have reviewed the recent literature on the humoral immune responses to a variety of subgingival plaque bacterial species in patients with destructive periodontal diseases. We do not feel that the information presently available on the specific antibody responses to proposed pathogens such as Bacteroides gingivalis and Actinobacillus actinomycetemcomitans allows antibody responses to be diagnostic. All control subjects without periodontal destruction have antibodies to candidate pathogens but the generally higher levels in patients are not sufficiently elevated to be diagnostic. Nor can they be used to predict the initiation of disease or the onset of new episodes of destruction where disease had previously occurred. Successful treatment of patients may lead to lower levels of antibodies to some organisms, including possible pathogens, and thus support a given species in the aetiopathogenesis of disease. It appears that unsuccessful treatment may be accompanied by continuing high antibody levels to some organisms and further studies may enable this observation to be used to monitor therapy. There is some evidence from serological studies that each destructive episode may be induced by a different bacterial species or consortium. The start of studies using single antigens and the techniques of molecular biology will provide not only antibody-based diagnostic methods but also allow us to determine which bacterial antigens are virulence factors and thus the role of the antibody responses, whether protective or damaging, in the periodontal diseases.

The histological evaluation of surgical biopsies from affected tissues is a standard way of assessing pathological change and determining treatment in many diseases. In most forms of periodontal disease, however, this approach finds limited application. Here, we review what uses the histopathological approach has in the study and evaluation of the periodontal diseases. Current understanding of the changes in epithelial anatomy during pocket formation, the cellular composition and dynamics of the inflammatory infiltrate and the mechanisms of bone resorption and repair are reviewed from the perspective of the information available from microscopical investigation, including the uses and potential application of modern immunocytochemical methods to these questions. The usefulness of histological study of biopsy material is reassessed in the light of advances made in immunohistochemical techniques and their application to gingival inflammatory infiltrates and epithelia. Such techniques offer immediately valuable research opportunities with potential for diagnostic applications, noteably the recognition of phases of destructive activity and their differentiation from periods of effective host defence.

Many factors have been hypothesised either to characterise groups and individuals at risk for periodontal disease or to be markers of periodontal breakdown. In order to identify these as associated either with disease status or progression, a statistical association between the factor and a measure of disease will have to be demonstrated. The statistical modelling of data arising from periodontal research presents special problems. These include the large number of measurements made in each subject, the large magnitude of measurement error compared to the changes in attachment level, the analysis of longitudinal studies, the lack of a measure of instantaneous rate of attachment loss and controversies over the nature of the progression of the disease. We consider statistical methods currently available in the light of these difficulties and identify areas in which further research is necessary.

Periodontal microbiology is reviewed with regard to the potential of certain characteristics to serve as markers of high risk groups or individuals for periodontal diseases. The generally accepted associations between particular organisms and the various periodontal diseases are discussed. The usefulness of various clinical study designs is reviewed. The ecology of the subgingival plaque microflora is discussed and a number of suggestions for future research are made. We have concluded that there is no monospecific aetiology to any of the various periodontal conditions. Nevertheless, we give particular attention to the role of the black-pigmented bacteroides based upon our belief that they, and Bacteroides gingivalis in particular, are fundamental to our understanding of the biology of periodontal diseases in humans and other animals. Consequently, the contribution of its various virulence factors and their potential as markers of disease susceptibility and activity is addressed.

The importance of malposition of teeth and plaque accumulation is still not established. The purpose of this study was to measure plaque accumulation on individual malpositioned teeth for comparison with contralateral nonmalpositioned teeth. Furthermore, the distribution of plaque in the anterior segments was measured and compared between aligned and nonaligned segments and the total mouth plaque score. Plaque scores and contact point indices were recorded from a total of 87 subjects of which 20 were drawn from dental and ancillary students and 67 from randomly chosen patients. For anterior teeth, in both groups significantly more plaque accumulated on malpositioned teeth compared with contralateral nonmalpositioned teeth. For the right-handed subjects (83), mean plaque scores for malpositioned teeth were greater than for nonmalpositioned teeth whether the malpositioned tooth was on the right or left of the anterior segment. This difference was significant in the patient group. The contact point index of the anterior segments correlated only with plaque accumulation in those subjects with a plaque index of less than 1. Upper and lower anterior segment plaque scores correlated with total mouth scores in both groups. However, the upper anterior segment scores had significantly less plaque than the total mouth score irrespective of the presence or absence of tooth malalignment, whereas the lower anterior segment always had significantly higher plaque scores than the total mouth score, irrespective of the presence or absence of malalignment. Finally, lower segments, whether aligned or malaligned, had significantly more plaque than upper anterior segments which were aligned or malaligned.

The use of saliva as a source of components that may identify subjects at risk of developing destructive periodontitis, or provide markers of disease potential or activity, has been reviewed. It was concluded that bacteria, their constituents or products are unlikely to be rewarding and that host-derived salivary factors such as enzymes cannot identify risk, as deficiency states for these do not exist. Secretory IgA, plasma IgA and IgG isotype levels and specific antibodies may be associated with risk, but probably only if levels fall below those which are protective or a specific antibody response is absent. More work is needed to distinguish between monomeric and dimeric IgA antibodies and to identify IgG antibodies in longitudinal clinical studies. In general, although saliva may prove to be useful as a source of indicators of current disease activity or as a means of assessing responses to treatment, it is unlikely to provide evidence for the existence of risk factors.

The fundamental concepts of measuring periodontal diseases and the interpretation of such information as an historical record of disease, rather than disease activity, emphasises the need for improved diagnostic and prognostic tests. Criteria for an indicator of disease activity were suggested and an index fulfilling these should allow sites to be categorised as "active", quiescent or healing, and enable one to predict the risk of future disease activity. The ability of current measurements and indices, routinely used during clinical assessments of periodontal diseases, to fulfill the suggested criteria was considered and rejected in all cases. It is concluded that clinical parameters are only capable of identifying disease retrospectively, indicating the need for longitudinal, rather than cross-sectional studies in the search for clinical and laboratory markers of disease activity and susceptibility.

Gingival crevicular fluid is regarded as a promising medium for the detection of markers of periodontal diseases activity. The collection protocols are straight forward and non-invasive and can be performed at specific sites of interest in the periodontium. Because the fluid accumulates at the gingival margin, it will contain potential markers derived not only from the host tissues and serum but also the subgingival microbial plaque, and thus an extremely broad range of candidate molecules may be investigated. However, the ability to successfully describe indicators of current disease activity and predictors of future disease is dependent not only upon the choice of the biochemical marker but also on the accurate description of the health status of the sample sites using currently available clinical and radiographic methods. Areas of study which currently show the most promise involve the analysis of host enzyme activities directed against components of the extracellular matrix, the nature of the glycosaminoglycans released into the sulcus and the concentration in gingival crevicular fluid of certain mediators of the inflammatory process, most notably prostaglandin E2.

It is argued that the periodontal diseases can no longer be regarded as universally prevalent conditions to which all members of the world's population are at equal risk if they fail to practise good oral hygiene. Rather, they should be regarded as a range of different diseases for each of which certain individuals, which together comprise certain minority groups, are at relatively high risk. The epidemiological evidence for the existence of high-risk groups is reviewed, from which it is concluded that world-wide the prevalence of severe destructive periodontitis is of the order of only 7-15% of the adult dentate population. A working classification of the different types of gingivitis and periodontitis is offered, as is a summary of the theoretically possible approaches to the detection of high-risk groups and individuals which are explored in detail in subsequent papers. Successful identification of such individuals will permit scientifically valid, rational and targetted prevention and treatment.

The evidence for systemic predisposition to periodontal diseases is reviewed in relation to cellular and humoral immunity, drug therapy, diet and nutrition and stress. It is concluded that, apart from defects of polymorphonuclear leukocytes (PMN) and Ehlers-Danlos Syndrome, little firm evidence exists for other diseases, though insulin-dependent diabetes and acquired immune deficiency syndrome (AIDS) may accelerate and/or potentiate the damage of existing disease. The precise rôle of drugs, diet and nutrition and stress remain to be elucidated, but recent advances in these areas offer the prospect of assessing risk using carefully controlled studies.

The total protein concentration of gingival crevicular fluid (GCF), sampled repeatedly over a 10-min period with the minimum of physical irritation to the sulcus, was evaluated in a group of 32 healthy adolescents. The mean concentration of the 1st sample was comparable to that of normal tissue fluids and lymph, irrespective of the state of inflammation of the sample site. However, during repeated sampling, the values rose to resemble serum protein levels, except at those sites with no clinically detectable inflammation. Gel electrophoretic analysis confirmed the increasing proportion of serum-derived molecules in the more proteinaceous GCF samples. The results demonstrate the extreme sensitivity of the gingival vasculature to GCF sampling and consequently the need for accurate standardisation of GCF collection protocols. This will apply particularly when compositional data is to be normalised with respect to the total protein content or when the levels of a serum constituent are being examined.