Established Periodontitis Research Articles

The influence of periodontitis case definition on the association between periodontal disease and glycaemic status.

The association between periodontitis and glycaemic control is complex, and often described as 'bidirectional'. Although epidemiological studies have examined this relationship extensively, a disagreement on periodontitis case definition still exists. This study aimed to assess the influence of case definition on the association between periodontal disease and glycaemic status. The study is a secondary analysis of data from the United States National Health and Nutrition Examination Survey (NHANES), 2009-2014 cycles. The association between periodontitis and glycated haemoglobin (HbA1c) was assessed using different periodontitis case definitions: the definition by the Centers for Disease Control and Prevention and the American Academy of Periodontology (CDC/AAP), Community Periodontal Index (CPI), ≥1 site with ≥3 mm clinical attachment loss (CAL) and ≥4 mm probing depth (PD), ≥1 site with ≥4 mm CAL and ≥4 mm PD, the 5th European Workshop definitions, Machtei et al. 'established periodontitis', the 2017 World Workshop classification, and self-reported periodontitis. The associations between periodontitis and HbA1c were compared across the case definitions. There was substantial variability in prevalence estimates of periodontitis, and in the strength of association between periodontitis and HbA1c when different case definitions were applied. The CDC/AAP and stage III/IV periodontitis were consistently significantly associated with elevated HbA1c. For stage III/IV, the adjusted odds ratios of prediabetes and diabetes HbA1c were 1.19 and 1.76, respectively. Comprehensive periodontitis case definitions that account for CAL and PD, such as the CDC/AAP and the 2017 classification, seem to better detect the association between periodontal disease and HbA1c.

S100A8 and S100A9 in saliva, blood and gingival crevicular fluid for screening established periodontitis: a cross-sectional study

BackgroundPeriodontitis is one of major oral diseases, which has no consensus on early screening tool. This study aimed to compare the association and screening ability of S100A8 and S100A9 in saliva, blood and gingival crevicular fluid (GCF) for periodontitis status.MethodsWe recruited 149 community Korean adults, 50 no or initial periodontitis (NIPERIO) and 99 established periodontitis (PERIO). Using clinical attachment loss and a panoramic radiograph, stage II–IV of new classification of periodontitis proposed at 2018 was considered cases as PERIO. Enzyme linked immunosorbent assay kit was used to quantify S100A8 and S100A9. T-test, analysis of covariance, Mann–Whitney test and correlation analysis were applied to compare the relationship of S100A8 and S100A9 in saliva, blood, and GCF for periodontitis. Receiver operating characteristic curve was applied for screening ability.ResultsAmong S100A8 and S100A9 in saliva, blood and GCF, S100A8 in saliva was significantly higher in PERIO than in NIPERIO (p < 0.05). However, S100A8 and S100A9 in GCF were higher in NIPERIO (p < 0.05). The screening ability of salivary S100A8 was 75% for PERIO, while that of GCF S100A8 was 74% for NIPERIO. Salivary S100A8 was positively correlated to blood S100A8 (p < 0.05).ConclusionSalivary S100A8 could be a potential diagnostic marker for established periodontitis and be useful for screening established periodontitis.

Subgingival Host-Microbial Interactions in Hyperglycemic Individuals

Type 2 diabetes mellitus (T2DM) is an established risk factor for periodontitis, yet its contribution to creating host-bacterial disequilibrium in the subgingival crevice is poorly understood. The present investigation aimed to quantify the impact of hyperglycemia on host-bacterial interactions in established periodontitis and to map shifts in these dynamics following mechanical nonsurgical therapy. Seventeen T2DM and 17 non-T2DM subjects with generalized severe chronic periodontitis were recruited along with 20 periodontally healthy individuals. Subjects with periodontitis were treated with scaling and root planing (SRP). Samples of subgingival biofilm and gingival crevicular fluid were collected at baseline and at 1-, 3-, and 6 mo postoperatively. Correlations were generated between 13.7 million 16S ribosomal DNA sequences and 8 immune mediators. Intermicrobial and host-microbial interactions were modeled using differential network analysis. Periodontal health was characterized by a sparse interbacterial and highly connected cytokine-bacterial network, while both normoglycemics and T2DM subjects with periodontitis demonstrated robust congeneric and intergeneric hubs but significantly fewer cytokine-bacterial connections. Following SRP, the cytokine-bacterial edges demonstrated a 2-fold increase 1 mo postoperatively and a 10-fold increase at 6 mo in normoglycemics. In hyperglycemics, there was a doubling at 1 mo but no further changes thereafter. These shifts accompanied an increasingly sparse interbacterial network. In normoglycemics, the nodes anchored by interleukin (IL)–4, IL-6, and IL-10 demonstrated greatest rewiring, while in hyperglycemics, IL-1β, IL-6, INF-γ, and IL-17 exhibited progressive rewiring. Thus, the present investigation points to a breakdown in host-bacterial mutualism in periodontitis, with interbacterial interactions rather than host-bacterial interactions primarily determining community assembly. Hyperglycemia further exacerbates this uncoupled mutualism. Our data also demonstrate that while nonsurgical therapy might not consistently alter microbial abundances or lower proinflammatory molecules, it “reboots” the interaction between the immunoinflammatory system and the newly colonizing microbiome, restoring a role for the immune system in determining bacterial colonization. However, this outcome is lower and delayed in hyperglycemics.

Comparative analysis of expression of microbial sensing molecules in mucosal tissues with periodontal disease

Host-derived pattern recognition receptors (PRRs) are necessary for effective innate immune engagement of pathogens that express microbial-associated molecular patterns (MAMP) ligands for these PRRs. This study used a nonhuman primate model to evaluate the expression of these sensing molecules in gingival tissues. Macaca mulatta aged 12–24 with a healthy periodontium (n = 13) or periodontitis (n = 11) provided gingival tissues for assessment of naturally-occurring periodontitis. An additional group of animals (12–23 years; n = 18) was subjected to a 5 month longitudinal study examining the initiation and progression of periodontitis, RNA was isolated and microarray analysis conducted for gene expression of the sensing PRRs. The results demonstrated increased expression of various PRRs in naturally-occurring established periodontitis. Selected PRRs also correlated with both bleeding on probing (BOP) and pocket depth (PD) in the animals. The longitudinal model demonstrated multiple TLRs, as well as selected other PRRs that were significantly increased by 2 weeks during initiation of the lesion. While gene expression levels of various PRRs correlated with BOP and PD at baseline and resolution of disease, few correlated with these clinical parameters during initiation and progression of the lesion. These findings suggest that the levels of various PRRs are affected in established periodontitis lesions, and that PRR expression increased most dramatically during the initiation of the disease process, presumably in response to the juxtaposed microbial challenge to the tissues and goal of reestablishing homeostasis.

Resveratrol derivative-rich melinjo seed extract induces healing in a murine model of established periodontitis.

Products of internal defense systems, like pro-inflammatory cytokines, reactive oxygen species, and leukocytes, are released which attack periodontal bacteria in periodontitis, but at the same time, lead to tissue destruction as well. We hypothesize that resveratrol derivative-rich melinjo seed extract (MSE), an edible plant extract that has antioxidant properties, should promote healing of periodontal bone loss and modulating immune-inflammatory systems that leads periodontal tissue destruction. We used an experimentally induced periodontitis (EP) model in mice. Ligatures were placed first for development of EP (15 days). MSE was intraperitoneally administrated (0.001% (w/w)) to reverse bone loss that had already occurred in established EP and mice were then sacrificed (day 17, 20 and 22). Morphometric outcomes revealed lower bone-loss in the MSE groups compared to control. Immunohistochemistry assays demonstrated lower oxidative stress in MSE groups. MSE also inhibited M-CSF/sRANKL mediated osteoclast formation and down-regulated osteoclast activity. Treatment with MSE in EP actually caused healing of bone, and these effects are probably related to decreases in local oxidative damage and osteoclast activity. Given MSE's positive effects on osteodifferentiation as well, these findings suggest that MSE could be a useful therapeutic agent for the management of periodontitis.

Resolvin E1 Reverses Experimental Periodontitis and Dysbiosis.

Periodontitis is a biofilm-induced inflammatory disease characterized by dysbiosis of the commensal periodontal microbiota. It is unclear how natural regulation of inflammation affects the periodontal biofilm. Promoters of active resolution of inflammation, including resolvin E1 (RvE1), effectively treat inflammatory periodontitis in animal models. The goals of this study were 1) to compare periodontal tissue gene expression in different clinical conditions, 2) to determine the impact of local inflammation on the composition of subgingival bacteria, and 3) to understand how inflammation impacts these changes. Two clinically relevant experiments were performed in rats: prevention and treatment of ligature-induced periodontitis with RvE1 topical treatment. The gingival transcriptome was evaluated by RNA sequencing of mRNA. The composition of the subgingival microbiota was characterized by 16S rDNA sequencing. Periodontitis was assessed by bone morphometric measurements and histomorphometry of block sections. H&E and tartrate-resistant acid phosphatase staining were used to characterize and quantify inflammatory changes. RvE1 treatment prevented bone loss in ligature-induced periodontitis. Osteoclast density and inflammatory cell infiltration in the RvE1 groups were lower than those in the placebo group. RvE1 treatment reduced expression of inflammation-related genes, returning the expression profile to one more similar to health. Treatment of established periodontitis with RvE1 reversed bone loss, reversed inflammatory gene expression, and reduced osteoclast density. Assessment of the rat subgingival microbiota after RvE1 treatment revealed marked changes in both prevention and treatment experiments. The data suggest that modulation of local inflammation has a major role in shaping the composition of the subgingival microbiota.

한국 성인에서 비타민 섭취와 치주염 유병간의 관련성

The aim of this study was to examine whether there is an association between vitamin intakes and established periodontitis in Korean adult population. The 6,245 subjects aged over 19 years old, who participated in health survey, oral examination and nutrition survey were selected for this study from the database of the Fourth Korean National Health and Nutrition Examination Survey. Established periodontitis was defined as ≥ code 3 in community periodontal index. Vitamin intake was assessed with the food-frequency questionnaire. In analysis, participants were classified by quintile of vitamin intakes. We also considered covariates as socio-demographic characteristics, health-related behaviors including physical activities, systemic diseases and oral health-related behaviors. Multiple logistic regression was performed to assess the crude and adjusted associations. All analyses considered a complex sampling design using SAS 9.2. In crude analysis, less intake of vitamin A, retinol and vitamin B2 significantly increased the risk of periodontitis (vitamin A, odds ratio (OR) Q1=1.00, Q2=0.73, Q3=0.80, Q4=0.77, Q5=0.78; retinol, OR: Q1=1.00, Q2=0.86, Q3=0.73, Q4=0.62, Q5=0.55; vitamin B2, OR: Q1=1.00, Q2=0.70, Q3=0.63, Q4=0.67, Q5=0.68). However, after adjusting for socio-demographics, general and oral health status and behaviors, only vitamin B2 was significantly associated with established periodontitis (OR: Q1=1.00, Q2=0.72, Q3=0.73, Q4=0.76, Q5=0.84). An adequate vitamin B2 intake was significantly associated with a decreased risk of periodontitis. This finding shows that nutrient intake is slightly correlated with periodontitis in Korean adult population. Further studies are needed to understand this association between nutrients intake and periodontitis in more details.

Comparison of circulating tumour necrosis factor superfamily cytokines in periodontitis patients undergoing supportive therapy: a case‐controlled cross‐sectional study comparing smokers and non‐smokers in health and disease

B-cells are prominent immune cells in established periodontitis lesions. Tumour necrosis factor superfamily (TNFSF) cytokines play roles in supporting B-cell function as well as bone re-modelling. The influence of smoking on factors that support B-cell function in periodontitis remains unclear. To investigate plasma concentrations of TNF (TNSF1A), soluble receptor activator of nuclear-factor Kappa-B ligand (sRANKL/TNFSF11), a proliferation-inducing ligand (APRIL/TNFSF13), B-cell activating factor (BAFF/TNFSF13B) and Osteoprotegerin (OPG/TNFRSF11B) in smokers and non-smokers with and without chronic periodontitis Plasma concentrations of TNFSF and OPG were evaluated in 200 systemically healthy subjects divided into four groups: non-smokers with periodontitis (n=101), smokers with periodontitis (n=55), healthy non-smokers (n=27) and healthy smokers (n=17). Periodontitis patients had significantly higher plasma sRANKL, TNF, APRIL and BAFF and lower OPG than healthy subjects (p<0.01). TNF and sRANKL were significantly greater in smokers with periodontitis (p=0.011, p=0.001) and OPG concentrations significantly lower (p=0.001), whereas APRIL or BAFF were little changed. Plasma APRIL, BAFF, sRANKL and TNF correlated with probing depth and clinical attachment loss. TNFSF cytokines correlate with periodontitis disease severity. However, only TNF, sRANKL and OPG levels were altered by cigarette smoking. APRIL and BAFF appear as good indicators of disease severity.

Association of periodontal disease with self-reported systemic disorders in Greece.

The aim of this retrospective investigation was to examine the occurrence of periodontal disease in patients referred to a specialist clinic for neurosurgery and to explore possible associations between common systemic disorders and periodontal disease in an adult population in Greece. The study sample consisted of 1,652 individuals, 760 males and 892 females, aged 40 to 68 years, with a mean age of 57.3 ± 4.7 years. Data were collected by means of an oral clinical examination and a self-administered questionnaire. Statistical analysis of questionnaire items was performed by using a multiple linear regression analysis model in order to estimate correlations between systemic disorders as independent variables, and the relative frequency of periodontal pockets of 5 mm or more and the frequency of clinical attachment loss of 6 mm or more as dependent variables. The relative frequencies of periodontal pockets >= 5.0 mm and clinical attachment loss >= 6.0 mm as expressed in terms of mean values were 76% and 70.2%, respectively, for individuals who suffer from cardiovascular disease and 62.3% and 52.9% respectively, for those who suffer from respiratory disease. The depth of periodontal pockets was significantly and positively correlated to the presence of respiratory diseases (P = 0.0001) and diabetes mellitus (P = 0.0001) after adjustment for age, gender and smoking, whereas clinical attachment loss was significantly and positively correlated to the presence of diabetes mellitus (P = 0.0001) and cardiovascular diseases (P = 0.037). Based on the clinical criteria for established periodontitis, the current study supports associations between periodontal disease and systemic disorders such as diabetes mellitus, cardiovascular and respiratory diseases.

Smoking and periodontal disease: Clinical evidence for an association

Purpose The aim of the present study was to assess the periodontal condition and smoking status, according to dose and duration information, and to estimate the percentage of subjects with periodontitis attributable to cigarette smoking in a representative adult rural population in southern Brazil. Materials and methods Bivariate statistical analysis was used to evaluate the association of smoking status with periodontitis in a cross-sectional study comprising 165 dentate individuals, aged 35 to 66 years, subjected to oral clinical examination of six sites per tooth in all sextants. Results The prevalence of periodontitis (having > or = 1 pocket of > or = 4 mm around the index teeth) in the population was 35.2%. Overall, 13.9% had a cumulative loss of attachment > 4 mm; 35.7% of subjects were current smokers, classified as heavy (average 25.3 pack years), moderate (average 14.6 pack years) and light smokers (average 3.1 pack years). Statistical analysis showed that current smokers had an 11 times (95% confidence interval [CI] = 4.69 to 26.62) and former smokers had a nine times (95% CI = 3.29 to 25.96) greater probability of having established periodontitis compared with non-smokers. The number of pack years (P = 0.0004) and years of smoking exposure (P = 0.0013) were associated with an increased prevalence of periodontitis. The number of current smokers with periodontitis might be reduced by 80%, had they not smoked cigarettes. Of the subjects with periodontitis, 64% could be prevented among current smokers by eliminating tobacco consumption. Conclusions Cigarette smoking was strongly associated with periodontitis, and there was a relationship with dose and duration of smoking. These findings contributed to the evidence of smoking as a risk factor for periodontal disease and support the importance of dose-response analysis on determining the strength of this association.

1‐Tetradecanol Complex: Therapeutic Actions in Experimental Periodontitis

The present study was planned to investigate the therapeutic actions of 1-tetradecanol complex (1-TDC), a novel monounsaturated fatty acid mixture, in established periodontitis in rabbits. Periodontitis was initiated in 18 New Zealand White rabbits using ligatures around mandibular second premolars, followed by topical Porphyromonas gingivalis application (10(9) colony forming units). After 6 weeks of disease induction (phase 1), three animals were sacrificed to assess the established periodontitis level. P. gingivalis application was discontinued, and the remaining 15 animals continued with topical treatment of 1-TDC (100 mg/ml; n = 5) or placebo (n = 5) or no treatment (n = 5) for an additional 6 weeks (phase 2). Mandibular block sections obtained after euthanasia were decalcified and embedded in paraffin. In addition to the macroscopic analyses, hematoxylin and eosin-stained sections were used to study cellular inflammatory infiltrate and quantitative histomorphometry. Tartrate-resistant acid phosphatase and osteocalcin were used to identify osteoclastic and osteoblastic activity, respectively. P. gingivalis application resulted in periodontal disease with gingival inflammation and bone loss (30% compared to baseline) at 6 weeks. Treatment with 1-TDC stopped the progression of the disease and resulted in a significant reduction in the macroscopic periodontal inflammation, attachment, and bone loss (10.1% +/- 1.8%), whereas periodontal disease progressed in the untreated and placebo groups (P <0.05). Histologic assessment and histomorphometric measurements demonstrated that 1-TDC inhibited inflammatory cell infiltration and osteoclastic activity (P <0.05). The findings suggest that topical application of cetylated monounsaturated fatty acid complex (1-TDC) is a potential therapeutic approach in controlling the progression of chronic periodontal disease.

Smoking and Periodontal Disease: Clinical Evidence for an Association

The aim of the present study was to assess the periodontal condition and smoking status, according to dose and duration information, and to estimate the percentage of subjects with periodontitis attributable to cigarette smoking in a representative adult rural population in southern Brazil. Bivariate statistical analysis was used to evaluate the association of smoking status with periodontitis in a cross-sectional study comprising 165 dentate individuals, aged 35 to 66 years, subjected to oral clinical examination of six sites per tooth in all sextants. The prevalence of periodontitis (having > or = 1 pocket of > or = 4 mm around the index teeth) in the population was 35.2%. Overall, 13.9% had a cumulative loss of attachment > 4 mm; 35.7% of subjects were current smokers, classified as heavy (average 25.3 pack years), moderate (average 14.6 pack years) and light smokers (average 3.1 pack years). Statistical analysis showed that current smokers had an 11 times (95% confidence interval [CI] = 4.69 to 26.62) and former smokers had a nine times (95% CI = 3.29 to 25.96) greater probability of having established periodontitis compared with non-smokers. The number of pack years (P = 0.0004) and years of smoking exposure (P = 0.0013) were associated with an increased prevalence of periodontitis. The number of current smokers with periodontitis might be reduced by 80%, had they not smoked cigarettes. Of the subjects with periodontitis, 64% could be prevented among current smokers by eliminating tobacco consumption. Cigarette smoking was strongly associated with periodontitis, and there was a relationship with dose and duration of smoking. These findings contributed to the evidence of smoking as a risk factor for periodontal disease and support the importance of dose-response analysis on determining the strength of this association.

The Association Between Gingival Crevicular Fluid TGF‐β1 Levels and Periodontal Status in HIV‐1+ Patients

The purpose of this study was to investigate the relationship between transforming growth factor-beta 1 (TGF-beta1) in gingival crevicular fluid (GCF) and the periodontal status of subjects who were positive for the human immunodeficiency virus (HIV)-1. Medical and demographic variables, including age, cigarette smoking, CD4 cell count, and viral load values, were recorded. At the baseline and 6-month visits, gingival index (GI), plaque index, bleeding on probing, probing depth (PD), and attachment loss (AL) were recorded, and GCF samples were taken with paper strips from three periodontitis sites (GI >0; PD > or =5 mm; AL > or =3 mm), three gingivitis sites (GI >0; PD < or =3 mm; AL = 0), and two healthy sites (GI = 0; PD < or =3 mm; AL < or =2 mm) in 25 subjects who were HIV-1(+). GCF TGF-beta1 levels were determined by enzyme-linked immunosorbent assays. A statistical software package was used to analyze the data. The mean amounts of GCF TGF-beta1 were greater in gingivitis and periodontitis sites than in healthy sites (P <0.0001). GCF levels of TGF-beta1 correlated with PD, AL, age, smoking pack-years, CD4 cell count, and viral load at the baseline and 6-month visits (0.0001 < P <0.05). An active site was defined as a site that had > or =2 mm new AL during the 6-month study period. An active patient was defined as a patient who had one or more active site(s) during the study period. Repeated-measures analysis of 18 active sites versus 182 inactive sites indicated that GCF TGF-beta1 levels were higher in active sites than in inactive sites (P <0.0001). Eleven of the 25 study subjects had active sites at the end of the 6-month study period. The mean GCF TGF-beta1 level and the mean AL and PD for these 11 active subjects were higher than for the 14 inactive subjects (P <0.0001). In subjects who are HIV-1(+), sites with high GCF levels of TGF-beta1 are at significantly greater risk for the progression of established periodontitis.

Resolvin E1 Regulates Inflammation at the Cellular and Tissue Level and Restores Tissue Homeostasis In Vivo

Resolvin E1 (RvE1) is a potent proresolving mediator of inflammation derived from omega-3 eicosapentaenoic acid that acts locally to stop leukocyte recruitment and promote resolution. RvE1 displays potent counter-regulatory and tissue-protective actions in vitro and in vivo. Periodontal disease is a local inflammatory disease initiated by bacteria characterized by neutrophil-mediated tissue injury followed by development of a chronic immune lesion. In this study, we report the treatment of established periodontitis using RvE1 as a monotherapy in rabbits compared with structurally related lipids PGE(2) and leukotriene B(4). PGE(2) and leukotriene B(4) each enhanced development of periodontitis and worsened the severity of disease. Promotion of resolution of inflammation as a therapeutic target with RvE1 resulted in complete restoration of the local lesion, and reduction in the systemic inflammatory markers C-reactive protein and IL-1beta. This report is the first to show that resolution of inflammation by a naturally occurring endogenous lipid mediator results in complete regeneration of pathologically lost tissues, including bone.

Association of periodontal disease to anxiety and depression symptoms, and psychosocial stress factors.

A cross-sectional study was conducted to investigate if anxiety, depression and hopelessness symptoms are associated with periodontal disease. A total of 160 subjects took part in this study. Probing depth and clinical attachment level were recorded at six sites per tooth and the gingival and plaque indices were also recorded. The instruments used to assess the psychological variables (anxiety, depression, stress, psychiatric symptoms and hopelessness) were: the State-Trait Anxiety Inventory, the Beck Depression Inventory, the Life Events Scale modified by Savoia, the Self-Report Screening Questionnaire-20 and the Beck Hopelessness Scale. There was no difference in scale score means between patients with and without established periodontitis. Results of the Ordinal Logistic Regression Analysis model that included age, plaque index, smoking and psychological factors showed that patients with psychiatric symptoms (odds ratio (OR) 1.24, 95% confidence interval (CI) 0.33-4.78), depression symptoms (OR 0.57, 95% CI 0.15-2.21) and with hopelessness (OR 0.70, 95% CI 0.13-3.84) were not at a greater risk of developing established periodontitis. In this sample, no evidence was found for an association between depression, hopelessness, psychiatric symptoms and established periodontitis. The association of periodontal disease to depression, anxiety and stress should be investigated in psychiatric populations, especially in those with depression and anxiety disorders.

Factors influencing the effect of race on established periodontitis prevalence.

This paper identifies differences in prevalence of established periodontitis and evaluates factors that might explain the differences between non-Hispanic African Americans (n = 232) and whites (n = 199) in the Detroit tricounty area. Subjects from a disproportionate probability sample of community-dwelling adults were interviewed regarding demographic, psychosocial and enabling factors, dental health-related behaviors, and other risk factors, and had comprehensive in-home dental examinations. The overall prevalence of established periodontitis was 20.8 percent; African Americans exhibited a significantly higher prevalence than whites (29.8% vs 17.7%). The crude association between race and prevalence of established periodontitis was significant (odds ratio [OR] for African Americans = 1.98; 95% confidence interval [CI] = 1.17,3.34). After controlling for other covariates, we found the effect of race may be modified by dental checkup visit frequency: African Americans with dental checkups at least once a year had almost a fourfold higher odds of established periodontitis (OR = 3.64; 95% CI = 1.43, 9.24) than their white counterparts with dental checkups at least once a year (the referent group); while African Americans with a dental checkups once every two years or less often were more than fourfold less likely to have established periodontitis (OR = 0.22; 95% CI = 0.08, 0.59) than their white counterparts in the referent group. This analysis supports the disparity in periodontal health as part of the black:white health disparity when taking other factors into account. However, periodontal health disparities may be more complex than previously recognized, requiring greater understanding of factors related to dental care utilization in future studies evaluating this disparity.

Longitudinal study of prognostic factors in established periodontitis patients.

Numerous indicators for disease progression have been described in the last decade. The purpose of this study was to examine, longitudinally, a large battery of clinical, microbiological, and immunological indicators, to try to determine whether the presence of one or a combination of these parameters at baseline, would correlate positively with increased attachment and or bone loss (true prognostic factors). Following initial screening, 79 patients with established periodontitis were monitored longitudinally for one year. Whole mouth clinical measurements, plaque gingival and calculus indices, together with pocket depth and attachment level measurements, were repeated every three months. Full mouth radiographic survey, performed at baseline and 12 months, served to determine changes in crestal bone height using an image enhancement technique. Subgingival plaque samples were taken at baseline and every 3 months. Immunofluorescence assays were performed for the a battery of target microorganisms. Serum and GCF samples for IgG subclasses analysis were obtained at each visit and assayed using ELISA techniques. Likewise blood, samples were also drawn at each visit for a quantitative analysis of serum cotinine level. The overall mean attachment loss (AL) and bone loss (BL) were almost identical (0.159 mm and 0.164 mm, respectively). Individual patients variation was large (-0.733 to +1.004 mm). An overall 6.89% of sites were active; individual patients' means ranged from 0-28.9%. Mean pocket depth (PD) showed minimal change over the study period (-0.033 mm) thus suggesting that most if not all the AL was accompained by concomitant gingival recession. Smokers exhibited greater AL and radiographic BL compared to non-smokers. Likewise, patients' cotinine level showed direct correlation with outcomes of progressive periodontal breakdown. Past severity of periodontal involvement, as reflected in the patients baseline PD, AL and crestal bone height, showed good correlation with longitudinal changes in the periodontium. This correlation was higher for crestal BL as the outcome variable, while somewhat smaller for change in AL as the outcome variable. Bacteroides forsythus (Bf.), Prevotella intermedia (Pi.) and Porphyromonas gingivalis (Pg.) were frequently found in these patients. The presence of these microorganisms at baseline was associated with further disease progression. Subjects with mean baseline pocket depth equal or greater than 3.2 mm were at greater risk for future bone loss 1 year later (O.R. 2.97; C.I. 1.02-8.70). Smokers were at significantly greater risk for further attachment loss when compared to non-smokers (O.R. 5.41; C.I. 1.50-19.5). Subjects that harbored B. forsythus at baseline, were at seven times greater risk for increased pocket depth (O.R. 7.84; C.I.1.74-35.3). In conclusion, past periodontal destruction, smoking habits, Bf., Pg., & Pi. are prognostic factors for further periodontal breakdown. When designing clinical trials, or when evaluating epidemiological data, it is most important to balance for these factors. Also, treatment strategies should attempt to eliminate or modify these factors.

Association of amyloid P protein with pathology in periodontal tissues

The lesion of chronic periodontitis is characterized by the persistence of perivascular collections of degenerate plasma cells. In this study, immunohistochemical demonstration of amyloid P (AP) component was used to define the distribution of this protein in established periodontitis lesions and in biopsies of non-destructive marginal gingivitis. Quantitative assessment of AP indicated significantly higher levels in periodontitis than in gingivitis for all regions of the tissue. This was associated with pathology as determined by the intensity of plasma cell accumulation and the extent of connective tissue matrix degradation. AP was concentrated in the deep connective tissue areas but perivascular accumulation was also noted, as was deposition associated with nerve bundles and, occasionally, in the extracellular matrix of the lining epithelium. These findings have potential significance in relation to the pathology of chronic periodontitis as AP has been shown to interact in a calcium-dependent manner with a number of ligands including fibronectin, elastic fibres, C-4 binding protein and amyloid fibrils.

The rate of periodontal attachment loss in subjects with established periodontitis.

A stepwise approach to determine attachment level changes was utilized to assess the nature of progression of periodontal disease. Following initial screening, 51 subjects with established periodontitis were monitored quarterly for 9 more months. Probing depth (PD) and relative attachment level (RAL) were recorded using an automated, pressure sensitive probe system. To establish intra-examiner error, repeated measurements were performed for all sites at the final visit. An overall standard deviation (SD) for RAL repeated measurements was initially calculated (0.76 mm) using all 6,935 double measurements. Sites were sorted by factors which contribute to the error of attachment level measurements; i.e., pocket depth (shallow, moderate, deep), tooth type (molar, non-molar) and location (buccal, lingual). Data were sorted by the above 12 groups, and SD for repeated measurements was calculated separately for them. The ratio between these SD and the overall SD served as the corrective factor. Each patient's initial threshold (2 SD) was multiplied by these corrective factors thus resulting in 12 thresholds for each subject. Next, linear, exponential and logarithmic regression models were tested for each site, and the regression model showing the highest R value was chosen for that site. AL changes were tested against the patient's threshold for that site. Sites with attachment loss exceeding the threshold were deemed active. Five hundred eighty-one sites (8.3%) exhibited attachment loss exceeding the various thresholds. Of these, linear progression occurred in 195, logarithmic in 224, and exponential in 162 sites. Individual patient's attachment loss ranged from 0.6 to 19.4% of all sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Alternative methods for screening periodontal disease in adults.

Clinical measurements of periodontal attachment loss, while not always representing the histological changes, are used to establish the diagnosis of adult periodontitis. Such measurements are difficult to perform accurately and are labor intensive. To counter these problems, index teeth and index sites have been employed in an attempt to estimate the severity of the periodontal condition without the need to resort to elaborate attachment measurements. Unfortunately, such indices usually tend to underestimate prevalence while often overestimating severity. The purpose of the present study was to examine the correlation of alternative clinical, radiographic and microbiological parameters, with periodontal disease using the diagnostic criteria of established periodontitis. 508 adults included in this study received thorough periodontal examination which included probing pocket depth, clinical attachment level, plaque, gingival and calculus scores, together with radiographic analysis and assays of subgingival periopathogenic microorganisms. Radiographic alveolar bone loss and probing pocket depth had the highest correlation with clinical attachment loss (phi = 0.72 and phi = 0.75 respectively). Plaque scores (phi = 0.17), like gingival scores (phi = 0.06) and calculus scores (phi = 0.42) had poor correlation with established periodontitis. Periodontopathogenic species demonstrated high specificity and negative predictive values; but low sensitivity and positive predictive values make for an overall low correlation of these species with established periodontitis. However, when used in a logistic regression model, the presence of P. gingivalis (odds ratio = 6.25) has shown to contribute significantly to the estimate of probability for established periodontitis. The use of these various alternative parameters for screening of periodontal disease is discussed in light of their sensitivity, specificity and predictive value.