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Root grooves: a risk factor in periodontal attachment loss.

Periodontal health reflects a balance between harmful and protective elements in the gingival margin area. The total plaque mass, specific periodontopathogens, and local environmental factors may challenge this balance. The aim of this retrospective study was to evaluate the effect of proximal root grooves as a risk factor in periodontal attachment loss. One-hundred and three (103) extracted, formalin-stored, single-rooted teeth showing loss of attachment and having one non-grooved and one grooved proximal root surface were selected for the study. Following staining in 0.1% toluidine blue to visualize attached periodontal ligament remnants, the teeth were examined in a light microscope under incident light. On each tooth, loss of attachment was measured along the long axis of the root from the cemento-enamel junction to the most coronal level of the stained periodontal ligament remnants on mesial as well as on distal surfaces. Incisors and premolars were grouped separately. For both groups, a statistically significant greater loss of attachment was present on grooved than on non-grooved surfaces (P < 0.0001). Generally, there was a direct relationship between groove location and maximum loss of attachment. The results indicate that proximal root grooves should be considered in periodontal diagnosis, prognosis, and treatment planning.

Bicuspid↗

Correlation between gingivain/gingipain and bacterial dipeptidyl peptidase activity in gingival crevicular fluid and periodontal attachment loss in chronic periodontitis patients. A 2-year longitudinal study.

The aim of this study is to determine whether either gingival crevicular fluid (GCF) bacterial gingivain/gingipain or dipeptidyl peptidase (DPP) levels, total activity (TA) and concentration (EC), predict progressive attachment loss (AL) in 75 patients with moderate periodontitis. GCF was collected from 16 molar and premolar mesiobuccal sites and then clinical attachment level (CAL) and probing depth (PD) were measured with an electronic constant pressure probe. Lastly, gingival, gingival bleeding, and plaque indices were scored. Prior to the baseline visit, patients were given basic periodontal treatment after which the above procedures were repeated. In addition, carefully localized radiographs were taken of the test teeth and repeated annually. Patients were then seen every 3 months for 2 years and the clinical measurements repeated at each visit. In 48 patients, 124 AL sites, 91 rapid AL (RAL), and 33 gradual AL (GAL) were detected. Gingivain/gingipain and bacterial DPP levels (TA and EC) at RAL sites were significantly higher (P < or = 0.0001) than at paired control sites at the attachment loss time (ALT) and prediction time (PT). Mean levels over the study period of both proteases (TA and EC) at GAL sites were significantly higher (P < or = 0.0001) than those at paired control sites. The GCF levels of gingivain/gingipain were always higher than those of DPP. Critical values (CV) of 5 microU/30 seconds (TA) and 30 microU/microL (EC) for both proteases showed high sensitivity and specificity values for TA and EC, which were the same at both ALT and PT. The positive predictive values were higher for gingivain/ gingipain. Mean site levels, over the course of the study, of both proteases (TA and EC) were significantly higher (P < or = 0.0001) at AL, RAL, and GAL sites than non-attachment loss (NAL) sites in AL patients and mean patient levels were significantly higher (P < or = 0.0001) in AL, RAL, and GAL patients than NAL patients. These results indicate that both of these bacterial proteases in GCF may be predictors of periodontal attachment loss.

Adhesins, Bacterial↗

The relationship between gingival crevicular fluid cathepsin B activity and periodontal attachment loss in chronic periodontitis patients: a 2-year longitudinal study.

This study aims to determine whether gingival crevicular fluid (GCF) cathepsin B levels, total activity (TA) and concentration (EC) predict progressive attachment loss (AL). Seventy-five previously untreated patients with moderate periodontitis were recruited. GCF was collected from 16 molar and premolar mesiobuccal sites and probing attachment level (PAL) and probing depth (PPD) were measured with an electronic probe. Gingival, gingival bleeding and plaque indices were then scored. Prior to baseline patients were given basic periodontal treatment after which the above procedures were repeated. Carefully localized radiographs were taken of the test teeth and repeated annually. Patients were seen 3-monthly for 2 yr and the procedures were repeated. One hundred and twenty-one AL sites, 90 rapid AL (RAL) and 31 gradual AL (GAL), in 49 patients were detected. Cathepsin B levels (TA & EC) at RAL sites were significantly higher (p < 0.0001) than paired control sites at the attachment loss time (ALT) and prediction time (PT). Mean levels (TA & EC) over the study period at GAL sites were significantly higher (p < 0.0001) than paired control sites. Using a critical value (CV) of 7.5 microU/30 s (TA) and 30 microU/microL (EC) showed a sensitivity of 100% and specificity of 99.83% (TA) and 100% and 99.75%(EC) at both ALT & PT. Mean cathepsin B levels (TA & EC) were significantly higher (p < 0.0001) at RAL and GAL sites than non-attachment loss (NAL) sites in AL patients in intrapatient comparisons and mean patient levels were significantly higher (p < 0.0001) in AL patients than NAL patients in interpatient comparisons. These results indicate that GCF cathepsin B may serve as a predictor of attachment loss.

Adult↗

Epidemiologic risk factors for periodontal attachment loss among adults in the United States.

OBJECTIVES: The objective of this study was to identify variables related to periodontal loss of attachment (LOA). MATERIALS AND METHODS: The study population consisted of a nationally representative sample of 12,325 US adults who participated in the National Health and Nutrition Examination Survey III. The analyses used survey multinomial logistic regression to account for the complex survey design. RESULTS: The adjusted odds ratio for a mean LOA of 3 mm or more associated with current smoking was 18.55 (95% CI 9.44-36.45) among 20-49-year olds. Among those aged 50 years or more, the odds ratio for a mean LOA of 4 mm or more was 25.64 (13.04-50.40). Prior smoking, untreated decayed surfaces (on both person and site levels), and male gender were also associated with LOA. There was no excess risk observed among non-Hispanic blacks or Mexican-Americans. The adjusted population attributable fractions due to current smoking were 60% for persons aged 20-49 with the worst 10% of LOA (1.58 mm or more), and 47% for those aged 50 plus (LOA of 3.39 mm or more). CONCLUSION: These results support earlier findings regarding the central role of cigarette smoking in the etiology of periodontal loss of attachment, a role due in large part to the substantial relationship between smoking and severe periodontal disease.

Adult↗

Problems in identifying "bursts" of periodontal attachment loss.

A theory of periodontal attachment loss which postulates discrete bursts of activity has recently been proposed. This paper identifies several problems in the interpretation of the experimental data that have been used to support the burst model. Major obstacles to valid inferences are associated with the following: substantial measurement error, insufficient evidence supporting a dichotomy of disease state and the use of diagnostic decision criteria with undesirable properties. The nature of these problems is discussed from the framework of receiver operating characteristic (ROC) analysis. "Bursts" of attachment loss can be explained, in whole or in part, by these factors in the absence of real change. Types of research evidence that would offer more compelling support for the burst model are identified. The questionable validity of evidence supporting the burst model may impact on both the direction of future research efforts and clinical applications.

Epithelial Attachment↗

The prevalence of periodontal attachment loss in an Iowa population aged 70 and older.

Survey dental examinations were conducted in 262 dentate elderly people aged 70 and older and residing in two rural Iowa counties. Over 60 percent of the elderly in these countries were dentate. Buccal and mesial sites of all teeth were assessed for gingival recession, pocket depth, and attachment loss. Mean loss of periodontal attachment was 2.1 mm, and was slightly greater in older age groups and in men. More gingival recession was found on buccal sites and deeper pocketing was found on mesial sites regardless of age group, sex, or tooth type. However, the clinical magnitude of these differences was small. The prevalence of advanced periodontal breakdown was relatively low, with less than 15 percent of the subjects having at least one site with attachment loss of 7 mm or more. However, moderate periodontal breakdown was highly prevalent in this older population.

Aged↗

Pulpal disease and bursts of periodontal attachment loss.

Progression of periodontitis is currently thought to occur during bursts of activity, followed by periods of remission, when healing may occur. This concept contrasts with the older hypothesis that periodontitis was continuously, but slowly, progressive throughout life. At present, there is no proof of the conventional (microbiological) hypothesis which gives a major role to site-specific bacteria in the initiation of bursts of attachment loss. An alternative hypothesis is presented in this paper which accounts for periodontal attachment loss by pathways that are independent of plaque. Severe lesions of the periodontium caused by pulpal pathoses (apical and retrograde periodontitis) are known to form at any level of the periodontium, not only at the root apex. When these lesions cause destruction of the periodontal tissues at the alveolar crest, and when plaque, calculus and gingivitis are also present, an endodontic origin is rarely suspected. Three pathways are proposed to account for the development of localized periodontal attachment loss consequent to pulpal disease. This hypothesis accounts for the sudden deterioration of periodontal sites under regular review, the strict localization of alveolar defects with normal alveolar bone immediately adjacent, the presence of site-specific bacteria (secondary colonizers of deep pockets) which cannot cause disease when transferred to healthy sites, and the antibody responses directed against them.

Acute Disease↗

The identification of periodontal attachment loss from clinical measurements.

Clinical readings of pocket depth and loss of periodontal attachment were recorded on the approximal sites of 21 teeth scheduled for extraction. Corresponding laboratory measurements of pocket depth and loss of periodontal attachment were made on the teeth after extraction. Clinical measurements were within 1mm of their corresponding laboratory values on 95% of occasions. Clinical readings of loss of periodontal attachment of 0 or 1mm showed poor agreement with corresponding laboratory measurements. It was concluded that the presence of loss of periodontal attachment can only be reliably identified where a clinical reading of 2mm or greater is recorded.

Adult↗

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)

Adult↗

The association between osteopenia and periodontal attachment loss in older women.

BACKGROUND: Recent research suggests that osteopenia may be a predisposing factor for periodontal tissue destruction. If so, then a relationship should exist between measures of systemic bone mineral density and periodontal tissue destruction. The purpose of the present cross-sectional study was to evaluate the association between systemic bone mineral density and the clinical signs of periodontal tissue destruction in a large population of elderly dentate women. METHODS: A total of 292 dentate women (average age 75.5 years) were randomly selected for a cross-sectional periodontal substudy from participants at the Pittsburgh Field Center of the Study of Osteoporotic Fractures (SOF), a prospective study of a cohort of elderly women (age > or =65 years at baseline) to determine risk factors for fractures. Bone mineral density (BMD) was measured using single photon absorptiometry (radius, calcaneus) and dual energy x-ray absorptiometry (hip, spine). Oral health examinations, including periodontal probings and an assessment of bleeding on probing, were made using an NIDR probe at 3 buccal sites of all teeth. Multiple regression models were used to assess the association between bone mineral density and measures of periodontal disease status while controlling for potential confounders. Periodontal status variables examined included: average loss of periodontal attachment (LOA); number of sites with at least 4 mm LOA; number of sites with at least 6 mm LOA; number of sites with bleeding on probing; and deepest probing depth per person. RESULTS: This study found no statistically significant association between the 5 indicators of periodontal disease and measures of systemic BMD at 8 anatomic sites after controlling for age, smoking, and number of remaining natural teeth. Some suggestive findings support a weak association between generalized osteopenia and periodontal disease. CONCLUSIONS: Systemic osteopenia is, at best, only a weak risk factor for periodontal disease in older non-black women.

Absorptiometry, Photon↗

Periodontal attachment loss assessed by linear and area measurements in vitro.

The aim of the present study was to investigate the relationship between linear and area measurements of periodontal attachment loss, and to determine the root surface area on different tooth-types. Extracted permanent teeth were collected in a national survey including a systematic random sample of 500 Norwegian dentists. The response rate was 70%. Altogether 329 teeth were received, 81 of them (excluding 3rd molars) were subjected to both linear and area measurements of attachment loss. Using a dissecting microscope (10 x), 4 to 8 duplicate linear measurements were recorded per tooth. The areas of both lost and remaining periodontal attachment were measured by a method based on controlled release of Cu and Co metal ions from coatings applied to the root surface. Linear loss of attachment for single-rooted teeth (n = 63) was mean = 44.0% and the area loss mean = 49.2%. The corresponding measurements for multi-rooted teeth (n = 18) were mean = 30.3% and mean = 35.1%, respectively. The correlation between linear and area loss was r = 0.78 for single-rooted and r = 0.75 for multi-rooted teeth (p < 0.01). The lower correlation in multi-rooted teeth is probably due to the more complex root anatomy. It is concluded that there is a strong correlation between linear loss of attachment and area of periodontal support lost for teeth with early to moderate loss of attachment, and that linear measurements tend to underestimate the remaining periodontal attachment.

Alveolar Bone Loss↗

Cemental tear: a risk factor in periodontal attachment loss.

The objective of this retrospective study was to evaluate the influence of cemental tear as a risk factor in periodontal attachment loss. Seventeen extracted, single-rooted teeth showing loss of attachment and having one cemental tear surface and one opposite intact surface were examined. The teeth were stained in 0.1% toluidine blue to visualize attached periodontal ligament remnants and examined in a light microscope under incident light. On each tooth, loss of attachment was measured along the long axis of the root from the cemento-enamel junction to the most coronal level of the periodontal ligament on intact as well as on defect surfaces. Cemental tear surfaces demonstrated a significantly greater loss of attachment than opposite intact surfaces (P < 0.0001). In one specimen, the cemental tear fragment was partially attached to the root after the extraction procedure. This specimen was processed for light microscopy to determine the location of the cemental tear fracture. Histological examination clearly revealed that the split between the root and the fragment had occurred along the cemento-dentinal border. The results indicate that cemental tear should be considered as a possible etiologic entity in localized rapid periodontal breakdown.

Dental Cementum↗

Etiologic models for incident periodontal attachment loss in older adults.

Etiologic factors for incident periodontal attachment loss (ALOSS) have not been conclusively identified. The purpose of this study was to develop etiologic models for ALOSS in older adults. Data on 697 older blacks and whites were obtained from 5 sequential examinations over 7 years in the Piedmont 65+ dental study, a complex random sample of older adults in North Carolina. Multivariable Poisson regression models were fit for average number of ALOSS events per person or site month at risk. In models for whites, molar sites, sites with adjacent caries, sites in persons who had: Porphyromonas gingivalis (P.g.) at least 2% of total microbial count (TMC), never had a dental checkup, more depression symptoms, fewer than 12 years of education, higher BANA score, or smoked, had significantly higher rates of ALOSS. In a separate model for blacks, interproximal and molar sites, sites in blacks who had: P.g. at least 2% of TMC, higher BANA score, never had a dental checkup, lower socioeconomic status (SES), or smoked, had significantly higher rates of ALOSS. These results confirm a multifactorial etiology for ALOSS in older adults and indicate that interventions aimed at infection, smoking, and preventive dental care utilization, may be most useful.

Black or African American↗

Serum cotinine levels, smoking, and periodontal attachment loss.

Cigarette smoking and tobacco use have been the subjects of numerous studies for many years. Smoking has also been associated with periodontal disease. However, no relationship between a reliable biochemical marker and increased severity of the periodontal condition has yet been described. It was thus the aim of this study to apply the measurement of cotinine, the major metabolite of nicotine, as a quantitative method to assess levels of smoking, and to correlate serum levels of cotinine with severity of periodontal disease. The degree of association between smoking and periodontal attachment loss was investigated in a study including 79 patients 25 to 64 years old suffering from periodontitis. Patients were examined and the following parameters recorded: Gingival Assessment (GA), Probing Pocket Depth (PPD), Clinical Attachment Level (CAL), and Bone Crest Height (BCH). In addition, self-reported histories of tobacco use as well as blood samples for quantitative analysis of serum levels of cotinine were taken. The serum samples were analyzed for cotinine content by means of a competitive-inhibition ELISA technique. The differences in mean cotinine levels were statistically significant (p = 0.0001) between smokers and non-smokers, showing no overlap between the groups. Severity of periodontal attachment loss was positively correlated with serum levels of cotinine for both measures of periodontal disease (CAL p = 0.005; BCH p = 0.008). Results from the present study indicate that serum cotinine levels used as a biochemical marker of smoking status are correlated with severity of periodontal attachment loss.

Adult↗

Periodontal attachment loss in HIV-infected patients is associated with the major histocompatibility complex 8.1 haplotype (HLA-A1,B8,DR3).

Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals.

Adult↗

Dental restorations: a risk factor for periodontal attachment loss?

BACKGROUND: Dental caries and restorations in proximal tooth surfaces often impinge upon the periodontal biological width. AIM: This study examines whether these factors may contribute to risk for periodontal attachment loss at these sites. METHODS: The study is based upon data from the Dunedin Multidisciplinary Health and Development Study, a long-standing cohort study. Approximal tooth surfaces of 884 study members were evaluated for restorations and caries at age 26 and again at 32 years, and probing depth and gingival recession were recorded in millimetres at age 32. Attachment loss was computed as the sum of pocket depth and gingival recession. Data were analysed using generalized estimating equations. RESULTS: Where a caries/restorative event had occurred on an inter-proximal tooth surface before age 26, the age-32 attachment loss at the corresponding periodontal site was approximately twice more likely to be >or=3 mm than if the adjacent tooth surface had remained sound to age 32. This was also true where a caries/restorative event had occurred subsequent to age 26. The association remained after controlling for potential confounders, including smoking. CONCLUSIONS: Site-specific periodontal attachment loss due to dental caries or restorative events occurs in adults in their third and fourth decades of life.

Adult↗

A community study on the relationship between stress, coping, affective dispositions and periodontal attachment loss.

BACKGROUND: Psychological factors may increase the risk for periodontal diseases. Contemporary conceptualization of the stress process supports the evaluation of stress at three levels: stressors, moderating and mediating factors, and stress reactions. OBJECTIVE: This study was undertaken to investigate the relationship of periodontal disease in terms of clinical attachment level (CAL) to psychosocial stress, making reference to the major components of stress process. METHODS: A cross-sectional study of 1000 subjects aged 25-64 years in Hong Kong was conducted. Subjects were asked to complete a set of questionnaires measuring stressors including changes, significant life event and daily strains, stress reactions including physiological and affective responses, and coping and affective dispositions. CAL was assessed. RESULTS: Individuals with high mean CAL values had higher scores on the job and financial strain scales than periodontally healthy individuals (P < 0.05), after adjusting for age, gender, cigarette smoking and systemic disease. Depression, anxiety trait, depression trait, problem-focused coping, and emotion-focused coping were also related to CAL. Logistic regression analysis indicated that all these factors were significant risk indicators for periodontal attachment loss, except problem-focused coping, which reduced the odds of CAL. Individuals who were high emotion-focused copers, low problem-focused copers, trait anxious, or trait depressive had a higher odds of more severe CAL. CONCLUSION: Chronic job and financial strains, depression, inadequate coping, and maladaptive trait dispositions are significant risk indicators for periodontal attachment loss. Adequate coping and adaptive trait dispositions, evidenced as high problem-focused coping and low anxiety/depression trait, may reduce the stress-associated odds.

Adaptation, Psychological↗

Radiographic periodontal attachment loss as an indicator of death risk in the elderly.

OBJECTIVES: Oral infections have been associated with serious systemic diseases and an increased risk of death. Our aims were to investigate whether radiographically-observed apical periodontitis lesions, carious teeth, periodontal attachment loss (horizontal bone loss, furcation lesions, number of teeth with infrabony periodontal pockets, the extent of infrabony periodontal pockets) and the sum of all these findings have any relationships with all-cause mortality within 4-year follow-up. MATERIAL AND METHODS: 292 community-dwelling elderly persons aged 76, 81 and 86 years. The number of deaths within 4 years was 54 (18.5%). In the dentate 169 subjects, of whom 32 (18.9%) deceased within 4 years, the mean number of teeth was 15.5 in men and 13.2 in women. The imaging method used was panoramic radiography supplemented by intraoral radiographs. RESULTS: 51% of the dentate subjects had infrabony pockets (mean 1.5, s.d. 2.2), and 40% had periapical periodontitis lesions (mean 1.0, s.d. 1.6). After controlling for age and gender, vertical bone loss judged as advanced infrabony pockets was associated with 4-year all-cause mortality (Odds ratio 2.2,1.0-4.7). Other associations were statistically insignificant. CONCLUSION: Periodontal attachment loss may indicate an increased risk of death in the elderly.

Aged↗