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Biomedical subjects

A D Haffajee

Publications and source records attributed to A D Haffajee.

At least 91 records · Page 5Linked to original sources
PubMed1988

Probing depth, attachment loss and gingival recession. Findings from a clinical examination in Ushiku, Japan.

The present investigation describes probing pocket depth, probing attachment level and recession data from 319 randomly selected subjects, aged 20-79 years, from Ushiku, Japan. The findings are reported as mean values, frequency distributions and percentile plots of the 3 parameters at buccal, interproximal and lingual surfaces of single rooted (incisors, canines, premolars) and molar teeth. Inter-as well as intra-examiner errors for probing pocket depth and probing attachment levels were assessed and found to be small. The data reported revealed that practically all subjects studied had one or more sites in the dentition affected by destructive periodontal disease and that the severity of disease increased with age. It was further observed that in each age group, molars had suffered more attachment loss than single rooted teeth and that the interproximal surfaces as a rule had lost more periodontal tissue support than corresponding buccal and lingual surfaces. The attachment loss difference observed between different surfaces of a given tooth or a group of teeth, however, was comparatively small. In the age groups between 20-59 years, advanced destructive periodontal disease was found in a small subgroup of the subject sample, while after the age of 60 years, widespread destructive periodontitis was common. An attempt was made to examine the progression of destructive disease with age by comparing the frequency distributions of sites with attachment loss of greater than or equal to 3 mm in subjects of different age groups. The data suggested that in younger subject groups, progression was confined to a subset of individuals, while in older age groups, more subjects and sites became involved. A major feature of destructive periodontal disease in older individuals was the accompaniment of attachment loss with recession at the gingival margin. Deep pockets were relatively infrequently detected, while advanced loss of attachment (with recession) occurred at many sites.

Adult↗
PubMed1987

Human serum antibody responses to oral microorganisms. IV. Correlation with homologous infection.

Recent microbiological studies of periodontal disease in humans have supported the concept of a specific bacterial etiology. While individual agents have not been unequivocally identified, numerous Gram-negative members of the subgingival microflora have been implicated. In addition, elevations in systemic antibody responses have been consistent with certain oral microorganisms being involved in an infectious process associated with the disease. This report delineates the relationship between elevated systemic antibody levels and oral colonization with the homologous microorganism at active disease sites. Thirty-four patients with various types of periodontal disease were examined. Using ELISA, each patient was shown to have an elevated antibody response to at least one organism from a battery of 18 oral microorganisms that were tested. Subsequently, subgingival plaque was cultured from disease-active and -inactive sites of each subject. The results demonstrated that the same microorganism to which the individual exhibited elevated serum antibody responses was detected in nearly 55% of the disease-active sites, while only 18% of the inactive sites showed the microorganism. Certain microorganisms including Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, Eikenella corrodens and Wolinella recta were primarily or exclusively correlated with active disease lesions. These findings support the hypothesis that elevated systemic antibodies to periodontopathic bacteria are reflective of subgingival colonization and exist as a response to a bacterial infection at disease-active sites.

Adolescent↗
PubMed1987

Difficulties encountered in the search for the etiologic agents of destructive periodontal diseases.

The present paper outlines some of the difficulties encountered in the search for the etiologic agents of destructive periodontal diseases. These include technical problems such as acquiring an appropriate microbial sample, as well as difficulties in the dispersion, cultivation and identification of isolates in that sample. Many of these difficulties are currently being successfully addressed. A second set of problems is more conceptual in nature. These include difficulties in distinguishing between periodontal diseases and determining the state of activity of periodontal lesions. In addition, complexes of organisms and/or sequences of species may be involved in the progress of lesions. A further problem is encountered in attempting to distinguish overgrowths of opportunistic species from increases in proportions of true pathogens. Finally, it appears likely that different infections occur at the same time in a single oral cavity. The technical and conceptual difficulties eventually filter down to the data analytical step and present numerous problems to the analyst. With all of these difficulties in mind, it is not surprising that the etiologic agents of destructive periodontal diseases are not clearly defined. However, improvement in technological assessments of the microbiota and clinical evaluation of the disease should permit reasoned approaches to be taken. The delineation of the etiologic agents of destructive periodontal diseases will be, of necessity, a multistage iterative process. Etiologic agents will be suggested by predominant cultivable studies and hypotheses concerning subsets of these agents tested using more specific procedures such as selective media, immunofluorescent techniques or DNA probes.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacteria↗
PubMed1986

Frequency distributions of periodontal attachment loss. Computer simulation.

3 patterns of attachment loss were described based on curve fitting the frequency distributions of baseline attachment level measurements of 61 subjects with destructive periodontal diseases. The frequency distributions of attachment level measurements of 30 group I individuals were satisfactorily fit by attachment level measurements of 30 group I individuals were satisfactorily fit by the sum of 2 normal curves, while those of 14 group II individuals were fit by the sum of 3 normal curves. Frequency distributions of 17 group III subjects were fit by a single normal curve. A computer algorithm was used to simulate attachment level loss frequency distributions by varying the "burst size" at active lesions and by imposing "immunity" for varying periods of time on sites which had been attacked. Frequency distributions of group I subjects could be simulated using burst sizes between 0.3 and 3.4 mm. These subjects could be divided into 2 groups: 14 subjects with localized minimal attachment loss required an average burst size of less than 1 mm, while 16 subjects with more destruction at diseased sites required an average burst size of greater than 1 mm to simulate their frequency distributions. Frequency distributions of 16 of 17 group III subjects could be simulated using an average burst size of less than 1 mm. However, the frequency distributions could also be simulated using larger burst sizes with the imposition of "immunity" for substantial periods of time at the attacked sites. The frequency distributions of group II subjects were more difficult to simulate.(ABSTRACT TRUNCATED AT 250 WORDS)

Computers↗
PubMed1986

Frequency distributions of periodontal attachment loss. Clinical and microbiological features.

The present investigation attempted to determine if the pattern of past periodontal destruction could be concisely summarized, and related to other clinical and microbiological parameters. 61 subjects between the ages of 12 and 61 years with destructive periodontal disease were evaluated at 6 sites per tooth for redness, plaque, suppuration, bleeding on probing, pocket depth, and attachment level. The frequency distribution of baseline attachment level measurements was computed for each individual. A curve fitting algorithm was used to fit the frequency distribution to 1-, 2-, and 3-term normal distributions. The parameters of the fit could be used to summarize concisely all of the frequency distributions. 3 major patterns of attachment loss could be distinguished. Pattern I required a two-term distribution with localized destruction at less than 34% of sites and was further divided into 3 groups, depending on average attachment loss at diseased sites. The means of the second peak for the subgroups were 2.7, 5.3, and 8.6 mm, respectively. Pattern II exhibited more widespread disease (greater than 33% of sites affected) with multiple peaks in the frequency distribution requiring a 3-term distribution for satisfactory fit. However, a significant proportion of sites was not affected. Pattern III exhibited a single-peaked normal distribution in which virtually all sites were affected. Mean attachment levels of the peaks in this group ranged from 2.7 to 8.4 mm. 23 of the 61 subjects showed significant attachment loss at 1 or more sites during the course of bi-monthly monitoring, as determined by the tolerance method of analysis. Subgingival plaque samples were taken from these active sites and matched with control sites prior to therapy. The proportions of Fusobacterium nucleatum, Streptococcus intermedius, and Eikenella corrodens were significantly elevated in active and control sites of subjects in groups II and III combined (the widespread disease groups), and proportions of Actinobacillus actinomycetemcomitans and Propionibacterium acnes were elevated in active and control sites of the more localized disease group I subjects. Group I subjects showed a 13- to 15-fold decrease in hazard rates of periodontal sites after Widman flap surgery and systemic tetracycline, whereas groups II and III subjects showed 2-to 6-fold decreases.

Adolescent↗
PubMed1986

Attachment level changes in destructive periodontal diseases.

The present communication attempts to summarize some of the features of attachment loss which are of interest to the clinician and the statistician analyzing data from clinical trials. These include the measurements employed to detect changes in attachment level, the nature of the destructive disease process and the effects of therapy on the attachment level measurements. Although there are several difficulties associated with the attachment level measurement, at the present time it appears to be the best estimator of periodontal attachment available. The overall standard deviation of this measurement in greater than 46,000 replicate measurements at periodontal sites in 58 subjects was 0.78 mm (range 0.4 to 1.2 mm). In the periodontally healthy subject, the length of the attachment measured around 28 teeth is approximately 700 mm. Therefore, there are approximately 1400 adjacent points along the periodontal attachment where a measurement could be made using a periodontal probe with a 0.5 mm diameter tip. If 6 measurements were recorded per tooth, then approximately 12% of the possible probable points would be evaluated. Recent data indicate that destructive periodontal diseases progress with acute bursts of activity rather than as slowly progressive, continual processes. Such findings suggest new models of attachment loss progression. In one likely model, destructive periodontal diseases would progress by asynchronous bursts of activity at individual sites which occur with greater frequency during a finite period of time in an individual's life. 3 major patterns of attachment loss could be distinguished when frequency distributions of attachment level measurements were constructed for 61 destructive periodontal disease subjects. Pattern I (30 subjects) exhibited a bimodal distribution with localized destruction occurring at less than 34% of sites. Pattern II (14 subjects) exhibited more widespread disease (greater than 33% of sites affected) with a trimodal frequency distribution. Pattern III (17 subjects) exhibited a unimodal distribution in which virtually all sites were affected. The proportions of Fusobacterium nucleatum, Streptococcus intermedius and Eikenella corrodens in subgingival plaque samples were significantly elevated in sites of subjects with patterns II and III (the widespread disease groups). Bacteroides intermedius, Streptococcus uberis and Actinobacillus actinomycetemcomitans were elevated in sampled sites of localized disease subjects (pattern I). The effects of therapy by Widman flap surgery and systemic tetracycline were examined by several statistical analyses.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Intraclass correlations of periodontal measurements.

Components of variance and intraclass correlation coefficients were computed for changes in attachment level, pocket depth, gingival and plaque index scores for 5 groups of treated periodontal disease patients and 1 group of untreated subjects with periodontal disease. The intraclass correlation coefficients for attachment level change ranged from 0.011 to 0.165 (median 0.067), while intraclass correlation coefficients for pocket depth changes ranged from -0.009 to 0.178 (median 0.071). These intraclass correlation coefficients were much lower than those computed for changes in measurements of plaque which ranged from 0.086 to 0.568 (median 0.268) or gingival inflammation which ranged from 0.119 to 0.522 (median 0.264). Intraclass correlation coefficients at baseline for pocket depths ranged from 0.000 to 0.199 (median 0.053), for plaque accumulation from 0.121 to 0.531 (median 0.222) and for gingival inflammation from 0.229 to 0.596 (median 0.391). The differences in the intraclass correlation coefficients between pocket depth and attachment level on the one hand and plaque accumulation or gingival inflammation on the other could not be explained on the basis of differences in the measurement scale employed, since collapsing measurement scales had little effect on the intraclass correlation coefficients. The observed larger intraclass correlation coefficients for changes in plaque and gingival indices suggest a larger rôle for host contribution to these measurements. In contrast, the data suggest that the major but by no means the sole factor determining the variability of attachment level or pocket depth changes is the nature of the local factors.

Chlorhexidine↗
PubMed1985

Gram negative species associated with active destructive periodontal lesions.

Apical subgingival plaque samples were taken from 19 subjects exhibiting active destructive periodontal disease. The predominant cultivable Gram negative species from 50 active sites were compared to 69 inactive sites of comparable pocket depth and attachment level loss. Active disease sites were chosen which showed a significant loss of attachment within a two-month interval. Proportions of Gram negative rods were higher in active periodontal disease sites than in inactive sites. Species which were found to be significantly elevated only in active sites were Bacteroides intermedius, "fusiform" Bacteroides, Actinobacillus actinomycetemcomitans and Wolinella recta. Fusobacterium nucleatum, Capnocytophaga gingivalis and Eikenella corrodens were found in significantly increased proportions in active sites of some subjects and inactive sites of others.

Adolescent↗
PubMed1985

Survival analysis of periodontal sites before and after periodontal therapy.

Periodontal diseases appear to progress with bursts of destructive activity at individual sites. One effect of treatment might be to diminish the frequency of such bursts. Survival analysis was employed to seek such effects on the periodontal sites of 16 individuals with prior evidence of destructive periodontal disease. The subjects were monitored at bi-monthly intervals and actively breaking down sites were detected using attachment level measurements and the tolerance method of analysis. When active sites were detected, control sites of equal pocket depth and attachment loss were selected and microbiological and immunological samples were taken. The subjects were treated by modified Widman flap surgery and systemically administered tetracycline. On completion of therapy, bi-monthly monitoring was reinstituted. Life tables were constructed for periodontal sites in each of the 16 subjects prior to and after therapy. A site losing more than 3 mm of attachment at any time interval was considered to have relapsed or "died". Survivor functions were calculated for each time period indicating the % of sites which survived at any time. The subjects were divided into 3 categories on the basis of post-therapy survivor functions. The annual hazard rate in 9 good treatment response subjects (group 1) was reduced from 0.10/year to 0.01/year. The hazard rate of 5 intermediate treatment response subjects (group 2A) was reduced from 0.16/year to 0.04/year and that of 2 poor treatment response subjects (group 2B) from 0.15/year to 0.07/year. Group 2A and 2B individuals were combined and differences were sought in clinical, microbiological and immunological parameters between the good and poor treatment response groups. 5 out of 7 of the poor responding individuals showed elevated humoral antibody responses to 3 or more gram-negative subgingival species tested. Many of the elevated responses in this group were to organisms which are widely distributed and return quickly after therapy such as Fusobacterium nucleatum, Eikenella corrodens, Bacteroides intermedius and Capnocytophaga sputigena. The predominant cultivable microbiota in subgingival samples taken prior to therapy from the good responding group had significantly greater proportions of Actinobacillus actinomycetemcomitans, C. ochracea and B. intermedius than the poor responding group. The latter group showed significantly elevated proportions of F. nucleatum, Peptostreptococcus micros and Streptococcus intermedius.

Adolescent↗
PubMed1985

Improved periodontal conditions following therapy.

The aim of the present clinical trial was to evaluate the effect of different modes of periodontal therapy on patients with moderately advanced periodontal disease and to express the findings in terms of probing pocket depth and attachment level alterations at periodontal sites with different initial probing depths. The material consisted of 16 patients, 35-65 years of age. Following a Baseline examination including assessments of oral hygiene status, gingival conditions, probing pocket depths and probing attachment levels, the patients were subjected to periodontal treatment. A "split-mouth" design approach of therapy was used and the jaw quadrants were randomly selected for the following different treatment procedures: (1) scaling and root planning, (2) scaling and root planing in conjunction with a gingivectomy procedure, (3) scaling and root planing in conjunction with an apically repositioned flap procedure without bone recontouring, (4) scaling and root planing in conjunction with an apically repositioned flap procedure including bone recontouring, (5) scaling and root planing in conjunction with a modified Widman flap procedure without bone recontouring and (6) scaling and root planing in conjunction with a modified Widman flap procedure including bone recontouring. The patients were following active treatment enrolled in a supervised maintenance care program including "professional tooth cleaning" once every 2 weeks during a 6-month period of healing, after which a final examination was performed. The investigation demonstrated that active therapy including meticulous subgingival debridement resulted in a low frequency of gingival sites which bled on probing, a high frequency of sites with shallow pockets (less than 4 mm) and the disappearance of pockets with a probing depth of greater than 6 mm. Between the Baseline examination and the 6-month re-examination, the probing attachment level for initially shallow pockets remained basically unaltered, but with a tendency of a minor apical shift. This occurred in all 6 treatment groups. For sites with initial probing depths of 4-6 mm and greater than 6 mm, there was in all groups some gain of probing attachment. This gain was most pronounced in the initially deeper (greater than 6 mm) pockets. With the use of regression analysis, the "critical probing depth" (CPD) value (i.e. the initial probing depth value below which loss of attachment occurred as a result of treatment and above which gain of probing attachment level resulted) was calculated for each of the 6 methods of treatment used. A comparison of the CPD-values between the 6 treatment groups did not reveal any major differences.

Adult↗
PubMed1985

Effect of subgingival scaling on systemic antibody responses to oral microorganisms.

The effects of scaling and root planing treatment on systemic antibody responses were studied in patients with periodontal disease and in normal subjects. Immunoglobulin G antibody in serum to a battery of oral microorganisms was assessed in an enzyme-linked immunosorbent assay before and after treatment in 31 individuals. The majority (96%) of the diseased patients exhibited elevated antibody to one or more of the microorganisms before the scaling regime. Significant increases in antibody levels in serum were noted in 16 of 19 patients after scaling, whereas only 2 of 12 nonscaled subjects showed similar changes during monitoring intervals of up to 3 years. The bacterial specificities of the increases were found to differ among the patients; however, a significant correlation to preexisting elevated antibody levels was observed. Peak levels of responses were noted at approximately 2 to 4 months posttreatment; antibody returned to pretreatment levels by 8 to 12 months. The predominant organisms for which changes were noted included the black-pigmented Bacteroides spp., Eikenella corrodens, Campylobacter concisus, and Actinobacillus actinomycetemcomitans. In 18 of 19 instances, the homologous microorganism was detected in the subgingival plaque when elevated antibody was present after treatment. These findings indicated that specific changes in host systemic responses accompany scaling and root planing treatment of periodontal disease patients. These alterations in the host response may provide an additional means by which successful therapy can be accomplished.

Actinobacillus↗
PubMed1984

The Papillon-Lefèvre syndrome: neutrophil dysfunction with severe periodontal disease.

Two cases of Papillon-LeF evre are described. Both siblings demonstrated neutrophil dysfunction and severe precocious periodontal disease. The neutrophil locomotion defect was characterized by a decreased migration toward a chemotactic factor and decreased random migration. Binding of the chemotactic factor, FMLP, to the neutrophil surface was unchanged. Both patients harbored Actinobacillus actinomycetemcomitans and showed elevated serum IgG levels. Both patients also demonstrated salivary and serum antibody to A. actinomycetemcomitans. The Papillon-LeF evre syndrome is compared with the more common localized juvenile periodontitis.

Actinobacillus↗
PubMed1984

Clinical, microbiological and immunological features associated with the treatment of active periodontosis lesions.

Clinical, microbiological and immunological factors were examined using data from a subject with periodontosis. The subject was monitored at bimonthly intervals for 26 months at 6 sites per tooth for redness, plaque, suppuration, bleeding on probing, pocket depth, and attachment level. Using attachment level measurements and the tolerance method of analysis, sites with active disease and control (inactive) sites of equal pocket depth were selected. Subgingival plaque samples were taken from these sites for predominant cultivable and dark field evaluation before, and 5 and 13 months after treatment by Widman flap surgery and systemic tetracycline. 50 isolates from each of 5 sites monitored before and after treatment were characterized and, if possible, identified. Active sites showed between 2 and 6 mm of attachment loss prior to therapy and "gained" between 2 and 9 mm of attachment after therapy. The control sites "gained" 0 to 1 mm of attachment after therapy. Bleeding on probing was significantly reduced after treatment, whereas plaque accumulation increased significantly in the sampled sites. Similar changes were seen in the remaining sites. The proportions of Actinobacillus actinomycetemcomitans and Selenomonas sputigena were elevated in active sites, while proportions of Bacteroides intermedius were elevated in control sites. 5 months after treatment, proportions of A. actinomycetemcomitans, S. sputigena and Eikenella corrodens were significantly decreased in the previously active sites and proportions of B. intermedius and E. corrodens were significantly decreased in the control sites. 13 months after therapy, the proportions of Fusobacterium nucleatum and Capnocytophaga species had increased. Multiple linear regression analysis was used to examine models which could "predict" the outcome, attachment level change in the previous monitoring period. The proportions of A. actinomycetemcomitans and S. sputigena, which were associated with destruction, coupled with the proportions of Streptococcus sanguis II and Campylobacter concisus which were associated with "gain" could predict prior attachment level change with an r2 of 0.93. Humoral antibody response to A. actinomycetemcomitans and C. sputigena significantly increased in a period in which multiple actively breaking down sites were detected. Antibody responses to 20 other species tested did not significantly change during the course of monitoring. Crevicular fluid and tissue levels of antibody to A. actinomycetemcomitans were elevated in 5 of 6 active destructive lesions prior to therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

New concepts of destructive periodontal disease.

The most common forms of destructive periodontal disease have been thought to slowly and continuously progress until treatment or tooth loss. Recently, data have become available which are inconsistent with this "continuous disease" hypothesis. Data from longitudinal monitoring of periodontal attachment levels and alveolar bone in humans and in animals suggest that periodontal disease progresses by recurrent acute episodes. In addition, rates of attachment loss have been measured in individual sites which are faster than those consistent with the continuous disease hypothesis or slower than those expected from estimates of prior loss rates. To account for these observations, a model of destructive periodontal disease is described in which bursts of activity occur for short periods of time in individual sites. These bursts appear to occur randomly at periodontal sites throughout the mouth. Some sites demonstrate a brief active burst of destructive periodontal disease (which could take a few days to a few months) before going into a period of remission. Other sites appear to be free of destructive periodontal disease throughout the individual's life. The sites which demonstrate destructive periodontal activity may show no further activity or could be subject to one or more bursts of activity at later time periods. Comparison of monitored loss rates for a year with mean loss rates prior to monitoring suggested that there may be relatively short periods in an individual's life in which many sites undergo periodontal destruction followed by periods of extended remission. An extension of the random disease model is also suggested in which bursts of destructive periodontal disease activity occur with higher frequency during certain periods of an individual's life.

Adult↗