Forms Of Periodontitis Research Articles

Immunoglobulin G profiles in different forms of periodontitis.

Races and Gm(23) allotypes can modify the serum levels of IgG subclasses. The average serum levels of IgG subclasses of African-Americans have been reported to be higher than those of Caucasians in both healthy young adults and patients with aggressive periodontitis; Gm(23)-positive subjects generally had higher IgG2 levels than Gm(23)-negative subjects. We examined serum immunoglobulin G (IgG) concentrations in Taiwanese patients with different forms of periodontitis. The serum levels of four IgG subclasses were determined by enzyme-linked immunosorbent assay and Gm(23) allotypes were verified by radial immunodiffusion tests in 50 patients with chronic periodontitis, 30 patients with aggressive periodontitis, and 74 healthy controls. There were no differences in the concentrations of four IgG subclasses in patients with chronic periodontitis compared with age-matched controls. However, in subjects younger than 35 years, levels of IgG2 were significantly elevated in patients with aggressive periodontitis compared with controls. We also found significant differences in IgG2 levels within the control group when stratified by age (< or = 35 years and > 35 years). Gm(23) allotypes were not correlated with the serum levels of IgG2 in either patient group. Microbial challenge might not provoke significant changes in systemic IgG response in patients with chronic periodontitis. However, in patients with aggressive periodontitis, IgG2 levels were increased when compared with age-matched controls. Gm(23) allotypes had no influence on IgG2 levels in well-established generalized chronic periodontitis or aggressive periodontitis.

Detection of highly and minimally leukotoxic Actinobacillus actinomycetemcomitans strains in patients with periodontal disease.

This study examined the prevalence of highly and minimally leukotoxic Actinobacillus actinomycetemcomitans in patients with periodontal disease. Pooled subgingival plaque samples from 136 patients with some form of periodontal disease were examined. Subjects were between 14 and 76 years of age. Clinical examinations included periodontal pocket depth (PD), plaque index (PI) and bleeding index (BI). The obtained plaque samples were examined for the presence of highly or minimally leukotoxic A. actinomycetemcomitans strains by the polymerase chain reaction (PCR). Chi-square and logistic regression were performed to evaluate the results. Forty-seven subjects were diagnosed with gingivitis, 70 with chronic periodontitis and 19 with aggressive periodontitis. According to chi-square there was no significant correlation detected between PD (chi2 = 0.73), PI (chi2 = 0.35), BI (chi2 = 0.09) and the presence of the highly leukotoxic A. actinomycetemcomitans. The highly leukotoxic A. actinomycetemcomitans strains were correlated with subjects that were 28 years of age and younger (chi2 = 7.41). There was a significant correlation between highly leukotoxic A. actinomycetemcomitans and aggressive periodontitis (chi2 = 22.06). This study of a Brazilian cohort confirms the strong association between highly leukotoxic A. actinomycetemcomitans strains and the presence of aggressive periodontitis.

HHV-6, HHV-7, HHV-8 in gingival biopsies from chronic adult periodontitis patients. A case-control study.

Recent reports have suggested that various herpesviruses may be involved in the occurrence and progression of different forms of periodontal disease. The objective of the present study was to investigate the presence of the novel herpesviruses HHV-6, HHV-7 and HHV-8 in gingival biopsies from patients affected by chronic adult periodontitis. As control, gingival biopsies from periodontally healthy subjects were analysed. Gingival biopsies were harvested from 23 volunteers: 13 patients affected by chronic adult periodontitis (CAP) and 10 periodontally healthy subjects. Each CAP patient contributed two biopsies involving the epithelium and connective tissue facing the sulcus/periodontal pockets: one biopsy from a site having a probing pocket depth (PPD) > or =5 mm and presenting with bleeding upon probing (affected site) at the time of biopsy collection, and the other biopsy from a site with PPD< or =3 mm and without bleeding on probing (nonaffected site). After DNA extraction, nested PCR was used in herpesvirus identification. HHV-6 DNA sequences were detected in one non-affected site (8%) and no affected sites (0%) of CAP patients. One biopsy (10%) in healthy subjects revealed HHV-6 positivity. Tissue specimens in 10/13 CAP patients (77%) and 7/10 healthy subjects (70%) contained HHV-7 DNA. HHV-7 prevalence in affected and nonaffected sites of CAP patients was 77% and 54%, respectively. HHV-8 was detected in 7.7% of CAP patients and 0% of healthy subjects. Gingival tissue may act as a reservoir for HHV-7. A high prevalence of HHV-7 was detected in both periodontally diseased and healthy individuals. The prevalence of HHV-6 and -8 was similarly low in both groups. Our data do not support an association of investigated herpesvirus species with destructive periodontal disease.

Biofilm growth and detachment of Actinobacillus actinomycetemcomitans.

The gram-negative, oral bacterium Actinobacillus actinomycetemcomitans has been implicated as the causative agent of several forms of periodontal disease in humans. When cultured in broth, fresh clinical isolates of A. actinomycetemcomitans form tenacious biofilms on surfaces such as glass, plastic, and saliva-coated hydroxyapatite, a property that probably plays an important role in the ability of this bacterium to colonize the oral cavity and cause disease. We examined the morphology of A. actinomycetemcomitans biofilm colonies grown on glass slides and in polystyrene petri dishes by using light microscopy and scanning and transmission electron microscopy. We found that A. actinomycetemcomitans developed asymmetric, lobed biofilm colonies that displayed complex architectural features, including a layer of densely packed cells on the outside of the colony and nonaggregated cells and large, transparent cavities on the inside of the colony. Mature biofilm colonies released single cells or small clusters of cells into the medium. These released cells adhered to the surface of the culture vessel and formed new colonies, enabling the biofilm to spread. We isolated three transposon insertion mutants which produced biofilm colonies that lacked internal, nonaggregated cells and were unable to release cells into the medium. All three transposon insertions mapped to genes required for the synthesis of the O polysaccharide (O-PS) component of lipopolysaccharide. Plasmids carrying the complementary wild-type genes restored the ability of mutant strains to synthesize O-PS and release cells into the medium. Our findings suggest that A. actinomycetemcomitans biofilm growth and detachment are discrete processes and that biofilm cell detachment evidently involves the formation of nonaggregated cells inside the biofilm colony that are destined for release from the colony.

Defining and classifying periodontitis: need for a paradigm shift?

The past two decades have witnessed a large number of proposals for the classification of periodontitis. These proposals are all founded in an essentialistic disease concept, according to which periodontitis is a link between the causes and the signs and symptoms of periodontitis. Essentialistic definitions are necessarily rather imprecise and thereby subject to multiple interpretations. Consequently, it remains unknown to what extent current knowledge regarding 'different' forms of periodontitis is based on the 'same' type of patients. However, periodontitis is a syndrome, the clinical manifestations of which may come in all sizes. Thereby, periodontitis has no diagnostic truth, just as there is no natural basis for a sharp distinction between health and disease or between 'different' forms of periodontitis. Recognition of these facts and adoption of a nominalistic approach to the definition of periodontitis is needed to provide a rational framework for the development of a classification system that meets the needs of both clinicians and scientists.

Constitutionally hyperreactive neutrophils in periodontitis.

Neutrophils constitute the first line of host defense, but their extracellular release of oxygen radicals and proteases may cause tissue destruction. Conflicting results have been reported on the neutrophilic production of oxygen radicals in periodontal patients. These may vary with different forms of periodontitis, the pathway of neutrophil activation studied, and the influence of smoking. Venous blood was taken from 15 patients with severe chronic periodontitis, treated with scaling, with or without surgery. They were matched by age and gender to periodontally healthy controls; all participants were non-smokers. Peripheral neutrophils from the participants were activated with IgG-opsonized bacteria, complement-opsonized zymosan, or phorbol myristate acetate (PMA). The total release of oxygen radicals was measured with luminol-enhanced chemiluminescence (CL) and the extracellular release of oxygen radicals with isoluminol-enhanced CL. Antibodies to endotoxin and the concentrations of interleukin (IL)-8 and acute phase proteins in plasma were analyzed to see if these parameters were related to hyperreactivity of the neutrophils. Neutrophils from periodontal patients had significantly higher CL when activated via the FcgammaR pathway, measured as both total generation of oxygen radicals and extracellular generation. The neutrophil generation of oxygen radicals was also higher in patients when complement-opsonized zymosan or PMA was used, but these differences were less pronounced. No significant differences in plasma proteins were found. Our findings suggest that the increased CL from peripheral neutrophils in periodontitis may be related to a constitutionally greater responsiveness of the Fcgamma-receptor.

Sister chromatid exchange (SCE) analysis in periodontitis.

Emerging data indicate that genetic factors may be associated with the etiopathogenesis of aggressive periodontitis. Sister chromatid exchange (SCE) is a sensitive method that might reflect an instability of DNA or a deficiency of DNA repair. The aim of the present study was to investigate SCE frequency of patients with different forms of periodontal disease and to determine whether this cytogenetic marker in patients with aggressive periodontitis can be differential compared to patients with chronic periodontitis and control subjects. SCE was analysed in peripheral blood lymphocyte chromosomes of 13 patients with generalised aggressive periodontitis (G-AP), 10 patients with chronic periodontitis (CP) and 10 control subjects. The periodontal parameters of probing depth, clinical attachment level, the presence of bleeding on probing and plaque were recorded. Peripheral blood lymphocytes obtained from both patient groups and control subjects were cultured in the presence of 5-Bromo-2-deoxyuridine in complete darkness for 72 h. For scoring SCE frequency, 20 metaphases were studied from each donor. The frequency of SCE was found to be 6.7 +/- 0.9 per cell in patients with G-AP, 6.5 +/- 1.5 per cell in CP patients and 6.9 +/- 1.1 in control subjects. No statistically significant differences were found between groups (p > 0.05). The data indicate that there the cyotogenetic damage in the aggressive type of periodontal disease is not greater than in chronic periodontitis and control subjects. Although no aberrant cytogenetic damage was observed in different forms of periodontitis compared to control, this does not discount the importance of other genetic factors in the pathogenesis of periodontal disease.

In vitro antioxidant activities of mouthrinses and their components.

Several forms of periodontal diseases (PD) are often associated with activated phagocytosing leukocytes and contemporary free radical production. Host antioxidant defenses could benefit from mouthrinses used as adjuncts to counteract plaque-associated bacteria. The aim of the present study was to determine possible antioxidant activity (AA) of a number of antiseptic mouthrinses and of their stated active principles (AP), regardless of their efficacy as antimicrobial agents. The antioxidant activities of 11 mouthrinses and their active principles were tested with a specific spectrophotometric method. Comet assay was used to test whether pure chemical antioxidant activity actually corresponded to prevention of in vitro DNA fragmentation. Methylsalicylate-containing mouthrinses were the most effective. Several compounds, and some vehicles, behaved as antioxidants. Fibroblast DNA fragmentation was limited by preincubation with methylsalicylate-containing mouthrinse but was unaffected by treatment with chlorexidine. The results described herein indicate that several mouthrinses possess AA; such a property could be ascribed to either AP or vehicles or both. All the data were obtained in systems in vitro and the demonstration of in vivo AA is necessary. These findings could be useful in the treatment of some forms of PD and should be considered when arranging new mouthrinse formulations.

The Use of Chemotherapeutic Agents in Localized Periodontal Pockets

Gingival diseases are the most widely dispersed diseases in the United States. In some patients, periodontal disease appears in a generalized form, but more often it appears in localized areas. Furthermore, after treatment with scaling and root planing in generalized cases, the disease is often reduced to a few local areas in the patient's mouth. Because periodontitis is a bacterial infection with known pathogenic microorganisms, the local delivery of antimicrobial agents has been considered to be a possible solution for treating and controlling localized forms of periodontal disease. Three local chemotherapeutic agents are reviewed in this paper: tetracycline fiber, doxycycline gel, and chlorhexidine chip. With the advancement of local drug delivery systems, restorative dentists, periodontists, and their patients have new alternatives for the treatment of periodontal disease. Local chemotherapeutic agents offer an additional mode of therapy and should be used on a case-by-case basis, not necessarily as an initial treatment.

Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment.

Periodontal disease is perhaps the most common chronic infection in adults. Evidence has been accumulating for the past 30 years which indicates that almost all forms of periodontal disease are chronic but specific bacterial infections due to the overgrowth in the dental plaque of a finite number of mostly anaerobic species such as Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. The success of traditional debridement procedures and/or antimicrobial agents in improving periodontal health can be associated with the reduction in levels of these anaerobes in the dental plaque. These findings suggest that patients and clinicians have a choice in the treatment of this overgrowth, either a debridement and surgery approach or a debridement and antimicrobial treatment approach. However, the antimicrobial approach, while supported by a wealth of scientific evidence, goes contrary to centuries of dental teaching that states that periodontal disease results from a "dirty mouth." If periodontal disease is demonstrated to be a risk factor for cardiovascular disease and stroke, it will be a modifiable risk factor since periodontal disease can be prevented and treated. Since the antimicrobial approach may be as effective as a surgical approach in the restoration and maintenance of a periodontally healthy dentition, this would give a cardiac or stroke patient and his or her physician a choice in the implementation of treatment seeking to improve the patient's periodontal condition so as to reduce and/or delay future cardiovascular events.

Elevated blood glucose levels in patients with severe periodontal disease.

The rôle of diabetes mellitus in various forms of periodontal disease was investigated intensively in the past; some studies have also indicated an impact of periodontal inflammation on diabetic balance. The purpose of this study was to evaluate the reciprocal relationship between abnormal serum glucose levels and elevated CPITN scores in non-diabetic patients. 10,590 subjects were analyzed for normal and abnormal (higher than 120 mg/dl) serum glucose levels, their periodontal status reflected as CPITN was correlated with their glucose level category. The results of the present study reflect a significant association between elevated blood glucose levels (higher than 120 mg/dl) and CPITN scores of 4.5 with an odds ratio of 2.46. A strong association exists between abnormal serum glucose level and periodontal disease as manifested by CPITN score.

Microbiological characteristics of subgingival microbiota in adult periodontitis, localized juvenile periodontitis and rapidly progressive periodontitis subjects

To describe the prevalence of the cultivable subgingival microbiota in periodontal diseases and to draw attention to the polymicrobial nature of periodontic infections. The study population consisted of 95 patients, 51 females and 44 males, aged 14-62 years. Twenty-nine patients exhibited adult periodontitis (AP), six localized juvenile periodontitis (LJP), and 60 rapidly progressive periodontitis (RPP). Two to four pooled bacterial samples were obtained from each patient. Samples were collected with sterile paper points from the deepest periodontal pockets. The samples were cultured under anaerobic and microaerophilic conditions using selective and non-selective media. Isolates were characterized to species level by conventional biochemical tests and by a commercial rapid test system. Prevotella intermedia and Capnocytophaga spp. were the most frequently detected microorganisms in all diagnostic groups. Porphyromonas gingivalis and Peptostreptococcus micros were found more frequently in AP and RPP patients, while Actinobacillus actinomycetemcomitans and Eikenella corrodens were associated with AP, LJP and RPP patients. The other bacterial species, including Actinomyces spp., Streptococcus spp. and Eubacterium spp., were detected at different levels in the three disease groups. The data show the complexity of the subgingival microbiota associated with different periodontal disease groups, indicating that the detection frequency and levels of recovery of some periodontal pathogens are different in teeth affected by different forms of periodontal disease.

Altered chemotactic behavior of crevicular PMNs in different forms of periodontitis.

Polymorphonuclear neutrophils (PMN) are the predominant host defence cells in the gingival sulcus. Previous work demonstrates that the in vitro phagocytosis of crevicular cells in localised early onset periodontitis (LEOP) and generalised early onset periodontitis (GEOP) lesions is diminished. The present study extends this work by characterizing the chemotaxis function of crevicular fluid (CF) PMNs in various forms of periodontitis. We investigated 7 patients with LEOP, 11 patients with GEOP, 12 patients with adult periodontitis (AP) and 2 age- and sex-matched healthy control groups. The two deepest sites of each quadrant in test and control subjects were selected for crevicular sampling. Chemotaxis was performed in a micro chamber (moist atmosphere, 5% CO2, 37 degrees C, 30 min) using N-formyl-methionyl-leucyl-phenylalanine (FMLP, 1 x 10(-7) mol FMLP/l) as a chemoattractant. The total chemotaxis was defined as the difference between the number of cells migrating towards FMLP minus the number of cells migrating towards PBS, counted in 20 randomly selected fields. Membranes were examined microscopically at 400 x magnification. The chemotactic activity in the adult periodontitis group was significantly higher compared to the age-related control group. However, we found a statistically significant reduction of chemotactic activity in LEOP and GEOP patients compared to the controls. These results indicate an increase of chemotactic activity from CF-PMN in patients with adult periodontitis, but on the other hand, a significant reduction of chemotactic responsiveness of these cells in LEOP and GEOP lesions.

Microbial comparison of smoker and non‐smoker adult and early‐onset periodontitis patients by polymerase chain reaction

A number of bacterial species are involved in the aetiology of periodontitis and include Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus and Treponema denticola. Several studies have shown differences in the microflora between the various forms of periodontal disease. It is recognised that smoking is a risk factor for periodontal disease, but there are conflicting reports on whether or not smoking has an effect on the periodontal microflora. We utilised the polymerase chain reaction to determine the presence of A. actinomycetemcomitans, P. gingivalis, P. intermedia, B. forsythus and T. denticola in subgingival plaque samples in 33 adult periodontitis (AP) patients and 24 generalized early-onset periodontitis (GEOP) patients prior to treatment. When GEOP and AP patients were compared there were significant differences in the number of positive patients and sites for both A. actinomycetemcomitans and B. forsythus (p=0.0023 and 0.00001, respectively). No statistically significant differences in the prevalence of these organisms were found between smoker and non-smoker groups. These results confirm that AP and GEOP sites harbour varied microflora, but show that B. forsythus and A. actinomycetemcomitans were detected to a significantly greater extent in this group of GEOP than in the AP patients investigated. Our findings do not support the hypothesis that smokers have significant differences in the prevalence of periodontal pathogens from non-smokers.

Passive immunization against dental caries and periodontal disease: development of recombinant and human monoclonal antibodies.

Indigenous micro-organisms in the oral cavity can cause two major diseases, dental caries and periodontal diseases. There is neither agreement nor consensus as to the actual mechanisms of pathogenesis of the specific virulence factors of these micro-organisms. The complexity of the bacterial community in dental plaque has made it difficult for the single bacterial agent of dental caries to be determined. However, there is considerable evidence that Streptococcus mutans is implicated as the primary causative organism of dental caries, and the cell-surface protein antigen (SA I/II) as well as glucosyltransferases (GTFs) produced by S. mutans appear to be major colonization factors. Various forms of periodontal diseases are closely associated with specific subgingival bacteria. Porphyromonas gingivalis has been implicated as an important etiological agent of adult periodontitis. Adherence of bacteria to host tissues is a prerequisite for colonization and one of the important steps in the disease process. Bacterial coaggregation factors and hemagglutinins likely play major roles in colonization in the subgingival area. Emerging evidence suggests that inhibition of these virulence factors may protect the host against caries and periodontal disease. Active and passive immunization approaches have been developed for immunotherapy of these diseases. Recent advances in mucosal immunology and the introduction of novel strategies for inducing mucosal immune responses now raise the possibility that effective and safe vaccines can be constructed. In this regard, some successful results have been reported in animal experimental models. Nevertheless, since the public at large might be skeptical about the seriousness of oral diseases, immunotherapy must be carried out with absolute safety. For this goal to be achieved, the development of safe antibodies for passive immunization is significant and important. In this review, salient advances in passive immunization against caries and periodontal diseases are summarized, and the biotechnological approaches for developing recombinant and human-type antibodies are introduced. Furthermore, our own attempts to construct single-chain variable fragments (ScFv) and human-type antibodies capable of neutralizing virulence factors are discussed.

A PRACTICAL APPROACH TO THE DIAGNOSIS AND TREATMENT OF PERIODONTAL DISEASE

Both nonsurgical and surgical periodontal therapies are important in the control of most forms of periodontal disease. Sometimes, nonsurgical therapy is adequate to control the disease in mild cases and to slow progression and maintain periodontal stability in more advanced cases. Other times, both therapies may be indicated to obtain satisfactory results. The author presents treatment guidelines and recommendations for periodontal therapy. The author searched the dental literature for information pertaining to periodontal therapy. The author found evidence-based data to support the effectiveness of nonsurgical and surgical periodontal therapy in controlling periodontal disease. Nonsurgical periodontal therapy requires time, effort, and good diagnostic and clinical skills to obtain satisfactory results. The results are determined by evaluating the patient's periodontal disease after active therapy, at which time additional surgical or nonsurgical treatment may be recommended. Evaluation should continue throughout the lifelong supportive phase of periodontal therapy. Clinicians should continue to develop and enhance their diagnostic skills, assess factors that affect diagnosis and prognosis, formulate a comprehensive treatment plan, render appropriate treatment, evaluate the outcome and determine when periodontal care is indicated. Failure to comply with monitoring the patient's periodontal status may lead to uncontrolled disease and eventually premature tooth loss. Premature tooth loss can be prevented through patient education and application of evidence-based nonsurgical and surgical therapy.

Analysis of In Situ Protease Activity in Chronic Adult Periodontitis Patients: Expression of Activated MMP‐2 and a 40 kDa Serine Protease

Periodontitis is characterized by extensive destruction of the gingival tissues and associated supporting structures of the teeth. Although the pathogenesis of the various forms of this disease is not completely understood, host-derived proteases are believed to have an important role. In this study, we analyzed human tissue samples from chronic adult periodontitis patients to assess the levels of specific proteases and determine the effect of pH and tetracyclines on their activity. Gingival tissue samples were obtained from patients with chronic adult periodontitis (probing depths ranged from 5 to 9 mm) and periodontally healthy controls. Tissue extracts were prepared and analyzed for protease activity by zymography and Western blotting. Maximal protease activity from clinically normal and diseased tissues was observed at pH 8. Latent matrix metalloproteinase (MMP)-9 and MMP-2 were expressed in all samples examined, while active MMP-2 was detected only in tissues obtained from patients with clinical disease. The MMP activities were differentially inhibited by derivatives of tetracycline. At pH 6, a protease with a mass of approximately 40 kDa was observed in diseased samples. The enzymatic activity was inhibited by phenylmethylsulfonyl fluoride, suggesting it is a serine protease. The results of the current study substantiate the proposed role of host-derived proteases in the pathogenesis of chronic adult periodontitis. Specifically, they indicate that activated MMP-2 and a 40 kDa serine protease are involved in tissue destruction associated with this form of periodontal disease and also suggest that tissue pH influences protease activity in situ.

Milestones in periodontal research and the remaining critical issues.

A significant recent development in periodontal research has been the convergence of basic and clinical research resulting in a logarithmic increase in the rate of progress. Scientific consensus has been reached in many areas. In most populations, moderate to severe periodontitis affects a relatively small segment of adults who are at high risk. The microbial etiology is accepted and the identity of the major pathogenic bacterial species is known. The mechanisms through which resistant individuals successfully fend off the microbial challenge are known, and the immuno-inflammatory pathways activated by bacteria that underlie destruction of the alveolar bone and the connective tissues of the periodontium are reasonably well understood. The evidence shows that these pathways are held in common by all forms of periodontitis. Therapeutic modulation of these pathways is now possible, and new treatments based on such modulation are now becoming available. Although bacteria are essential for disease to occur, they are insufficient; a susceptible host is also necessary. Host susceptibility, disease progression and response to treatment are determined predominantly by heredity and environmental and acquired risk factors. Some of these can be changed while others are immutable. Concepts and procedures for treatment are generally scientifically based and appropriately applied. Preventive measures are largely successful and widely practiced in industrialized countries. Clearly, control of these ancient chronic diseases is now within our reach. In spite of the tremendous progress, many unresolved issues remain. The purpose of this paper is to summarize some of the major accomplishments of periodontal research, and identify and discuss some of the more important critical issues that still need to be addressed.

The microbiology of periodontal disease.

Periodontal disease result from mixed bacterial infections, in which both host resistance barriers and bacterial interactions are important. Approximately ten bacterial species are strongly implicated with various forms of periodontal disease, although species that cannot yet be cultivated are likely also to be relevant. New technologies have shown that pathogenic bacterial species are present in defined complexes within subgingival plaque, thus identifying specific targets for therapeutic intervention. In light of increasing antibiotic resistance amongst oral bacteria, new strategies for control of periodontal bacterial complexes must be developed that inhibit the bacterial factors necessary for colonization and destruction of host tissues.

Actinobacillus actinomycetemcomitans serotype e--biotypes, genetic diversity and distribution in relation to periodontal status.

Actinobacillus actinomycetemcomitans isolates from 356 individuals were screened for identification of serotype e in order to investigate its distribution in relation to periodontal status. From subjects with serotype e, 1-6 isolates per subject (n = 61) were genotyped using arbitrarily primed-polymerase chain reaction (AP-PCR) and apaH gene polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) analysis to determine the genetic heterogeneity within the serotype. Furthermore, one serotype e strain per subject was tested for fermentation of 8 carbohydrates for biotyping. Among patients with adult periodontitis (n = 219), localized juvenile periodontitis (n = 55) and other forms of early-onset periodontitis (n = 18) serotypes b, a and c, respectively, were the most frequently detected serotypes. Non-periodontitis subjects (n = 64) were predominantly colonized with serotype c. Serotype e was found in 30 (14%) adult periodontitis patients, 2 (11%) early-onset periodontitis patients and in 5 (8%) non-periodontitis individuals, but in none of the 55 localized juvenile periodontitis patients. AP-PCR distinguished 3 and apaH gene PCR-RFLP analysis 2 genotypes among the 61 A. actinomycetemcomitans serotype e isolates, one genotype per subject. The AP-PCR genotypes 1 and 3 represented the apaH genotype 1 and the AP-PCR genotype 2 the apaH genotype 2. On the basis of variable fermentation of galactose and xylose, 3 biotypes among A. actinomycetemcomitans serotype e were established. Contrary to the absence of A. actinomycetemcomitans serotype e in localized juvenile periodontitis patients, its detection frequency was comparable among other forms of periodontitis and periodontal health. Clinical serotype e isolates form at least 2 genetic types and 3 biotypes.