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PubMed1993

Juvenile periodontitis--pattern of progression and relationship to clinical periodontal parameters.

The present investigation was carried out 1) to identify subjects with juvenile periodontitis (JP) in a group of schoolchildren from a community with a high prevalence of periodontal diseases and with no access to preventive dental care, and 2) to study the clinical features of the disease and the progression pattern during a period of 1 yr, and the relationship of JP to clinical periodontal parameters. The periodontal condition of a group of 502 Iraqi schoolchildren (260 girls and 242 boys) was assessed radiographically and clinically at baseline. Children showing > or = 3 mm arc-shaped angular radiographic bone loss at the proximal surfaces of two or more first molars and who showed clinical attachment loss at the same sites were regarded as JP patients. A second group of children with no signs of JP were randomly chosen from the study material. One year later, the JP and the non-JP groups were re-examined radiographically and clinically to assess plaque, gingivitis and presence of calculus. The results showed that nine children (1.8%) had JP. The ratio of girls to boys was 3.5:1, and of localized to generalized forms 2:1. Mesial surfaces of first molars were more often affected than distal surfaces. Clinical assessments showed a more profound loss than was depicted radiographically. All JP patients exhibited evidence of periodontal disease progression during the following year. There were no differences between JP and non-JP children with respect to gingival inflammation, dental plaque, or calculus deposits on teeth.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Immunopathogenesis of chronic inflammatory periodontal disease: cellular and molecular mechanisms.

Recent studies of the cellular mechanisms involved in chronic inflammatory periodontal disease (CIPD) have contributed significantly to our understanding of the pathogenesis of the disease process. Functional studies have demonstrated polymorphonuclear neutrophil (PMN) chemotactic defects in some 70% of subjects with localized juvenile periodontitis while chemiluminescence data have suggested that peripheral blood PMNs from young subjects with adult periodontitis (AP) may be in a metabolically active state. Further studies have shown that stimulation of PMNs with a number of periodontopathic bacteria resulted in the production of an IL-1 inhibitor suggesting a possible regulatory role for PMNs in CIPD in addition to their established protective role. Most work on the immunoregulation of CIPD has, however, concentrated on T-cells. Recent limit dilution analysis has demonstrated the presence of periodontopathic bacteria-specific T cells in peripheral blood and the involvement and homing of these cells to the local lesions of CIPD is currently the focus of many studies. In animal studies, Actinobacillus actinomycetemcomitans (Aa)-specific T-cell clones home to the gingival tissues where they may exert a protective role. Homing and retention of lymphocytes to and in specific sites is dependent upon the expression of adhesion molecules. Recent data indicate however, that while there are increasing levels of ICAM-1, LECAM-1 and PECAM-1 expression with increasing degrees of inflammation, there are no differences between gingivitis and periodontitis lesions. Cytokine profiles may be related to the role of T-cell clones homing to the gingiva in CIPD.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggressive Periodontitis↗
PubMed1984

Host responses in periodontal diseases.

Great progress has been made in our understanding of the pathogenesis of periodontal disease, the primary role of bacteria as etiologic agents, and the critical modifying role of host responses. It is useful to consider several stages in the pathogenesis of periodontal disease - (a) colonization, (b) invasion, (c) destruction, and (d) healing - and to place into perspective the various host responses as they may affect each of these four stages (Table 5). With respect to colonization, although very little direct evidence is available, it is reasonable to suggest that antibodies, either secretory or serum-derived, acting by virtue of their ability to block attachment, could inhibit colonization by immune reduction of adherence mechanisms. With respect to invasion of the tissue, it appears that phagocytes, particularly the neutrophils, are important, acting in concert with opsonic antibody and complement in ingesting and killing the periodontal microflora before or during the early invasive process. A major advance in our understanding of the pathogenesis of periodontal diseases is the realization that the virulence of periodontopathic bacteria relates to their leukaggressive properties, allowing them to evade neutrophil protective mechanisms. Invasion of the periodontal tissues by bacterial products may be inhibited by the complexing of these products with antibody with the formation of antigen-antibody complexes that are phagocytosed and digested, particularly by scavenger phagocytes such as the macrophage. With respect to the destructive phase of periodontal disease, it is clear that the direct effect of lymphocytes mediated either through direct cytotoxic activity, or through biologically-active destructive lymphokines (such as alpha-lymphotoxin and osteoclast activating factor), can lead to tissue destruction. Macrophages, through the production of monokines, collagenase, and reactive oxygen species, can also lead to tissue destruction. The direct effects of bacterial toxins or enzymes which can lead to tissue destruction can be inhibited by complexing with antitoxic or enzyme-neutralizing antibodies. With respect to healing and fibrosis, very little direct information is available; however, it is possible that the lymphocytes and macrophages affect fibrosis by the production of chemotactic factors for fibroblasts which would be expected to bring them to the area of periodontal inflammation and also by production of fibroblast-activating factors, which then cause the fibroblasts to proliferate and produce collagen which replaces lost collagen or results in fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Aggressive Periodontitis↗
PubMed1994

The humoral response in patients with periodontitis: effects of treatment and prospects for a vaccine.

Research indicates that human periodontitis is caused by bacteria. Although the roles of host factors are not clear, these factors are important in the development of this disease. The immune response that occurs in patients with infectious diseases, and that eventually arrests the process of the infection, does not appear to happen in patients with periodontitis. This article presents the results of studies that attempted to determine if periodontitis patients mount a humoral response during the course of their infection, if the antibodies produced are protective, and, if not, why these reactions fail to occur or why they are ineffective in halting the disease.

Aggressive Periodontitis↗
PubMed1996

Clinical success in regeneration: report of a case.

Occasionally in clinical periodontics we are confronted with exceptional examples of the potential for healing. This is the report of one such instance in a young patient with a history of juvenile periodontitis and significant localized bone loss. Following relatively simple treatment, marked bone fill of a periodontal defect was observed over the course of 1 year. The factors which contributed to the remarkable healing response are considered, and the techniques used during therapy are presented.

Adult↗
PubMedDate not supplied

The role of Actinobacillus actinomycetemcomitans in periodontal disease.

The different forms of periodontitis are all associated with a distinct bacterial flora. However, a clear relationship is described between localized juvenile periodontitis (LJP) and Actinobacillus actinomycetemcomitans. Eleven LJP patients all harboured A. actinomycetemcomitans. The arrest of LJP is often impossible, due to the inability to eliminate A. actinomycetemcomitans. Therefore, antibiotic treatment was introduced in combination with the initial treatment. We studied the effect of periodontal treatment on the microflora and clinical status of periodontal disease patients using different therapies. Group 3 attained the best results (initial treatment and a combination metronidazole and amoxicillin), the group to eliminate A. actinomycetemcomitans effectively.

Actinobacillus↗
PubMed1997

Presence of bacteriophage Aa phi 23 correlates with the population genetic structure of Actinobacillus actinomycetemcomitans.

Several bacteriophages associated with the oral bacterium Actinobacillus actinomycetemcomitans have been identified. Lysogeny might affect the virulence of this bacterium, which has been implicated in the etiology of juvenile and adult periodontitis. We have determined the presence of bacteriophage Aa phi 23-related DNA sequences among 185 A. actinomycetemcomitans strains belonging to 2 well-characterized collections and have related the findings to the population genetic structure of the collections. 2 cloned Aa phi 23-specific DNA probes were used in Southern blot hybridization experiments to detect homologous sequences in whole-cell DNA of the strains. DNA from 65 (35%) of the 185 strains hybridized to either of the DNA probes. The majority (74%) of the hybridizing strains showed an identical hybridization pattern, indicating presence of phage Aa phi 23. Whole-cell DNA from the remaining hybridizing strains hybridized to the probes with different patterns, indicating that DNA sequences related to but different from phage Aa phi 23 occur in these strains. The majority (81%) of the strains which harbored phage Aa phi 23 were of serotype a, whereas serotype d strains appeared to be resistant to infection with this phage. There was a clear correlation between hybridization patterns and genetic subdivisions based on our previous population genetic analyses of A. actinomycetemcomitans. However, there was no significant correlation between occurrence of Aa phi 23 among A. actinomycetemcomitans strains and the periodontal status of the patients from whom the isolates were obtained, suggesting that this bacteriophage does not significantly influence the virulence of A. actinomycetemcomitans.

Abscess↗
PubMed1999

Smoking and patterns of bone loss in early-onset periodontitis.

BACKGROUND: The aims of this study were to investigate the extent and distribution of bone loss in subjects with early-onset periodontitis (EOP) referred for periodontal care and to study the relationship between smoking and EOP. METHODS: A total of 71 consecutive referrals (21 male, 50 female) under 35 years old, who were otherwise healthy, with a clinical diagnosis of severe periodontitis were recruited for the study. Bone loss was measured from available radiographs using a Schei ruler to identify 2 patterns of destruction: localized (LEOP) in 41 (58%) and generalized early-onset periodontitis (GEOP) in 30 (42%) subjects. RESULTS: The study population had a mean of 25.0 (SD 2.4) teeth, excluding third molars, and mean bone loss of 28.7% (SD 13.0). Bone loss was more severe in the maxilla, 30.9% (SD 13.8) compared with 26.6% (SD 14.0) in the lower arch. More than one-third (36%) of the teeth examined had at least 30% bone loss. Mean smoking experience was 9.2 pack years (SD 5.6), and 39 (55%) of the EOP subjects smoked. Smokers had significantly more maxillary bone loss than non-smokers. A much higher proportion of GEOP (70%) currently smoked compared with 44% of LEOP, P = 0.029. CONCLUSIONS: It is concluded that young adults with early-onset forms of periodontitis often have advanced periodontal destruction before they are referred for specialist care. In addition, there was a relationship between smoking and severe bone destruction in subjects with EOP, particularly those with generalized disease.

Adolescent↗
PubMed2000

Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized juvenile and other forms of early-onset periodontitis.

BACKGROUND: Actinobacillus actinomycetemcomitans leukotoxin is thought to be an important virulence factor in the pathogenesis of localized juvenile and other forms of early-onset periodontitis. Some highly leukotoxic A. actinomycetemcomitans strains produce 10 to 20 times more leukotoxin than other minimally leukotoxic strains. The distribution, clonality, and intrafamilial transmission of highly leukotoxic A. actinomycetemcomitans were examined in order to determine the importance of leukotoxin in the pathogenesis of periodontitis. METHODS: The polymerase chain reaction (PCR) was used to differentiate highly leukotoxic from minimally leukotoxic strains in examining 1,023 fresh A. actinomycetemcomitans isolates and strains from our culture collection. These were obtained from 146 subjects including 71 with localized juvenile periodontitis (LJP), 4 with early-onset periodontitis, 11 with post-localized juvenile periodontitis, 41 with adult periodontitis, and 19 periodontally normal subjects. The arbitrarily primed polymerase chain reaction (AP-PCR) analysis of 30 oral isolates from each of 25 subjects was used to determine the intraoral distribution of A. actinomycetemcomitans clones. AP-PCR was also used to examine the transmission of A. actinomycetemcomitans in 30 members of 6 families. The clonality of 41 highly leukotoxic A. actinomycetemcomitans strains was evaluated by both AP-PCR and ribotyping. RESULTS: Highly leukotoxic A. actinomycetemcomitans was found only in subjects with localized juvenile and early-onset periodontitis. Fifty-five percent of the LJP subjects harbored highly leukotoxic A. actinomycetemcomitans isolates. Seventy-three percent of the A. actinomycetemcomitans isolates in these subjects were highly leukotoxic. Highly leukotoxic A. actinomycetemcomitans infected younger subjects (mean age 13.95 years, range 5 to 28 years) than minimally leukotoxic (mean age 35.47 years, range 6 to 65 years). Most subjects were infected with only one A. actinomycetemcomitans genotype. However, PCR of whole dental plaques and subsequent analysis of up to 130 individual oral isolates suggested a possible shift in A. actinomycetemcomitans over time in that a few subjects harbored both highly leukotoxic and minimally leukotoxic strains. AP-PCR analysis was consistent with intrafamilial A. actinomycetemcomitans transmission. Ribotyping and AP-PCR analysis confirmed a previous report that highly leukotoxic A. actinomycetemcomitans consists of a single clonal type. CONCLUSIONS: This study suggests that localized juvenile and other forms of Actinobacillus-associated periodontitis are primarily associated with the highly leukotoxic clone of A. actinomycetemcomitans.

Actinobacillus Infections↗
PubMed2001

Human fibroblasts ubiquitously express glutamic acid decarboxylase 65 (GAD 65): possible effects of connective tissue inflammation on GAD antibody titer.

BACKGROUND: Type 1 diabetes is caused by a destruction of pancreatic beta cells due to autoimmunity. Autoantibody against glutamic acid decarboxylase (GAD) 65 expressed in pancreatic beta cells is widely used as a predictive marker for pancreatic destruction. In this study, we hypothesized that if certain cells in periodontal tissues could express GAD, then it may influence GAD antibody titer. METHODS: We used: 1) reverse transcription-polymerase chain reaction (PCR) analysis to detect GAD 65 mRNA in various cells; 2) nucleotide sequencing analysis to confirm that amplified PCR product is the gene encoding GAD; and 3) Western blotting to determine the expression of GAD 65 protein in human gingival fibroblasts. Immunohistochemical staining of GAD 65 protein in normal and inflamed gingiva was performed to examine the potential influence of periodontal inflammation on GAD 65 expression. GAD antibody titer in sera of periodontal patients as well as healthy subjects was measured to determine if periodontal patients could develop autoantibody against GAD 65. RESULTS: Cultured human gingival, periodontal, and dermal fibroblasts and mesangial cells expressed GAD mRNA. Nucleotide sequencing analyses confirmed the amplified PCR product as GAD 65. Western immunoblotting analyses and immunohistochemical staining revealed that the GAD 65 protein was expressed in vitro and in vivo. The expression of GAD 65 in inflamed tissue was higher than that in normal tissues. Two of 62 periodontal patients without diabetes showed an increased antibody titer against GAD 65, while none of the systemically healthy subjects showed an increased antibody titer against this antigen. CONCLUSIONS: We concluded that periodontal inflammation may result in higher levels of GAD and influence GAD antibody titer, and, hence, affect diabetic diagnosis based upon GAD antibody production.

Actins↗
PubMed1992

Microbial etiology of periodontal diseases. Where are we? Where are we going?

Many studies indicate a strong association of Actinobacillus actinomycetemcomitans with localized juvenile periodontitis. Species associated with adult periodontitis include Bacteroides forsythus, Porphyromonas gingivalis, Prevotella intermedia, A. actinomycetemcomitans, and Wolinella recta. Capnocytophaga species may be important in pubertal gingivitis. An unnamed spirochete related to Treponema pallidum has been identified in acute necrotizing ulcerative gingivitis lesions. Species isolated from prepubertal periodontitis, peri-implantitis, pericoronitis, and human immunodeficiency virus gingivitis and periodontitis are similar to those isolated from periodontal and gingival infections. Species identification in combination with clinical characteristics facilitates periodontal diagnosis. DNA probes, immunoassays, and benzoyl-arginine naphthylamide reactivity methods can be used to indicate putative pathogens in plaque samples. Microbial identification aids in antibiotic selection and planning a treatment regimen.

Actinomyces↗
PubMed2000

Phagocytosis of periodontopathogenic bacteria by crevicular granulocytes is depressed in progressive periodontitis.

BACKGROUND: The aim of this study was to examine crevicular polymorphonuclear neutrophils (PMN) of patients with rapidly progressive periodontitis (RPP) for their in vitro phagocytic activity and intracellular killing of Porphyromonas gingivalis ATCC 33277 and two strains of Actinobacillus actinomycetemcomitans (NCTC 9710 - type strain and Tanner FDC 44 - leukotoxin producing strain). PATIENTS AND METHODS: 18 patients with RPP and nine healthy controls were included in the study. Phagocytosis and intracellular killing were assessed by fluorescence microscopy after staining with acridine orange. The percentage of phagocytosing PMN was determined. The phagocytic cells were then separated into two groups; those containing < 10 phagocytosed bacteria and those containing > 10 bacteria. The percentage of PMN containing viable bacteria was also determined. RESULTS: The leukotoxic A. actinomycetemcomitans strain was phagocytosed to a lesser degree than the corresponding type strain. The number of phagocytosing cells obtained from the RPP patients did not differ from the controls. However, in healthy subjects there were more phagocytes with more than ten ingested P. gingivalis than in RPP patients. The intracellular killing was diminished in the periodontitis group for P. gingivalis and for both A. actinomycetemcomitans strains. CONCLUSION: The PMN of patients with RPP show deficiencies in phagotcytic activity and in the intracellular killing or peridontopathogenic bacteria.

Aggregatibacter actinomycetemcomitans↗
PubMed2002

Sequence diversity in the major fimbrial subunit gene (flp-1) of Actinobacillus actinomycetemcomitans.

Cells of the periodontal pathogen Actinobacillus actinomycetemcomitans exhibit tight adherence to surfaces such as glass, plastic and hydroxyapatite, a property that probably plays an important role in the ability of this bacterium to colonize teeth and other surfaces. Tight adherence is mediated by long fibrils of bundled pili (fimbriae) that form on the surface of the cell. The flp-1 gene encodes the major pilin protein component of A. actinomycetemcomitans fimbriae. In this study we compared flp-1 DNA sequences from 43 strains of A. actinomycetemcomitans isolated in Europe, Japan and the United States and identified seven distinct flp-1 allelic classes. DNA and predicted protein sequences were almost completely conserved within each flp-1 class but were highly divergent between classes. Most amino acid substitutions occurred in the C-terminus of the pilin protein, a region that has been shown to be important for the bundling and adhesive properties of the pili. flp-1 classes correlated with serotypes and 16S rRNA genotypes in most strains. At least five strains showed evidence of horizontal transfer of flp-1 between strains of different serotypes and 16S rRNA genotypes. Four of the seven flp-1 classes were present in geographically diverse isolates. Strains representing all seven flp-1 classes, but not a strain carrying a transposon insertion in flp-1, bound avidly to polystyrene in an in vitro adherence assay. Strains representing six of the seven flp-1 classes were isolated from localized juvenile periodontitis patients, suggesting that phylogenetically diverse strains carry pathogenic potential. Our findings provide a framework for future biochemical, immunological and genetic studies of A. actinomycetemcomitans fimbriae.

Actinobacillus Infections↗
PubMed1988

Microbiological and clinical effects of surgery plus doxycycline on juvenile periodontitis.

It was previously determined that surgery plus the antibiotic doxycycline were effective in eliminating or suppressing Actinobacillus actinomycetemcomitans (Aa), an organism strongly associated with disease in localized juvenile periodontitis (LJP). Eight patients with LJP participated in this surgical study. Patients were reexamined three and 12 months following therapy. The results of this study strongly suggest that surgery plus doxycycline effectively eliminate Aa from periodontal pockets. This elimination results in clinical improvement and attachment gain at three and 12 months following surgery. Further destruction was seen in individuals who continued to harbor high levels of Aa.

Actinobacillus↗
PubMed1994

Sequential manifestation of different forms of early-onset periodontitis. A case report.

Pathogenic bacteria constitute the primary extrinsic agent in the etiology of early onset periodontitis. However, the risk of developing periodontal disease is not equal for all individuals, suggesting host factors are involved in determining an individual's disease susceptibility. In this report, a case of an otherwise healthy female, who exhibited prepubertal periodontitis (PPP) at age 10, juvenile periodontitis (JP) at age 13, and rapidly progressive periodontitis (RPP) at age 29 years, is presented. Microbial, immunological, and genetic features of the case are presented. PPP, JP, and RPP are considered distinct disease entities, albeit with similar pathology and pathogenesis, yet all were manifest sequentially in the same individual. This report presents the idea that certain individuals are predisposed to early-onset periodontal diseases and the early identification of risk factors is important in the management of these individuals.

Adolescent↗
PubMed1999

[Post-cure response in periodontal practice in Belgium].

The recall response of patients with prosthetic rehabilitation on implants (n = 530) and patients treated for periodontal disease (n = 2364) in a periodontal private practice was evaluated. The recall response over 7 years following treatment showed that (1) with time the response to treatment diminished for all patient groups, (2) (post) juvenile periodontitis patients responded poorly to follow-up, (3) patients with rapidly progressing periodontitis were most eager to regularly visit the periodontist, (4) implant patients with complete rehabilitation responded better than those with partial restorations who in turn responded better than those with a single crown on an implant.

Aggressive Periodontitis↗
PubMed2002

Mouthrinses and periodontal disease.

It is known that mouthwashes can influence gingivitis; however, their role in the three different kinds of periodontitis is unclear. Some solutions have demonstrated some effect on necrotising periodontitis, yet none have been shown to influence early onset periodontitis. The literature provides us with a wide range of in vitro concentrations of substances used pure or in various mixtures in mouthwashes. Although only a few solutions can be used in a curative approach, most mouthwashes represent an essential tool in prophylaxis and thus also in post-periodontal treatment (maintenance phase). However, severe qualitative differences exist between the diverse families of mouthwashes. Many studies have shown that the use of a mouthwash associated with regular tooth cleaning was more beneficial than the utilisation of mouthrinse alone.

Aggressive Periodontitis↗
PubMed1992

Papillon-Lefèvre syndrome.

Papillon-Lefèvre syndrome, also known as hyperkeratosis palmaris et plantaris or hyperkeratosis palmoplantaris, is a devastating dermatological disease characterized by a thickening of the stratum corneum of the skin on the palms of the hands and soles of the feet. In addition, some patients manifest excessive sweating (hyperhidrosis), the growth of fine body hair and the development of dirty-colored skin on the affected parts. Calcification of the falx cerebri of the dura mater, as well as other areas of the brain, have been reported. From a dental standpoint, young patients with Papillon-Lefèvre syndrome have juvenile or precocious periodontosis, with severe destruction of the alveolar bone in both deciduous and permanent dentitions. Bone loss has been observed as early as two years of age, with premature exfoliation of the teeth. There is usually gingival enlargement, gingival ulceration and the formation of deep periodontal pockets; but in some cases, there is no inflammatory reaction and only the periodontium of the secondary teeth is affected. This disease eludes all known forms of therapy and results in edentulousness after only a few years.

Aggressive Periodontitis↗