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PubMed1996

Periodontal implications: medically compromised patients.

The presence of systemic disease in patients requiring periodontal therapy creates challenges for management. Alteration of treatment plans, with emphasis on physician consultation and preventive periodontal care, is frequently needed to minimize the impact of periodontal disease on the systemic condition. Conversely, detection and treatment of systemic disorders may impact upon the status of the periodontium and the success of periodontal therapy. The goal of holistic patient management is facilitated by a free flow of information between the patients and their medical and dental health care providers.

Adolescent↗
PubMedDate not supplied

[The nonspecific resistance of the oral cavity in adolescents].

Nonspecific resistance of the oral cavity was studied in 83 adolescents with catarrhal gingivitis, generalized or focal periodontitis, and intact periodontium. Mixed salivary and gingival fluid pools were examined. Immunoglobulins A and G, secretory immunoglobulin A, salivary and gingival fluid lysozyme, B lyse activity, and salivary excretion rate were measured. The findings evidence activation of local defense factors in catarrhal gingivitis at the expense of nonspecific defense factors, and a reduction of nonspecific defense parallelled by activation of the specific factors (secretory IgA) in periodontitis, which fact may be explained by augmentation of the antigenic stimulus at the expense of bacterial plaque dissemination under the gingiva.

Adolescent↗
PubMed1990

Probe-specific DNA fingerprinting applied to the epidemiology of localized juvenile periodontitis.

Although Actinobacillus actinomycetemcomitans has been recognized as a primary etiological agent in localized juvenile periodontitis, questions remain concerning the source of infection, mode of transmission, and relative virulence of strains. DNA fingerprinting analysis, using a randomly cloned chromosomal DNA fragment as a probe, revealed that previously characterized strains of A. actinomycetemcomitans displayed significant restriction site heterogeneity which could be applied to the typing of clinical isolates of this bacterium such that individual strains or variants could be traced within subjects from localized juvenile periodontitis families. Hybridization data derived from an analysis of bacterial isolates obtained from families participating in an ongoing longitudinal study of the disease showed that a single individual could be infected with more than one strain or variant of A. actinomycetemcomitans and that various members of the same family could harbor different strains or variants of the bacterium. In several cases the clinical isolates were matched to characterized laboratory strains by comparing hybridization patterns generated by digestion of the DNA with several restriction enzymes in independent reactions. Thus, probe-specific DNA fingerprinting of A. actinomycetemcomitans will permit us to determine if particular strains or variants are frequently associated with sites of periodontal destruction. Attention could then be focused on determining the virulence properties of those strains or variants that have in vivo significance.

Actinobacillus↗
PubMed1990

An in vivo study of neutrophil locomotion in relation to periodontal disease status and local chlorhexidine.

Neutrophil migration from skin window abrasions was studied in 10 patients with no history of periodontitis, 10 with localised juvenile or post-juvenile periodontitis, and 10 with chronic adult periodontitis. Filters contained either saline or chlorhexidine (0.002% or 0.02%). The leading front was measured in filters placed for 30 min after cell migration had been established for 2 h. Subjects in the juvenile/post juvenile group showed a reduced range of migration distances, but were still within the normal range when compared with the other 2 groups. Chlorhexidine at 0.002% tended to increase leading front distances, and 0.02% to decrease them. We conclude that: 1) migrating neutrophils in vivo may move less far in patients with a history of juvenile periodontitis; 2) chlorhexidine may inhibit cell migration, possibly decreasing the host response in vivo if applied at current therapeutic concentrations.

Adolescent↗
PubMed1999

Localized adhesion molecule expression and circulating LFA-3 levels in adult and early onset forms of periodontitis.

Because of their importance in mediating cellular interactions in chronic inflammatory diseases, this study has examined the expression of a number of adhesion molecules in adult (n=11), generalized early onset (n=5) and localized early onset (n=2) forms of periodontitis. In comparison with immunostaining profiles of cryostat sections of healthy gingival tissue (n=7), the beta 1 integrins VLA-1, VLA-2 and VLA-4 were found to be up-regulated in periodontitis, with VLA-6 being markedly elevated. Although only small differences were observed in ICAM-1 and LFA-3 expression in the gingival epithelium, there was particularly notable up-regulation of these adhesion molecules within the inflammatory infiltrates of the diseased tissues. However, there were no statistically significant differences between the serum levels of a soluble form of LFA-3 in periodontitis patients (n=47) compared with healthy control subjects (n=40), although the generalized early onset and adult periodontitis groups exhibited wider ranges of circulating LFA-3. These findings show that there is localized modulation of adhesion molecule expression in the chronic inflammatory periodontal diseases studied, but that the levels of LFA-3 in the circulation nevertheless remain unaffected.

Adolescent↗
PubMed1999

Clonal diversity of Actinobacillus actinomycetemcomitans isolates from young adults with minimal periodontal disease.

Actinobacillus actinomycetemcomitans is a major periodontal pathogen which is associated with both early-onset periodontitis and adult cases refractory to conventional periodontal therapy, although the organism has also been shown to be widely distributed among dentate healthy individuals. The observed disease status may be associated with a variation in virulence of different strains or clones. The aim of the present study was to analyse genotype distribution as assessed by an arbitrarily primed polymerase chain reaction (AP-PCR) among 51 isolates of A. actinomycetemcomitans recovered from more than 200 young adult recruits with no or minor periodontal disease. In addition, isolates from 25 periodontitis patients as well as reference strains were genotyped. Primers amplifying (i) a specific sequence in the ltxA region, (ii) a specific 16S rRNA sequence and (iii) sequences in the leukotoxin promoter region were used to verify species identity of the strains. Three random oligonucleotide primers were employed to analyse genomic polymorphisms of the organism by means of PCR. A total of 19 genotypes could be distinguished, which were grouped by cluster analysis into 5 major clusters based on genetic similarity and a complete linkage sort. Whereas 3 clusters assembled A. actinomycetemcomitans genotypes isolated from both healthy subjects and periodontitis patients, one cluster containing 4 different genotypes exclusively comprised isolates from healthy or gingivitis subjects. Another cluster with 2 genotypes consisted of strains originating from periodontitis patients (p < 0.05). One strain characterized by a specific 530 bp deletion in the promoter region of the leukotoxin region was identified in a Ghanese patient with localized juvenile periodontitis. It was concluded that there is considerable clonal diversity of A. actinomycetemcomitans strains isolated from healthy or periodontally diseased subjects, and that genetically closely related groups might be associated with health or disease.

Actinobacillus Infections↗
PubMed1986

1985 Kreshover lecture. Molecular factors influencing neutrophil defects in periodontal disease.

Major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of localized juvenile periodontitis (LJP). Several lines of evidence suggest that LJP is an infectious process closely associated with Actinobacillus (Haemophilus) actinomycetemomitans as a causative agent, although other organisms may also participate. The immunologic profile of LJP patients suggests that a cell-associated neutrophil locomotory dysfunction is a key underlying immunodeficiency resulting in increased susceptibility to periodontal infection. In addition, LJP patients often exhibit cervical lymphadenopathy and IgG-hypergammaglobulinemia, and a markedly elevated antibody response to the infecting organism, A. actinomycetemcomitans, is found in the serum and crevicular fluid of most patients. Evaluation of the locomotory properties of LJP neutrophils shows that random migration and chemokinesis are normal; however, about 70% of the LJP patients suffer from a defect in chemotaxis, with their neutrophils responding poorly to bacterial chemotactic factors, synthetic chemotactic peptides, and complement fragments (C5a). Depressed chemotaxis of LJP neutrophils is paralleled by their reduced capacity to bind the synthetic chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP), as well as C5a. Furthermore, there is a reduction in the amount of glycoprotein 110, a neutrophil membrane matrix component and differentiation antigen which is associated with FMLP- and possibly also C5a-mediated chemotaxis. Reduction of C5a and of FMLP ligand binding, decreased expression of GP-110, and reduced neutrophil chemotaxis are consistent with a stem cell maturation error in LJP patients. This is further supported by studies demonstrating increased expression of CR2, the C3d/EBV receptor, on peripheral blood neutrophils of LJP patients. CR2 receptors are normally present on immature human neutrophils but are lost during the maturation process. These alterations in neutrophil surface components and their reduced chemotaxis may result from a genetically determined abnormality. Studies demonstrating the familial nature of both the neutrophil chemotactic disorder and the clinical entity represented by localized juvenile periodontitis point to a strong role for genetic determinants in the disease which affect neutrophil surface receptors.

Aggressive Periodontitis↗
PubMed1996

Alterations in phagocyte function and periodontal infection.

A review of phagocytic cells-polymorphonuclear leukocytes and monocytes-in the inflammatory process is presented. Examples of phagocyte defect-related pathology serve as a framework for understanding the role of these cells in periodontal infection. The role of alterations in neutrophil function in localized juvenile periodontitis is presented as a model system for understanding periodontal pathology as a result of host-related functional abnormalities. Two topical alternative hypotheses for periodontal breakdown are presented in which macrophage control of the chronic lesion is altered by an absence of T cells or the influence of bacterial superantigens.

Aggressive Periodontitis↗
PubMed1988

[Proteases and their inhibitors in rapidly progressive and in juvenile periodontitis].

The purpose of this work was to study the elastase content of PMNs, the elastase alpha1-protease inhibitor complex, and the protease inhibitors in the plasma of patients with periodontal disease as compared with healthy subjects. We examined 11 patients with localized juvenile periodontitis (LJP), 15 patients with rapidly progressive periodontitis (RPP), and 22 healthy control subjects (HS). Our findings showed a significantly higher value for elastase like protease (ELP) complex in both patient groups than for the control group. In RPP patients, the ELP content of PMNs was below that in healthy subjects. Correlation between the ELP complex and the ELP content of PMN's was significantly positive. No such correlation could be discovered in the LJP group between the quantity of a1Pl and its inhibitory capacity, which may suggest a functional disorder involving the a1Pl of these patients. The imbalance existing between the different protease inhibitors is perhaps an explanation of the extensive tissue destruction occurring in periodontal disease as a result of the unrestrained effect of released granulocyte enzymes in the case of defective inhibition.

Adolescent↗
PubMed1999

Specific primer for AP-PCR identification of Actinobacillus actinomycetemcomitans.

We used arbitrarily-primed polymerase chain reaction (AP-PCR) to design and construct a specific primer pair for the identification of Actinobacillus actinomycetemcomitans. We analyzed 25 DNA samples of A. actinomycetemcomitans isolated from patients with localized-juvenile periodontitis. From 90 AP-PCR primers screened, one amplification product was selected, cloned in pCR II vector, and sequenced. The sequence was used to design a single pair of specific primers. The sequence was compared with GenBank entries using BLAST and showed no significant matches. PCR amplification using the new primer pair AA1416 produced a characteristic 3.5-Kb band in all A. actinomycetemcomitans DNAs tested. Primer pair AA16S produced no or different amplicon profiles using DNA samples from bacterial species other than A. actinomycetemcomitans. Our results show that this single primer pair AA1416 can be used in PCR to identify A. actinomycetemcomitans isolates and differentiate them from other periodontal bacteria. These approaches appear promising in facilitating laboratory identification and taxonomy of putative periodontopathogens.

Aggregatibacter actinomycetemcomitans↗
PubMed2001

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

BACKGROUND, AIMS: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Adolescent↗
PubMed1993

Transmission of Actinobacillus actinomycetemcomitans in families of adult periodontitis patients.

At present Actinobacillus actinomycetemcomitans is regarded as an important microorganism in the etiology of some forms of periodontitis. The purpose of the present investigation was to study the number of Restriction Endonuclease Analysis (REA)-types present in the oral cavity of A. actinomycetemcomitans positive subjects and to study the possibility of transmission of A. actinomycetemcomitans within families of adult periodontitis patients. DNA of A. actinomycetemcomitans isolates was digested with a combination of the restriction endonucleases PstI and BamHI, after which the DNA fragments were separated by agarose gel-electrophoresis. To study the number of REA-types, multiple A. actinomycetemcomitans isolates obtained from 8 different sites in the oral cavity of five subjects were typed. The results showed that in most cases only one REA-type is present. In the 13 families investigated in 4 of the 26 children (15%) and in 1 of the 13 spouses (8%) of the adult periodontitis patients an indistinguishable REA-type was found within the families. This suggests that also in the case of adult periodontitis transmission of A. actinomycetemcomitans is possible, but does not seem to occur easily.

Actinobacillus Infections↗
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↗
PubMed1999

Association of a vitamin D receptor gene polymorphism with localized early-onset periodontal diseases.

BACKGROUND: Early-onset periodontal diseases (EOP) are caused by interactions between host factors, specific microbial pathogens, and environmental factors. It is, therefore, of interest to investigate the nature of host factors as they may provide useful risk markers and reveal important information regarding the disease pathogenesis. Genetic polymorphisms in the vitamin D receptor (VDR) gene are associated with parameters of bone homeostasis and with diseases in which bone loss is a cardinal sign, in particular osteoporosis. Rapidly progressive bone loss is one feature of EOP. We, therefore, sought to determine whether EOP is associated with a polymorphism in the VDR gene. METHODS: A restriction fragment length polymorphism (RFLP) for Taq I in exon nine of the VDR gene was analyzed by PCR, followed by restriction digestion with Taq I and gel electrophoresis. We analyzed the genotypes of 69 EOP patients, including 20 patients with unequivocal evidence of localized disease (L-EOP), and 72 controls with no history of EOP. RESULTS: The genotype distribution in the L-EOP patient group was 7 (35%), 5 (25%) and 8 (40%) and in the control group 31 (43.1%), 36 (50.0%) and 5 (6.9%) for TT, Tt and tt respectively (where t and T represent the alleles with and without the Taq I RFLP respectively). Chi2 analysis indicated that the distribution of the genotypes between these two groups was highly significantly different (P = 0.001). Allele frequencies were 47.5% and 52.5% for T and t in the L-EOP group; 68.1% and 31.9% in the control group, showing a significant association between the prevalence of the less frequent allele (t) and L-EOP (P = 0.017). There was no significant difference in the genotype distribution or the allele frequencies between the control samples and the larger EOP patient group (n = 69) which included patients with generalized and localized disease. CONCLUSIONS: These data indicate that carriage of the less frequent allele of the Taq I RFLP (t) in the VDR gene significantly increases the risk of developing L-EOP. However, VDR genotype may not affect the incidence of all cases of EOP. These findings contribute to our understanding of the genetic basis for periodontal disease and may help define sub-groups of this disease which share common pathogenic factors.

Adolescent↗
PubMed1991

[A case of severe periodontal disease in adolescence associated with hypophosphatasia].

Hypophosphatasia is an inherited disorder characterized by defective bone mineralization, deficiency of alkaline phosphatase (ALP) activity, increased excretion of phosphoethanolamine (PEA) in the urine and premature loss of the deciduous teeth. A male hypophosphatasia patient aged 15 years 6 months, with premature exfoliation of the deciduous teeth and manifesting severe periodontal destruction in the permanent dentition, was examined. Antibody titers against seven strains by the enzyme-linked immunosorbent assay (ELISA), monocyte and neutrophil chemotaxis studies and cellular immunity tests were performed. Low levels of ALP in serum and PEA in the urine were found. Radiographic examination showed a similar pattern of alveolar bone loss to that of the localized juvenile periodontitis. Suppressed monocyte and neutrophil chemotaxis were not detected. Slightly depressed CD2+, CD3+ and CD4+ and slightly elevated activity of NK cells were found. An elevated level of antibody to Porphyromonas gingivalis was observed and this antibody titer was decreased by periodontal treatments. The affected sites of the patient showed resistance to conventional periodontal therapy. P. gingivalis was estimated to associate as an important pathogen in the etiology of periodontal destruction in this hypophosphatasia patient in addition to the dental abnormalities such as abnormal enamel, dentin, or cementum formation.

Adolescent↗
PubMed2002

The relationship between juvenile and non-juvenile periodontitis, ABO blood groups and haemoglobin types.

This study was carried out to investigate the relationship between juvenile and non-juvenile peridontitis (JP, non-JP), ABO blood groups and haemoglobin type. The heamoglobin electrophoresis was determined by routine technique using cellulose acetate paper and tris buffer at pH 8.5. Tile blood grouping was carried out on all specimens. Forty Nigerian adolescent individuals were investigated, twenty of which were diagnosed as having JP while the remaining 20 were diagnosed a having plaque-induced chronic periodontitis (non JP). This latter group was used as the control group. All the JP patients were either of blood group B/AB, rhesus positive while the non-JP subjects had B rhesus positive/negative, O rhesus positive/negative or AB rhesus positive. The differences between the results of the test and the control groups were statistically significant P < 0.05. All the forty subjects (JP and non-JP) had the haemoglobin type A and none of them exhibited the S and C haemoglobin types. There is a need to further investigate the relationship between juvenile periodontitis, ABO blood group and the common haemoglobin types (A, AS, S, C, and SS) at molecular level.

ABO Blood-Group System↗
PubMed1996

Periodontal diseases affecting children and young adults.

There is a group of periodontal diseases affecting children and young adults that is characterized by onset prior to age 35, often with a rapid rate of periodontal destruction. Although a wide variation in patterns of presentation exist, these diseases can be described under the broad categories of (a) early onset periodontitis (juvenile periodontitis), (b) necrotizing ulcerative gingivitis/periodontitis, (c) periodontitis associated with systemic diseases. A discussion of each of these categories is followed by two case reports which illustrate possible clinical presentations of these diseases.

Adolescent↗