Periodontal disease in children and adolescents: introduction and classification.
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Adolescent↗
Biomedical subjects
D F Kinane
Publications and source records attributed to D F Kinane.
Etiopathogenesis of periodontitis in children and adolescents.
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Adolescent↗
Humoral immune response in early-onset periodontitis: influence of smoking.
Sixty-five patients with generalised early-onset periodontitis (G-EOP) (age range 16-42 years, 32 smokers and 33 non-smokers) were assessed for antibody titres and avidity to a panel of five suspected periodontal pathogens (Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Treponema denticola and Bacteroides forsythus). Thirty-four of these patients were untreated (17 smokers and 17 non-smokers), and thirty-one were in the maintenance phase of periodontal therapy (15 smokers and 16 non-smokers). Previous studies have investigated the effect of smoking on IgG levels in periodontitis patients in the context of the more extensive periodontal destruction seen in smokers. Based on this literature our hypothesis was that smokers would have depressed serum IgG levels directed against recognised periodontal pathogens compared with non-smokers. Antibody titres were measured by ELISA deploying fixed whole cells as coating. The IgG response was detected with biotin-anti-human IgG and avidin-peroxidase; avidity was determined by elution with ammonium thiocyanate. Median titres to A. actinomycetemcomitans, P. intermedia and T. denticola were significantly lower in maintenance patient smokers (p= 0.02, 0.02 and 0.002 respectively) but not in untreated patients. Avidity to P. gingivalis was also lower in smoking maintenance patients (p = 0.003) but not in untreated patients. These findings may imply some interruption of immune maturation in smokers following periodontal treatment.
Adolescent↗
Anti-inflammatory cytokine IL-10 and T cell cytokine profile in periodontitis granulation tissue.
Th2 cells are more abundant than Th1 cells in periodontitis lesions, but the relative importance of the Th1 and Th2 subsets in periodontal disease is not understood. In addition, the role of proinflammatory and anti-inflammatory cytokines in this disease process is unclear. Biopsies were obtained from 10 patients with early onset periodontitis (EOP) and 10 patients with adult periodontitis (AP). From all of the patients in the AP group we were able to obtain and section the gingival tissue to serve as controls. We used polyclonal monospecific antibodies to detect cells expressing IL-2, IL-4, IL-6, IL-10 and IL-15, tumour necrosis factor (TNF-alpha) and interferon-gamma (IFN-gamma) in formalin-fixed, paraffin-embedded sections of granulation tissue from periodontitis lesions. We also employed a series of oligonucleotide probes to detect cells expressing the cytokine transcripts in the same tissue biopsies. Cells that expressed IL-4 or IL-6 were more numerous than cells expressing either IL-2 or IFN-gamma. Th2 cells were more numerous in EOP and AP tissues. IL-15 substitutes for IL-2 in a number of biological activities related to the Th1 immune response, and interestingly, in periodontal lesions the IL-15-expressing cells outnumbered IL-2-expressing cells, suggesting that this is the pattern of immune regulation by T cells in the periodontium. The functional balance in the T cell subsets detected by their cytokine profiles underlies the importance of the anti-inflammatory mechanisms taking place in the diseased tissue. The numbers of inflammatory leucocytes that express the anti-inflammatory cytokine IL-10 are much more widely distributed than those that express the proinflammatory cytokines IL-6 and TNF-alpha. This study suggests that large numbers of infiltrating inflammatory cells as well as accessory cells are involved in the down-regulation of the inflammatory and immune response in periodontitis.
Adult↗
Clinical, pathological and immunological aspects of periodontal disease.
The inflammatory and immune responses during the development and progression of periodontitis are reviewed. Susceptibility to periodontitis may be related to whether plasma cells predominate in the tissues of an individual, or a site, in response to the microbial insult from dental plaque. The tendency for an individual or site to form an extensive plasma cell infiltrate may indicate an inability to defend against periodontopathogenic bacteria and thus a predisposition to periodontitis. Selected pertinent areas of current interest in cellular and humoral immunology are considered within the periodontal context. These topical issues include (a) homing of immune and inflammatory cells to target tissues; (b) the local proliferation and synthetic activity of immune and inflammatory cells; (c) the cytokine profile of the inflammatory and immune cells; and (d) the immunoglobulin subclasses of locally produced antibodies.
Antibodies, Bacterial↗
Periodontal manifestations of systemic disease.
Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.
Calcium Channel Blockers↗
Immunodominant antigens in periodontal disease: a real or illusive concept?
The humoral arm of the immune system provides protection from many medically significant pathogens. The antigenic epitopes of the pathogens which induce these responses, and the subsequent characteristics of the host response, have been extensively documented in the medical literature, and in many cases have resulted in the development and implementation of effective vaccines or diagnostic tests. There is a substantial body of literature on the humoral immune response in periodontal disease, which is targeted at micro-organisms present within periodontal pockets. However, the significance and specificity of the immune response in periodontal disease have proved difficult to elucidate, due to the large number of potential pathogens in the plaque biofilm and the apparent commensal nature of many of these opportunistic pathogens. This review addresses our current knowledge of the approaches and strategies which have been used to elucidate and examine the concept of immunodominant antigens in medical infections and, more recently, periodontal disease. An identification/understanding of the immunodominant antigens would be informative with respect to: (i) the relative importance of the implicated pathogens, (ii) new approaches to immunological diagnosis, (iii) specific bacterial virulence determinants, (iv) natural protective responses, and (v) the selection of potential vaccine candidate antigens. We conclude that immunodominance of antigens in periodontal disease may be relevant to our understanding of periodontal disease pathogenesis, but due to the complexity and diversity of the 'pathogenic microbial ecology', it is currently an enigmatic topic requiring a multidisciplinary approach linking clinical, microbiological, and immunological investigations. We also conclude, after assessing the literature available on the topic of immunodominance, that it is a term that, if used, must be clearly defined and understood, since it is often used loosely, leading to a general misinterpretation by readers of oral and medical literature.
Aggregatibacter actinomycetemcomitans↗
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.
Adult↗
Effect of subgingival scaling during supportive therapy.
BACKGROUND, AIMS: This prospective study was designed to investigate the rôle of root débridement at 3 month intervals for patients with periodontitis whose disease had persisted following the completion of conventional periodontal treatment. METHODS: 39 maintenance patients with at least 4 pockets at least 4 mm deep were assigned to coronal scaling (CS) and subgingival scaling (SS) groups. Probing depths (PD), bleeding on probing (BOP) and relative attachment levels (RAL) were recorded at all eligible sites at baseline and 3, 6, 9 and 12 months later. Plaque index scores were recorded at the 12-month visit. At every visit, following data collection, both groups received a coronal scaling and the SS group, in addition, received a thorough subgingival débridement. In the CS group, subgingival débridement was performed only for 'loser' sites which inhibited loss of attachment > or = 2 mm relative to baseline values. Due to low compliance, only 31 patients completed the study. Thus, data analyses were carried out for 130 sites in 17 CS group patients and 146 sites in 14 SS group patients. RESULTS: During the course of the study, 21 loser sites were identified in each group, but the difference in proportion of loser sites between groups was not significant. Furthermore, although there was a trend toward PD reduction in both groups throughout the study, mean PD, RAL and BOP values were not significantly different from baseline values at any time point, and there were no significant differences between groups with respect to these variables. Mean plaque scores measured at the 12-month visit revealed no significant differences between groups. CONCLUSION: These findings call into question the value of performing repeated subgingival scaling at 3-month intervals for patients with persistent disease.
Adult↗
Antibody responses against Porphyromonas gingivalis infection in patients with early-onset periodontitis.
BACKGROUND, AIMS: The aim of this study was to evaluate antibody responses against Porphyromonas gingivalis (P. gingivalis) infection in early-onset periodontitis (EOP) patients to elucidate further the host-parasite interactions in the pathogenesis of EOP. METHOD: 16 P. gingivalis-infected EOP and 20 adult periodontitis (AP) patients, and 18 periodontally healthy subjects (HS) participated in this study. Serum immunoglobulin G (IgG) antibody levels and avidities against extracted P. gingivalis whole cells were measured. The components of P. gingivalis outer membrane antigens (OMA) reacting to patients' sera were analysed from the molecular weights by Western blotting. Serum antibody levels against P. gingivalis lipopolysaccharide (LPS) were also measured. The ability of the patients' sera to block interleukin-1beta (IL-1beta) production by human mononuclear cells in response to P. gingivalis LPS was examined. RESULTS: Antibody levels were positively correlated with antibody avidities in both EOP and AP patients (r=0.91, r=0.72, p<0.0005, respectively), while not significantly so in HS (r=0.09). There was variability in the antigen recognition of P. gingivalis OMA in EOP and AP patients. Smear and 53-kDa protein were more frequently recognized by sera of EOP and AP patients rather than that of HS (p<0.05). The smear was partly diminished by absorption with P. gingivalis LPS, indicating the smear antigen was partly composed of LPS. There was high correlation between antibody levels against P. gingivalis whole-cell extracts and LPS in EOP and AP patients (r=0.81, p=0.0002, r=0.87, p<0.0001, respectively), while not significant in HS (r=0.22). The sera of EOP and AP patients with high IgG titre to P. gingivalis LPS blocked IL-1beta production more effectively than that of the patients with low IgG titre to P. gingivalis LPS. CONCLUSIONS: These results indicate that EOP patients' antibody response against P. gingivalis infection does not differ significantly from that of AP patients. The person-to-person heterogeneous antibody production against P. gingivalis LPS could contribute to our understanding of the relationship between the defensive ability of EOP patients and their chronic infection with this pathogen.
Adolescent↗
Cytokine expression in periapical granulation tissue as assessed by immunohistochemistry.
The aims of this study were to investigate the expression of pro-inflammatory, anti-inflammatory and immune-related cytokines present in periapical lesions. We investigated the expression of cytokines: namely interleukins IL-2, IL-4, IL-6, IL-10 and interferon-gamma (IFN-gamma) in formalin-fixed, paraffin-embedded sections of periapical granulation tissue. The study samples were biopsies from 24 patients with periapical lesions: 12 with periapical granulomas and 12 patients with radicular cysts. Immunohistochemistry was also performed on tonsillar tissue which served as a control. We utilised a set of specific monoclonal antibodies and polyclonal monospecific antibodies to detect cells that expressed the different cytokines within the tissues. We also considered the nature of the periapical immune response by investigation of the T-helper 1 (Th-1) and T-helper 2 (Th-2) lymphocyte subsets using their cytokine profile, i.e., Th-1: IL-2 and IFN-gamma and Th-2: IL-4, IL-5 and IL-6. Only a few cells were weakly positive for the IL-2 protein in each of the tissue sections. Cells that expressed IL-4 or IL-6 were far more numerous than cells that expressed either IL-2 or IFN-gamma. Thus, we demonstrated a greater number of Th-2 cells in periapical lesions. This relative ratio of the T-cell subsets underlines the importance of the anti-inflammatory mechanisms taking place in the diseased tissue manifested by the wide array of IL-10-expressing cells: B cells, T suppressor cells (CD8 (+)) and tissue macrophages. The numbers of inflammatory cells expressing the anti-inflammatory molecules far outnumbered the cells that expressed pro-inflammatory cytokines. Thus, the downregulation of the inflammatory response and the predominant Th-2 or humoral immune response in periapical periodontitis may be important features that dictate the outcome of the disease process in the periapical lesion.
Adult↗
How periodontal disease may contribute to cardiovascular disease.
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Arteriosclerosis↗
Regulators of tissue destruction and homeostasis as diagnostic aids in periodontology.
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Biomarkers↗
Inducible nitric oxide synthase expression in periodontitis.
Recently, nitric oxide (NO) has been shown to be vital in inflammatory processes. Nitric oxide synthase (NOS) exists in three different isoforms, two constitutively produced with physiological roles, and an inducible form, iNOS, which is involved in inflammation. This study examined the localisation of iNOS in biopsies from patients with periodontitis using immunohistochemistry, and compared these with healthy tissue biopsies. Biopsies were obtained from 16 periodontitis patients undergoing periodontal surgery and from clinically healthy tissues of 5 patients having crown lengthening procedures. The periodontitis diseased tissue demonstrated a greater level of iNOS expression than the healthy tissue. The source of iNOS in the periodontal tissues was determined by our monoclonal antibody to be the macrophage, with the endothelial cells also contributing. A role for NO in the inflammatory response of periodontal tissues is suggested, but the precise role requires further elucidation.
Case-Control Studies↗
Clinical and genetic analysis of a large North European Caucasian family affected by early-onset periodontitis.
Genetic studies of early-onset periodontitis (EOP) are hampered by several factors. These include delayed onset of the trait, an upper age limit of expression of the disease, and lack of phenotypic information for edentulous family members. Segregation analyses of families with EOP support a major locus hypothesis but fail to define clearly the criteria used for diagnosis of the relatives. Confirmation of a proposed mode of inheritance and the identification of risk genes is awaited by means of family linkage studies. It is suggested that a system can be developed for the current and retrospective diagnosis of relatives of EOP probands. In addition, it is hypothesized that the large family presented here is suitable for a linkage study. Relatives of the proband who were unavailable for a full periodontal examination, were edentulous, or were deceased, were diagnosed by means of documented clinical evidence of periodontal disease or from reported case histories. Segregation analysis was performed. Analysis of the power of the pedigree to detect linkage was carried out by means of the SIMLINK program. Three different categories were defined according to the reliability of diagnosis of EOP. Segregation analysis indicated either autosomal-dominant or X-linked-dominant inheritance in this family. The simulations showed lod scores above 3.0 for all locations of the disease gene, and for each category of diagnosis. In conclusion, a method has been developed which can be used for the diagnosis of relatives of EOP probands when ideal clinical data are unavailable. The simulations suggest that this family is suitable for a genetic linkage study with the aim of identifying the location of one or more susceptibility genes.
Adult↗
Cytokine responses of oral epithelial cells to Porphyromonas gingivalis infection.
Accumulating evidence indicates that epithelia are not merely mechanical barriers but also important elements of the innate immune system. The present study was performed to examine cytokine responses of oral epithelial cells after infection with the periodontal pathogen Porphyromonas gingivalis. The KB-cell line and primary cultures of periodontal pocket epithelium were infected with P. gingivalis for assessment of bacterial invasion by an antibiotic protection assay, and examination of expression of interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha by in situ hybridization and immunohistochemistry. We observed that P. gingivalis induces a strong cytokine response, positively correlated with the adhesive/invasive potential of the infecting strain, in both KB cells and primary cultures. These findings indicate that the epithelial cells of the periodontal pocket are an integral part of the immune system, eliciting cytokine responses to a bacterial challenge. In this context, the adhesive/invasive phenotype of P. gingivalis appears to contribute to pathogenicity.
Bacterial Adhesion↗
Smoking and periodontal disease.
Numerous investigations of the relationship between smoking and periodontal disease have been performed over the last 15 years, and there now exists a substantial body of literature upon which this current review is based. From both cross-sectional and longitudinal studies, there appears to be strong epidemiological evidence that smoking confers a considerably increased risk of periodontal disease. This evidence is further supported by the data emanating from patients who stop smoking. These patients have levels of risk similar to those of non-smokers. Numerous studies of the potential mechanisms whereby smoking tobacco may predispose to periodontal disease have been conducted, and it appears that smoking may affect the vasculature, the humoral immune system, and the cellular immune and inflammatory systems, and have effects throughout the cytokine and adhesion molecule network. The aim of this review is to consider the evidence for the association between smoking and periodontal diseases and to highlight the biological mechanisms whereby smoking may affect the periodontium.
Bone Regeneration↗
Periodontal diagnostics.
Periodontitis affects a subset of the population and our current thinking is that progression of periodontal disease may be either continuous or cyclical (burst hypothesis). These features make screening and diagnostic tools desirable in the management of this disease. Although many potential markers exist, several difficulties hamper our ability to declare them diagnostic tests with proven utility. The 'gold standard' for active periodontal disease is not available and inflammation due to gingivally confined lesions (gingivitis) and periodontal inflammation which results in attachment loss is a potential confounder of any test based on assessing the host response elements of the disease. The current absence of proof for the progression of periodontal disease i.e., whether or not the burst hypothesis is correct, is a further problem. Although much is written about the need for markers of current or future disease which will prevent us from overtreating pockets, the time, effort and cost involved in testing these sites has to be balanced against the relative ease and speed of routine therapy such as root planing. In addition, we are still some way from the development and validation of reliable host or microbial testing methods. In terms of screening tests for diseases such as the early-onset forms of periodontitis, the research and development on diagnostic tools involving genetic polymorphisms, specific genes, systemic antibodies or leucocyte cell surface markers of the patients, may become a clinical reality in time. One could envisage chairside tests using blood from thumb pricks being capable of determining a young individual's risk of developing disease at a later age, and thus the need for a timely prevention programme. Before applying any test we should reconsider what treatment planning effects a positive or negative result will have, and any test which does not influence the treatment plan is redundant. Whether periodontal diagnostic tests will be developed which will indicate to the clinician the need for various treatment regimes other than root planing, is still an open question. For example, in the future, a test of specific antibody levels in patients prior to treatment might indicate their likely response to therapy and thus the need for additional therapeutic agents such as antibiotics. Periodontal diagnostic tests are still at an early stage of development and much work remains to be performed to fully validate their utility such that they become an important and cost effective aspect of clinical treatment planning, screening or patient monitoring.
Aggressive Periodontitis↗