Colocalization of Porphyromonas gingivalis with CD4+ T cells in periodontal disease.

Porphyromonas gingivalis, an anaerobic, asaccharolytic gram-negative bacterium, is a causative agent in chronic periodontitis. It has many virulence factors that facilitate infection of the gingiva, but little is known about the local immune cells that respond to this bacterium. The aims of this study were to quantify P. gingivalis in gingival biopsies from patients with periodontitis using laser capture microdissection (LCM) plus qRT-PCR and to determine the phenotype of immune cells associated with the bacteria using immunofluorescence. The presence of P. gingivalis was confirmed in periodontitis gingival tissue from 10 patients, and differences in bacterial distribution in the epithelium and connective tissue with or without inflammatory infiltrates were observed. Immune cells found in the biopsy tissues, including CD20+ mature B cells and CD138+ plasma cells, were associated with the Th2-type immune response. Most P. gingivalis was in direct contact with CD4+ T cells. This study revealed for the first time the colocalization of P. gingivalis with immune cells. Use of LCM combined with qRT-PCR enabled quantitative analysis of bacteria in a selected area of a biopsy sample without any tissue degradation. Observation of the immune cells associated with these bacteria was also performed by immunofluorescence.

Relationship between the gingival sulcus depth and interleukin-1 isoform concentrations within the adjacent gingival tissue.

BACKGROUND AND OBJECTIVE: While there is substantial information concerning the concentrations of interleukin-1 isoforms within gingival crevicular fluid, there is little information concerning their concentrations within either normal or diseased gingival tissues. Therefore, the aim of this study was to evaluate the relationship between the concentrations of gingival interleukin-1 isoforms and the adjacent sulcular depth. MATERIAL AND METHODS: Interdental gingival papillae were excised and grouped based on adjacent pocket depth and the presence of bleeding on probing. Gingiva adjacent to a sulcus of < or = 3 mm without bleeding on probing were classified as 'normal'; gingiva adjacent to a 3-mm sulcus with bleeding on probing were classified as 'diseased-slight'; gingiva adjacent to a 4-6-mm sulcus featuring bleeding on probing were classified as 'diseased-moderate'; and gingiva adjacent to a sulcus of > 6 mm featuring bleeding on probing were classified as 'diseased-severe'. Tissues were solublized and the concentrations of interleukin-1beta, interleukin-1alpha, interleukin-1 receptor antagonist and interleukin-6 were assessed by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance, the post-hoc Tukey test and the Pearson's correlation test. RESULTS: Gingival concentrations of interleukin-6, interleukin-1 receptor antagonist, interleukin-1alpha- and interleukin-1beta were significantly greater at diseased-severe sites than at normal, diseased-slight, or diseased-moderate sites (p < 0.05); the gingival concentrations of interleukin-1 receptor antagonist and interleukin-1alpha were significantly greater at diseased-severe than at diseased-moderate sites (p < 0.05). Interleukin-1 receptor antagonist concentrations were significantly correlated with both interleukin-1alpha and interleukin-1beta concentrations. The ratios of concentrations of the interleukin-1 isoforms were different at the various stages of inflammation. CONCLUSION: Our data indicated a progressive increase in gingival concentrations of interleukin-1 isoforms with increased adjacent sulcular depth. However, within 'diseased' tissues, the proportional concentrations of interleukin-1alpha and -beta to interleukin-1 receptor antagonist were lowest within diseased-severe tissues.

Evidence for a specific crevicular lymphocyte profile in aggressive periodontitis.

BACKGROUND AND OBJECTIVE: It is undisputed that the periodontal pocket is a particular region of the host defense that is dominated by polymorphonuclear leukocytes. However, little is known about the lymphocytes in the crevice. It was the aim of this study to analyse the proportions of T cells (CD3+), T-helper cells (CD4+), T-suppressor cells (CD8+), and B cells (CD20+) in the crevice of patients with localized aggressive periodontitis (LAP), generalized aggressive periodontitis (GAP), and generalized chronic periodontitis (CP). The results were compared with those obtained from periodontally healthy controls. MATERIAL AND METHODS: Crevicular cells were collected according to a previously described method. The lymphocyte subpopulations were analysed by using an indirect immunofluorescence method. RESULTS: Significant differences were established between the test groups and the controls regarding the mean number of CD8+ lymphocytes (LAP > CP and controls; p < 0.05) and CD20+ lymphocytes (LAP/GAP > CP, p < 0.05 and LAP/GAP > controls; p < 0.001). Significant variations in the CD4+/CD8+ ratio were observed (LAP < controls and GAP < controls; p < 0.01), as well as a correlation between the number of T cells and the degree of inflammation. CONCLUSION: In the present study, patients with LAP and patients with GAP were found to have increased numbers of crevicular T-suppressor/cytotoxic and B cells. This supports the hypothesis of a changed immune pathology in patients with aggressive periodontitis.

The changes in T lymphocyte subsets following periodontal treatment in patients with chronic periodontitis.

OBJECTIVE: The aim of this study was to determine whether there was any change in T-lymphocyte subsets in patients with chronic periodontitis after applying different periodontal treatment methods. PATIENTS AND METHODS: Twenty-four patients with chronic periodontitis were included in the study. In every phase of the treatment (pretreatment, initial treatment, curettage and flap operations) the biopsy samples were taken from the gingival tissues at sites of chronic periodontitis. Then CD4(+) and CD8(+) lymphocyte and CD4(+)/CD8(+) ratio values were determined using flow cytometry in the biopsy samples. At the same time, gingival pocket depth, Löe-Silness gingival index, and Silness-Löe plaque index scores were recorded to assess the periodontal status in patients. To determine the correlation between the clinical measurements and the laboratory results obtained before the treatment, after initial treatment, after curettage and after flap operations, we conducted an analysis using a paired t-test. RESULTS: Flow cytometry findings in the patients with chronic periodontitis showed that CD4(+) and CD8(+) lymphocyte values before treatment were under the normal value and the CD4(+)/CD8(+) ratio was within the normal distribution interval. The CD4(+)/CD8(+) ratio decreased postcurettage and postflap operation. This decrease was statistically significant (p < 0.001). The CD4(+) and CD8(+) lymphocyte values were increased postcurettage and postflap operation. This increase was also statistically significant (p < 0.001). CONCLUSIONS: These findings suggest that local immune response was poor in the patients with chronic periodontitis. CD4(+) and CD8(+) T-lymphocytes could play a significant role in chronic periodontitis pathobiology.

Interleukin-11 and IL-17 and the pathogenesis of periodontal disease.

BACKGROUND: Interleukin (IL)-11 and IL-17 are cytokines that modulate the inflammatory process and have not been assessed within normal or inflamed gingival tissues. Our purpose was to compare concentrations of human IL-11 and IL-17 within healthy and diseased human gingiva to determine their possible role in the initiation or progression of periodontal diseases. METHODS: Biopsies from healthy (non-hemorrhagic gingiva adjacent to a < or = 3 mm gingival sulcus) and diseased gingiva (hemorrhagic gingiva adjacent to a > or = 3 mm periodontal pocket) were studied. IL-11, IL-17, RANTES, and IL-6 concentrations were assessed within solubilized gingival biopsies by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance and a post-hoc Tukey honestly significant difference (HSD) test. Regression analysis and partial correlation analysis (adjusted for sample weight) were also used to determine correlations between the variables. RESULTS: Interleukin-11 concentrations were highest within gingiva adjacent to 3 mm diseased pockets (P < 0.001), and IL-17 concentrations were highest at 4 to 5 mm sites compared to other sites (P < 0.001). Gingival concentrations of both cytokines were significantly lower in gingiva adjacent to a > or = 6 mm pocket. RANTES concentrations were significantly greater in gingiva adjacent to > or = 6 mm pockets than in tissues derived from other sites (P < 0.001). IL-11, IL-6, and RANTES concentrations were significantly correlated with sulcular depth. CONCLUSIONS: Gingival concentrations of IL-11 and IL-17 are different in diseased gingiva adjacent to 3, 4 to 5, and > or = 6 mm pockets, suggesting that their concentrations change as a consequence of the progression of gingivitis to periodontitis and that both cytokines could have a significant role in this progression. These data may be useful for the design of procedures for prevention of periodontal disease.

Flow-cytometric analysis of T-lymphocyte subsets after different treatment methods in smokers and non-smokers with chronic periodontitis.

AIM: To determine any change in T-lymphocyte subsets after applying different treatment methods in smokers and non-smokers with chronic periodontitis. PARTICIPANTS: 50 adults with chronic periodontitis. METHOD: The subjects were divided into smokers and non-smokers. Biopsy samples were taken from the gingival pocket wall tissues at sites with chronic periodontitis before treatment, after initial treatment, after curettage and after flap operation and tested for CD4+, CD8+ lymphocyte and CD4/ CD8 ratio values. Gingival pocket depth, gingival index (GI-Löe-Silness) and plaque index (PI-Silness-Löe) scores were also recorded. Analysis aimed at determining the relation between the clinical measurements and the laboratory results. RESULTS: Flow cytometry findings in both groups showed that CD4+ and CD8+ lymphocyte values before treatment were under the normal value while the CD4+/CD8+ ratio was within normal distribution interval. The lymphocyte values observed in the smokers were found to be lower than those in the non-smokers. After treatment the difference between the lymphocyte values in smokers and non-smokers was found to be statistically significant. However, the difference between the CD4/CD8 rate obtained in smokers and non-smokers was not found to be statistically significant. CONCLUSIONS: The lymphocyte values observed in smokers were found to be lower than those in non-smokers after applying different treatment methods and the local immune response was poor in the smokers.

Topical distribution of Fc gammaRI, Fc gammaRII and Fc gammaRIII in inflamed human gingiva.

The topical distribution of Fc gamma receptor types I, II and III (Fc gammaRI-III) was analyzed by means of immunohistochemistry in human gingival tissue obtained from 12 patients with chronic periodontitis. CD68+ macrophages expressing all three classes of Fc gammaR were found throughout the whole gingival connective tissue (CT), whereas dense infiltrates of polymorphonuclear granulocytes (identified by staining for neutrophil elastase) with strong staining for Fc gammaRIII and Fc gammaRII were found subjacent to the apical part of the pocket epithelium (PE) and in the PE itself. CD19+ B lymphocytes with variable staining intensity for Fc gammaRII were observed in clusters subjacent to the PE and extending into the central part of the CT. Only a few scattered CD3+ T lymphocytes stained for Fc gammaRIII. Some spindle-shaped cells (CD68-, therefore non-macrophages) and apparently non-cellular fibrous tissue elements stained for Fc gammaRI and Fc gammaRII. In the epithelium, Fc gammaRII+ dendritic cells were frequently observed in the entire oral gingival epithelium and in the coronal part of the PE. Occasionally, some keratinocytes which stained for Fc gammaRII and Fc gammaRIII were found. The observations indicate that Fc gammaR of the various classes are amply expressed on numerous cell types in inflamed gingival tissue. The specific distribution pattern detected suggests that Fc gammaRs may play a role in the mediation of chronic inflammation in the periodontal lesion.

Some effects of periodontal therapy on local and systemic immunological parameters.

The aim of the present investigation was to study the effect of nonsurgical periodontal therapy on some local (gingival) and systemic host defense characteristics in subjects with advanced periodontal disease. 16 individuals with advanced periodontal disease were recruited. Following a clinical examination, the 3 deepest interproximal sites in the upper and lower premolar- or molar segments were selected for further analysis. Samples from the subgingival microbiota were obtained from the pocket of the selected sites and were prepared for a microbiological examination. The gingival tissue at one of the selected sites was also biopsied. Each excised soft tissue specimen was snap frozen and prepared for immunohistochemical analysis. A sample of peripheral blood was obtained from each individual and prepared for immunohistochemical analysis. Following the baseline examination, all 16 patients received periodontal therapy including oral hygiene instruction and scaling and root planing. Re-examinations regarding the clinical parameters were performed, the subgingival microbiota harvested from the sampling sites and one gingival biopsy was collected at 12 months and 24 months, respectively, among the selected sites. Samples of peripheral blood were obtained from the subjects at the 24-month re-examination. It was demonstrated that non-surgical periodontal therapy effectively reduced symptoms such as gingivitis and probing pocket depth in the subject sample and improved the overall probing attachment level. The treatment applied also markedly reduced (i) the total number of micro-organisms present in selected gingival pockets as well as (ii) the relative proportions of A. actinomycetemcomitans, P. gingivalis and P. intermedia of the subgingival microbiota. The improved clinical condition was, in addition, accompanied by a substantial reduction in the size of the inflammatory lesion (P-ICT) which in the soft tissue samples harvested at baseline was found to reside lateral to the pocket epithelium. Also qualitative alterations occurred in the lesions. Hence, following therapy (i) both the density of CD19 positive cells and the proportion of CD3 positive cells expressing TCR Vbeta genes were reduced in the P-ICT. while (ii) the overall relative number of CD3 positive cells remained unchanged. In conclusion, non-surgical periodontal therapy markedly changed the size and composition of the plaque associated lesion in the gingival tissue but apparently failed to affect the relative distribution of lymphocyte subsets in peripheral blood.

The relationship between concentrations of proinflammatory cytokines within gingiva and the adjacent sulcular depth.

The objective of this study was to determine and compare concentrations and ratios of 3 proinflammatory cytokines, interleukin (IL) IL-1beta, IL-6, and IL-8 within gingival tissue biopsies adjacent to < or = 3, 4 to 6, or >6 mm sulci. All gingiva adjacent to > or = 4 mm sulci had clinical evidence of active inflammation. Factorial analysis of variance suggested significant effects of sulcus depth on the type and concentration of the three cytokines in the adjacent gingiva (P < 0.001). IL-8 concentrations were highest in gingiva adjacent to < or = 3 and lowest adjacent to >6 mm sulci (P < 0.001). In contrast, IL-6 concentrations were lowest in gingiva adjacent to < or = 6 mm and highest adjacent to >6 mm sites. IL-1beta concentrations were highest in gingiva adjacent to >6 mm and lowest adjacent to 4 to 6 mm sites; they were also higher adjacent to < or = 3 mm than adjacent to 4 to 6 mm sites (P < 0.01). Multiple regression analysis suggested that sulcular depth, type of cytokine, and cytokine concentration were significantly correlated (P < 0.001). Ratios of gingival cytokines changed with increased sulcular depth. In gingiva adjacent to < or = 6 mm sites, IL-8 was the most and IL-6 the least prevalent. In gingiva adjacent to > or = 6 mm sites, IL-8 was the least and IL-1-beta the most prevalent. The data suggest that the characteristics of the gingival cytokine network are affected by adjacent sulcular depth. These data could be used to design adjunct diagnostic tests for progression of periodontal diseases.

Serum IgG antibody response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis: implications for periodontal diagnosis.

The relationship of the serum antibody titer and avidity to the putative periodontal pathogens Actinobacillus actinomycetemcomitans (Aa) strains Y4 and 29523 and Porphyromonas gingivalis (Pg) strain 381 were examined in relation to clinical parameters in 26 gingivitis and 28 periodontitis patients. The relationship of antibody titer and avidity to infection with the homologous organism was also examined in a subset of 30 patients. Antibody titer was determined by an enzyme-linked immunosorbent assay, and antibody avidity was assessed using a dissociation assay. Considering all patients, there was a significant negative correlation between mean probing depth and antibody titer (r=-0.28) and avidity (r=-0.28) to Aa Y4. There was a significant positive correlation of probing depth and antibody titer (r=0.46) and avidity (r=0.46) to Pg. The correlation of antibody titer and avidity to Aa and infection with Aa Y4 (r=-0.32, r=-0.21) and Aa 29523 (r=-0.35, r=-0.39) was negative, while the correlations of titer and avidity to Pg and presence of the organisms was strongly positive (r=0.40, r=0.35). These data indicate that the relationship of serum antibody titer and avidity to clinical parameters of periodontal disease severity and the level of infection with the homologous organism appears to be different for Aa and Pg. The development of an antibody response to Aa appears to protect the individual from infection with the organism. In contrast, the development of an antibody response to Pg was not able to eliminate the infection. These results should be considered when developing a diagnostic strategy for periodontal disease utilizing the humoral immune response.

A comparison of IgG antibody reactive with Bacteroides forsythus and Porphyromonas gingivalis in adult and early-onset periodontitis.

Recent work has indicated that Bacteroides forsythus and Porphyromonas gingivalis are significant local risk factors for periodontitis. Several reports find that both organisms are frequently associated with periodontitis lesions and often are present together. We have previously shown that early-onset periodontitis patients seropositive for P. gingivalis have less attachment loss than seronegative patients. In this study, we determined serum IgG antibody concentrations reactive with B. forsythus in adult and early-onset periodontitis patients using an ELISA and used P. gingivalis in the same populations as a positive control. The results for P. gingivalis were consistent with previous work and indicated that 47%, 36%, and 33% of adult, generalized early-onset, and localized juvenile patients were seropositive, respectively. Mean serum IgG concentrations for the three groups were 5.36 microg/ml, 5.65 microg/ml, and 5.44 microg/ml for adult, generalized early-onset, and localized juvenile patients, respectively. In contrast, for B. forsythus only 11%, 14%, and 10% of adult, generalized early-onset, and localized juvenile patients were seropositive, with mean serum IgG concentrations of 0.46 microg/ml, 0.46 microg/ml, and 0.47 microg/ml, respectively. This suggests that B. forsythus is either poorly immunogenic or less invasive than P. gingivalis. If most patients fail to mount an immune response to B. forsythus and it is invasive, it may explain why this organism is a risk factor for disease.

Life and death in the three millimeter pocket.

Periodontal diseases are, in part, the result of an interaction of the patient's immune system with the local bacterial population. We can measure the result of the interaction and sometimes repair it. We can identify the bacteria involved in the process. What we cannot do is measure the patient's immune regulators; therefore we cannot predictably measure the recrudescence of disease activity or differentiate before hand the presence of refractory disease. We need fast, comfortable, inexpensive methods to measure the patient's immune regulators.

Immunohistochemical characterization of lymphocyte subsets in chronic adult periodontitis.

It is well known that interactions between microbial dental plaque and the host immune system play a major role in the etiopathogenesis of periodontal disease. The aim of the present study was to analyze the phenotypic properties of gingival T lymphocytes and subsets in patients with chronic inflammatory adult periodontitis (AP) showing various degrees of inflammation and to relate the results to the immunopathogenesis of AP. Gingival biopsies were obtained from patients aged between 26 and 52 yr who were grouped according to gingival index scores (GI) of 1, 2, and 3. Using immunohistochemical techniques, T cells (CD2+), T-helper cells (CD4+) and T-suppressor cells (CD8+) were identified in three well-defined areas of the biopsy samples. Moreover, peripheral blood was collected from the same patients, and relative counts of B cells (CD19+), HLA-DR+ cells and IL-2R+ cells as well as CD3+, CD4+, CD8+ cells were determined using three color flow cytometry. While the blood results were found to be within the normal ranges, the relative counts of CD4+ cells showed statistically significant decreases as the GI score increased. Similarly, the CD4+/CD8+ ratio also decreased. Moreover, gingival T lymphocyte and subset counts appeared to be related to the severity of gingival inflammation. Particularly, CD4+ cells showed a significant increase with the GI score. Furthermore, the CD4+/CD8+ ratio beneath the pocket epithelium was apparently correlated with increasing GI score (p < 0.05). The cytotoxic effect of CD8+ cells seems to be more prominent at the local level while the suppressor effect is more active systematically. This means that the price of systemic protection appears to be local destruction.

Antibody responses to suspected periodontal pathogens in elderly subjects with periodontal disease.

Little is known about the relationship of aging to periodontal disease. The immune response undergoes aging-related changes resulting in loss of functional capacity. The aim of this study was to investigate the relationship between levels of serum IgG antibodies against suspected periodontal pathogenic microorganisms to the presence or absence of periodontal disease in an elderly (65-75 yrs) population. From this study, we obtained information concerning: (1) the ability to differentiate elderly individuals without disease from those with disease by their levels of antibodies against periodontal pathogens and (2) which periodontal pathogen(s) triggered those responses. IgG anti- Porphyromonas gingivalis (strains W83 and 381) levels in the serum of elderly patients with severe periodontal disease were the only antibody responses measured which were elevated compared to the elderly control group of subjects with no periodontal disease. Anti- Prevotella intermedia IgG levels in both elderly patient groups were depressed compared to anti- P. intermedia levels in the young normal control subjects. Serum IgG antibody levels to six other plaque microorganisms did not differentiate between diseased and normal, elderly or young subjects. This data suggested that P. gingivalis was associated with periodontal disease in this elderly group of individuals and that those elderly individuals were able to respond with a normal IgG immune response.

Immunohistochemical study of gamma delta T cells in human gingival tissues.

The distribution and the density of gamma delta T cells in human gingival tissues were examined immunohistochemically in biopsy samples obtained from 20 subjects. Few gamma delta T cells were observed in gingival tissue free from inflammatory cell infiltration, but were found, albeit in low numbers, in association with inflammatory cell infiltration, especially T cells. This relationship with T cells was confirmed statistically. The ratios of gamma delta T cells to T cells in the epithelia and in the connective tissue were calculated in the sections in which more than 500 CD3-positive cells were identified. Seven of eight such epithelial specimens showed a ratio of less than 1% and one less than 2% (mean +/- SD; 0.8% +/- 0.4). In the connective tissue, 8 of 13 such specimens showed less than 1%, three less than 2%, one 3%, and one 7% (1.4% +/- 1.9). These results suggest that basically gamma delta T cells are not resident cells in the gingival epithelium such as comprise the first defense line against exogenous irritation. They may play some role in the pathogenesis of periodontal disease collaborating with alpha beta T cells in the inflammatory response.

Immunoglobulin isotypes in gingival crevicular fluid: possible protective role of IgA.

In order to simultaneously assess the local humoral immune and polymorphonuclear leukocyte (PMN) responses in periodontal disease, IgG, IgM, and IgA, as well as the PMN lysosomal enzyme beta-glucuronidase (beta G), were examined in gingival crevicular fluid (GCF) from patients with varying degrees of periodontal pathology. Evaluations were made before and after conservative therapy (scaling and root planing). Thirty patients with varying degrees of periodontal pathology, ranging from mild inflammatory gingivitis to moderate periodontitis, were studied. GCF was collected from the mesial surfaces of all teeth. The presence of the 3 immunoglobulin isotypes was determined by enzyme linked immunosorbent assays (ELISA), while total beta G activity in GCF was determined by a fluorometric assay. Clinical parameters were obtained from 6 sites per tooth. Our data indicate that prior to treatment, total beta G activity is strongly related to the severity of periodontal disease as measured by mean probing attachment level (AL; r = 0.89; P < .005), mean probing depth (PD; 4 = 0.89; P < .0005) and percentage of sites exhibiting bleeding on probing (% BOP; r = 0.49; P < .005). Following treatment, no statistically significant relationship of disease severity and beta G is found. The concentrations of IgG and IgM in GCF do not follow a specific pattern when related to disease severity. In contrast, prior to treatment the concentration of IgA is negatively correlated to mean AL (r = -0.54; P < .005), mean PD (r = -0.59; P < .005), and % BOP (r = -0.47, P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)

[The phagocytosis of polymorphonuclear neutrophilic granulocytes in progressive periodontitis]. / Phagozytose der polymorphkernigen neutrophilen Granulozyten bei der progressiven Parodontitis.

The aim of this paper was the evaluation of the phagocytic activity of neutrophils in blood and in gingival pocket fluid in patients suffering from rapidly progressive periodontitis (RPP) and postjuvenile periodontitis (PJP). Prior to periodontal treatment the authors evaluated the capacity to phagocytose latex particles of peripheral blood neutrophils from 21 patients with RPP, 51 with PJP and 59 healthy subjects (control group) as well as the phagocytic activity of neutrophils in pocket fluid from 21 patients with RPP, 14 with PJP and from 20 healthy subjects. This phagocytic activity was significantly lower in all examined groups in comparison with the control group. A similar evaluation executed 3 months after treatment revealed normal phagocytosis of blood neutrophils from patients with RPP. In patients receiving complementary pharmacotherapy (spiramycine combined with metronidazol), a better improvement of phagocytosis was noted, than that observed in patients treated only surgically.

Distribution of ICAM-1, LFA-3 and HLA-DR in healthy and diseased gingival tissues.

Cell adhesion molecules are involved in recognition and effector aspects of the host response, including the control of migration of leukocytes into inflammatory sites. In this study we have demonstrated that the distribution of three cell-surface molecules involved in cell interactions, ICAM-1, LFA-3 and HLA-DR is distinct and different in healthy and diseased gingival tissue. ICAM-1 was consistently expressed by junctional epithelial cells in healthy gingiva and by pocket epithelium in diseased gingiva but was not detectable on the majority of keratinocytes in external gingival epithelium. ICAM-1 was also expressed by endothelial cells of gingival blood vessels and a subset of leukocytes in the infiltrated connective tissue in both healthy and diseased gingiva. HLA-DR and LFA-3 were also expressed by epithelial cells and endothelial cells but in patterns which were distinctly different from ICAM-1.

Local immunoglobulin synthesis in juvenile periodontitis: initial findings.

An electro-immunoassay technique was used to determine simultaneously immunoglobulin G (IgG) and albumin concentrations in serum and extracts of gingival tissue comprising the pocket wall. Assays of samples obtained from seven patients with juvenile periodontitis (mean age, 18 years) indicated that local synthesis accounted for 72% of the IgG found in the gingiva.