Assessment of interleukin-6 receptor inhibition therapy on periodontal condition in patients with rheumatoid arthritis and chronic periodontitis.

BACKGROUND: Overproduction of interleukin (IL)-6 may play a pathologic role in rheumatoid arthritis (RA) and chronic periodontitis (CP). The present study assesses IL-6 receptor (IL-6R) inhibition therapy on the periodontal condition of patients with RA and CP. METHODS: The study participants were 28 patients with RA and CP during treatment with IL-6R inhibitor, and 27 patients with RA and CP during treatment without IL-6R inhibitor. Periodontal and rheumatologic parameters and serum levels of cytokine and inflammatory markers and immunoglobulin G against periodontopathic bacteria were examined after medication with IL-6R inhibitor for 20.3 months on average (T1) and again 8 weeks later (T2). RESULTS: No differences were observed between the groups in any parameter values at T1, except for serum IL-6 levels. The anti-IL-6R group showed a significantly greater decrease in gingival index, bleeding on probing (BOP), probing depth (PD), clinical attachment level (CAL), and serum levels of IL-6 and matrix metalloproteinase (MMP)-3 from T1 to T2 than the control group (P <0.05). A significant correlation was found between changes in serum anticyclic citrullinated peptide levels and those in PD and CAL in the anti-IL-6R group (P <0.05), whereas both groups exhibited a significant association between changes in serum MMP-3 levels and those in BOP (P <0.05). CONCLUSION: Changes in periodontal and serum parameter values were different between the patients with RA and CP during treatment with and without IL-6R inhibitor.

Assessment of the plasma/serum IgG test to screen for periodontitis.

Chronic periodontitis is a silent infectious disease prevalent worldwide and affects lifestyle-related diseases. Therefore, efficient screening of patients is essential for general health. This study was performed to evaluate prospectively the diagnostic utility of a blood IgG antibody titer test against periodontal pathogens. Oral examination was performed, and IgG titers against periodontal pathogens were measured by ELISA in 1,387 individuals. The cut-off value of the IgG titer was determined in receiver operating characteristic curve analysis, and changes in periodontal clinical parameters and IgG titers by periodontal treatment were evaluated. The relationships between IgG titers and severity of periodontitis were analyzed. The best cut-off value of IgG titer against Porphyromonas gingivalis for screening periodontitis was 1.682. Both clinical parameters and IgG titers decreased significantly under periodontal treatment. IgG titers of periodontitis patients were significantly higher than those of healthy controls, especially in those with sites of probing pocket depth over 4 mm. Multiplied cut-off values were useful to select patients with severe periodontitis. A blood IgG antibody titer test for Porphyromonas gingivalis is useful to screen hitherto chronic periodontitis patients.

Antibody responses to periodontopathic bacteria in relation to rheumatoid arthritis in Japanese adults.

BACKGROUND: Periodontopathic bacteria have been implicated as contributory to the etiology of rheumatoid arthritis (RA). Anticyclic citrullinated peptide (CCP) antibodies and rheumatoid factor (RF) were shown to be associated with RA. This study examines whether serum levels of antibodies to periodontopathic bacteria may affect clinical and laboratory profiles of RA. METHODS: The study participants consisted of 80 patients with RA, and 38 age-, sex-, smoking status-, and periodontal condition-balanced healthy controls. After periodontal and rheumatologic examination, serum levels of immunoglobulin G (IgG) antibodies to Porphyromonas gingivalis (Pg), Prevotella intermedia, Aggregatibacter actinomycetemcomitans (Aa) (previously Actinobacillus actinomycetemcomitans), and Eikenella corrodens (Ec) and those of anti-CCP antibodies and RF were determined by an enzyme-linked immunosorbent assay. RESULTS: Patients with RA showed significantly higher levels of anti-Pg and anti-CCP antibodies than controls (P = 0.04 and P <0.0001). In contrast, IgG responses to Aa and Ec in patients with RA were significantly lower than those in controls (P <0.0001 and P = 0.0001). Multiple logistic regression analysis revealed a significant association of anti-Pg and anti-Aa IgG responses with RA, after adjustment for age, sex, and smoking (P = 0.005 and P = 0.02). Anti-Pg titer displayed a significant correlation with RF levels, probing depth, and clinical attachment level (P = 0.03, P = 0.03, and P = 0.02). CONCLUSION: These results suggest that serum levels of anti-Pg IgG antibodies were associated with RA, and might affect serum levels of RF and periodontal condition in patients with RA.

Granulocyte chemotactic protein 2 (gcp-2/cxcl6) complements interleukin-8 in periodontal disease.

BACKGROUND AND OBJECTIVE: Mucosal inflammatory responses are orchestrated largely by pro-inflammatory chemokines. The chemokine granulocyte chemotactic protein 2 (CXCL6) is involved in neutrophil recruitment and migration. Previous studies have shown that granulocyte chemotactic protein 2 is up-regulated during mucosal inflammation (e.g. in inflammatory bowel disease), similarly to the functionally and structurally related chemokine interleukin-8. Nevertheless, unlike interleukin-8, a role of granulocyte chemotactic protein 2 in gingival inflammation has not been yet demonstrated. In this study we aimed to evaluate the expression of the chemokine granulocyte chemotactic protein 2 in clinically healthy vs. diseased gingival tissues and to explore possible correlations with clinical and microbiological markers of periodontitis. MATERIAL AND METHODS: Gene expression in 184 'diseased' and 63 'healthy' gingival tissue specimens from 90 patients with periodontitis was analyzed using Affymetrix U133Plus2.0 arrays. The expression of granulocyte chemotactic protein 2 was further confirmed by real-time reverse transcription-polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay, while the localization of granulocyte chemotactic protein 2 in gingival tissues was analyzed by immunohistochemistry. Plaque samples from the adjacent periodontal pockets were collected and evaluated for 11 species of periodontal bacteria using checkerboard DNA-DNA hybridizations. RESULTS: Among all known chemokines, GCP-2 expression was the most up-regulated (3.8-fold, p < 1.1 x 10(-16)), in 'diseased' vs. 'healthy' tissue as compared to a 2.6-fold increased expression of interleukin-8 mRNA (p < 1.2 x 10(-15)). Increased expression of granulocyte chemotactic protein 2 correlated with higher levels of 'red' and 'orange' complex pathogens and with increased probing depth, but not with attachment loss. Immunohistochemistry showed that granulocyte chemotactic protein 2 was expressed in gingival vascular endothelium. CONCLUSION: The level of expression of granulocyte chemotactic protein 2 correlates with the severity of periodontitis and appears to act as a hitherto unrecognized functional adjunct to interleukin-8 in diseased gingival tissues.

Streptococcus cristatus attenuates Fusobacterium nucleatum-induced interleukin-8 expression in oral epithelial cells.

BACKGROUND AND OBJECTIVE: Oral epithelial cells may be invaded by a polymicrobial intracellular flora, including pathogens together with commensals. Various oral pathogens can induce the production of interleukin-8, a potent neutrophil chemotractant, in oral epithelial cells. Evidence from the gut suggests that commensal species may modulate inflammatory responses to pathogens. The aim of this study was to examine the interleukin-8 responses of oral epithelial cells to an oral pro-inflammatory species, Fusobacterium nucleatum, in combination with an oral commensal, Streptococcus cristatus. MATERIAL AND METHODS: KB, TERT-2, TR146 and SCC15 cells were cocultured with F. nucleatum and S. cristatus, either alone or in combination, at 37 degrees C in 5% CO2 under various conditions. The mRNA expression of interleukin-8 was analyzed by reverse transcription-polymerase chain reaction and protein secretion was measured by enzyme-linked immunosorbent assay. RESULTS: F. nucleatum alone evoked a potent interleukin-8 response, whereas S. cristatus alone did not induce significant interleukin-8 expression in oral epithelial cells. When present together, S. cristatus attenuated the F. nucleatum-induced interleukin-8 production in the four oral epithelial cell lines to varying degrees. The inhibitory effect of S. cristatus was independent of its viability and its co-aggregation with F. nucleatum, was not related to soluble bacterial products and appeared to require bacterial contact with epithelial cells. Similar effects were seen with several other species of oral streptococci. CONCLUSION: Our data suggest that S. cristatus may exert immunomodulatory effects on the interleukin-8 response of oral epithelial cells to F. nucleatum challenge.

Susceptibility of various oral bacteria to antimicrobial peptides and to phagocytosis by neutrophils.

BACKGROUND AND OBJECTIVE: The aim of this study was to compare the susceptibility of nonperiodontopathic and periodontopathic bacteria to major defense mechanisms for bacterial clearance in gingival sulcus. MATERIAL AND METHODS: Twenty strains of 13 oral bacterial species were studied for their susceptibility to phagocytosis by human neutrophils and to the antimicrobial peptides LL-37 and human beta defensin-3. The minimum inhibitory concentrations of LL-37 and human beta defensin-3 were determined by a liquid dilution assay, and susceptibility to phagocytosis was examined by a flow cytometric phagocytosis assay. RESULTS: The minimum inhibitory concentrations of LL-37 and human beta defensin-3 varied greatly, depending on the strain and species. Although a significant difference between the non- and periodontopathic groups was not observed, the red-complex bacteria were more resistant to LL-37 than the others (p=0.004). The susceptibility of oral bacteria to phagocytosis was quite variable, depending on the species but not on the strains. The periodontopathic bacteria, especially Actinobacillus actinomycetemcomitans and the red-complex triad, were more resistant to phagocytosis than were the nonperiodontopathic bacteria (p=0.0003). In addition, bacteria resistant both to antimicrobial peptides and to phagocytosis were more common in the periodontopathic group. CONCLUSION: Our results indicate that immune evasion may contribute to the pathogenicity of some periodontopathic bacteria.

Antibody-based diagnostic for 'refractory' periodontitis.

OBJECTIVE: About 10-15% of US adults are 'refractory' to therapy for chronic periodontitis. Recently, studies suggest that these patients have elevated lysine decarboxylase activity in the sulcular microbiota. The aim of this study was to determine whether an elevated IgG antibody response to lysine decarboxylase, alone or with antibody to other bacterial antigens and baseline clinical measurements, would predict 'refractory' patients with high accuracy. METHODS: Chronic periodontitis patients were treated using scaling and root planing (SRP) followed by maintenance SRP and 3-monthly re-examinations. If there was a loss of mean full mouth attachment or more than three sites appeared with > 2.5 mm new loss within a year, the subjects were re-treated (modified Widman flap surgery and systemically administered tetracycline). If attachment loss as above recurred, the subjects were 'refractory'. Baseline clinical measurements and specific antibody responses were used in a logistic regression model to predict 'refractory' subjects. RESULTS: Antibody to a peptide portion of lysine decarboxylase (HKL-Ab) and baseline bleeding on probing (BOP) prevalence measurements predicted attachment loss 3 months after initial therapy [pIAL = loss (0) or gain (1)]. IgG antibody contents to a purified antigen from Actinomyces spp. (A-Ab) and streptococcal d-alanyl glycerol lipoteichoic acid (S-Ab) were related in 'refractory' patients (R2 = 0.37, p < 0.01). From the regression equation, the relationship between the antibodies was defined as linear (pLA/S-Ab = 0) or non-linear pLA/S-Ab = 1). Using pLA/S-Ab, pIAL and age, a logistic regression equation was derived from 48 of the patients. Of 59 subjects, 37 had 2-4 mm attachment loss and were assigned as 'refractory' or successfully treated with 86% accuracy. CONCLUSION: HKL-Ab facilitated an accurate prediction of therapeutic outcome in subjects with moderate periodontitis.

Associations between serum antibody levels to periodontal pathogens and early-onset periodontitis.

BACKGROUND: The role of antibodies to periodontal microorganisms in the development of periodontal tissue destruction is still unclear. The aim of this study was to investigate the association between serum levels of IgG, IgA, and IgM antibodies to 6 periodontal microorganisms and clinical subtypes of varying severity of early-onset periodontitis (EOP) in young African American adults. METHODS: The study group consisted of 159 African Americans aged 19 to 25 years (mean 22 years) and included 97 cases with EOP and 62 controls with no clinical signs of EOP. These subjects were selected from a nationally representative sample of adolescents who received an oral examination as part of the National Survey of Oral Health of United States Children in 1986-1987. The group was examined clinically a second time 6 years later and blood samples were collected. Serum levels of IgG, IgA, and IgM reactive to Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Campylobacter rectus, Eikenella corrodens, and Fusobacterium nucleatum were assessed. RESULTS: Serum levels of IgG and IgA antibody reactive to P. gingivalis and A. actinomycetemcomitans and IgA antibody to P. intermedia were significantly higher in generalized EOP cases compared to healthy controls. IgM antibody levels did not show any significant associations with EOP for any of the 6 bacterial species tested. There were no significant differences in antibody levels between controls and the 13 subjects in our study who were classified with localized EOP. CONCLUSIONS: The findings suggest that antibodies to P. gingivalis, P. intermedia, and A. actinomycetemcomitans may play a significant role in the pathogenesis of EOP. Substantial longitudinal studies that monitor antibody levels and avidity prior to disease onset, during progression, and following clinical intervention will be necessary to fully understand the role of this component of the immune response in protection versus tissue destruction and the potential use in EOP risk assessment and disease management.

Serum phenytoin concentration and IgG antibody titre to periodontal bacteria in patients with phenytoin-induced gingival overgrowth.

Epileptic patients taking phenytoin with gingival-overgrowth and those without gingival-overgrowth were compared for daily drug dose, plasma total phenytoin concentration, plasma free-phenytoin concentration and serum IgG antibody titre against 13 periodontal bacteria. Significantly higher daily drug dose was noted in patients with gingival overgrowth (P < 0.05) when compared with those without overgrowth. In addition, both total and free forms of plasma phenytoin concentration were significantly higher in sera of patients with gingival growth than of those without overgrowth (P < 0.01). Strong positive correlation was found between daily drug dose and serum phenytoin concentration in patients with gingival overgrowth, while weak correlation was found in patients without gingival overgrowth, suggesting a difference in drug metabolism in these two groups. However, no differences were found in serum IgG antibody titres to 13 periodontal bacteria examined between two groups. These results suggest that metabolic ability of phenytoin is one of the factors for developing gingival overgrowth, and that periodontal infection may not be a primary causative factor for gingival overgrowth but act as an additive factor which increase tissue mass for this unwanted side effect.

[Analysis using ELISA test of antibody response to Fusobacterium nucleatum and Eikenella corrodens in subjects with periodontal disease]. / Análisis mediante una prueba de ELISA de la respuesta de anticuerpos frente a Fusobacterium nucleatum y Eikenella corrodens en sujetos con enfermedad periodontal.

BACKGROUND: To know the synthesis of IgG, IgA, and IgM to Fusobacterium nucleatum and Eikenella corrodens in serum, crevicular liquid and saliva in subjects with periodontal disease, using ELISA test. PATIENTS AND METHODS: We studied 26 patients with high bias to the disease aged less than 35 years and 30 individuals with comparable age and with scarce bias to the disease. RESULTS: No differences were found for IgG and IgM titers between the groups, except for IgM to E. corrodens. For IgA, differences were found when the saliva and crevicular liquid were studied for both bacteria, as occurred in serum IgA compared to E. corrodens. In all the cases antibody levels were lower in the patients. CONCLUSIONS: The lower synthesis of IgM and IgA, fundamentally the latter, to F. nucleatum and E. corrodens in patients with periodontal disease would contribute to the pathogenesis of this illness.

Interleukin-6 (IL-6) and IL-8 are induced in human oral epithelial cells in response to exposure to periodontopathic Eikenella corrodens.

Periodontitis is the inflammatory response in periodontal tissues elicited by bacterial colonization in periodontal pockets. In this response, pocket epithelial cells are the first cells to come into contact with bacteria. To elucidate this mechanism, we determined the adherence of the periodontopathic bacterium Eikenella corrodens 1073, which has a GalNAc-sensitive lectin-like adhesin (EcLS), to a human oral epithelial carcinoma cell line (KB) and the induction of proinflammatory cytokine production in the cells following exposure to this bacterium in vitro. In the adherence assay, EcLS played a role as the adhesin of this bacterium in adherence to KB cells. In a reverse transcriptase PCR, significant interleukin-8 (IL-8) and IL-6 mRNA levels were induced in response to exposure to this bacterium. In an enzyme-linked immunosorbent assay after an 8-h bacterial exposure, the IL-8 and IL-6 protein levels were 13.5- and 8.3-fold higher than those in the nonexposed controls, respectively. These protein responses were time dependent. Interestingly, when E. corrodens was separated from KB cells by cell culture inserts, a slight stimulation of the IL-6 and IL-8 mRNA and secreted protein levels was seen. These results imply that the direct contact of E. corrodens 1073 with oral epithelial cells is not necessarily required for the stimulation of IL-6 and IL-8 secretion. We suggest that E. corrodens induces the epithelial cells to secrete proinflammatory cytokines which serve as an early signaling system to host immune and inflammatory cells in underlying connective tissues.

Periodontal findings and systemic antibody responses to oral microorganisms in Behçet's disease.

BACKGROUND: Behçet's disease is a multisystem disorder of unknown etiology, affecting predominantly the oral mucosa, skin, and eyes. Recurrent and painful episodes of oral ulcerations interfere with regular oral hygiene leading to rapid bacterial plaque accumulation. The aims of this study were to evaluate the periodontal status of patients with Behçet's disease and determine serum antibody responses to selected oral microorganisms, including major periodontopathogens in these patients. METHODS: Thirty-three patients with Behçet's disease and 15 healthy subjects were included in the study. Plaque, sulcular bleeding, periodontal index scores, probing depths, and total number of teeth were recorded. Serum IgG antibody levels to a panel of 13 oral microorganisms were determined. RESULTS: Significantly higher values for each of the clinical measures were observed in patients with Behçet's disease compared to healthy subjects (P <0.0001). Antibody levels to selected members of plaque, including Actinomyces viscosus, Streptococcus mutans, Streptococcus sanguis, Streptococcus oralis, Eikenella corrodens, Campylobacter rectus, and Prevotella intermedia were significantly lower in patients with Behçet's disease than in controls (P <0.001-0.05). In contrast, these patients exhibited significantly elevated antibody levels to Actinobacillus actinomycetemcomitans Y4 compared to controls (P <0.01). CONCLUSIONS: Our data indicate that the patients with Behçet's disease generally exhibit clinical findings of established periodontal disease. Decreased antibody responses to early colonizers of both supra- and subgingival plaque were observed along with the elevation in antibody levels to A. actinomycetemcomitans. These results suggest that the bacterial plaque ecology and/or immune responses to these microorganisms may be affected in Behçet's disease which could lead to changes in the expression of periodontal disease.

Analysis of serum antibody responses to periodontopathogens in early-onset periodontitis patients from different geographical locations.

Serum antibody specificity to oral micro-organisms was used to delineate the pathogens associated with early-onset periodontal diseases in a Turkish population. Additionally, comparison of the findings to those derived from a clinically similar US patient population described differences in bacterial specific antibody between these 2 geographic regions. Serum from 89 (LJP), 86 (RPP) and 94 (normal) subjects was analyzed (ELISA) to determine IgG antibody to 14 oral micro-organisms. All LJP patients from Turkey exhibited elevated antibody levels to A. actinomycetemcomitans (serotypes c and a significantly increased), while antibody levels to A. actinomycetemcomitans Y4 and JP2 (serotype b) were significantly higher in US LJP patients. 50% of the Turkish RPP patients also showed elevated anti-A. actinomycetemcomitans antibody, although the US RPP patients exhibited significantly higher antibody levels and frequency of elevated antibody to the A. actinomycetemcomitans serotypes. Healthy subjects and LJP and RPP patients from the US exhibited higher antibody levels to all 3 P. gingivalis serogroups compared to those from Turkey, although, the frequency of elevated antibody to the P. gingivalis serogroups was significantly higher in LJP and RPP patients from Turkey than from the US. Interestingly, 87% and 77% of the LJP patients in the Turkish population had elevated antibody responses to P. gingivalis and E. corrodens, respectively, which was not observed in the US LJP patients. These data suggested that considerable variation exists in the systemic antibody levels to periodontopathogens between these 2 countries. This supports potential differences in subgingival colonization or antigenic composition of these pathogens between patient populations from different geographical regions.

Variable serum immunoglobulin G immune response to genetically distinct Eikenella corrodens strains coexisting in the human oral cavity.

This study examined the variable serum immunoglobulin G (IgG) levels to genetically distinct autologous Eikenella corrodens strains by enzyme-linked immunosorbent assay (ELISA). Twenty subjects, including 10 adult periodontitis patients, 5 juvenile periodontitis patients and 5 periodontally healthy subjects were examined. Each subject was colonized by 2-8 genetically distinct E. corrodens strains. The serum IgG levels to autologous E. corrodens within individuals were significantly different in 7 adult periodontitis patients, 4 juvenile periodontitis patients and a periodontally healthy subject. Poor correlation was found in diseased subjects between serum IgG levels to autologous strains and to reference strains ATCC 23834 or FDC 373. Four adult periodontitis patients and two juvenile periodontitis patients exhibited significant serum IgG levels to autologous E. corrodens strains (two standard deviations above the mean for periodontally healthy subjects); two of these six diseased subjects exhibited low serum IgG levels to reference strains and would have been classified as low immune responders if only reference strains had been used in ELISA. This study showed the importance of using autologous E. corrodens strains in the assessment of serum IgG immune responses to this organism.

Molecular analysis of the gene encoding a protein component of the Eikenella corrodens adhesin complex that is close to the carbohydrate recognition domain.

A monoclonal antibody against a lectin-like substance (LS) of Eikenella corrodens (Ec) was used for screening the Ec DNA library. Three positive clones that carried an identical 12-kb segment were obtained. A 25-kDa protein, which specifically binds to the antibody, was overproduced in all of the Escherichia coli clones. Deletion analysis showed that the gene encoding the 25-kDa protein was located within a 1.2-kb segment. The nucleotide (nt) sequence of this segment contained an open reading frame encoding a protein of 24600 Da. We purified the 25-kDa protein from the cloned E. coli strain. The sequence of the first 10 amino acids(aa) from the N-terminus of the purified 25-kDa protein agreed with that deduced from the nt sequence. Since the monoclonal antibody used in this study inhibits the physiological activity of EcLS, we concluded that the 25-kDa protein is a component of the adhesin complex, which is located near the carbohydrate recognition domain of lectin in EcLS.

An Eikenella corrodens toxin detected by plaque toxin-neutralizing monoclonal antibodies.

Bacterial plaque from the gingival region of teeth contains cytotoxic agents which lyse undifferentiated human HL60 cells. A small panel of monoclonal antibodies (MAbs) was found to abrogate much of this activity and to detect antigens in certain strains of Streptococcus mitis and Eikenella corrodens. The aim of this study was to determine whether these bacterial antigens might be involved in HL60 cells cytolysis. Saline extracts were obtained by homogenizing washed, stationary-phase cells in 65 mM NaCl with a tight-fitting Potter-Elvehjem homogenizer. The extracts of E. corrodens were toxic to HL60 cells, whereas similar extracts of S. mitis were nontoxic. Adding plaque toxin-neutralizing MAb 3hE5 blocked the toxic effect of E. corrodens extract S. mitis extracts contained a single, strongly reactive antigen of 140 kDa (s140K antigen) detected on Western blots (immunoblots) by three MAbs from the panel. Rabbit antibodies raised to this antigen excised from the gel (anti-s140K serum) detected larger antigens in addition to s140K. E. corrodens extracts contained a number of antigens detected by the MAbs. Immunoglobulin G (IgG) was purified from anti-s140K serum by passage through DE52 cellulose. A 100-fold excess (by weight) of the purified IgG to E. corrodens protein specifically cross-precipitated an 80-kDa antigen plus a nonantigenic 16-kDa protein, presumably attached noncovalently. The remaining supernatant fraction had no toxic activity. A similar ratio of control IgG (from nonimmunized rabbits) did not precipitate these proteins, and the supernatant fraction had the same activity as the extract not treated with IgG. The proteins of 80 and 16 kDa were also detected in the anti-s140K immunoprecipitate by rabbit IgG antibodies to E. corrodens whole cells. The 80-kDa antigen, alone or complexed with the 16-kDa protein, may be involved in mediating the toxic activity in E. corrodens and plaque extracts.

Effect of periodontal treatments on serum IgG antibody titers against periodontopathic bacteria.

Serum IgG antibody titers to 7 periodontopathic bacteria in periodontitis patients were measured at the 1st visit and after various periodontal treatments with clinically successful improvement, in order to evaluate what kind of factors are associated with changes of serum antibody titers. 20 patients (10 male and 10 female from 23 to 61 years old) with adult, rapidly progressive periodontitis were enrolled in this study. All patients received initial preparation and most of them also underwent surgical procedure. After the treatments, the mean probing pocket depths decreased from 3.72 mm to 1.56 mm. Serum samples were collected from patients at the initial and final examinations. Serum IgG antibody titers against sonicated antigens of Porphyromonas gingivalis FDC 381, Prevotella intermedia ATCC 25611, Prevotella loescheii ATCC 15930, Fusobacterium nucleatum subspecies nucleatum ATCC 25586, Actinobacillus actinomycetemcomitans FDC Y4, Eikenella corrodens FDC 1073 and Capnocytophaga ochracea # M 12 were determined by enzyme-linked immunosorbent assay. The mean antibody titers to P. gingivalis and P. intermedia decreased significantly after the treatment as compared to their pretreatment levels. The antibody titer to P. gingivalis, especially, decreased in all of the patients examined. A significant relationship was found between the decreased antibody titer to P. gingivalis and the number of teeth which received periodontal surgery, as well as treatment length, and the relationship between the decreased antibody titer to P. intermedia and the number of extracted teeth was also significant. These results suggest that the changes of serum IgG titers against P. gingivalis and P. intermedia are related to the suppression of such pathogens in subgingival plague.

Some suspected periodontopathogens and serum antibody response in adult long-duration insulin-dependent diabetics.

The subgingival microflora and serum antibody response were examined in long-duration insulin-dependent diabetics and age- and sex-matched non-diabetics. The material consisted of 9 diabetics aged 40-49 years and 19 aged 50-59 years, 13 non-diabetics aged 40-49 years and 21 aged 50-59 years. The bacterial species studied (Actinobacillus actinomycetemcomitans, Campylobacter rectus, Capnocytophaga spp, Eikenella corrodens, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia) were recovered in diabetics as well as in non-diabetics. Significantly more diabetics in both age groups harboured P. gingivalis compared to non-diabetics. Prevalence of P. gingivalis was associated with deepened periodontal pockets among non-diabetics but not among diabetics. In diabetics and non-diabetics, the serum antibody titres for most antigens were similar.