Search

Objective: This study aimed to investigate the association of GCF TREM‐1, PGLYRP1, and IL‐1β levels with periodontal health in pre‐ and postmenopausal women. Background: Triggering receptor expressed on myeloid cells 1 (TREM‐1), activated through its ligand peptidoglycan recognition protein 1 (PGLYRP1), stimulates proinflammatory cytokine production, such as interleukin (IL)‐1β, during periodontal inflammation. Postmenopausal changes may modulate these immune‐inflammatory functions. No clinical study has yet investigated the effect of menopause on TREM‐1, PGLYRP1, and IL‐1β levels in gingival crevicular fluid (GCF). Methods: This cross‐sectional study included 148 women (age range = 35–65 years), divided into postmenopausal women (PMW) (n = 76, mean age = 54 ± 5 years) and regularly menstruating premenopausal women (RMPW) (n = 72, mean age = 40 ± 4 years). Clinical periodontal parameters were recorded. TREM‐1, PGLYRP1, and IL‐1β levels were quantified with enzyme‐linked immunosorbent assays. Pearson's Chi‐squared test and Mann–Whitney‐U test were used to compare categorical and numerical variables, respectively. Spearman's Rho correlation analysis was used to test the linear relationship between variables. Analyte level data were categorized based on the periodontal diagnosis and menopause status (2 × 2 nonparametric factorial ANOVA). Results: No significant differences in TREM‐1, PGLYRP1, and IL‐1β levels between PMW and RMPW were observed (p >.05). Mean values of periodontal indexes including probing depth did not differ significantly between PMW and RMPW groups (p =.474). TREM‐1 levels were significantly higher in both PMW and RMPW with periodontitis, compared to gingivitis or health (p =.0021). Conclusion: Menopause‐related changes have no observable effect on GCF levels of TREM‐1, PGLYRP1, and IL‐1β. Higher GCF TREM‐1 levels in women with periodontitis regardless of their menopausal status indicate that TREM‐1 may be an indicator for periodontitis both in premenopausal and postmenopausal women. [ABSTRACT FROM AUTHOR]

Background and objective: Periodontitis (PD) is a dysbiotic disease of tooth-supporting structures that has been associated with various systemic diseases including rheumatoid arthritis (RA). To date, evidence demonstrated increased prevalence of RA among PD patients and postulated PD to have a role in the development of autoantibodies in RA patients. Therefore, a systematic review was conducted to assess the available evidence to ascertain the effect of PD on levels of autoantibodies in the serum, saliva and gingival crevicular fluid (GCF) of RA patients. Material and methods: The systematic review was conducted in compliance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement guidelines. Relevant literature was searched from PubMed, Web of Science, Scopus and Ebscohost databases from inception until 31 August 2020. The risk of bias in each study was determined based on the Newcastle–Ottawa Scale tool. Results from random-effect meta-analyses were presented as summary estimates of odds ratios (ORs) for seropositivity and standardised mean difference (SMD) of autoantibody levels with 95% confidence intervals. Sensitivity tests and meta-regression were performed to assess the robustness of the results and potential cause of heterogeneity. Results: The electronic and manual searches gathered 932 articles. Following screening and full-text assessment, a total of 29 studies were included in the analysis. Twenty-eight published observational studies were included in the quantitative analysis in the form of random-effect meta-analysis which revealed that PD was associated with anti-citrullinated proteins autoantibodies (ACPAs) and Rheumatoid Factor (RF) seropositive RA patients (OR for ACPA seropositivity: 1.82; 95% CI: 1.13–2.93) (OR for RF seropositivity: 1.53; 95% CI: 1.05–2.24). Also, RA patients with PD had increased serum levels of ACPA and RF. However, high heterogeneity among studies' results, partially ascribed to the unstandardised case definition of PD and laboratory testing of autoantibodies. Apart from ACPA and RF in serum, studies which reported on other RA-related autoantibodies, as well as autoantibody levels in saliva and GCF were scarce. Conclusion: RA patients with PD tend to have greater ACPA and RF levels in their serum when compared with the RA patients without PD supporting the plausible role of PD in the development of systemic autoimmunity in RA patients. [ABSTRACT FROM AUTHOR]

Periodontitis is a chronic inflammatory condition that destroys the tooth‐supporting tissues and eventually leads to tooth loss. As one of the most prevalent oral conditions, periodontitis endangers the oral health of 70% of people throughout the world. Periodontitis is also related to various systemic diseases, such as diabetes mellitus, atherosclerosis, and rheumatoid arthritis, which not only has a great impact on population health status and the quality of life but also increases the social burden. Porphyromonas gingivalis (P. gingivalis) is a gram‐negative oral anaerobic bacterium that plays a key role in the pathogenesis of periodontitis. Porphyromonas gingivalis can express various of virulence factors to overturn innate and adaptive immunities, which makes P. gingivalis survive and propagate in the host, destroy periodontal tissues, and have connection to systemic diseases. Porphyromonas gingivalis can invade into and survive in host tissues by destructing the gingival epithelial barrier, internalizing into the epithelial cells, and enhancing autophagy in epithelial cells. Deregulation of complement system, degradation of antibacterial peptides, and destruction of phagocyte functions facilitate the evasion of P. gingivalis. Porphyromonas gingivalis can also suppress adaptive immunity, which allows P. gingivalis to exist in the host tissues and cause the inflammatory response persistently. Here, we review studies devoted to understanding the strategies utilized by P. gingivalis to escape host immunity. Methods for impairing P. gingivalis immune evasion are also mentioned. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to assess associations between neutrophil‐related primary immunodeficiencies (PIDs) and the presence of periodontal disease and other oral diseases and response to periodontal treatment. Background: Presence of neutrophil‐related PIDs is thought to be a major risk factor for development of periodontitis. Methods: This study had both a cross‐sectional and cohort design. Twenty‐four children (age 4–16) with PIDs and 24 age‐matched systemically healthy subjects received a dental clinical examination, including measures of probing pocket depths (PPD), clinical attachment loss (CAL) and bleeding on probing (BOP). Those found to be affected by periodontal disease were offered periodontal treatment and reassessed 6 months later. Results: Diagnosis of PIDs was associated with increased odds of presence of periodontal disease (p =.008 adjusted for age, gender, plaque, OR = 10.0, 95% CI = 1.83–54.38) and with continuous measures of periodontal disease such as number of PPDs >4 mm, mean PPD and mean CAL (all p <.001) and BOP (p =.001). However, only 7 out of 24 children were diagnosed with periodontitis. PIDs were also associated with a history of oral ulcers (p =.001, OR 12.47, 95% CI 2.71–57.29). An improvement in periodontal parameters (PPD and CAL) was detected following oral hygiene instructions and non‐surgical periodontal therapy. Conclusion: Although children affected by neutrophil‐associated PIDs exhibited a higher prevalence of periodontal disease compared with systemically healthy children, severe periodontitis was rarely seen. This suggests that good systemic control of the PIDs may reduce their impact on the periodontium. [ABSTRACT FROM AUTHOR]

PMN migration into the gingival sulcus is a tightly regulated process aimed at selectively increasing leukocyte availability at the site of bacterial plaque aggression, i.e. the superficial portion of the junctional epithelium. The evidence reviewed in this paper indicates that, besides the action of complement fragments, arachidonic acid metabolites, formyl peptides and other bacterial products, the establishment of a gradient of ICAM-1 expression across the junctional epithelium and the expression of IL-8 in its superficial layers probably represent important regulatory mechanisms leading to PMN migration into the gingival sulcus. Such mechanisms can be regulated by the autocrine and paracrine action of some pro-inflammatory cytokines and could possibly be initiated by specific bacteria-keratinocyte interactions. The advantage of such a redundant regulatory mechanism leading to PMN transepithelial migration is probably related to the key role of the neutrophil in the maintenance of a local host-parasite equilibrium on one side, and on the tissue injury associated with PMN persistence or random migration within periodontal tissues on the other. Several investigations are in progress aimed at identifying the initial environmental stimuli leading to PMN recruitment into the gingival sulcus and at further exploring the important regulatory events. [ABSTRACT FROM AUTHOR]

The principal aim of this work was to analyze the host systemic immune response to an oral infection of A. viscosus T14V. Previous work had established a Balb/c mouse model for A. viscosus T14V oral infection. Animals were infected and the splenocyte response to A. viscosus T14V antigens, LPS, and Con A were assessed in the lymphoblast assay. Splenocytes from mice infected with A. viscosus T14V exhibited an altered response pattern to the antigens and mitogens. The responses were enhanced or suppressed when compared to the uninfected control splenocyte response. The effluent cells from a nylon wool column were unresponsive to A. viscosus antigens but LPS did respond to Con A. This response pattern was true for splenocytes from infected and uninfected animals. These results suggest that A. viscosus T14V is a potent immunomodulater when analyzed within the BaIb/c mouse model system. [ABSTRACT FROM AUTHOR]

Background and Objective There is a substantial magnitude of data implicating the role of interleukin-23 ( IL-23) in the initiation and progression of periodontal disease. The main aim of this study was to evaluate the levels of IL-23 in the gingival crevicular fluid of systemically healthy subjects in periodontal health and disease. In addition, we explored the effectiveness of periodontal interventional therapy on the levels of IL-23 in subjects with chronic periodontitis to obtain a deeper insight into the possible role of IL-23 in three separate periodontal conditions in three different populations. Material and Methods In this study, 54 individuals, satisfying the study inclusion and exclusion criteria, were recruited. They were categorically divided, on the basis of gingival index, probing pocket depth and relative attachment loss, into three groups: Group 1 (patients with a clinically healthy periodontium, n = 18); Group 2 (patients with gingivitis, n = 18); and Group 3a (patients with chronic periodontitis, n = 18). Samples taken from all 18 subjects of Group 3a, 3 mo after the initial therapy, constituted Group 3b. All clinical parameters were recorded at baseline and 3 mo after scaling and root planing. Gingival crevicular fluid samples were obtained in which the IL-23 concentration was measured using ELISA. Results The highest mean IL-23 concentration in gingival crevicular fluid was found for Group 3a (16448.69 pg/mL) and the lowest for Group 1 (2565.28 pg/mL). The mean IL-23 concentrations in Group 2 (5425 pg/mL) and Group 3b (6272.22 pg/mL) lay between the maximum and minimum values. This implies a positive correlation between the gingival crevicular fluid IL-23 concentration and relative attachment loss ( p < 0.05). Conclusion A noteworthy increase in the gingival crevicular fluid IL-23 concentration was seen that was proportional to the amount of periodontal tissue damage. As the IL-23 concentration in gingival crevicular fluid is directly proportional to the severity of the periodontal affliction, it can be speculated that IL-23 has a possible role in the pathogenesis of periodontal disease. [ABSTRACT FROM AUTHOR]

The response of peripheral blood leukocytes to various concentrations of whole cells of Candida albicans (particulate antigen), and of PPD and ultrasonicates of Veillonella parvula, Bacteroides melaninogenicus, Actinomyces viscosus, and Fusobacterium nucleatum (soluble antigens) was studied in vitro by means of two different leukocyte migration tests: The capillary tube technique and the agarose plate technique. Using the capillary tube technique migration inhibition to Candida cells was significant in persons with a delayed hypersensitivity skin reaction to this antigen;, however, migration inhibition to PPD or the soluble antigens of dental plaque bacteria was not detected in persons with mild periodontal inflammation. With the agarose plate technique the migration of leukocytes from tuberculin positive persons was inhibited by PPD, while no inhibition of cells from tuberculin negative persons was found. Migration inhibition to soluble V. parvula antigen was significant in persons with mild gingivitis as compared with edentulous persons,. Migration inhibition to antigens from the other dental plaque bacteria was not significant. Blocking of protein synthesis by means of puromycin prevented migration inhibition by PPD and V. parvula. The results suggest that the leukocyte migration test in agarose is suitable faor detection of cell-mediated immunity to bacteria involved in periodontal disease. [ABSTRACT FROM AUTHOR]

An immunoradiometric assay (IRMA) was used for quantifying dog serum antibodies to antigens from dental plaque collected, from full-grown dogs. The antigens were adsorbed onto the inner surface of plastic tubes and then incubated with dog-anti-plaque serum. 1251I-labelled anti-dog plasma-immunoglobulin was used for quantification of the specific antibodies. Four 10 months old Beagle dogs in excellent gingival health were immunized for 10 weeks with ultrasonicated dog dental plaque. The anibody levels in antisera sampled 6, 8, 10 and 11 weeks after the first antigen injection were 2 to 5 times as high as those recorded before the immunizing period. The variability of the assay as judged from the difference between duplicate samples was found to be 18 % ± 4 (p < 0.01) of the mean value and the variability between the same serum ran on different test occasions 13 % ± 7 (p < 0.01). The specificity of the antigen-antibody reaction in the immuno assay was tested by inhibition experiments. Pre-incubation of the antisera with dental plaque antigen significantly inhibited the antigen-antibody reaction in the IRMA, while bovine serum albumin! did not. [ABSTRACT FROM AUTHOR]

Recently van Winkelhoff et al. (1) described 3 novel serotypes in virulent Porphyromomas gingivalis Strains, which were based on different polysaccharide antigens. These antigens probably represent capsular structures and have been designated K1, K2 and K3. In the present study we report on 3 novel capsular serotypes, which are represented by P. gingivalis strains ATCC 49417, HG 1690 and HG 1691. The strains, isolated from patients with periodontitis, showed obvious encapsulation in wet India ink preparations. Thermostable antigens could be detected in the supernatant fractions of autoclaved cells. These antigens appeared to be negatively charged, sensitive to periodate degradation, and resistant to proteinase K treatment. On the basis of these characteristics we conclude that the antigens are probably extra-cellular polysaccharides representing a bacterial capsular structure. These K-antigens did not cross-react with K1, K2 or K3 immunesera of P. gingivalis, with the exception of the K2 antiserum, which partially recognized K5- and K6-antigens. In contrast, K5 and K6 antisera did not react with the K2-antigen. After absorbtion of the K2 antiserum with cells of strains HG 1690 (K5) and HG 1691 (K6) cross-reactivity was no longer present. We propose these novel serotypes to be designated: K4 (ATCC 49417), K5 (HG 1960) and K6 (HG 1691). [ABSTRACT FROM AUTHOR]

Extracts of gingival tissue from periodontal patients can generate chemotactic factors from guinea pig serum for mononuclear leukocytes. Both the classical and alternative pathways of complement activation are triggered. The data do not preclude the fact that other components of the gingival extract (bacterial and/or tissue enzymes, immune complexes and endotoxin) may also play a role in the generation of chemotactic factors from complement. [ABSTRACT FROM AUTHOR]

The local immune response to challenge antigen injection in sensitized mice was investigated. Challenge injection was administered through the maxillary labial mucosa. The influence of non-specific inflammation on the challenge response was studied when both were present simultaneously in a local oral tissue site. The results indicate that inflamed tissues react more violently to the presence of horse ferritin-anti horse ferritin complexes than do non-inflamed tissues. Although the challenge reaction in non-inflamed tissues incited an acute in-flammatory lesion, this same reaction occurring in inflamed tissue induced an Arthus reaction.

The symposium on host resistance to commensal bacteria will be held in the Hume Tower, George Square, Edinburgh during the Spring Meeting of the British Society of Periodontology during the period of March 22-24, 1972. Six sessions will be devoted to ecology of the commensal microflora of the body, host resistance to and infection by commensal bacteria, the systemic immune response, the enzymic basis of cellular resistance and antibiotics and commensal infection.