Virulence factors of Porphyromonas gingivalis.

The microbial challenge in periodontitis

To investigate the role of cytokines in interactions between lactic acid bacteria and the immune system, we measured production of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-10 from human peripheral blood mononuclear cells after stimulation with live or glutaraldehyde-fixed bacteria. Production of tumor necrosis factor alpha, IL-6, and, in some cases, IL-10 was induced in amounts even greater than those obtained with lipopolysaccharide as a stimulant. Our results suggest that lactic acid bacteria can stimulate nonspecific immunity.

Production of human tumor necrosis factor alpha, interleukin-6, and interleukin-10 is induced by lactic acid bacteria.

In 1993, the 1st European Workshop on Periodontology explicitly recognized that there was insufficient knowledge to differentiate truly different forms of periodontal disease from differences in the presentation/severity of the same disease. In spite of recent progress in our understanding of periodontal diseases, the issue is far from having been resolved. Classification of periodontal diseases, therefore, remains based upon the definition of specific clinical syndromes. Early-onset periodontitis (EOP) is one such syndrome and comprises a group of pathological conditions leading to loss of periodontal tissues early in life. The notion that classifies periodontitis syndromes as "early-onset" or "adult" is primarily epidemiological in nature and is based on the observation that periodontitis is rather infrequent in children and young adults. Nevertheless, considerable epidemiological evidence indicates that periodontitis does affect children and young adults to a level of severity that may lead to premature exfoliation of primary and/or permanent teeth. Clinical presentation of periodontitis early in the life of an individual is thought to indicate that the etiologic agents have been able to cause considerable tissue damage over a relatively short period of time. It also implies either infection with highly virulent bacteria and/or a highly susceptible subject. The purpose of this review is to discuss the criteria generally utilized to classify EOP, provide the rationale to designate EOP as a distinct disease entity, and to review the evidence justifying a subclassification into particular subgroups of EOP.

Early-onset periodontitis.

Health claims of lactic acid bacteria (LAB) used in functional foods and pharmaceutical preparations are based on the capacity of these microorganisms to stimulate the host immune system. In this study, the antigenic effect of LAB (Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus delbrueckii ssp. bulgaricus and Streptococcus thermophilus) on the gut immune system of BALB/c mice was evaluated. A dose-dependent increase of the Bcl2 protein was observed with all LAB assayed. Furthermore, the analysis of cytokine-producing cells in the lamina propria of gut showed that TNFalpha and INFgamma values, determined in macrophages cultured from Peyer patches, were enhanced for all the LAB assayed. An important increase of interleukins IL-10 and IL-4 was observed mainly in mice fed with Lactobacillus delbrueckii ssp. bulgaricus or Lactobacillus casei, while a significant induction of IL-2 and IL-12 was only observed with L. acidophilus (P<0.01). These effects were dose dependent. The role of produced cytokines in the balance Th1/Th2 was determined by a systemic antibody response against parenterally injected ovoalbumin. L. casei, L. delbrueckii ssp. bulgaricus and L. acidophilus enhanced the IgG1 response favouring Th2 balance, while L. acidophilus also increased the IgG2a response inducing Th1 balance. S. thermophilus did not influence the balance Th1/Th2. Our studies showed that lactic acid bacteria induce distinct mucosal cytokine profiles showing different adjuvant capacity among them. Thus, selection of probiotic strain with immunological properties must be well defined to influence cytokine expression that favour the claimed immune response.

Interaction of lactic acid bacteria with the gut immune system

Macrophages respond to bacterial lipopolysaccharides (LPS) and activate several host defense functions through production of mediators. However, it is not clear whether the degree of macrophage responsiveness to different sources of LPS is equivalent to or varies with the source of LPS. Therefore, in this report, we examined the extent of the human monocyte response to LPS derived from two oral pathogens, Actinobacillus actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg). Additionally, due to its well-established ability to activate monocytes, we used LPS from Escherichia coli (Ec). Human monocytes, when activated with a specific source of LPS, exhibited rapid expression of mRNA for IL-1 beta, TNF-alpha, and IL-8, which was followed by IL-6, as measured by RNA-PCR. Moreover, the expression of mRNA for these cytokines was followed by cytokine synthesis. Monocytes from the same subject, when activated with LPS from Pg, Aa, or Ec expressed quantitatively different levels of mRNA and proteins for all four cytokines. A given LPS induced either high or low expression of the battery of cytokines tested, indicating that the expression of these pro-inflammatory cytokines may be regulated by a single or a cluster of gene(s). However, no apparent differences in the time course of mRNA expression for these cytokines were observed in response to any of the LPS tested. Furthermore, the relative ability of the different sources of LPS to induce mRNA for cytokines varied throughout a wide range of LPS concentrations. This suggests that differences exist in the sensitivity of monocytes to a specific LPS, rather than in the kinetics of the secretory process itself.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential expression of IL-1 beta, TNF-alpha, IL-6, and IL-8 in human monocytes in response to lipopolysaccharides from different microbes.

Localized juvenile periodontitis (LJP) is an aggressive periodontal disease of familial nature. Neutrophils from a majority of patients with this disease exhibit decreased Chemotaxis with increased adherence, oxidative burst, and degranulation in response to opsonized bacteria. It is proposed that the biological basis for these altered neutrophil functions in LJP may be due either to intrinsic cell abnormalities or to the effect of factors present in the sera of LJP patients, which can modulate neutrophil functions. LJP neutrophils exhibit a lower number of receptors for chemoattractants and GP-110 molecules which are known to facilitate Chemotaxis. Furthermore, these cells exhibit lower signal transduction in response to a biological stimulus. These observations suggest that intrinsic cellular defects may be responsible for altered neutrophil functions in LJP. However, healthy neutrophils, when treated with very low concentrations of proinflammatory cytokines, also exhibit the characteristics of altered or "defective" LJP neutrophils. Additionally, healthy neutrophils, when treated with LJP serum, also exhibit many of the characteristics associated with LJP neutrophils. Attempts to identify these factors have shown that cytokines like TNF-α and/or IL1 β in LJP sera may be at least partially responsible for modulating neutrophil functions in LJP. These cytokines are primarily produced by activated macrophages, indicating a role for these cells in the etiology of LJP. The hyper-responsiveness of these cells to an immunologic challenge can result in local increases in cytokines leading to excessive bone loss and tissue damage at the site of infection, while systemic elevations in cytokines would lead to decreased neutrophil Chemotaxis, both of which are observed in LJP. Present evidence indicates that neutrophil functions are indeed altered in the majority of LJP patients. However, the biological basis for the alteration may not be due to the neutrophils themselves but, rather, a consequence of an inherent hyperactive immune response during the host-pathogen interaction. J Periodontol 1996;67:337-344.

Altered Neutrophil Function in Localized Juvenile Periodontitis: Intrinsic or Induced?

Dental professionals have an opportunity to screen for substance use, provide targeted feedback based on patients' oral health, provide patient education, and refer for further assessment as needed. The aim of this study was to assess the impact on dental hygiene students of an interprofessional Screening, Brief Intervention, and Referral to Treatment (SBIRT) educational intervention with standardized patients as a tool for initiating discussions on alcohol and drug use with patients. Starting in 2015, dental hygiene students in two classes at the University of Pittsburgh participated with nursing students in one and a half hours of didactic instruction followed within a ten-week period by SBIRT simulation scenarios utilizing standardized patients, with subsequent debriefing of students by faculty. Students' attitudes were assessed before and after the didactic session and immediately after the SBIRT simulation, using the Alcohol and Alcohol Problems Perceptions Questionnaire and the Drug and Drug Problems Perceptions Questionnaire. All 67 dental hygiene students in the program at the time participated in the educational intervention and surveys. The results showed significant positive changes in role security, defined as the acceptance of SBIRT delivery as part of their role identity as dental hygienists, following the intervention. This study found that the IPE intervention with dental hygiene and nursing students improved the dental hygiene students' attitudes through using SBIRT.

Effect on Dental Hygiene Students of a Substance Use Simulation Conducted with Nursing Students.

The known actions of cytokines suggest that these molecules hold a great potential for modulating the host immune response and enhancing tissue regeneration. These molecules would be useful in controlling the adverse effects of the host immune response and/or augmenting the regenerative potential of cytokines. Once the technology is optimized, it may be possible for dentists to apply cytokine therapy to resolve periodontal infections. Such therapeutic measures hold promise not only in the resolution of periodontal infections, but also in the treatment of other diseases of the oral cavity.

Role of cytokines in periodontal diseases.

https://www.dental.theclinics.com/article/S0011-8532(05)00094-7/pdf

Angelina E. Riccelli

Papers

Differential expression of IL-1 beta, TNF-alpha, IL-6, and IL-8 in human monocytes in response to lipopolysaccharides from different microbes.

Altered Neutrophil Function in Localized Juvenile Periodontitis: Intrinsic or Induced?

Effect on Dental Hygiene Students of a Substance Use Simulation Conducted with Nursing Students.

Role of cytokines in periodontal diseases.

Prevention Strategies for Dental Caries in the Adolescent