A.M.G.A. Laheij

Healthcare-associated viral and bacterial infections in dentistry

Infection prevention in dentistry is an important topic that has gained more interest in recent years and guidelines for the prevention of cross-transmission are common practice in many countries. However, little is known about the real risks of cross-transmission, specifically in the dental healthcare setting. This paper evaluated the literature to determine the risk of cross-transmission and infection of viruses and bacteria that are of particular relevance in the dental practice environment. Facts from the literature on HSV, VZV, HIV, Hepatitis B, C and D viruses, Mycobacterium spp., Pseudomonas spp., Legionella spp. and multi-resistant bacteria are presented. There is evidence that Hepatitis B virus is a real threat for cross-infection in dentistry. Data for the transmission of, and infection with, other viruses or bacteria in dental practice are scarce. However, a number of cases are probably not acknowledged by patients, healthcare workers and authorities. Furthermore, cross-transmission in dentistry is under-reported in the literature. For the above reasons, the real risks of cross-transmission are likely to be higher. There is therefore a need for prospective longitudinal research in this area, to determine the real risks of cross-infection in dentistry. This will assist the adoption of effective hygiene procedures in dental practice.

Viral loads and antiviral resistance of herpesviruses and oral ulcerations in hematopoietic stem cell transplant recipients

Ulcerative oral mucositis and infection are frequent complications in hematopoietic stem cell transplant (HSCT) recipients. The aim of this study was to investigate the relationship between oral ulcerations and HSV-1, EBV and CMV excretion and the presence of aciclovir-resistant HSV-1 strains in HSCT recipients. This prospective observational study included 49 adult patients who underwent allogeneic HSCT. In total, 26 patients received myeloablative and 23 received non-myeloablative conditioning. Ulcerations on non-keratinized and keratinized oral mucosa were scored and oral rinsing samples were taken twice weekly. Viral loads were determined by real-time PCR. Samples from patients remaining HSV-1 positive despite antiviral treatment were studied for resistance to antivirals. Having an HSV-1 or EBV DNA–positive sample was a significant predictor for ulceration of keratinized mucosa. HSV-1 was a significant predictor for ulcerations on non-keratinized mucosa as well. Persistent HSV-1 infection occurred in 12 of 28 patients treated with antiviral medication and aciclovir-resistant HSV-1 was found in 5 persistent infections. In conclusion, HSV-1 is a predictor of ulcerations on non-keratinized as well as keratinized oral mucosa following HSCT. The role of EBV deserves further study. Persistent HSV-1 replication despite antiviral treatment is common and is due to resistance in 18% of treated patients.

The Influence of Oral Bacteria on Epithelial Cell Migration In Vitro

Oral ulcerations often arise as a side effect from chemo- and radiation therapy. In a previous clinical study, Porphyromonas gingivalis was identified as a positive predictor for oral ulcerations after hematopoetic stem cell transplantation, possibly incriminating P. gingivalis in delayed healing of the ulcerations. Therefore, it was tested whether P. gingivalis and its secreted products could inhibit the migration of oral epithelial cells in an in vitro scratch assay. To compare, the oral bacteria Prevotella nigrescens, Prevotella intermedia, Tannerella forsythia, and Streptococcus mitis were included. A standardized scratch was made in a confluent layer of human oral epithelial cells. The epithelial cells were challenged with bacterial cells and with medium containing secretions of these bacteria. Closure of the scratch was measured after 17 h using a phase contrast microscope. P. gingivalis, P. nigrescens, and secretions of P. gingivalis strongly inhibited cell migration. A challenge with 1000 heat-killed bacteria versus 1 epithelial cell resulted in a relative closure of the scratch of 25% for P. gingivalis and 20% for P. nigrescens. Weaker inhibitory effects were found for the other bacteria. The results confirmed our hypothesis that the oral bacteria may be involved in delayed wound healing.

In situ Remineralisation of Enamel and Dentin after the Use of an Amine Fluoride Mouthrinse in Addition to Twice Daily Brushings with Amine Fluoride Toothpaste

It is often claimed that 3 fluoride moments a day significantly reduce the caries risk compared to 2 daily fluoride moments. However, previous research is not conclusive. Therefore, the aim of this study was to compare the effect on lesion progression of 2 versus 3 fluoride moments a day. A double-blind, randomized, cross-over in situ experiment was designed. The experiment comprised 2 in situ periods of 3 weeks with a washout period of 3 weeks in between. Sixteen participants wore an enamel and a dentine specimen with a preformed lesion placed buccally in their partial prosthesis. The participants brushed twice a day with a 1,400 ppm F (amine fluoride) toothpaste and rinsed once a day with either 250 ppm F (amine F/NaF) or a placebo rinse. At the end of the experiment the specimens were retrieved for fluoride analysis and the assessment of integrated mineral loss with transversal microradiography. The fluoride analysis showed a statistically significant increase in structurally bound fluoride in dentine, but not in enamel, when comparing the fluoride mouthrinse group with the placebo rinse group. The amounts of loosely bound, KOH-soluble fluoride were not different between both groups neither for enamel nor for dentine. In dentine IML gain was significantly (p < 0.05) higher for the fluoride mouthrinse group than for the placebo mouthrinse group. In enamel no statistically significant differences in IML gain were found. For dentine a third fluoride moment may be beneficial in enhancing remineralisation, even under the remineralising conditions as in this study.

Can the oral microflora affect oral ulcerative mucositis

Purpose of reviewOral mucositis is one of the most prevalent toxicities after hematopoietic stem cell transplantation. Mucositis is initiated by the chemotherapy or radiotherapy preceding the transplantation. It is commonly accepted that microorganisms play a role in the process of oral mucositis. Despite the upcoming techniques to determine the whole oral bacterial ecosystem, the exact role of the microflora in mucositis is not yet understood. This article provides an overview of the state-of-the-art research on the oral microflora and mucositis. Recent findingsA shift in microflora, in both the intestine and the oral cavity, can be found after chemotherapy or radiation therapy. The presence of oral ulcerative mucositis coincides with the presence of periodontitis-associated bacteria, in particular Porphyromonas gingivalis. Moreover, this bacterium can inhibit wound healing processes in an in-vitro model. SummaryWe come to realize that some diseases are associated with a shift in the microflora. The role of the microflora in oral and intestinal mucositis is gaining more attention in recent literature. In the oral cavity, periodontitis-associated bacteria may influence the healing of ulcerations and the role they play in mucositis may be more subtle and complicated than was previously thought.

Free available chlorine concentration in sodium hypochlorite solutions obtained from dental practices and intended for endodontic irrigation: are the expectations true?

OBJECTIVE Sodium hypochlorite (NaOCl) is an important tool in root canal disinfection although it is well known that the shelf-life of NaOCl is limited. In this study, NaOCl solutions that were collected from dental practices and were intended for endodontic irrigation were investigated to see whether they contained the expected concentration of free available chlorine. METHOD AND MATERIALS NaOCl solutions were collected from dental practices. The concentration of available chlorine per sample was determined with iodometric titration and the pH was measured. Each participating dentist completed a questionnaire that requested data on a range of issues relating to the assumed concentration of NaOCl and handling of the sample. RESULTS Eighty-four samples with questionnaires were received. NaOCl was purchased from supermarkets and drugstores (36%), dental suppliers (48%), or pharmacies (16%). The median expected concentration was 2% (n = 36). On average, 27% less available chlorine was measured than the dentist assumed was in the sample (P < .001). Fifteen percent of samples contained less than 1% available chlorine, which is needed for tissue dissolution and disinfection. The average pH was 11.5. CONCLUSION The greatest differences in concentrations were found in NaOCl sourced from supermarkets or drugstores. Future studies should elucidate the cause of this discrepancy. CLINICAL RELEVANCE In the meantime it is recommended to purchase NaOCl from professional suppliers, because this group showed the most reliable content of free available chlorine.

A scoping review on bio-aerosols in healthcare and the dental environment

Background Bio-aerosols originate from different sources and their potentially pathogenic nature may form a hazard to healthcare workers and patients. So far no extensive review on existing evidence regarding bio-aerosols is available. Objectives This study aimed to review evidence on bio-aerosols in healthcare and the dental setting. The objectives were 1) What are the sources that generate bio-aerosols?; 2) What is the microbial load and composition of bio-aerosols and how were they measured?; and 3) What is the hazard posed by pathogenic micro-organisms transported via the aerosol route of transmission? Methods Systematic scoping review design. Searched in PubMed and EMBASE from inception to 09-03-2016. References were screened and selected based on abstract and full text according to eligibility criteria. Full text articles were assessed for inclusion and summarized. The results are presented in three separate objectives and summarized for an overview of evidence. Results The search yielded 5,823 studies, of which 62 were included. Dental hand pieces were found to generate aerosols in the dental settings. Another 30 sources from human activities, interventions and daily cleaning performances in the hospital also generate aerosols. Fifty-five bacterial species, 45 fungi genera and ten viruses were identified in a hospital setting and 16 bacterial and 23 fungal species in the dental environment. Patients with certain risk factors had a higher chance to acquire Legionella in hospitals. Such infections can lead to irreversible septic shock and death. Only a few studies found that bio-aerosol generating procedures resulted in transmission of infectious diseases or allergic reactions. Conclusion Bio-aerosols are generated via multiple sources such as different interventions, instruments and human activity. Bio-aerosols compositions reported are heterogeneous in their microbiological composition dependent on the setting and methodology. Legionella species were found to be a bio-aerosol dependent hazard to elderly and patients with respiratory complaints. But all aerosols can be can be hazardous to both patients and healthcare workers.

The impact of virulence factors of Porphyromonas gingivalis on wound healing in vitro

Background Porphyromonas gingivalis inhibits oral epithelial wound healing in vitro more strongly than other oral bacteria, but it is unknown why P. gingivalis is such a potent inhibitor of wound healing. Objective Therefore, the aim of this study was to investigate the influence of major virulence factors of P. gingivalis on wound healing in an in vitro wound-healing model. The influence of the capsular polysaccharide, the Arg- and Lys- gingipains, the major fimbriae and lipopolysaccharide (LPS) was investigated. Design A standardized scratch was made in a confluent layer of human oral epithelial cells HO-1-N-1. The epithelial cells were then challenged with different concentrations of several P. gingivalis wild-type strains and knockout mutants. Closure of the scratch was determined after 17 h and compared to control conditions without bacteria. Results The P. gingivalis strains ATCC 33277, W83, and W50 significantly inhibited wound healing. The presence of a capsular polysaccharide lowered significantly the inhibition of epithelial cell migration, while gingipain activity significantly increased the inhibition of cell migration. LPS and the major fimbriae did not influence epithelial cell migration. None of the tested P. gingivalis strains completely prevented the inhibition of cell migration, suggesting that other characteristics of P. gingivalis also play a role in the inhibition of wound healing, and that further research is needed. Conclusions The capsular polysaccharide and the Arg- and Lys- gingipains of P. gingivalis influenced the capacity of P. gingivalis to hinder wound healing, while LPS and the major fimbriae had no effect.

Candida and Porphyromonas gingivalis: the effect on wound closure in vitro

ABSTRACT Microorganisms play a role in oral mucositis after cancer therapy. The current study explored the hypothesis that Candida spp. alone and together with Porphyromonas gingivalis cause delayed healing of oral ulcerations due to the inhibition of wound closure. An in vitro scratch assay model was used to study the influence of viable and heat-killed Candida glabrata, Candida kefyr, and Candida albicans on cell migration of oral epithelial cells. Separately, the effect of conditioned medium of Candida spp. and the effect of a mixed infection of Candida spp. with P. gingivalis on wound closure was studied. In the presence of 10 viable C. glabrata or C. kefyr versus one epithelial cell, with a multiplicity of infection (MOI) of 10, the relative closure of the scratch was 26% and 17%, respectively. At a MOI of 1, this was 60% for C. glabrata and 78% for C. kefyr. The inhibition of oral epithelial cell migration challenged with either C. glabrata or C. kefyr together with P. gingivalis was stronger than the inhibition caused by one of both organisms separately. Candida spp. inhibit cell migration in vitro. A combination of Candida spp. and P. gingivalis inhibited cell migration more than either microorganism separately.