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Oral microbiota and systemic disease
... Ognisko zakażenia jest definiowane jako obszar, który zawiera mikroorganizmy patogenne, pojawia się w dowolnym miejscu ciała i nie powoduje zazwyczaj objawów klinicznych (1,2,3). Wielu autorów uznaje jamę ustną za potencjalne źródło zakażenia i stanu zapalnego, które wpływa na ogólny stan zdrowia (1,4,5,6,7,8,9). ...
... Ognisko zakażenia jest definiowane jako obszar, który zawiera mikroorganizmy patogenne, pojawia się w dowolnym miejscu ciała i nie powoduje zazwyczaj objawów klinicznych (1,2,3). Wielu autorów uznaje jamę ustną za potencjalne źródło zakażenia i stanu zapalnego, które wpływa na ogólny stan zdrowia (1,4,5,6,7,8,9). Pierwotne ogniska zakażenia (foci infectiosi primarii) mogą prowadzić do powstania ognisk wtórnych (foci secundarii), które nazywa się chorobami odogniskowymi (morbus focalis) (5,10). ...
... Problem ten był znany w Asyrii, Babilonie, Egipcie i Grecji (9,10,12,13). W pismach Hipokratesa można znaleźć opis wyleczenia zapalenia stawów po usunięciu "zakażonego zęba" (1,2,6,9,10,13). ...
The study describes opinions dealing with the connections between the existence of primary foci of infection in the oral cavity and the development of diseases of organs and systemic diseases. There is a description of potential complications of foci of infection coming from the teeth and of methods of discovering them and their treatment.
... Open-angle glaucoma is the most common variant; it is painless, advances slowly, and often results in blindness if treatment is not received. The drainage angle gradually closes in closed-angle glaucoma as the peripheral iris bows forward either abruptly or gradually, whereas in open-angle glaucoma the iridocorneal angle promotes unrestricted fluid outflow within the eyes [14,15]. Abrupt oblique ophthalmosis is characterized by a middilated pupil, redness of the eye, intense discomfort in the eye, and nausea. ...
... Abrupt oblique ophthalmosis is characterized by a middilated pupil, redness of the eye, intense discomfort in the eye, and nausea. Reduced vision loss from glaucoma is irreversible and is caused by the loss of axons in the ganglion cell layer as a result of a narrower neuro-retinal margin on the optic nerve [11][12][13][14]. ...
Periodontitis, marked by the deterioration of the tissues bordering the surfaces of the teeth, is one of the most prevalent diseases. The presence of pathogenic bacteria, also known as "periopathogens," in the gingival sulcus region is the main cause of periodontitis. Analyzing the relationship between ocular disorders, chronic tonsillitis and periodontitis has been the subject of few investigations.
The aim of this study was to evaluate the association between periodontitis, glaucoma and chronic tonsillitis. This study evaluated periodontal health in glaucoma and chronic tonsillitis patients among ageing adults and the elderly population. It was a case-control study in which there was an evaluation of the correlation between periodontitis glaucoma and chronic tonsillitis. 120 clinically diagnosed cases of glaucoma and 120 clinically healthy individuals were taken as controls. 123 cases of clinically diagnosed cases of chronic tonsillitis were taken as controls. In every clinically diagnosed case, there was a thorough periodontal examination by measuring the following parameters. PI: periodontal index. CAL: Clinical attachment loss. BI: Bleeding index. There was a collection of biofilm specimens from the buccal surface of the maxillary first molar, second molar and mandibular anterior for evaluation of colonies of Streptococcus mutans. The specimens were cultured in agar plates. The CFU/ml was calculated. Logistic regression analysis revealed that there was statistically significant difference in values of PI (p<0.001) indicating poor periodontal health in glaucoma patients and chronic tonsillitis patients. There was statistically significant difference in values of BI (p<0.001), indicating increased bleeding from gums in glaucoma patients and chronic tonsillitis patients. In our study there was statistically significant difference in values of CAL indicating increased attachment loss in glaucoma patients and chronic tonsillitis patients. There was statistically significant difference in values of CFUs of Streptococcus mutans in plaque samples indicating increased CFUs of Streptococcus mutans in chronic tonsillitis and glaucoma patients. This study demonstrated the link between periodontitis glaucoma and chronic tonsillitis and offered a potential explanation. To solve this study's shortcomings, more research would be required. Examining individuals with chronic tonsillitis and glaucoma requires determining the oral cavity's state and computing dental indices, of which the periodontal index is crucial. Recommending extensive therapy for patients suffering from periodontitis, glaucoma, and chronic tonsillitis is imperative by ophthalmologists, ENT professionals and periodontists.
Keywords: Periodontal health, glaucoma, chronic tonsillitis, aging adults, old population
... Nor is it peculiar that bacterial DNA has been identified in distant sites of the cardiovascular system such as heart valves and atherosclerotic plaques in patients with untreated periodontitis (43;44). This has collectively been referred to as the focal infection theory, which stress that members of the oral microbiota are capable of inducing disease at distant body sites, if they gain access to these areas of the human organism (45). The focal infection theory is definitely not the new kid on the block. ...
... The focal infection theory is definitely not the new kid on the block. In fact, the focal infection theory dates back as long as to Hippocrates, and today it is still considered the explanatory model of endocarditis and pneumonia caused by oral microorganism (45). ...
... [8][9][10] Microbiome (microbial population) of intestine and mouth could affect all activities of cells and organs near or far of intestines with creating different kinds of diseases including systemic inflammatory events, rheumatoid arthritis, localized disease, oral and pharyngeal cancers. 5,[11][12][13] Poor oral and periodontal health has also been proposed to increase malignant tumors in parts other than the oral or gastrointestinal system. 14 Presence of P. gingivalis in saliva have been proposed as a predictor of head and neck squamous cell carcinoma (HNSCC), colon cancer, and a risk of cancer death. ...
... Oral hygiene is neglecting in high percent of people, 12 causing many complications, including periodontitis, dental loss, and in turn oral and colon cancers, and other complicate diseases such as cardiovascular disease, and preterm birth. 5,[7][8][9]11,[16][17][18][19][32][33][34] In this regard, relationships between oral health such as dental loss and periodontitis with oral, lung, upper gastrointestinal, and pancreas cancers have been reported in different studies. 5,[8][9]14,35 For example, presence of periodontal pathogen Porphyromonas gingivalis was evaluated and proposed as a predictor of death in orodigestive tract cancers. ...
The purpose of this study was to investigate the relationship between oral and dental health in cancer patients and control group, which was conducted in Tabriz Shahid Gazi hospital. A researchers-made and validated questionnaire including oral and dental health criteria, was filled by the cancer patients (201 cases) and healthy controls (199 cases). Then, the results of the study were analyzed by SPSS software, and reported as Odds ratios (95 % confidence intervals) in tow groups. The results indicate that comparison of filled tooth, tooth extraction, dental caries, and gingival problems including bleeding, gum surgery and inflammation in cancer and controls were significantly meaningful. However, the comparison between the two groups was not significant in terms of the type of the tooth (natural or denture) and the number of daily toothbrushes, but they were considered as risk factors due to statistical results. Environmental factors, and especially oral hygiene, can play an important role in the incidence of different cancers. Among these, the type of oral microorganisms, and their overgrowth and released antigens should be studied further in the emergence of different kinds of cancer in humans.
... Bacteria used to test the antibacterial activity herein reported belonging to gram-positive and gram-negative types of the oral cavity. For Kumar (2013), there are more than 1000 species of bacteria in the oral cavity of a human being, and these bacteria are displaced to other parts of the body causing other diseases such as inflammation of the prostate, asthma, pneumonia, endocarditis, diabetes, etc. [9]. Thus, it is necessary to investigate and use new compounds that are capable of inhibiting the growth of these bacteria. ...
... Bacteria used to test the antibacterial activity herein reported belonging to gram-positive and gram-negative types of the oral cavity. For Kumar (2013), there are more than 1000 species of bacteria in the oral cavity of a human being, and these bacteria are displaced to other parts of the body causing other diseases such as inflammation of the prostate, asthma, pneumonia, endocarditis, diabetes, etc. [9]. Thus, it is necessary to investigate and use new compounds that are capable of inhibiting the growth of these bacteria. ...
Cercospora brachiata is a phytopathogenic fungus. To know more about the metabolites produced by this fungus, the objective of this work was to identify, isolate and characterize substances present in extracts of the growth broth and mycelium, using gas chromatography with mass spectrometry (GC-MS) and nuclear magnetic resonance (NMR). It was also objective to evaluate the antibacterial activity of the extracts. Among the compounds identified, fatty acids, esters, and steroids can be highlighted. The main compounds identified are 9-hexadecenoic, hexadecenoic, oleic, octadecanoic, lauric, myristic, palmitic, doceno-13-enoic, stearic, linoleic, and nonadecanoic acids present in almost all extracts. For the antibacterial activity, the broth microdilution method was used. The ethyl acetate extract of the mycelium presented inhibitory concentrations (MICs) against the bacterium Actinomyces naeslundii (100 μg mL−1) and Streptococcus sanguinis (200 μg mL−1). Finally, two steroids were isolated and identified in the hexane extract of mycelium: ergosta-6,22-dien-3β,5α,8α-triol and brassicasterol.
... Grau et al. [18] found that individuals with periodontitis had a greater risk of developing stroke by 400% than those with caries. Another study found a correlation between intimal thickening (used as a surrogate measure of atherosclerosis) and periodontal pathogens, but not health-compatible organisms [19]. Systemic antibody levels have been linked to periodontal pathogens, as well as the incidence of coronary heart disease and subclinical atherosclerosis. ...
... Systemic antibody levels have been linked to periodontal pathogens, as well as the incidence of coronary heart disease and subclinical atherosclerosis. This data suggests a connection between periodontal pathogens and the incidence of cardiovascular disease [19]. ...
To date, coronavirus disease 2019 (COVID-19) has affected over 6.2 million individuals worldwide, including 1.46 million deaths. COVID-19 complications are mainly induced by low-grade inflammation-causing vascular degeneration. There is an increasing body of evidence that suggests that oral dysbiotic taxa are associated with worse prognosis in COVID-19 patients, especially the Prevotella genus, which was retrieved from nasopharyngeal and bronchoalveolar lavage samples in affected patients. Oral dysbiosis may act by increasing the likelihood of vascular complications through low-grade inflammation, as well as impairing respiratory mucosal barrier mechanisms against SARS-CoV-2. Salivary markers can be used to reflect this oral dysbiosis and its subsequent damaging effects on and the lungs and vasculature. Salivary sampling can be self-collected, and is less costly and less invasive, and thus may be a superior option to serum markers in risk stratification of COVID-19 patients. Prospective studies are needed to confirm such hypothesis.
Video Abstract: http://links.lww.com/CAEN/A28
... Additionally, not only bacteria can be introduced into bloodstream, but their bacterial products and endotoxins can also be released into systemic circulation. This can trigger inflammatory responses in specific sites elevating the risk of producing systemic diseases (35). A good illustration of a commensal oral-systemic relationships mediated by bacteria products, relates to the metabolism of nitrates from diet into nitrites. ...
... These evidences caused the resurgence of the so called "focal infection theory". This theory explains how "bacteria and/or bacterial products are disseminated from this source to distant parts, leading to disease in these organ systems" (35). However, it is from epidemiological studies that new questions arose about how oral health exerts an influence on general health. ...
In the first part of this literature review, published in October 2019 in this journal, we summarized the conceptual background of the oral microbiota, and the main methods used in microbiology to characterize oral organisms. We also presented the most studied bacteria species in the oral microbiota. In this second part, we will discuss the evidence regarding the biological plausibility linking the oral microbiota dysbiosis and systemic diseases, as well as the main factors and mechanisms suspected in this association.
... In the mouth, bacteria aggregate into biofilms within distinct niches, each supporting specific microbial populations shaped by unique environmental conditions. This dynamic nature of the oral microbiome makes defining a general composition difficult [5][6][7][8]. ...
Objectives
To evaluate the effect of coconut oil on the oral bacteriome and inflammatory response in patients with periodontitis by integrating next-generation sequencing analyses of pathogenic bacterial shifts and quantification of inflammatory markers, thereby assessing its potential as a natural adjunct to standard nonsurgical periodontal therapy.
Materials and methods
A triple-blind clinical trial was conducted with 30 participants diagnosed with periodontitis, randomized into 3 groups: (1) coconut oil, (2) chlorhexidine and (3) placebo. Saliva and gingival crevicular fluid (GCF) samples were collected before treatment, one month after treatment, and one month post-non-surgical periodontal therapy. Bacterial DNA was extracted, and the V3-V4 region of the 16 S rRNA gene was PCR-amplified and sequenced using Illumina MiSeq technologies. Inflammatory biomarkers, including Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), were quantified from GCF samples.
Results
Coconut oil treatment significantly reduced pathogenic bacterial families such as Spirochaetaceae and Tannerellaceae while promoting beneficial bacteria such as Streptococcaceae. At the genus and species levels, coconut oil reduced pathogens such as Tannerella forsythia and Treponema denticola along with increase in beneficial bacteria such as Streptococcus. The subgingival microbial dysbiosis index improved significantly in both coconut oil and chlorhexidine groups. Furthermore, the coconut oil demonstrated a reduction in IL-6 and TNF-α levels, indicating decreased local inflammation.
Conclusions
Coconut oil treatment significantly modulated the oral microbiome and reduced inflammatory markers in patients with periodontitis, suggesting its potential as a natural and effective adjunct in periodontal therapy.
Clinical relevance
This study highlights coconut oil’s potential as a natural adjunct in periodontal therapy, effectively reducing pathogenic bacteria and inflammatory markers (IL-6, TNF-α). It offers a safe alternative to chlorhexidine, promoting microbiome balance and improved periodontal health.
... 1,2 During the progression of periodontal disease, gram-negative bacteria are able to modify their environment to enhance survival by developing a microbial shift eliciting the host inflammatory response. [3][4][5][6] This microbial dysbiosis, combined with predisposing factors, results in the release of proinflammatory cytokines, negatively affecting the periodontium. 7,8 Elevated levels of proinflammatory cytokines are associated with the release of acute phase reactants such as high-sensitivity C-reactive proteins (hsCRPs) and haptoglobin (Hp). ...
... Moreover, it is not just bacteria that can enter the bloodstream; their bacterial byproducts and endotoxins can also be discharged into the systemic circulation. This has the potential to initiate inflammatory reactions in particular locations, thereby heightening the risk of developing systemic diseases (80). On the other hand, systemic diseases can significantly influence the composition and dynamics of the oral microbiota, this is attributed to the high level of inflammation associated with these conditions affects the oral microbiota, leading to significant alterations (81). ...
The oral microbiome is a complex community of microorganisms residing in the oral cavity interacting with each other and with the host in a state of equilibrium. Disruptions in this balance can result in both oral and systemic conditions. Historically, studying the oral microbiome faced limitations due to culture-dependent techniques that could not capture the complexity and diversity of the microbial community. The emergence of advanced genomic technologies and the ease of sample collection from the oral cavity has revolutionized the understanding of the oral microbiome, providing valuable insights into the bacterial community in both health and disease. This review explores the oral microbiome in children, discussing its formation and dynamics in both states of health and disease, its role in various conditions such as dental caries, periodontal disease, oral cancer, cleft lip and palate, and explores its connection to several systemic consequences.
... Oral health is an important issue when being evaluated for HTx and LVAD due to their risk for developing systemic infectious complications [5][6][7][8]. Oral bacteria are a potential risk and/or source for systemic infections, especially in the case of (severe and extended) periodontal inflammation [25]. Thus, bacteremia can occur related to dental treatment or daily oral hygiene measures [26,27]. ...
Background: This study aimed to evaluate the diagnostic value of pre-existing computed tomography (CT) examinations for the detection of dental pathologies compared with clinical dental examination in patients with end-stage heart failure. Methods: For this purpose, 59 patients with end-stage heart failure and pre-existing non-dental CT images of the craniofacial region were included. Virtual orthopantomograms (vOPG) were reconstructed. Dental pathologies were analyzed in vOPG and source-CT images. Imaging and clinical findings less than 6 months apart were compared (n = 24). Results: The subjective image quality of vOPG was more often rated as insufficient than CT (66%; 20%; p < 0.01). Depending on examination (CT, vOPG or clinic), between 33% and 92% of the patients could require dental intervention such as treatment of caries and periodontitis or tooth extraction. vOPG led to a higher (80%) prevalence of teeth requiring treatment than CT (39%; p < 0.01). The prevalence of teeth requiring treatment was similar in CT (29%) and clinic (29%; p = 1.00) but higher in vOPG (63%; p < 0.01). CT (stage 3 or 4: 42%) and vOPG (38%) underestimated the stage of periodontitis (clinic: 75%; p < 0.01). Conclusions: In conclusion, available CT images including the craniofacial region from patients with end-stage heart failure may contain valuable information regarding oral health status. The assessability of vOPGs might be insufficient and must be interpreted with caution.
... Dentistry has evolved significantly over the years, shifting from a focus solely on oral health to an integrated approach that considers the intricate connections between the mouth and the rest of the body. The oral cavity often serves as a window to overall health, with many systemic diseases manifesting initial symptoms in the mouth [1]. As such, dentists are in a unique position to detect early signs of systemic diseases, which can lead to timely referrals and interventions, ultimately improving patient outcomes [2]. ...
Dentists play a vital role in detecting early signs of systemic diseases that present in the oral cavity, extending their influence beyond
oral health. This article delves into how dentists identify systemic conditions such as diabetes mellitus, cardiovascular diseases,
autoimmune disorders, oral cancer, gastroesophageal reflux disease (GERD), hematologic disorders, and nutritional deficiencies.
By recognizing oral manifestations such as gum disease, oral infections, dry mouth, tooth erosion, mucosal changes, and unusual
bleeding, dentists can prompt timely referrals and interventions. The connection between oral and systemic health highlights the
need for thorough oral examinations and continuous education for dental professionals, fostering an integrated healthcare approach.
Innovations in diagnostic tools, collaborative care, and patient education enhance dentists' ability to detect and manage systemic
diseases early. This multidisciplinary strategy not only improves patient health outcomes but also emphasizes the critical role of
dentists in the comprehensive healthcare system.
... The implications of these findings extend beyond oral health. The oral microbiota has been increasingly recognized as a potential contributor to systemic diseases, including diabetes and cardiovascular disease [19]. The dysbiosis observed in the oral microbiota of individuals with T2DM may have broader implications for their overall health and well-being [20]. ...
The cross-sectional study on the oral microbiota in patients with Type 2 Diabetes Mellitus (T2DM) reveals
important insights into the potential dysbiosis and differences in the oral microbiota composition between
individuals with T2DM and those without. The study highlights the higher abundance of periodontal pathogens,
such as Porphyromonas gingivalis and Prevotella intermedia, in the oral microbiota of the T2DM group, suggesting
an increased risk of periodontal disease. Conversely, beneficial bacteria like Streptococcus salivarius and
Lactobacillus acidophilus were found to be lower in abundance in the oral microbiota of the T2DM group. These
findings have implications for the increased risk of periodontal disease and dental caries in individuals with T2DM.
The study emphasizes the importance of targeted interventions, such as probiotic supplementation and improved
oral hygiene practices, in managing oral health in individuals with T2DM. Furthermore, the dysbiosis observed in
the oral microbiota of individuals with T2DM may have broader implications for their overall health and wellbeing, including the potential impact on systemic diseases like diabetes and cardiovascular disease. Longitudinal
studies and further research are needed to explore the dynamic nature of the oral microbiota and its relationship
with T2DM, as well as to develop novel therapeutic strategies for restoring oral microbiota balance and improving
oral health outcomes in individuals with T2DM.
... From a molecular perspective, oral health may be composed of different microbial and metabolomic profiles [105]. In addition, the composition of the oral microbiota is highly site-specific [106], and influenced not only by oral health status, but also by general medical disorders and age [107][108][109]. Moreover, frequency and mode of delivery are of critical importance, as probiotic supplements will most likely have the most pronounced effect in situations where the oral biofilm is also being mechanically disrupted. ...
Data from systematic reviews and meta-analyses show that probiotics positively impact clinical parameters of oral diseases such as gingivitis, dental caries, and periodontitis. However, the working mechanism of probiotics is not fully understood, but is hypothesized to be mediated by direct and indirect interactions with the oral microbiota and the human host. In the present narrative review, we focused on the microbiological effect of probiotic supplements based on data retrieved from randomized clinical trials (RCTs). In addition, we assessed to what extent contemporary molecular methods have been employed in clinical trials in the field of oral probiotics. Multiple RCTs have been performed studying the potential effect of probiotics on gingivitis, dental caries, and periodontitis, as evaluated by microbial endpoints. In general, results are conflicting, with some studies reporting a positive effect, whereas others are not able to record any effect. Major differences in terms of study designs and sample size, as well as delivery route, frequency, and duration of probiotic consumption, hamper comparison across studies. In addition, most RCTs have been performed with a limited sample size using relatively simple methods for microbial identification, such as culturing, qPCR, and DNA–DNA checkerboard, while high-throughput methods such as 16S sequencing have only been employed in a few studies. Currently, state-of-the-art molecular methods such as metagenomics, metatranscriptomics, and metaproteomics have not yet been used in RCTs in the field of probiotics. The present narrative review revealed that the effect of probiotic supplements on the oral microbiota remains largely uncovered. One important reason is that most RCTs are performed without studying the microbiological effect. To facilitate future systematic reviews and meta-analyses, an internationally agreed core outcome set for the reporting of microbial endpoints in clinical trials would be desirable. Such a standardized collection of outcomes would most likely improve the quality of probiotic research in the oral context.
... Oral microbes cling to the teeth and gums to avoid entering the stomach for protection from acids (Cui et al. 2013). Microbes exist in mouth tissues, creating colonies (Kumar 2013). Saliva is essential in colony formation and biofilm development (Cepoi et al. 2016). ...
... Overall, the potential underlying mechanism seems plausible; an oral disease, such as periodontitis, leads to a transient bacteraemia [9]. In cases of severe periodontal inflammation, this is increasingly caused by the loss of integrity and thus higher permeability of the junctional epithelium [30]. In this respect, identic clones of periodontal bacteria have been detected in periodontal pockets and synovial fluid, which is especially evident for common potential pathogens such as Fusobacterium nucleatum [5]. ...
Objective: The aim of this cross-sectional cohort study was to evaluate a comprehensive dental examination and referral concept for patients prior to endoprosthesis (EP) implantation in an interdisciplinary setting. Methods: Patients, who were prepared for EP surgery in the clinic for orthopaedics, were referred to the dental clinic for a dental examination. Thereby, dental and periodontal treatment need, radiographic and temporomandibular joint findings were assessed. Based on oral and radiographic investigation, a risk classification for potential source of prosthetic infection was performed. If potential oral foci of EP infection were present (e.g., apically radiolucent teeth, severe periodontitis or additional inflammatory findings), patients were classified as at high risk for EP infection with oral origin. Those individuals were allocated to their family dentist or special clinic for dental treatment prior to EP surgery. Results: A total of 311 patients were included (mean age: 67.84 ± 10.96 years, 51% male). A dental treatment need of 33% was found, while the periodontal treatment need was 83%. Thirty-one percent of patients showed at least one apical radiolucency (a sign of chronic infection/inflammation). Furthermore, additional findings such as radiographic signs of sinusitis maxillaris were found in 24% of patients. Temporomandibular disease was probable in 17% of individuals. One-third (34%) were assigned to the high risk group for an EP infection with oral origin. Conclusion: German patients before EP have a high periodontal treatment need and show frequently (34%) a potential oral focus of infection, underlining the necessity of including dental examination and risk stratification as part of the pre-operative assessment prior to EP implantation. Therefore, an approach as applied in this study appears reasonable for those individuals.
... Esta microbiota juega un papel crucial en el mantenimiento de la homeostasis oral, previniendo y protegiendo a la cavidad oral del desarrollo de enfermedades (Jia et al., 2018). Un desequilibrio en este ecosistema oral se ha visto asociado a numerosas enfermedades tanto orales (Schwabe & Jobin, 2013) como extraorales, entre ellas, alteraciones inmunológicas, endocrinas, neurológicas, digestivas, cardiovasculares y particularmente neoplásicas (Kumar, 2013). ...
In this Scoping Review, we present the evidence recorded in the literature about that oral microbiota can generate a carcinogenic action, acting through three main mechanisms: on the extracellular space, activating intracellular signaling pathways and/or generating direct action on DNA, and that the principal pathogens studied are Fusobacterium nucleatum and Porphyromona gingivalis. Nowadays, there is sufficient evidence about the association between oral microbiota and several types of cancer, however, there is not much knowledge about the mechanisms by which this microbiota participates in its development. We present a compilation of different mechanisms of action used by oral cavity bacteria in the process of carcinogenesis in four different types of cancer. It is of great importance to increase the knowledge about the etiological role of the oral microbiota in the development of cancer disease because it would be established as a new carcinogenic agent and its knowledge could be used as a valuable tool in the detection and treatment of this disease.
... Periodontal pathogens may induce a local inflammatory response and activate innate immunity through the activation of Toll-like receptors (TLRs), which may result in the production of proinflammatory cytokines and the recruitment of phagocytes and lymphocytes into the inflammatory zones [13]. Simultaneously, in the retinal immune system, retinal pigment epithelium cells may play a significant role in immune response and express Toll-like receptors along with a rich source of pro-inflammatory cytokines, chemokines, and growth factors (Figure 3) [14,15]. The complement system is the backbone of the innate immune system. ...
Periodontitis has been associated with several medical conditions. For some of these medical conditions, periodontitis has been hypothesized to share important pathogenic mechanisms with other systemic conditions affecting the body. Recently, advances in technology have led to the identification of novel inflammatory mediators implicated in some chronic medical conditions associated with periodontitis. The potential identification of these systemic inflammatory mediators in periodontitis would offer additional support to the potential periodontal-systemic disease association. In recent years, the term oral foci of infection has attained an upturn in terms of systemic morbidities, while finite scrutinization indicates the implication of chronic oral inflammation in the pathogenesis of eye diseases. Initially, there is a singularity for the mechanistic understanding of the reported link between periodontal diseases and ocular comorbidities. There is a limited number of scientific evidence in the literature that suggests a relationship between glaucoma and periodontitis, and they share a common pathway/link based on inflammatory markers. Based on a molecular biological technique, it was believed by researchers and clinicians that eye diseases were a result of oral infections. Furthermore, this review will try to focus on the concept of oral dysbiosis in the progression of inflammatory eye diseases such as diabetic retinopathy, scleritis, uveitis, glaucoma, and age-related macular degeneration (AMD).
... Overall, the potential underlying mechanism seems plausible; an oral disease, such as periodontitis, leads to a transient bacteraemia [9]. In cases of severe periodontal inflammation, this is increasingly caused by the loss of integrity and thus higher permeability of the junctional epithelium [30]. In this respect, identic clones of periodontal bacteria have been detected in periodontal pockets and synovial fluid, which is especially evident for common potential pathogens such as Fusobacterium nucleatum [5]. ...
Objective:
The aim of this cross-sectional cohort study was to evaluate a comprehensive dental examination and referral concept for patients prior to endoprosthesis (EP) implantation in an interdisciplinary setting.
Methods:
Patients, who were prepared for EP surgery in the clinic for orthopaedics, were referred to the dental clinic for a dental examination. Thereby, dental and periodontal treatment need, radiographic and temporomandibular joint findings were assessed. Based on oral and radiographic investigation, a risk classification for potential source of prosthetic infection was performed. If potential oral foci of EP infection were present (e.g., apically radiolucent teeth, severe periodontitis or additional inflammatory findings), patients were classified as at high risk for EP infection with oral origin. Those individuals were allocated to their family dentist or special clinic for dental treatment prior to EP surgery.
Results:
A total of 311 patients were included (mean age: 67.84 ± 10.96 years, 51% male). A dental treatment need of 33% was found, while the periodontal treatment need was 83%. Thirty-one percent of patients showed at least one apical radiolucency (a sign of chronic infection/inflammation). Furthermore, additional findings such as radiographic signs of sinusitis maxillaris were found in 24% of patients. Temporomandibular disease was probable in 17% of individuals. One-third (34%) were assigned to the high risk group for an EP infection with oral origin.
Conclusion:
German patients before EP have a high periodontal treatment need and show frequently (34%) a potential oral focus of infection, underlining the necessity of including dental examination and risk stratification as part of the pre-operative assessment prior to EP implantation. Therefore, an approach as applied in this study appears reasonable for those individuals.
... and 89.46-90. 24 for the M1 and the M2 materials, respectively. It is worth noting that the presence of the adhesive material itself caused a decrease in the L* parameters of the brackets. ...
Orthodontic appliances discolour over treatment time, and a yellowish plaque builds up on the contact area of the brackets, adhesive and teeth. Brilliant Blue-based plaque-staining agents (BBPSAs), which increase tooth brushing efficiency, have the potential to support the maintenance of proper oral hygiene during orthodontic treatment. However, they exhibit strong colouring properties, and their impact on the aesthetics of braces remains unclear. Therefore, the aim of this study was to investigate the influence of commercially available BBPSAs on the colour of aesthetic orthodontic materials. A light-cured, colour-changing orthodontic adhesive and new-generation, monocrystalline, sapphire brackets were chosen for the experiments. The effect of the staining agent on the tested materials was investigated in terms of the reaction temperature and time, as well as the presence of black tea-induced impurities on the materials. The CIELAB (Commission Internationale de L’éclairage L* a* b*) colour system parameters were measured, and the colour differences (ΔE*ab and ΔE00—the Commission Internationale de L’éclairage 2000 colour-difference) were determined for the materials under several experimental conditions. The braces’ green-red colour expression was positively affected by the BBPSA. Under in vitro conditions, the regular use of the BBPSA for 90 days visibly improved the unfavourable colour change caused by the black tea.
... Notably, the presence of a densely connected cluster of oral colonisers -some of which were identified to have interspecies spatial associations [52] -may point to a potential reservoir of sepsis pathogens. This also suggests the possibility of opportunistic infections from the human microbiota and dysbioses that could affect disease severity, given that oral infections are a known risk factor for systemic disease [53,54]. This hypothesis is in line with the reported changes in nasal microbiomes in septic individuals [55] and the associations of intestinal dysbiosis with increased susceptibility to sepsis [56]. ...
Our understanding of the host component of sepsis has made significant progress. However, detailed study of the microorganisms causing sepsis, either as single pathogens or microbial assemblages, has received far less attention. Metagenomic data offer opportunities to characterize the microbial communities found in septic and healthy individuals. In this study we apply gradient-boosted tree classifiers and a novel computational decontamination technique built upon SHapley Additive exPlanations (SHAP) to identify microbial hallmarks which discriminate blood metagenomic samples of septic patients from that of healthy individuals. Classifiers had high performance when using the read assignments to microbial genera [area under the receiver operating characteristic (AUROC=0.995)], including after removal of species ‘culture-confirmed’ as the cause of sepsis through clinical testing (AUROC=0.915). Models trained on single genera were inferior to those employing a polymicrobial model and we identified multiple co-occurring bacterial genera absent from healthy controls. While prevailing diagnostic paradigms seek to identify single pathogens, our results point to the involvement of a polymicrobial community in sepsis. We demonstrate the importance of the microbial component in characterising sepsis, which may offer new biological insights into the aetiology of sepsis, and ultimately support the development of clinical diagnostic or even prognostic tools.
... An orchestrated series of dysbiotic polymicrobial interactions can promote the colonization of a pathogenic microbial community below the gum line, leading to periodontitis, an infection-driven inflammatory disease of the periodontal tissues and alveolar bone, imposing adverse systemic effects on human health [1][2][3][4][5] . Various etiological models suggest that the Gram-negative anaerobe Porphyromonas gingivalis may play a central role in the onset of periodontitis via orchestrating a pronounced ecophysiological change below the gingival margin 6,7 ; however, the mechanistic basis of such a microbial shift has not been elucidated. ...
Our understanding of how the oral anaerobe Porphyromonas gingivalis can persist below the gum line, induce ecological changes, and promote polymicrobial infections remains limited. P. gingivalis has long been described as a highly proteolytic and asaccharolytic pathogen that utilizes protein substrates as the main source for energy production and proliferation. Here, we report that P. gingivalis displays a metabolic plasticity that enables the exploitation of non-proteinaceous substrates, specifically the monocarboxylates pyruvate and lactate, as well as human serum components, for colonization and biofilm formation. We show that anabolism of carbohydrates from pyruvate is powered by catabolism of amino acids. Concomitantly, the expression of fimbrial adhesion is upregulated, leading to the enhancement of biofilm formation, stimulation of multispecies biofilm development, and increase of colonization and invasion of the primary gingival epithelial cells by P. gingivalis. These studies provide the first glimpse into the metabolic plasticity of P. gingivalis and its adaptation to the nutritional condition of the host niche. Our findings support the model that in response to specific nutritional parameters, P. gingivalis has the potential to promote host colonization and development of a pathogenic community.
... Various microorganisms inhabit the oral cavity, which has a microbial diversity secondary only to the gut microbiome (25). The oral microbiome has been associated with human health and diseases, including oral cancer (26), pancreatic cancer (27), and systemic disease (28). One prospective study that assessed the association between the oral microbiome and CRC risk was conducted in an African American population, where the oral microbiome was represented by mouth rinse samples (29). ...
Background:
Emerging evidence demonstrates that the salivary microbiome could serve as a biomarker for various diseases. To date, the oral microbiome's role in the diagnosis of colorectal cancer (CRC) has not been fully elucidated. We aimed to illustrate the salivary microbiome's role in diagnosing and predicting the risk of CRC.
Methods:
We collected preoperational saliva from 237 patients [95 healthy controls (HCs) and 142 CRC patients] who underwent surgical resections or colorectal endoscopy in Renji Hospital from January 2018 to January 2020. Clinical demographics, comorbidities, and oral health conditions were obtained from medical records or questionnaires. Salivary microbial biomarkers were detected using quantitative polymerase chain reaction (qPCR) after DNA extraction. Multivariate logistic regression analysis was employed to analyze the risk factors for CRC. A predictive model for the risk of developing CRC was constructed based on logistic regression analysis. Predictive accuracy was internally validated by bootstrap resampling. A clinical nomogram was constructed to visualize the predictive model.
Results:
Logistic regression analysis demonstrated that the risk factors associated with CRC included age at diagnosis, male sex, poor oral hygiene, and relative salivary Desulfovibrio desulfuricans abundance. The predictive model had good discriminative (0.866) and calibration abilities (0.834) after bias correction.
Conclusions:
The model based on age, sex, oral hygiene index (OHI), and the salivary Desulfovibrio desulfuricans level, which is visualized by a clinical nomogram, can predict the risk of CRC. Developing good oral hygiene habits might reduce the risk of CRC.
... The biofilm is composed of more than 1,000 different species of microorganisms but some strictly anaerobic bacteria such as Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola and Aggregatibacter atinomycetemcomitans are frequently associated with the initiation and perpetuation of periodontitis (10)(11)(12). ...
The purpose of this research was to assess the correlation between glycemic control and clinical periodontal characteristics in type 2 diabetics with generalized chronic periodontitis. A total of 182 patients with type 2 diabetes mellitus and generalized chronic periodontitis were included in our study. The clinical examination included full-mouth plaque accumulation, bleeding on probing (BoP), probing depth (PD), presence of suppuration (SUP), clinical attachment level (CAL) and number of remaining teeth. Blood analyses were conducted for glycated hemoglobin (HbA1c) and fasting plasma glucose (FPG). The correlation between the extent of periodontitis, defined as the percentage of PD and CAL sites ≥5 mm, and glycemic control was also analyzed. In addition, clinical parameters were compared between two (<7 and ≥7%) glycemic subsets. The frequency of uncontrolled diabetic subjects (HbA1c ≥7%) was higher than that of the well-controlled subjects (HbA1c <7%), 57.15 vs. 42.85%. Among the clinical parameters evaluated, mean full-mouth plaque accumulation was significantly higher among patients without glucose control (74.2±25.2 vs. 62.5±28.7%, P<0.01), as well as mean PD (3.78±0.9 vs. 3.42±0.8 mm, P<0.01) and mean CAL (4.5±1.2 vs. 4.1±1.2 mm, P= 0.02). The sites with PD ≥5 mm were statistically more prevalent among patients with HbA1c ≥7% compared with patients with HbA1c <7% (27.8±6.2 vs. 23.4±5.8%, P<0.01). The mean number of remaining teeth was statistically significantly lower in patients with HbA1c ≥7% compared with patients with HbA1c <7% (18.5±3.2 vs. 20.4±4.1, P<0.01). In conclusion, the severity and extension of generalized chronic periodontitis was higher in type 2 diabetes mellitus patients with poor glucose control compared with those with good glucose control.
... For these patients, oral health issues might be of particular importance. On the one hand, inflammatory diseases of the oral cavity can be related to a risk of infectious complications [4]. It has been reported that DNA of potentially periodontal pathogens, which are related to periodontal diseases, can be detectable in cardiac tissues [5]. ...
Objectives
The aim of this cross-sectional study was to compare oral health-related quality of life (OHRQoL) of patients with left ventricular assist device (LVAD) and heart failure (HF).
Material and methods
Seventy-four patients with LVAD were recruited from University Department for Cardiac Surgery, Leipzig Heart Center, Germany. A group of 72 patients with HF was composed by matching (age, gender, smoking). The German short form of oral health impact profile (OHIP G14) was applied. Health-related quality of life (HRQoL) was measured by short form 36 survey (SF-36). Dental conditions (decayed-, missing- and filled-teeth [DMF-T]), remaining teeth and periodontal findings were assessed. Statistics: t -test, Mann-Whitney U test, Kruskal-Wallis test, chi-square or Fisher test, linear regression.
Results
Age, gender, smoking, underlying disease, co-morbidities and oral findings were comparable between groups ( p > 0.05). OHIP G14 sum score was 3.53 ± 6.82 (LVAD) and 2.92 ± 5.35 (HF; p = 0.70), respectively. The scales SF-36 physical functioning ( p = 0.05) and SF-36 social functioning ( p < 0.01) were worse in LVAD. In the LVAD group, the DMF-T and remaining teeth negatively correlated with OHIP G14 sum score ( p < 0.01). In HF patients, positive correlations were found between OHIP G14 and D-T ( p < 0.01) and remaining teeth ( p = 0.04). Moreover, DMF-T ( p = 0.03) and remaining molars/premolars ( p = 0.02) were negatively correlated with SF-36 scales in HF.
Conclusions
Oral health and OHRQoL was comparable between LVAD and HF; thereby, OHRQoL reflected the clinical oral status.
Clinical relevance
Dental care, with beginning in early stage of HF, should be fostered to preserve teeth and support quality of life before and after LVAD implantation.
... Dental diseases, including persistent periapical infection, are biofilm-mediated infections, which have been associated with the etiology of several systemic diseases, ranging from arthritis to neurodegenerative diseases [1][2][3][4]. Biofilm is a community of bacteria enclosed in the self-produced polymeric matrix and adhered to the surface. Growth inside biofilm facilitates bacteria to survive and produce chronic infection [5]. ...
Quaternary ammonium methacrylates (QAMs) are useful antimicrobial compounds against oral bacteria. Here, we investigated the effects of two QAMs, dimethylaminododecyl methacrylate (DMADDM) and dimethylaminohexadecyl methacrylate (DMAHDM), on biofilm formation, survival and development of tolerance by biofilm, and survival and development of tolerance against QAMs after prolonged starvation. Enterococcus faecalis (E. faecalis), Streptococcus gordonii (S. gordonii), Lactobacillus acidophilus (L. acidophilus), and Actinomyces naeslundii (A. naeslundii) were used. Minimum inhibitory concentration (MIC) of QAMs against multispecies biofilm was determined. Biofilm formed under sub-MIC was observed by crystal violet staining and confocal laser scanning microscopy (CLSM). Metabolic activity was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and lactic acid production measurement. Development of tolerance was determined by MIC values before and after exposure to QAMs or after prolonged starvation. It was found that E. faecalis and S. gordonii could survive and form biofilm under sub-MIC of QAMs. Lactic acid production from biofilms formed under sub-MIC was significantly higher than control specimens (p
... e neuroinflammatory response activated by microglia is believed to play a leading role in the pathophysiology of glaucoma. Activated microglia induce secretion of proinflammatory cytokines (IL-1, IL-6, and TNF-α) and trigger innate immune responses through TLRs [25][26][27]. Inflammation and innate immunity are essential for understanding the link between periodontitis and glaucoma. In addition, oxidative stress is a potential common pathophysiology for the two conditions. ...
The objective of this cross-sectional study was to evaluate the association between periodontitis and glaucoma. This prospective cohort study used epidemiological data from the Korean Genome and Epidemiology Study performed between 2004 and 2016. Among 173,209 participants, 9572 patients with periodontitis and 115,332 controls (nonperiodontitis) were selected. We analysed the history of glaucoma in periodontitis and control participants. The participants were interviewed regarding their history of hypertension, diabetes mellitus, hyperlipidaemia, periodontitis, glaucoma, smoking, and alcohol consumption by trained interviewers. A logistic regression model was created to analyse the odds ratio of having a history of glaucoma among patients with periodontitis. Two-tailed analyses using chi-square and independent t-tests were used for statistical analysis. The adjusted odds ratio of periodontitis as a risk factor for glaucoma was 3.44 (95% confidence interval = 2.99–3.97, p < 0.001 ). This study demonstrated that glaucoma was associated with periodontitis.
... Periodontitis is one of the main causes of tooth loss (Hajishengallis et al., 2012). As the sixth largest infectious disease in the world, it is also closely related to systemic diseases such as rheumatoid arthritis, atherosclerosis, and Alzheimer's disease (Kumar, 2013;Kassebaum et al., 2014;Hussain et al., 2015;Leech and Bartold, 2015;Singhrao et al., 2015). Periodontitis is caused by subgingival plaque biofilm, which is rich in abundant and diverse microorganisms (Flemming and Wingender, 2010;Valm, 2019). ...
As one of the main pathogens of periodontitis, Porphyromonas gingivalis often forms mixed biofilms with other bacteria or fungi under the gingiva, such as Candida albicans. Heme is an important iron source for P. gingivalis and C. albicans that supports their growth in the host. From the perspective of heme competition, this study aims to clarify that the competition for heme enhances the pathogenic potential of P. gingivalis during the interaction between P. gingivalis and C. albicans. Porphyromonas gingivalis single-species biofilm and P. gingivalis-C. albicans dual-species biofilm were established in a low- and high-heme environment. The results showed that the vitality of P. gingivalis was increased in the dual-species biofilm under the condition of low heme, and the same trend was observed under a laser confocal microscope. Furthermore, the morphological changes in P. gingivalis were observed by electron microscope, and the resistance of P. gingivalis in dual-species biofilm was stronger against the killing effect of healthy human serum and antibiotics. The ability of P. gingivalis to agglutinate erythrocyte was also enhanced in dual-species biofilm. These changes disappeared when heme was sufficient, which confirmed that heme competition was the cause of thepathogenicy change in P. gingivalis. Gene level analysis showed that P. gingivalis was in a superior position in the competition relationship by increasing the expression of heme utilization-related genes, such as HmuY, HmuR, HusA, and Tlr. In addition, the expression of genes encoding gingipains (Kgp, RgpA/B) was also significantly increased. They not only participate in the process of utilizing heme, but also are important components of the virulence factors of P. gingivalis. In conclusion, our results indicated that the pathogenic potential of P. gingivalis was enhanced by C. albicans through heme competition, which ultimately promoted the occurrence and development of periodontitis and, therefore, C. albicans subgingival colonization should be considered as a factor in assessing the risk of periodontitis.
... Interestingly, bacterial strains involved in oral and gut dysbiosis are known to play key roles in the development and progression of systemic diseases such as heart valvulopathies, diabetes mellitus, pre-eclampsia, rheumatoid arthritis and AD, among others [75,[87][88][89][90]. Thus, local dysbiosis of oral and gut microbiota is known to not only impact local tissues but also affect distant organs, and there is mounting evidence that microbial elements may be associated with the development of neuroinflammation and neurodegeneration within the brain. ...
Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Creutzfeldt–Jakob disease (CJD) are brain conditions affecting millions of people worldwide. These diseases are associated with the presence of amyloid-β (Aβ), alpha synuclein (α-Syn) and prion protein (PrP) depositions in the brain, respectively, which lead to synaptic disconnection and subsequent progressive neuronal death. Although considerable progress has been made in elucidating the pathogenesis of these diseases, the specific mechanisms of their origins remain largely unknown. A body of research suggests a potential association between host microbiota, neuroinflammation and dementia, either directly due to bacterial brain invasion because of barrier leakage and production of toxins and inflammation, or indirectly by modulating the immune response. In the present review, we focus on the emerging topics of neuroinflammation and the association between components of the human microbiota and the deposition of Aβ, α-Syn and PrP in the brain. Special focus is given to gut and oral bacteria and biofilms and to the potential mechanisms associating microbiome dysbiosis and toxin production with neurodegeneration. The roles of neuroinflammation, protein misfolding and cellular mediators in membrane damage and increased permeability are also discussed.
... An interesting approach to establish a possible relationship between periodontal infections and systemic disease, consisting on epidemiological studies, demonstrated a strong association between chronic periodontitis and cardiovascular disease, respiratory diseases, diabetes, osteoporosis [36], preterm low birth weight [37], and more recently, pancreatic cancer [38], metabolic syndrome [39], chronic kidney disease [40], rheumatoid arthritis [41], and Alzheimer's disease [42]. ...
The "focal infection theory" is a historical concept based on the assumption that some infections may cause chronic and acute diseases in different districts of the body. Its great popularity spanned from 1930 to 1950 when, with the aim to remove all the foci of infection, drastic surgical interventions were performed. Periodontitis, a common oral pathology mainly of bacterial origin, is the most evident example of this phenomenon today: in fact, bacteria are able to migrate, develop and cause health problems such as cardiovascular and respiratory diseases, diabetes, and osteoporosis. The aim of this narrative report is to verify the hypothesis of the association between oral infections and systemic diseases by different ways of approach and, at the same time, to propose new kinds of treatment today made possible by technological progress. The analysis of the literature demonstrated a strong relationship between these conditions, which might be explained on the basis of the recent studies on microbiota movement inside the body. Prevention of the oral infections, as well as of the possible systemic implications, may be successfully performed with the help of new technologies, such as probiotics and laser.
... This form of survival implies greater protection against external agents and tensions by limiting the penetration of antimicrobial agents and by providing mechanical resistance to shear generated by saliva flow [3]. Some of these bacteria are the main etiological agents of caries and periodontal diseases, being among the most prevalent diseases in humans [4,5]. Depending on its location, two types of dental plaque can be found, the supragingival plaque and the subgingival plaque. ...
Silver nanoparticles (AgNPs) have been proposed as new alternatives to limit bacterial dental plaque because of their antimicrobial activity. Novel glutathione-stabilized silver nanoparticles (GSH-AgNPs) have proven powerful antibacterial properties in food manufacturing processes. Therefore, this study aimed to evaluate the potentiality of GSH-AgNPs for the prevention/treatment of oral infectious diseases. First, the antimicrobial activity of GSH-AgNPs against three oral pathogens (Porphyromonas gingivalis, Fusobacterium nucleatum, and Streptococcus mutans) was evaluated. Results demonstrated the efficiency of GSH-AgNPs in inhibiting the growth of all bacteria, especially S. mutans (IC50 = 23.64 μg/mL, Ag concentration). Second, GSH-AgNPs were assayed for their cytotoxicity (i.e., cell viability) toward a human gingival fibroblast cell line (HGF-1), as an oral epithelial model. Results indicated no toxic effects of GSH-AgNPs at low concentrations (≤6.16 µg/mL, Ag concentration). Higher concentrations resulted in losing cell viability, which followed the Ag accumulation in cells. Finally, the inflammatory response in the HGF-1 cells after their exposure to GSH-AgNPs was measured as the production of immune markers (interleukins 6 and 8 (IL-6 and IL-8) and tumor necrosis factor-alpha (TNF-α)). GSH-AgNPs activates the inflammatory response in human gingival fibroblasts, increasing the production of cytokines. These findings provide new insights for the use of GSH-AgNPs in dental care and encourage further studies for their application.
... P. gingivalis is one of the major causative agents of periodontal disease and with this newly discovered ability to escape from macrophages, may have several clinical implications beyond the oral cavity. P. gingivalis is able to enter the bloodstream through sores and lesions within inflammation sites [89] and numerous studies have linked P. gingivalis to multiple systemic diseases [50][51][52][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68]. The association between periodontitis and Chronic Obstructive Pulmonary Disease, an inflammation-driven respiratory disease with a high mortality rate, has been widely recognized in the past twenty years [62,64,[90][91][92][93][94][95][96]. ...
Macrophages are phagocytic cells that play a key role in host immune response and clearance of microbial pathogens. Porphyromonas gingivalis is an oral pathogen associated with the development of periodontitis. Escape from macrophage phagocytosis was tested by infecting THP-1-derived human macrophages and RAW 264.7 mouse macrophages with strains of P. gingivalis W83 and 33277 as well as Streptococcus gordonii DL1 and Escherichia coli OP50 at MOI = 100. CFU counts for all intracellular bacteria were determined. Then, infected macrophages were cultured in media without antibiotics to allow for escape and escaping bacteria were quantified by CFU counting. P. gingivalis W83 displayed over 60% of the bacterial escape from the total amount of intracellular CFUs, significantly higher compared to all other bacteria strains. In addition, bacterial escape and re-entry were also tested and P. gingivalis W83, once again, showed the highest numbers of CFUs able to exit and re-enter macrophages. Lastly, the function of the PG0717 gene of P. gingivalis W83 was tested on escape but found not related to this activity. Altogether, our results suggest that P. gingivalis W83 is able to significantly avoid macrophage phagocytosis. We propose this ability is likely linked to the chronic nature of periodontitis.
... (10)(11)(12)(13) These substances should help in avoiding the proliferation of anerobic pathogens in protected oral niches (spaces where mechanical cleaning is more difficult), which may act as reservoir of aggressive bacteria in susceptible individuals . (14) As a matter of fact, the reduction in the use of antibiotics should be one of the goals of current medical and dental therapy, considering the increased risk of developing resistant strains. (15)(16) Among different mouthwashes chlorhexidine (CHX) remains gold standard among all. ...
... Recently, dysbiosis of colonic microbiota was also suggested to be affected by oral microbiota (Koliarakis et al. 2019) pointing out that oral-colon interaction should be studied in detail, especially for the evaluation of oral bacteria-mediated systemic inflammatory responses. Therefore, the development of functional probiotics and probiotic products capable of fostering a healthy oral microbiota is a special area of interest not only for treating periodontal diseases but also for treating systemic diseases Kumar 2013). ...
M18 strain of Streptococcus salivarius is a bacterial replacement probiotic that has been suggested for use in the oral cavity. Here, we have shown that S. salivarius M18 cell-free supernatant reduced the growth of the two most common human pathogens Pseudomonas aeruginosa and Klebsiella pneumonia and sensitized the pathogenic bacteria to antibiotic. Besides, the supernatant inhibited biofilm formation of P. aeruginosa drastically. For pinpointing the biomolecular changes that occurred in P. aeruginosa incubated with the probiotic supernatant, attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy was used. Unsupervised learning algorithms, principal component analysis (PCA) and hierarchical cluster analysis (HCA), and intensity analyses of individual spectral bands exhibited comprehensive alterations in the polysaccharide and lipid contents and compositions of P. aeruginosa cultivated with S. salivarius M18 cell-free supernatant. These results indicate that S. salivarius M18 has the potential for the prevention or alleviation of different pathogen-induced infections along with the infections of oral pathogens.
... According to the World Health Organization (WHO), oral health contributes to general health and quality of life. Poor oral hygiene and its consequences on the individual such as periodontitis is a recognized public health problem [1][2][3], as periodontal pathogens can reach the bloodstream and contribute to the progression of systemic diseases [4][5][6]. Additionally, in the absence of treatment, periodontal diseases can lead to tooth mobility, tooth loss, and halitosis that negatively affect patient lifestyle with social, physical, and psychological repercussions [7][8][9]. Tobacco use and poor oral hygiene combined an increase the risk of periodontitis not only by initiating but also by fostering disease progression and affecting response to treatment [10,11]. ...
Background:
Oral hygiene instructions (OHI) and periodontal nonsurgical treatment (PNST) play pivotal roles in the management of periodontitis. The study aims to discern their respective effects on periodontal clinical parameters and patient-reported outcome measures (PROMs).
Methods:
Ninety-one patients were included, 34 non-smokers (NS), 25 former smokers (FS) and 32 current smoker (CS). Clinical parameters such as probing depth (PD) and bleeding on probing (BOP) were collected, and the periodontal inflamed tissue area (PISA) was calculated. Clinical parameters and PROMs were recorded before and after receiving OHI, with electronic tooth brush and interdental brushes, as well as 3 months after debridement.
Results:
Smokers presented a significantly higher proportion of severe periodontitis (64.7%) with generalized extension (76.5%) and with a rapid rate of progression (97.1%) compared to NS and FS. OHI led to a significant decrease of PD, BOP, and PISA (p < 0.0001) only in NS and FS. Debridement reduced PD and the percentage of PD >6 mm in all groups (p < 0.0001). OHI induced significant improvement of oral hygiene, frequency of interdental cleaning, and PROMs (p < 0.0001). Further debridement induced significant additional improvement PROMs in FS and NS (p < 0.0001).
Conclusion:
OHI and debridement improved periodontal clinical parameters and PROMs in both NS and FS. Former smokers had comparable outcomes to non-smokers, suggesting that smoking cessation should be encouraged.
... Oral microbiome has been associated with human health and diseases, including oral cancer 37 , pancreatic cancer 38 and systemic diseases 39 . One prospective study of oral microbiome and colorectal cancer risk was conducted in African American populations 31 , nevertheless the oral microbiome was represented by mouth rinse samples and low-income populations were recruited so selection bias was possible. ...
Background: Mounting evidence have shown that fecal microbiome can act as biomarkers for diagnosing colorectal cancer (CRC). Recent studies demonstrate that oral microbiome is concordant with gut microbiome. The role of oral microbiome in colorectal cancer has not been fully illustrated.
Methods: We collected preoperational saliva with a final cohort of 237 patients who underwent surgical resections or colorectal endoscopy in XX Hospital from January 2018 to January 2020. Clinical demographics, comorbidities and oral conditions were obtained from medical records or questionnaires. Salivary microbial biomarkers were detected by quantitative polymerase chain reaction (PCR) after DNA extraction. Multivariate logistics regression analysis was employed to analyze the risk factors for colorectal cancer. A four-variable prediction model was constructed based on the logistics analysis.
Results: Among the 237 patients enrolled, there were 95 endoscopy confirmed healthy control and 142 pathologically confirmed colorectal adenocarcinoma patients. Logistics regression analysis demonstrated that the risk factors associated with CRC included age at diagnosis (OR=1.111, 95%CI=1.072-1.151), male sex (OR=2.111, 95%CI=1.068-4.175), oral hygiene index (OR=1.769, 95%CI=1.116-2.804) and relative salivary Desulfovibrio desulfuricans (Dd) abundance (OR=1.156, 95%CI=1.05-1.272), based on which a four-variable model was developed. The four-variable model had good discriminative (Brier score=0.144, Concordance index=0.866) and calibration (0.834) abilities after bias correction.
Conclusions: Elevated salivary Dd level is an independent risk factor for CRC. We have developed a four-variable model that could help identify at-risk patients for CRC.
Objectives
The priming mechanism of adaptive immunity in oral mucositis remains unclarified. This study aimed to elucidate the mechanisms of oral lichen planus (OLP), with a specific focus on the role of inducible tertiary lymphoid structures (iTLSs) and stromal‐immune microenvironments within OLP.
Materials and Methods
We employed single‐cell RNA sequencing and multiplex immunofluorescence staining to characterize the spatial characteristics and transcriptional signature of iTLSs in OLP. To investigate whether the presence of iTLSs influences the disease severity of OLP, we retrospectively collected clinical data from OLP patients.
Results
Based on single‐cell resolution analysis, we identified distinct cellular compositions and fibroblast‐immune cells interactions within the iTLSs of OLP. We highlighted the critical role of CCL19 ⁺ fibroblasts in T‐cell chemotaxis, promoting the development of iTLSs. Lymphotoxin was demonstrated to activate fibroblasts expressing CCL19. We revealed a significant correlation between the presence of iTLSs and increased severity of OLP, marked by more atrophic‐erosive forms and higher disease scores in patients with iTLSs.
Conclusions
The present research proposed the fibroblast‐immune cell interactions within iTLSs as essential factors in OLP's inflammatory milieu, indicating iTLSs as the priming structure of T‐cell immunity in the local oral mucosa.
A dysbiotic microbial community whose members have specific/synergistic functions that are modulated by environmental conditions, can disturb homeostasis in the subgingival space leading to destructive inflammation, plays a role in the progression of periodontitis. Filifactor alocis , a gram‐positive, anaerobic bacterium, is a newly recognized microbe that shows a strong correlation with periodontal disease. Our previous observations suggested F. alocis to be more resistant to oxidative stress compared to Porphyromonas gingivalis . The objective of this study is to further determine if F. alocis , because of its increased resistance to oxidative stress, can affect the survival of other ‘established’ periodontal pathogens under environmental stress conditions typical of the periodontal pocket. Here, we have shown that via their interaction, F . alocis protects P. gingivalis W83 under H 2 O 2 ‐induced oxidative stress conditions. Transcriptional profiling of the interaction of F. alocis and P. gingivalis in the presence of H 2 O 2 ‐induced stress revealed the modulation of several genes, including those with ABC transporter and other cellular functions. The ABC transporter operon ( PG0682–PG0685 ) of P. gingivalis was not significant to its enhanced survival when cocultured with F. alocis under H 2 O 2 ‐induced oxidative stress. In F. alocis , one of the most highly up‐regulated operons ( FA0894–FA0897 ) is predicted to encode a putative manganese ABC transporter, which in other bacteria can play an essential role in oxidative stress protection. Collectively, the results may indicate that F. alocis could likely stabilize the microbial community in the inflammatory microenvironment of the periodontal pocket by reducing the oxidative environment. This strategy could be vital to the survival of other pathogens, such as P. gingivalis , and its ability to adapt and persist in the periodontal pocket.
Background:
This study tests the effects of scaling and root planing (SRP) versus SRP plus minocycline hydrochloride microspheres (SRP+MM) on 11 periodontal pathogens and clinical outcomes in Stage II-IV Grade B periodontitis participants.
Methods:
Seventy participants were randomized to receive SRP (n = 35) or SRP+MM (n = 35). Saliva and clinical outcomes were collected for both groups at baseline before SRP, 1-month reevaluation, and at 3- and 6-month periodontal recall. MM were delivered to pockets ≥5 mm immediately after SRP and immediately after the 3-month periodontal maintenance in the SRP+MM group. A proprietary saliva test* was utilized to quantitate 11 putative periodontal pathogens. Microorganisms and clinical outcomes were compared between groups using generalized linear mixed-effects models with fixed effects and random effects terms. Mean changes from baseline were compared between groups via group-by-visit interaction tests.
Results:
Significant reduction in Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum, Prevotella intermedia, Parvimonas micra, and Eikenella corrodens were identified at the 1-month reevaluation after SRP+MM. Six months after SRP with a re-application of MM 3 months after SRP, Fusobacterium nucleatum, Prevotella intermedia, Campylobacter rectus, and Eikenella corrodens were significantly reduced. SRP+MM participants had significant clinical outcome reductions in pockets ≥5 mm at the reevaluation, 3- and 6-month periodontal maintenance, and clinical attachment loss gains at the 6-month periodontal maintenance.
Conclusion:
MM delivered immediately after SRP and reapplication at 3 months appeared to contribute to improved clinical outcomes and sustained decreased numbers of Fusobacterium nucleatum, Prevotella intermedia, Campylobacter rectus, and Eikenella corrodens at 6 months.
Objectives:
Collagen triple helix repeat containing-1 (CTHRC1) is a glycoprotein that can be secreted extracellularly and is involved in the regulation of collagen matrix in a variety of diseases. The expression level of CTHRC1 in periodontitis was detected in the present study.
Materials and methods:
The gingival tissues from clinically healthy subjects (15 cases) and those with periodontitis (30 cases) were taken for immunohistochemical staining. Lipopolysaccharide of the Porphyromonas gingivalis was added in the periodontal ligament fibroblast culture in vitro. Cells were collected and the mRNA levels of the intracellular CTHRC1 and protein expression of the extracellular CTHRC1 were detected.
Results:
The protein expression of CTHRC1 in the periodontitis group was higher than that of the clinically healthy group. The in vitro cell experiments showed that 10 μg/mL of P.g LPS could induce a significant increase in protein secretion of CTHRC1, and 5 μg/mL P.g LPS had a significant effect on promoting the mRNA expression of CTHRC1.
Conclusion:
CTHRC1 might be involved in the development of periodontitis and the expression level might be significantly correlated with the stimulation of P.g LPS on fibroblasts. Different stimulation intensities of P.g LPS might result in different expression patterns of CTHRC1.
En esta revisión sistemática exploratoria, presentamos la evidencia registrada en la literatura, de que la microbiota oral puede generar una acción carcinogénica, actuando a través de tres mecanismos principales: sobre el medio extracelular, activando vías de señalización intracelular y / o generando acción directa sobre el ADN, y que las principales bacterias estudiadas corresponden a Fusobacterium Nucleatum y Porphyromona Gingivalis. En la actualidad hay evidencia suficiente acerca de la asociación entre microbiota oral y distintos tipos de cáncer, sin embargo, no hay gran conocimiento de los mecanismos por los cuales esta microbiota participa en su desarrollo. Presentamos una recopilación de los diversos mecanismos de acción que utilizan las bacterias de la cavidad oral en el proceso de carcinogénesis en cuatro tipos diferentes de cáncer.
Filifactor alocis is an emerging member of the periodontal community and is now proposed to be a diagnostic indicator of periodontal disease. However, due to the lack of genetic tools available to study this organism, not much is known about its virulence attributes.
Measurement of saliva microbes is promoted as a way to detect oral and systemic disease, yet there is a multitude of factors that affect the oral microbiome. The salivary microbiome is influenced by biofilm of shedding (epithelial) and non-shedding (tooth) surfaces. Methods for study of the salivary microbiome are by no means standardized, and differences in sample collection, storage, and processing can all affect results to some degree. Here we describe one method of saliva collection that has been validated for reproducibility. Standard 16S rRNA gene analysis is done using the Human Oral Microbiome Database library which results in analysis that is straightforward. Everything about this procedure except the library synthesis and DNA sequencing itself can easily be done in-house. To gauge the ability of salivary microbial analytics to distinguish between edentulous and dentate oral conditions, differences in the saliva microbiome of subjects with and without teeth were examined. Fifty-two dentate and 49 edentulous subjects provided stimulated saliva samples. 16S rRNA gene sequencing, QIIME-based data processing, and statistical analysis were done using several different analytical approaches to detect differences in the salivary microbiome between the two groups. Bacteria diversity was lower in the edentulous group. Remarkably, all 31 of the most significant differences in taxa were deficits that occurred in the edentulous group. As one might expect, many of these taxa are attributed to dental plaque and gingival sulcus-associated bacteria verifying that the measurement of 16S rRNA genes in the bacteria of the saliva can be used to reproducibly measure expected differences in the oral microbiome that occur with edentulism or other conditions and diseases.
Bacteriophages are viruses that specifically lyse bacteria. They have demonstrated potential in applications as antibacterial agents in medicine, agriculture, and environmental remediation. Due to the complex and dynamic nature of the oral microbiome, antibiotic treatment of chronic, polymicrobial oral diseases may lead to dysbiosis. In these diseases, bacteriophages may provide targeted activity against oral bacteria without such disruption to the broader microbial community. In this chapter, we describe the methods for screening samples that may contain bacteriophages against oral pathogenic bacteria, and using the example of FNU1, the bacteriophage we isolated against Fusobacterium nucleatum, describe the process of bacteriophage purification and characterization.
Background
Oral microbiota has largely escaped attention in Parkinson’s disease (PD), despite its pivotal role in maintaining oral and systemic health.
Objective
The aim of our study was to examine the composition of the oral microbiota and the degree of oral inflammation in PD.
Methods
Twenty PD patients were compared to 20 healthy controls. Neurological, periodontal and dental examinations were performed as well as dental scaling and gingival crevicular fluid sampling for cytokines measurement (interleukine (IL)-1β, IL-6, IL-1 receptor antagonist (RA), interferon-γ and tumor necrosis factor (TNF)-α). Two months later, oral microbiota was sampled from saliva and subgingival dental plaque. A 16S rRNA gene amplicon sequencing was used to assess bacterial communities.
Results
PD patients were in the early and mid-stage phases of their disease (Hoehn & Yahr 2–2.5). Dental and periodontal parameters did not differ between groups. The levels of IL-1β and IL-1RA were significantly increased in patients compared to controls with a trend for an increased level of TNF-α in patients. Both saliva and subgingival dental plaque microbiota differed between patients and controls. Streptococcus mutans, Kingella oralis, Actinomyces AFQC_s, Veillonella AFUJ_s, Scardovia, Lactobacillaceae, Negativicutes and Firmicutes were more abundant in patients, whereas Treponema KE332528_s, Lachnospiraceae AM420052_s, and phylum SR1 were less abundant.
Conclusion
Our findings show that the oral microbiome is altered in early and mid-stage PD. Although PD patients had good dental and periodontal status, local inflammation was already present in the oral cavity. The relationship between oral dysbiosis, inflammation and the pathogenesis of PD requires further study.
Matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) is a rapid and accurate method to identify microorganisms in clinical laboratories. This study isolates yeast-like microorganisms in the oral washes that are collected from non-bedridden nursing home residents, using CHROMagar Candida plates, and identifies them using Bruker MALDI-TOF MS. The ribosomal DNA sequences of the isolates are then examined. Three hundred and twenty yeast isolates are isolated from the oral washes. Candida species form the majority (78.1%), followed by Trichosporon/Cutaneotrichosporon species (8.8%). Bruker MALDI-TOF MS gives a high-level confidence, with a log(score) value of ≥1.8, and identifies 96.9% of the isolates. There are six inconclusive results (1.9%), and those sequences are verified as rare clinical species, including Candida ethanolica, Cutaneotrichosporon jirovecii, Exophiala dermatitidis, and Fereydounia khargensis. Almost all of the isolates have a regular color on the CHROMagar Candida plates. If the colonies are grouped by color on the plates, a specific dominant yeast species is present in each color group, except for purple or orange isolates. In conclusion, MALDI-TOF MS is verified as a fast, accurate and practical method to analyze oral yeasts in elderly subjects.
Rheumatoid arthritis and periodontitis are two common chronic inflammatory diseases affecting human population worldwide. The association between the two conditions have been the focus of many researches, trying to explore the possible mechanisms underlying this association. Prolactin hormone, besides its known lactogenic effects acts as a cytokine secreted from various tissues other than the pituitary gland with multiple pleotropic actions in immunity and inflammation. Several data showed that prolactin levels are increased significantly in the synovial and periodontal tissues, and this increase is correlated with disease activity and tissue destruction. Our hypothesis suggests that local prolactin can represent a link between the two conditions. In this work, we suggest a possible mechanistic interactions, hypothesized to form a common path linking between rheumatoid arthritis, periodontitis and prolactin. This is because of the need to develop new treatment strategies for the most effective long term control of inflammation in both conditions.
OmpA-like proteins located in the outer bacterial membrane are potential virulence factors from the major periodontal pathogens Porphyromonas gingivalis and Tannerella forsythia. Our previous studies have shown that OmpA-like proteins are glycosylated by O-linked N-acetylglucosamine (O-GlcNAc) and are strongly reactive to wheat germ agglutinin (WGA) lectin, which shows sugar specificity to GlcNAc. Utilizing this property, we have developed a separation method for OmpA-like proteins by affinity chromatography using WGA lectin-agarose. The purity of enriched native OmpA-like proteins were confirmed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE) and Coomassie Brilliant Blue (CBB) staining. More importantly, the purified OmpA-like proteins formed a unique trimeric structure keeping their bioactivity intact. In this chapter, we describe a detailed procedure to separate OmpA-like proteins, which may be used to further progress the biological studies of OmpA-like proteins.
Recent evidence suggests that smoking affects the composition of the disease-associated subgingival biofilm, yet little is known about its effects during the formation of this biofilm. The present investigation was undertaken to examine the contributions of smoking to the composition and proinflammatory characteristics of the biofilm during de novo plaque formation. Marginal and subgingival plaque and gingival crevicular fluid samples were collected from 15 current smokers and from 15 individuals who had never smoked (nonsmokers) following 1, 2, 4, and 7 days of undisturbed plaque formation. 16S rRNA gene cloning and sequencing were used for bacterial identification, and multiplex bead-based flow cytometry was used to quantify the levels of 27 immune mediators. Smokers demonstrated a highly diverse, relatively unstable initial colonization of both marginal and subgingival biofilms, with lower niche saturation than that seen in nonsmokers. Periodontal pathogens belonging to the genera Fusobacterium, Cardiobacterium, Synergistes, and Selenomonas, as well as respiratory pathogens belonging to the genera Haemophilus and Pseudomonas, colonized the early biofilms of smokers and continued to persist over the observation period, suggesting that smoking favors early acquisition and colonization of pathogens in oral biofilms. Smokers also demonstrated an early proinflammatory response to this colonization, which persisted over 7 days. Further, a positive correlation between proinflammatory cytokine levels and commensal bacteria was observed in smokers but not in nonsmokers. Taken together, the data suggest that smoking influences both the composition of the nascent biofilm and the host response to this colonization.
Systematic review on periodontal disease as a risk factor for pre-eclampsia
The subgingival microbiome is largely uncultivated, and therefore, cultivation-based and targeted molecular approaches have limited value in examining the effect of smoking on this community. We tested the hypothesis that the subgingival biofilm is compositionally different in current and never-smokers by using an open-ended molecular approach for bacterial identification. Subgingival plaque from deep sites of current and never-smokers matched for disease was analyzed by 16S sequencing. Smokers demonstrated greater abundance of Parvimonas, Fusobacterium, Campylobacter, Bacteroides, and Treponema and lower levels of Veillonella, Neisseria, and Streptococcus. Several uncultivated Peptostreptococci, Parvimonas micra, Campylobacter gracilis, Treponema socranskii, Dialister pneumosintes, and Tannerella forsythia were elevated in this group, while Veillonella sp. oral clone B2, Neisseria sp. oral clone 2.24, Streptococcus sanguinis, and Capnocytophaga sp. clone AH015 were at lower levels. The microbial profile of smoking-associated periodontitis is distinct from that of non-smokers, with significant differences in the prevalence and abundance of disease-associated and health-compatible organisms.
A recent clinical trial (Obstetrics and Periodontal Therapy [OPT] Study) demonstrated that periodontal therapy during pregnancy improved periodontal outcomes but failed to impact preterm birth. The present study evaluated seven target bacteria, Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia (previously T. forsythensis), Prevotella intermedia, Campylobacter rectus, and Fusobacterium nucleatum, in subgingival dental plaque of pregnant women in the OPT Study and their association with birth outcomes.
Pregnant women were randomly assigned to receive periodontal treatment before 21 weeks' gestation or after delivery. Subgingival plaque was sampled at baseline (13 to 16 weeks; 6 days of gestation) and at 29 to 32 weeks. We analyzed subgingival plaque samples from women who experienced fetal loss, delivered a live preterm infant (preterm women), or delivered a full-term infant (full-term women). Samples were analyzed using quantitative polymerase chain reaction. Associations between preterm birth and bacterial counts and percentages were tested using multiple linear regression.
No significant differences were observed at baseline between preterm and full-term women for any measured bacterial species or group of species, after accounting for multiple comparisons. Changes in bacterial counts and proportions during pregnancy also were not associated with birth outcomes. In full-term and preterm women, periodontal therapy significantly reduced (P <0.01) counts of all target species except for A. actinomycetemcomitans.
In pregnant women with periodontitis, non-surgical periodontal therapy significantly reduced levels of periodontal pathogens. Baseline levels of selected periodontal pathogens or changes in these bacteria resulting from therapy were not associated with preterm birth.
Of four groups of chickens, two (groups I and II) were infected with MDV and two were not (groups III and IV). Groups I and III were fed diets low in lipid, and groups II and IV were fed cholesterol-supplemented diets. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of infected normocholesterolemic and hypercholesterolemic chickens (groups I and II). In contrast, grossly visible atherosclerotic lesions were not seen in uninfected normocholesterolemic chickens (group III), nor in uninfected hypercholesterolemic chickens (group IV). Microscopically, arterial changes in the infected animals were characterized by occlusive fibromuscular intimal thickening which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in man. These results may have important bearing on our understanding of the etiology and pathogenesis of human arteriosclerosis since there is widespread and persistent infection of human populations with up to five different herpes-viruses.
There are four cases of Actinobacillus actinomycetemcomitans pulmonary infections reported in the English literature prior to 1990. We report a case of A actinomycetemcomitans pulmonary infection with invasion of overlying soft tissue, rib, and sternum. This manifestation has not been previously reported. The clinical manifestation is similar to that of Actinomyces israelii, which may be misinterpreted as malignancy initially. The portal of entry of A actinomycetemcomitans may be via hematogenous spread or aspiration. The diagnosis depends on culture after prolonged incubation of the involved tissue obtained by aspiration or biopsy. Elevated serum antibody is helpful for diagnosis of active infection. A actinomycetemcomitans is susceptible to most antibiotics, but is frequently resistant to penicillin, vancomycin, clindamycin, and erythromycin. Isolation of the organism and an in vitro drug sensitivity testing are important in managing the patient. Our patient recovered after a three-month regimen of penicillin.
Patients with bacteremia after dental extraction, third-molar surgery, dental scaling, endodontic treatment, and bilateral tonsillectomy were studied by means of lysis-filtration of blood samples with subsequent aerobic and anaerobic incubation. Samples were obtained before, during, and 10 min after treatment. Bacteremia was observed in 100% of patients after dental extraction, 55% of patients after third-molar surgery, 70% of patients after dental scaling, 20% of patients after endodontic treatment, and 55% of patients after bilateral tonsillectomy. Anaerobic microorganisms were isolated more frequently than aerobic microorganisms were, and viridans group streptococci were the most commonly isolated bacteria. Ten minutes after treatment, the frequency as well as the magnitude of bacteremia showed pronounced reduction.
Known risk factors for coronary heart disease do not explain all of the clinical and epidemiological features of the disease. To examine the role of chronic bacterial infections as risk factors for the disease the association between poor dental health and acute myocardial infarction was investigated in two separate case-control studies of a total of 100 patients with acute myocardial infarction and 102 controls selected from the community at random. Dental health was graded by using two indexes, one of which was assessed blind. Based on these indexes dental health was significantly worse in patients with acute myocardial infarction than in controls. The association remained valid after adjustment for age, social class, smoking, serum lipid concentrations, and the presence of diabetes. Further prospective studies are required in different populations to confirm the association and to elucidate its nature.
The periodontal status of maxillary first molars in 284 young adults demonstrating near-health to early disease was evaluated, and supragingival and subgingival plaque samples were collected. Plaque samples were processed anaerobically, enumerated microscopically for bacterial morphotypes, and cultivated on various media to enumerate the microflora. Although haemophili were ubiquitous (recovered in 98.5 and 96.2% of the supragingival and subgingival plaque samples, respectively), 50% of the respective samples had proportions of less than or equal to 1.5% and less than or equal to 0.33% total Haemophilus spp. based on total cultivable microflora. To study the distribution of Haemophilus spp., 377 colonies were identified from modified chocolate agar (selective for oral haemophili) from 14 supragingival and corresponding subgingival samples from 14 subjects. The most prevalent species, Haemophilus parainfluenzae, was found in significantly higher proportions, based on total haemophili on modified chocolate agar, in supragingival and subgingival samples from teeth with shallower probing depths (less than or equal to 3.0 mm) versus deeper probing depths (greater than or equal to 3.0 mm). Additional statistically significant findings included Haemophilus segnis in higher proportions in supragingival samples from deeper sites, Haemophilus aphrophilus in higher proportions in subgingival samples from deeper sites, and Haemophilus paraphrophilus in higher proportions in subgingival samples from shallower sites. Scatter diagrams illustrating the bivariate distributions of proportions of haemophili with proportions of dark-pigmented Bacteroides spp., spirochetes, and streptococci demonstrated that high proportions of haemophili were never recovered from sites with high proportions of Bacteroides spp. or spirochetes. All levels of haemophili, however, were recovered from sites with all levels of streptococci. Two potential systems for interpreting haemophili data were hypothesized for predicting periodontal probing depths. There was highly significant agreement between the two systems. Small but statistically significant correlations were found between the gingival index, probing depth, and attachment level, and proportions of total Haemophilus species in the respective samples.
Chlamydia pneumoniae, a common human respiratory pathogen, has been associated with atherosclerosis in several seroepidemiological studies. Moreover, its presence in lesions of vessel walls has been demonstrated by culture, immunohistochemistry, PCR, and electron microscopy. In this study, we infected intranasally with C. pneumoniae New Zealand White rabbits which had been fed a normal diet. Reinfection was given 3 weeks later. Six of the nine reinfected animals showed inflammatory changes consisting of intimal thickening or fibroid plaques resembling atherosclerosis in 2 to 4 weeks after reinfection. One rabbit had calcified lesions. Immunohistochemistry for C. pneumoniae was strongly positive in the three older affected animals. No lesions were seen in the controls. The results suggest that C. pneumoniae infection is capable of inducing inflammatory atherosclerosis-like changes in the aortas of infected rabbits.
An increasing body of evidence has linked infections to atherosclerosis and thrombosis. Herpesviruses cause atherosclerosis
in experimental animals. Herpesviruses can also be detected in atherosclerotic lesions in humans. Cytomegalovirus may play
a role in arteriosclerosis in transplanted hearts, and this virus, together with tumor suppressor protein p53, can be found
in restenosis lesions following angioplasty. Chlamydia pneumoniae and dental infections are associated with coronary heart disease in cross-sectional and longitudinal studies, and preceding
respiratory infections are associated with ischemic stroke. Infections may favor formation of atherosclerosis and thrombosis
by elevation of blood levels of fibrinogen, leukocytes, clotting factor, and cytokines and by alteration of the metabolism
and functions of endothelial cells and monocyte macrophages. Low-grade infections may also be one of the causes of the inflammatory
reaction observed in atherosclerotic lesions and acute ischemic symptoms, reflected in elevated levels of C-reactive protein.
These observations warrant further studies in this field.
An increasing body of evidence supports the concept that host-produced PGE2mediates much of the tissue destruction that occurs in periodontal disease. PGE2levels within the crevicular fluid can serve as a static assessment of ongoing disease activity; i.e., rate of attachment loss and bone resorption. New insights into the mechanisms that regulate PGE2synthesis provide an altered paradigm of periodontal disease which places the emphasis on host response, rather than the bacterial etiology, as the principal determinant of disease expression. We describe a PGE2host response model as a hypothetical framework to discuss new, possible explanations for host susceptibility to periodontal disease. J Periodontol 1993;64:432-444.
Although it has been established that aspiration of pharyngeal bacteria is the major route of infection in the development of nosocomial pneumonia, colonization of the pharyngeal mucosa by respiratory pathogens has been shown to be a transient phenomenon. It has been suggested that the dental plaque may constitute an additional, possibly more stable, reservoir of respiratory pathogens. The purpose of this study was to assess the prevalence of oral colonization by potential respiratory pathogens in a group of elderly (mean age = 75.9 yrs) chronic-care-facility residents (n = 28) and a group of age-, gender-, and race-matched outpatient control subjects (n = 30), with specific attention to plaque present on tooth, denture, and oral mucosal surfaces. Plaque scores on teeth and dentures were significantly higher in the chronic-care-facility (CCF) subjects than in the dental outpatient control (DOC) subjects (Pll 2.3 vs. 1.2 and denture plaque 1.4 vs. 0.3). While no subjects in the DOC group were found to be colonized with respiratory pathogens (> 1.0% of the cultivable aerobic flora), 14.3% (4/28) of the CCF subjects were found to be colonized. Oral colonization with respiratory pathogens in CCF subjects was associated with the presence of chronic obstructive pulmonary disease (COPD) and higher plaque scores. These results suggest that deficient dental plaque control and the presence of COPD may be related to respiratory pathogen colonization of dental plaque in chronic-care-facility residents.
The subgingival bacterial flora from 2 gingival sites was cultured and characterized monthly in twenty periodontitis-free women during pregnancy and again post-partum. Monthly plaque samples were also cultured in eleven age and disease matched non-pregnant women. Plaque was processed anaerobically on selective and nonselective media and the predominant colony types were characterized. A portion of each plaque sample was tested for bacterial uptake of C14-estradiol and C14-progesterone. Plasma levels of estrogens and progesterone were measured four times in each subject. The number of gingival bleeding sites, the Gingival Index and the Plaque Index were determined at each sampling period.
In the second trimester there was a significant increase in gingivitis, the ratio of anaerobic to aerobic bacteria, and the proportional levels of Bacteroides melaninogenicus ss. intermedius. In the third trimester both gingivitis and the levels of B. melaninogenicus ss. intermedius decreased. Plaque uptake of C14-steroids increased significantly during pregnancy and paralleled the plaque levels of B. melaninogenicus ss. intermedius. In the second trimester, recovery of B. melaninogenicus ss. intermedius was strongly correlated with plasma levels of estrogens and progesterone. No changes were observed in clinical parameters or the subgingival flora of non-pregnant subjects.
Pregnancy and specifically steroid hormones appear capable of influencing the normal bacterial flora and inducing alterations in the subgingival ecology.
Kunnen A, van Doormaal JJ, Abbas F, Aarnoudse JG, van Pampus MG, Faas MM. Periodontal disease and pre-eclampsia: a systematic review. J Clin Periodontol 2010; 37: 1075–1087. doi: 10.1111/j.1600-051X.2010.01636.x
Aim: This review evaluates the possible relationship between periodontal disease and pre-eclampsia, a major pregnancy complication. A generalized inflammatory response plays an important role in the pathogenesis of pre-eclampsia. Because periodontal disease is a low-grade inflammatory state, periodontal disease might contribute to the pathogenesis of pre-eclampsia.
Main Findings and Conclusion: A literature search of PubMed, EMBASE and CINAHL until August 2010 revealed 12 eligible observational studies and three randomized-controlled trials (RCTs). It appeared difficult to compare these studies, due to variations in definitions of periodontal disease and pre-eclampsia, timing of periodontal examination and inadequate control for confounding factors. Eight observational studies reported a positive association, while four studies found no association. None of the RTCs reported reductions in pre-eclamptic rate after periodontal therapy during pregnancy. Therefore, it is questionable whether periodontal disease plays a causal role in the pathogenesis of pre-eclampsia. The observed association in eight observational studies might be the result of induction of periodontal disease due to the pre-eclamptic state or it may be an epiphenomenon of an exaggerated inflammatory response to pregnancy. Larger RCTs with pre-eclampsia as the primary outcome and pathophysiological studies are required to explore causality and to dissect biological mechanisms involved.
The general systemic distribution of micro-organisms in certain diseases with a localized focus is well established, but the factors which determine the localization of bacteria after they gain entrance into the circulation are obscure.In this paper I wish to record a summary of the results obtained from the intravenous injection, under a standard technic, of streptococci isolated from appendicitis, ulcer of the stomach and duodenum, cholecystitis, rheumatic fever, erythema nodosum, herpes zoster, epidemic parotitis, myositis and endocarditis, and to discuss the bearing of these results on localization of streptococci.TECHNIC
The streptococci were usually grown from sixteen totwenty-four hours at 37 C. in tall columns of ascites (10 per cent.) dextrose (0.2 per cent.) broth (0.6+ to 0.8+) to which sterile tissue (guinea-pig kidney or heart muscle) was often added; the sterility of the ascites fluid and broth containing the tissue was always proved beforehand. After incubation smears were
A patient is described in whom there developed a pulmonary infiltrate and constrictive pericarditis caused by a combined Actinomyces and Actinobacillus actinomycetemcomitans infection, presumably originating from his poor dentition. The diagnosis was only made following repeated thoracotomy. After surgery, long-term treatment with antibiotics led to complete clinical recovery. None the less, some months later he was found to have a brain abscess which resolved during a further course of antibiotics. The variable clinical picture of actinomycosis is discussed, as well as the role of other bacteria frequently associated with actinomycotic infection, in particular Actinobacillus actinomycetemcomitans. The therapeutic implications are described.
To assess the prevalence of oral colonization by respiratory pathogens in a group of ICU patients, with specific attention to dental plaque and the oral mucosa.
Prospective, nonrandomized study with age-matched controls.
Medical ICU in a tertiary-care Veterans Affairs Medical Center and a dental school outpatient preventive dentistry clinic.
Nonconsecutive, unselected patients admitted to the medical ICU during a 2-month period; controls were age-matched patients seen for the first time in the preventive dentistry clinic.
None.
Oral hygienic status was assessed in both groups using a semiquantitative system. Quantitative cultures of dental plaque and buccal mucosa were done within 12 hrs of medical ICU admission and every third day thereafter until discharge/death from the medical ICU. In controls, cultures of plaque and buccal mucosa were done on the initial visit only. Severity of illness of medical ICU patients was quantitated using the Acute Physiology and Chronic Health Evaluation (APACHE II) system and McCabe-Jackson criteria.
Oral hygiene of medical ICU patients was poor. These patients had a mean plaque score (1.9 +/- 0.2) that was significantly greater than that same score seen in outpatients of the preventive dentistry clinic (1.4 +/- 0.1; p less than .005). Plaque and/or oral mucosa of 22 (65%) of 34 medical ICU patients were colonized by respiratory pathogens, in contrast to only four (16%) of 25 preventive dentistry clinic patients (p less than .005). The potential respiratory pathogens cultured from medical ICU patients included methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa, and ten genera of Gram-negative bacilli. Colonization by respiratory pathogens was statistically associated with concomitant antibiotic therapy within the medical ICU group of patients, but not with severity of illness. Although medical ICU patients tended to have more dental plaque than preventive dentistry clinic patients, there was no statistically significant association noted between the presence of dental plaque and respiratory pathogen colonization.
These findings suggest that bacteria commonly causing nosocomial pneumonia colonize the dental plaque and oral mucosa of intensive care patients. In many cases, this colonization occurs by large numbers of bacteria. Dental plaque may be an important reservoir of these pathogens in medical ICU patients. Efforts to improve oral hygiene in medical ICU patients could reduce plaque load and possibly reduce oropharyngeal colonization.
The purpose of this study was to determine the incidence of bacteremia after a single professional subgingival irrigation with a 0.12% chlorhexidine gluconate mouthrinse (CHX) as well as after a subsequent scaling and root planing (S/RP) during the same visit. Thirty subjects each with at least 1 site that probed 4 mm or more and bled on probing were randomly assigned to the following groups: 1) irrigation with 0.12% CHX; 2) irrigation with sterile water; and 3) non-irrigated controls. To begin the study blood was drawn just before and 2 minutes after irrigation. Thirty minutes later, blood was drawn again just before and 2 minutes after S/RP at the same site. Specimens were cultured for anaerobic and aerobic microorganisms using standard cultural techniques. Eighteen blood cultures from 15 subjects yielded positive cultures resulting in 23 isolates. Gram-positive rods comprised 34.8% of the total isolates; Gram-positive cocci 34.8%, Gram-negative rods 21.7%, and Gram-negative cocci 8.7%. In the CHX group, bacteremia was detected in 5 subjects after irrigation and in 2 other subjects after S/RP. In the water group, bacteremia was detected in one subject after irrigation and in 4 subjects after S/RP. The control group had 3 bacteremias after S/RP. There was no significant difference between the incidence of bacteremia associated with irrigation by CHX or sterile water (P = 0.141). There was also no significant difference in the incidence of bacteremia after S/RP between the CHX and sterile water irrigation groups and in patients who did not receive irrigation (control group) (P = 0.88).(ABSTRACT TRUNCATED AT 250 WORDS)
Herpesviral infection of endothelial cells (ECs) induces arterial injury. We now demonstrate that such infection promoted enhanced monocyte-endothelial adhesion. Enhanced adhesion was blocked by monoclonal antibodies to the viral-encoded cell surface glycoprotein gC but not by antibodies to gD or gE. Adhesion was also blocked by treating ECs with specific thrombin inhibitors or by growing cells in prothrombin-depleted serum. We found that gC bound and promoted activation of factor X on infected ECs, thereby contributing to thrombin generation. Factor X also bound to transfected L cells that were induced to express gC. Cross-linking and immunoprecipitation studies demonstrated factor X-gC complex formation on the surface of these cells. We suggest that gC-dependent thrombin generation by herpes-infected endothelium may be an important mediator of vascular pathology during viral infection.
The study aims to assess the correlation between dental pathologies and ophthalmic diseases. Based on a statistical evaluation, the study examines the presence of dental diseases in patients suffering from optic neuritis or uveitis in comparison to a control group of subjects. The possible interactions between the two ophthalmic pathologies and dental diseases are then analyzed in order to highlight possible clinical signs which may be useful for their identification.
Infection of normocholesterolemic, specific-pathogen-free chickens with Marek's disease herpesvirus (MDV) has been shown histologically to lead to chronic atherosclerosis like that in humans. The development of herpesvirus-induced atherosclerosis in vivo and the presence of specific Marek's antigen within aortic cells suggested that MDV infection may modify lipid metabolism and lead to significant lipid accumulation. Experiments reported herein were designed to determine the types and quantity of lipid present in aortas from MDV-infected and uninfected chickens between 2 and 8 months of age following infection and assess one possible mechanism of lipid accumulation by evaluating the effect of MDV infection on aortic cholesterol and cholesteryl ester (CE) metabolism. Chromatographic-fluorometric analyses indicated that at 4 and 8 months of age after MDV inoculation, MDV-infected animals had a significant (P less than 0.05) two-fold to threefold increase in total aortic lipid accumulation characterized by significant increases in cholesterol, CE, triacylglycerol, and phospholipid as compared with aortas from uninfected animals. At 8 months of age, similar increases in aortic lipid accumulation were observed in MDV-infected animals as compared with those animals vaccinated with turkey herpesvirus and later challenged with MDV. CE synthetic activity was increased significantly by 50% at 4 months of age in the MDV-infected group as compared with the uninfected group, which could explain the initial increase in CE accumulation. By 8 months of age, the authors also observed a twofold increase in CE synthetic activity and a 30% and 80% reduction in lysosomal and cytoplasmic CE hydrolytic activities, respectively, in aortas of MDV-infected chickens as compared to controls. Moreover, infection with MDV blocked the activation of cytoplasmic CE hydrolytic activity by dibutyryl cyclic AMP or exogenous cyclic AMP-dependent protein kinase. Taken together, these results suggest that lipid accretion in aortas of MDV-infected chickens results, in part, from alterations in cholesterol/CE metabolism during early stages of the disease. These findings support the hypothesis that human atherosclerosis may result from specific herpesvirus infection which can alter lipid metabolism and lead to lipid accretion.
The type and rate of bacteremia following dental extractions, dental cleaning, or other dental/oral surgical procedures were studied in 124 patients with valvular heart disease following parenteral antibiotic prophylaxis (penicillin G potassium with or without streptomycin sulfate, or vancomycin hydrochloride) as recommended by the American Heart Association in 1977. Generally, under penicillin G prophylaxis with or without streptomycin, detection of bacteremia in blood culture media containing no penicillinase was low (14.7% to 16.1% at five minutes and 3.1% to 9.0% at 30 minutes after the procedure). The number and types of organisms recovered from patients who received penicillin prophylaxis alone or with streptomycin were similar. Anaerobes were recovered twice as frequently as aerobes. Polymicrobial bacteremia was rare and only one patient had streptococci detected in the blood culture. Addition of penicillinase to one blood culture medium, however, and comparing it with a similar medium without penicillinase was accompanied with a sixfold greater recovery from patients of both aerobic and anaerobic bacteria, including six patients with streptococcal bacteremia. Vancomycin prophylaxis was accompanied with bacteremia in only one patient.
Nosocomial pneumonias are a particularly problematic group of infections. The pathogenesis of these pneumonias, including mechanisms of colonization and pulmonary defense mechanisms, is discussed. An approach to the hospitalized patient with fever and infiltrates, based on the clinical setting, the nature of the host defense defect, the radiographic findings, and the results of invasive diagnostic procedures, is presented. Antimicrobial agents available to treat patients with nosocomial pneumonia are reviewed.
Periodontitis is an inflammatory disease of the periodontium which is characterized by a progressive destruction of the tissues supporting the tooth. Its primary etiology is an ill-defined series of microbial infections which may be composed of only some of the more than 300 species of bacteria currently recognized in the oral cavity. The disease is currently considered to progress as periodic, relatively short episodes of rapid tissue destruction followed by some repair, and prolonged intervening periods of disease remission. Despite the apparent random distribution of episodes of disease activity, the resulting tissue breakdown exhibits a symmetrical pattern of alveolar bone loss and pocket formation which is common to several forms of periodontitis, although the distribution of the most affected teeth and surfaces may vary among diseases (e.g., juvenile periodontitis versus adult periodontitis or rapidly progressive periodontitis). Several reports have indicated that bacterial cells can be found in the pocket wall of periodontitis lesions. The translocation of bacteria into the tissues from the pocket environment is quite common, as evidenced by the common occurrence of bacteremias in patients with periodontitis following relatively minor events such as chewing and oral hygiene procedures. However, it is important to distinguish between the passive introduction of bacteria into periodontal tissues and frank invasion as might occur in an acute infection, since the pathological implications may be quite different.
Comparison of the naturally occurring atherosclerotic plaques of human beings and birds with the reparative response of mammalian aorta to injury led to the consideration of an alternative to the injury repair hypothesis currently in vogue. This was based upon the following considerations: cells of spontaneous lesions differ from cells of normal arterial wall media and also from cells populating a repair site. They differ in size and arrangement of cells, in composition of associated extracellular material. In particular the cells of the plaque are smaller than those of the media and appear to produce abundant collagen and little or no elastin. Intercellular junctions between cells of the plaque are reduced in number or absent. These apparent differences in the cell populations encouraged consideration of the possibility that the focal proliferative lesions of atherosclerosis are either derived from a different group of cells than those populating the media or are an altered cell population, the change being similar to that occurring in benign smooth muscle cell tumors. Benign smooth muscle tumors, uterine leiomyomas, and other preneoplastic lesions appear to originate from a single precursor cell, i.e., are monoclonal in origin. Recent developments in the understanding of somatic cell genetics and the capacity to analyze these in human material made the question concerning the cell composition of plaques susceptible to an answer. Data from 30 plaques from 3 cases and 50 samples of nonplaque intima from 4 cases showed that fibrous caps, even of relatively large plaques, appear to be composed of cells that produce solely or predominately one enzyme type. On the other hand, the arterial media seems regularly to be composed of a mixture of cell types in samples as small as 0.1 cubic mm of tissue. Further experiments provide consistent support of the original data: analysis of 12 more plaques from 4 more cases including one coronary plaque yielded enzyme patterns consistent with a monoclonal character of the plaques against a background of mixtures of the 2 cell types for the intima and inner media. The apparent monoclonal character of the atherosclerotic plaques led to the idea that these proliferative lesions have properties resembling benign neoplasms. One feature of neoplasms expressed by some on culture of their cells in vitro is an apparently infinite capacity to divide. The cells of the atherosclerotic plaques and the cells of the leiomyomas behave in an identical manner under conditions of culture, but both exhibited a finite life span.
The main cellular elements of atherosclerotic plaques are smooth muscle cells. Because these plaques differ from their precursors in the underlying artery wall in several ways, we have asked the question: Are human atherosclerotic plaques polyclonal or monoclonal in their origin? The X-linked glucose-6-phosphate dehydrogenase (EC 1.1.1.49) in heterozygotic females has been used to obtain an answer. 30 Plaques of different degrees of complexity and 59 samples of normal aorta and iliac artery walls from four females, 25-79 years old, were investigated. The data show that fibrous caps even of relatively large atheromatous plaques, 0.5 cm or greater in diameter, are composed of cells that produce solely or predominantly one enzyme type, whereas samples of artery wall media and intima as small as 0.1 mm(3) are regularly composed of a mixture of cell types. If plaques were a response to injury akin to a healing wound, a reaction to a growth stimulant, or formed due to an organization of a mural thrombus, they would be expected to be polyclonal. Hence, the results imply that atherosclerotic plaques in human beings arise by another mechanism. The mechanism compatible with the monoclonal nature of atherosclerotic plaques is mutation, and the likely causes are chemical mutagens or viruses.
The subgingival bacterial flora from 2 gingival sites was cultured and characterized monthly in twenty periodontitis-free women during pregnancy and again post-partum. Monthly plaque samples were also cultured in eleven age and disease matched non-pregnant women. Plaque was processed anaerobically on selective and nonselective media and the predominant colony types were characterized. A portion of each plaque sample was tested for bacterial uptake of C14-estradiol and C14-progesterone. Plasma levels of estrogens and progesterone were measured four times in each subject. The number of gingival bleeding sites, the Gingival Index and the Plaque Index were determined at each sampling period. In the second trimester there was a significant increase in gingivitis, the ratio of anaerobic to aerobic bacteria, and the proportional levels of Bacteroides melaninogenicus ss. intermedius. In the third trimester both gingivitis and the levels of B. melaninogenicus ss. intermedius decreased. Plaque uptake of C14-steroids increased significantly during pregnancy and paralleled the plaque levels of B. melaninogenicus ss. intermedins. In the second trimester, recovery of B. melaninogenicus ss. intermedius was strongly correlated with plasma levels of estrogens and progesterone. No changes were observed in clinical parameters or the subgingival flora of non-pregnant subjects. Pregnancy and specifically steroid hormones appear capable of influencing the normal bacterial flora and inducing alterations in the subgingival ecology.
This paper traces the history of the theory of focal infection--which related a number of general conditions to septic foci from which toxic products spread to different parts of the body--and its application to dental diseases in early 20th century Britain. Bad teeth were said to be one of the major sources of infection and a cause of many diseases. The paper focuses on the social and professional context in which the theory emerged and flourished. It shows that in spite of its lack of scientific foundation, the theory of focal sepsis was readily accepted by the dental profession and used to advance its claims for professional recognition. Thus the paper attempts to illustrate the point that the acceptance of a medical theory by health practitioners is as much determined by social and economic factors as by its therapeutic potential or its scientific validity.
This study was designed to determine the role of dental flossing in producing transient bacteremias. An improved protocol that provides for repeated samplings of blood was developed. Four patients had 32 blood cultures taken (16 before flossing and 16 after). Two of the patients had no periodontal disease and two had only marginal gingivitis. The results showed that the patients who flossed daily developed no bacteremias but that patients who delayed flossing from 1 to 4 days developed bacteremias 86% of the time. It is important that patients who have a history of rheumatic fever and those who have internal prosthetic devices be cautioned regarding sporadic flossing. While gingival bleeding was not significantly related to bacteremias in this study, further investigation is needed to ascertain how flossing in various types of periodontal disease relates to bacteremias.
This study characterizes oral microorganisms believed to have spread from the root canal into the blood stream during and after endodontic therapy of teeth with Asymptomatic apical periodontitis. Microbiological samples were taken under aseptic conditions from the root canal of 26 single-rooted teeth in 26 patients. In the endodontic treatment of 13 of the patients (Group 1), the first 3 reamers, sizes 15, 20 and 25, were used to a level 2 mm beyond the apical foramen. In the other 13 patients (Group 2), the instrumentation ended inside the root canal 1 mm short of the apical foramen. Blood samples were taken from the patients during the instrumentation and 10 min after the treatment was completed. Anaerobic microorganisms were isolated from all root canals. In 7 patients of Group 1, Propionibacterium acnes, Peptostreptococcus prevotii, Fusobacterium nucleatum, Prevotella intermedia and Saccharomyces cerevisiae were recovered from the blood. In 4 patients of Group 2, P. intermedia, Actinomyces israelii, Streptococcus intermedius and Streptococcus sanguis were isolated from the blood. Biochemical tests and antibiograms revealed that the isolates from the root canal and blood had identical profiles within the patients, strongly suggesting that the microorganisms isolated from the blood had the root canal as their source.
The most important epidemiological, aetiological and diagnostic problems related to nosocomial pneumonia in the intensive care unit and its significance are reviewed. Areas of uncertainty are identified, as are methods for improving our understanding of this complex condition.
The so-called classic risk factors of coronary heart disease (CHD) do not explain all its clinical and epidemiological features. Recent evidence suggests that certain infections, among them dental infections, are involved in the pathogenesis of CHD. Case-control studies have revealed an association between dental infections and acute myocardial infarction and chronic coronary heart disease. A large epidemiological survey revealed an association between missing teeth and CHD and a recent 14-year follow-up of 9760 individuals showed that periodontitis is associated with an increased risk of coronary heart disease. Preliminary results suggest that the severity of dental infections correlates with the extent of coronary atheromatosis. Individuals with severe dental infections also have higher level of von Willebrand factor antigen, leukocytes and fibrinogen. Streptococcus sanguis has been shown to aggregate human platelets in vitro. The mechanism behind the association between dental infections and CHD could be the effect of bacteria on the cells taking part in the pathogenesis of atherosclerosis and arterial thrombosis.
Although patients with refractory periodontitis have been widely reported, no clear biologic profile of these patients has been noted. The purpose of the present study was to evaluate host responsiveness of a well-defined group of refractory periodontitis patients by determining the effect of a lipopolysaccharide (LPS) challenge on monocyte surface receptor density and on the release of inflammatory mediators. Venous blood was obtained from 7 refractory periodontitis, 8 stable periodontal maintenance, and 8 gingivitis patients with no evidence of periodontitis. Mononuclear cells were cultured in either control media or media treated with Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), or Salmonella typhimurium (S. typh) LPS. At 0 and 24 hours supernatants were assayed for prostaglandin-E2 (PGE2) and interleukin-1 beta (Il-1 beta) release by ELISA. Using flow cytometry the density of specific monocyte surface receptors were assayed with Mo3e and LeuM3 monoclonal antibodies (mAb); T-cell CD4/CD8 ratios were assayed with OKT-3, OKT-4, and OKT-8 mAb. After 24 hours incubation with Pg or S. typh LPS, the upregulation of the Mo3e receptor was significantly decreased for refractory periodontitis patients (P < 0.05) when compared to gingivitis and to stable maintenance patients. In refractory periodontitis patients the T-cell CD4/CD8 ratio was decreased. Upon stimulation with Pg or S. typh LPS, monocytes from stable maintenance and refractory periodontitis patients released more Il-1 beta (P < 0.05) and PGE2 (P = 0.13 and 0.15) than monocytes from gingivitis subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
An increasing body of evidence supports the concept that host-produced PGE2 mediates much of the tissue destruction that occurs in periodontal disease. PGE2 levels within the crevicular fluid can serve as a static assessment of ongoing disease activity; i.e., rate of attachment loss and bone resorption. New insights into the mechanisms that regulate PGE2 synthesis provide an altered paradigm of periodontal disease which places the emphasis on host response, rather than the bacterial etiology, as the principal determinant of disease expression. We described a PGE2 host response model as a hypothetical framework to discuss new, possible explanations for host susceptibility to periodontal disease.
Streptococci that colonize the mouth and upper respiratory tract tend to beconsidered harmless commensals. In 45 cases of
acute pneumonia and/or pulmonary abscess and 25 cases of thoracic empyema, the predominant speciesrecoveredwere anaerobic
bacteria and the Streptococcus milleri group, which encompassesthe oral species Streptococcus anginosus, Streptococcus constellatus, and Streptococcus intermedius. The isolation of most S. milleri organisms along with oral anaerobes indicated synergy betweenthese groups. Studies in a mouse model of pneumonia demonstrated
this synergy; mortality was higher, histopathologic abnormalities were more marked (reflecting acute pneumonia followed by
pulmonary abscessor empyema), and viable bacteria were more numerous in the lungs of mice with mixed infectionscaused by the
S. milleri group and anaerobes than in the lungs of those with monomicrobial infection. In vitro studies elucidated a possible mechanism
of this synergistic effect: anaerobes may enhance the growth of the S. milleri group and/or inhibit the bactericidal activity of the host. We conclude that the S. milleri group is more important in pulmonary infections than has previously been recognized.
Bacteremia resulting from dental extraction is regarded as an important cause of bacterial endocarditis, and it is therefore recommended that patients undergoing tooth extraction be given prophylactic antibiotics. As dental procedures other than extractions may also cause bacteremias, we studied a variety of dental procedures routinely used in pediatric dentistry. Blood samples for cultures were obtained 30 s after each of 13 dental operative procedures in 735 anesthetized children aged 2-16 years. Four procedures used for conservative dentistry caused bacteremias significantly more often than the baseline value of 9.4%: polishing teeth 24.5%, intraligamental injection 96.6%, rubber dam placement 29.4%, and matrix band with wedge placement 32.1%. In comparison, toothbrushing alone caused a bacteremia on 38.5% of occasions. The organisms isolated were typical of odontogenic bacteremias in that 50% of the isolates were identified as varieties of viridans streptococci. These data show that a wider variety of dental procedures than was previously documented cause bacteremia.