MedicalResearch.com Interview with:
ANGELA R. KAMER, DMD, MS, PhD
Associate Professor
Periodontology and Implant Dentistry
NYU Dentistry
MedicalResearch.com: What is the background for this study? Response: The accumulation of amyloid β plaques and neurofibrillary pathology in the brain are pathognomonic to Alzheimer's disease (AD). Brain amyloid deposition begins decades before cognitive dysfunction and is thought to be the first AD pathological feature followed by tau tangle accumulations and other pathologies.
The mechanisms by which brain amyloid develops are incompletely understood although inflammation and bacterial imbalances (known as dysbiosis) of the gut and oral cavity may be involved. Periodontal disease affecting more than 50% of elderly is an inflammatory, chronic condition characterized by periodontal tissue destruction and bacterial imbalances. Using PET studies, we showed previously that measures of periodontal destruction were associated with brain amyloid retention in the brain [1]. In this study, we sought to investigate whether subgingival (under the gum line) bacteria associated with Alzheimer’s disease specific pathology, namely amyloidosis and tauopathy. (more…)
MedicalResearch.com Interview with:
Francesco D’Aiuto
Professor/Hon Consultant
Head of Periodontology Unit
UCL Eastman Dental InstituteMedicalResearch.com: What is the background for this study? Response: This study was set out to further our understanding of the link between gum disease and high blood pressure. Recent evidence suggested that individuals with gum disease had a 20-70% increased risk of hypertension and systemic inflammation seemed to be a driver in mediating this association. Further research on the matter was needed. We recruited two relatively large groups of otherwise healthy participants (without a confirmed diagnosis of hypertension) who had gum disease one and healthy gums the other.
We found that diagnosis of periodontitis (gum disease) was consistently linked to higher systolic blood pressure independent of other cardiovascular risk factors.
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MedicalResearch.com Interview with:
Prof. Michael Glogauer, D.D.S., Ph.D
Faculty of Dentistry, University of Toronto
Toronto, ON Canada
MedicalResearch.com: What is the background for this study? Response: Periodontal disease (PD) affects between 20% and 50% of the global population, with growing evidence supporting its association with other inflammatory diseases, including heart disease, arthritis, and diabetes.
Several studies have shown how untreated periodontal disease leads to increased medical care costs for nonoral conditions, including patient hospitalization rates. The interaction of inflammatory diseases with PD suggests a shared, underlying pathology that may be exploited to better manage patients and reduce the economic burden. However, the mechanisms through which these diseases interact are unclear.
In periodontal disease, tissue and bone destruction in the mouth is driven by elevated recruitment of white blood cells called polymorphonuclear neutrophils (PMNs), which are activated by the oral disease and recruited from the circulation to sites of inflammation.(more…)
MedicalResearch.com Interview with:
Robert Margolskee, MD, PhD
Director and President
Monell Center
Adjunct Professor, Department of Systems Pharmacology and Translational Therapeutics
University of Pennsylvania Perelman School of Medicine
MedicalResearch.com: What is the background for this study? What are the main findings?Response: We found chemical-sensing cells in the gums that protect the mouth by standing guard against infections that damage soft tissue and destroy the bone that supports the teeth. With the help of bitter taste receptors that also detect byproducts from harmful bacteria, these special gum cells trigger the immune system to control the amount and type of bacteria in the mouth. This knowledge could one day lead to personalized dental treatments against gum disease.
Periodontitis is a serious gum disorder caused by an imbalance in the bacteria and other microorganisms of the mouth. We hope that our new information can help to combat this sixth-most prevalent infectious disease and most common cause of tooth loss worldwide.
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MedicalResearch.com Interview with:Jean Wactawski-Wende, PhD
Dean, SUNY Distinguished Professor
Professor, Department of Epidemiology and Environmental Health
School of Public Health and Health Professions
University of Buffalo
MedicalResearch.com: What is the background for this study? What are the main findings?Response: There has been a growing interest in the role of periodontal disease in system chronic diseases, including cancer. We explored the association of periodontal disease history and incident cancer in the women's health initiative study of postmenopausal women. We found that women reporting periodontal disease history were at increased risk of developing cancer overall. In addition they were found to have significant increased risk of specific cancers including cancers of the lung, breast, esophagus, gallbladder and melanoma. The risk persisted after control for many other factors. In addition, the risk was seen in women regardless of their smoking history. Both ever smokers and never smokers were found to have increased risk of cancer associated with periodontal disease history.
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MedicalResearch.com Interview with:
Dana T. Graves DDS
Department of Periodontics
School of Dental Medicine
University of Pennsylvania
Philadelphia, PA
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: It was previously thought that diabetes did not have a significant effect on oral bacteria. We found that diabetes caused a change in the composition of the oral bacteria. This change caused resulted in a bacterial composition that was more pathogenic and stimulated more inflammation in the gums and greater loss of bone around the teeth.
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MedicalResearch.com Interview with:
Bradley F. Bale, M.D.
Texas Tech Health Science Center
School of Nursing, Lubbock, Texas
1002 Montrose Drive
Gallatin, TN 37066
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: It has been known for some time that periodontal disease is associated with higher risk for arterial disease. It was shown decades ago that the germs in the mouth frequently seed into our blood stream with simple activities such as chewing and brushing our teeth. During the last decade, it was discovered certain high risk periodontal pathogens are associated with various cardiovascular (CV) risk factors such as blood pressure, lipid levels, insulin resistance and endothelial dysfunction. These studies elucidated that the CV risk stems from the bacteria involved in the periodontal disease and not the clinical signs such as pocket depth, bleeding of gums and loose teeth.
The above knowledge demonstrated that high risk periodontal pathogens can adversely influence two of the three elements in the atherogenic triad. Those factors are concentration of apoB and endothelial inflammation and dysfunction. Then approximately two years ago it was published that the high risk pathogen Porphyromonas gingivalis (P.g.) can enhance the third element. This portion is the transformation of contractile smooth muscle cells (SMCs) in the medial layer of artery into migratory secretory SMCs. These morphed cells enter the deep layer of the intima and enrich it with proteoglycans which are the ‘velcro’ that traps cholesterol particles in the arterial wall and initiates the formation of arterial disease.At that point, there was solid evidence that the high risk pathogens boost every element in the triad to create atherosclerosis. With that knowledge these pathogens must be considered a contributory cause of arterial disease. When a condition is causal it demands diagnosis and management to reduce the disease risk.
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MedicalResearch.com Interview with:
Maximilian F. Konig, MD
Division of Rheumatology,
Johns Hopkins University School of Medicine
Current affiliation:
Department of Medicine
Massachusetts General Hospital
Harvard Medical School
MedicalResearch.com: What is the background for this study?Response:The idea that rheumatoid arthritis (RA), an autoimmune disease that leads to chronic joint inflammation and destruction, may be initiated by a bacterial infection is not novel, but has been posited for more than a century. Based on the clinical observation that patients with RA frequently have severe periodontal disease (gum disease), gum inflammation has long been thought to contribute to disease development in RA. However, limited understanding of the mechanisms that fuel and sustain the autoimmune attack in RA made it difficult to pinpoint a specific bacterial trigger.
In recent years, our understanding of the abnormal immune response that attacks the joints in patients with RA has grown exponentially, and we now know that disease-specific autoantibodies (ACPAs) target modified self-proteins (this modification is known as citrullination). It is this abnormal immune response against citrullinated proteins that appears to drive the joint (and sometimes lung) inflammation seen in rheumatoid arthritis. Recent studies from our laboratory at The Johns Hopkins University (led by principle investigator Felipe Andrade, MD, PhD) suggested that an immune cell called the neutrophil, which normally protects us from infection at sites like the oral cavity or anywhere else in the body, also appears to be the source of the proteins attacked in RA. We were therefore interested to understand what drives the association of gum disease, an inflammation commonly triggered by bacteria, with RA.
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MedicalResearch.com Interview with:
Boxi Zhang PhD Student
School of Health and Medical Sciences
Örebro University Medical Research: What is the background for this study? What are the main findings?
Response: In the past decade, many studies raise concerns about the increased prevalence of cardiovascular disease and mortality among patients with periodontitis. Porphyromonas gingivalis is the major pathogen causing periodontal disease. This bacterium also plays a significant role in the pathogenesis of atherosclerosis. In this study, we infect human aortic smooth cells with P. gingivalis and show that this periodontal pathogen affects gene and protein expression in human aortic smooth muscle cells associated with increased inflammation and atherosclerosis.
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MedicalResearch.com Interview with:
Daniel Grenier, Ph.D.
Professeur titulaire
Oral Ecology Research Group, Faculty of Dentistry, and Institute of Nutrition and Functional Foods, Université Laval
Quebec City, QC, Canada
Medical Research: What is the background for this study? Dr. Grenier: Periodontal diseases (gingivitis and periodontitis) are major public health problems because of their high prevalence and incidence in all regions of the world. According to epidemiological studies, approximately 5% of North Americans suffer from severe generalized periodontitis, which can lead to tooth loss, while mild to moderate periodontitis affects up to 35% of adults. Given emerging data indicating that there is a relationship between periodontal diseases and systemic health problems such as diabetes, cardiovascular diseases, and preterm birth, studies on preventive and therapeutic strategies targeting periodontal diseases are highly relevant.
Medical Research: What are the main findings?Dr. Grenier: Using various in vitro models, we brought clear evidence that a blueberry extract enriched in proanthocyanidins can act on the two etiological components of periodontal disease. We first showed that these polyphenols inhibit the growth of Fusobacterium nucleatum as well as its ability to form a biofilm, which can provide to the bacterium a resistance to antimicrobial agents and immune cells. Interestingly, F. nucleatum has been associated with various forms of periodontitis as well as to a number of extra-oral infections, including endocarditis, inflammatory bowel disease, and brain abscesses. Moreover, the blueberry extract attenuated the inflammatory response of human macrophages challenged with F. nucleatum, resulting in a decreased secretion of inflammatory cytokines (IL-1β, IL-6, TNF-α) and tissue destructive enzymes (MMP-8, MMP-9). Evidence was brought that this property is likely related to the ability of the blueberry polyphenols to block the activation of the NF-κB signaling pathway that play a key role in inflammatory reactions.
Over the last decade, my laboratory has been investigating the potential benefits of various classes of polyphenols for oral health. Polyphenols are a large group of natural substances found in plants and characterized by the presence of more than one phenol unit per molecule. Given that wild blueberries (Vaccinium angustifolium Ait), a popular berry fruit in Quebec, are particularly rich in a specific class of polyphenols, called proanthocyanidins, we tested their effect on the two major etiological factors involved in the pathogenesis of periodontitis: a limited group of Gram negative anaerobic bacteria, and an uncontrolled host immune response to these pathogens that results in the secretion of high amounts of inflammatory mediators which modulate the progression and severity of periodontitis.
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MedicalResearch.com Interview with: Xiaodan Mai MBBS
University at Buffalo, The State University of New York
Buffalo, NY
MedicalResearch: What is the background for this study? What are the main findings?
Response: Periodontal disease is a condition that is highly prevalent amongst the elderly, and is characterized by chronic polymicrobial infection and inflammation of gum tissue. Periodontal disease has been associated with increased cancer risk, and these findings may be partially explained by extra-oral translocation of subgingival bacteria that subsequently modulates host cell environment and function. However, there is limited research on whether the presence of certain subgingival bacteria influences cancer risk. .
Oral bacteria have been categorized into color-coded complexes by their timing of colonization and strength of association with periodontal disease. Using data from an ancillary study of the Women’s Health Initiative conducted in Buffalo, New York (a cohort of 1300 postmenopausal women), we therefore investigated the associations between the presence of three early-colonizing periodontal pathogens (Fusobacterium nucleatum, Prevotella intermedia, and Campylobacter rectus, i.e., "orange complex" bacteria moderately associated with PD), the presence of two late-colonizing periodontal pathogens (Porphyromonas gingivalis, Tannerella forsythia, i.e., "red complex" bacteria strongly associated with PD) in dental plaque and cancer risk. We found borderline associations between presence of any early-colonizing pathogens and increased risk of total cancer and lung cancer. Individual pathogens were not associated with total cancer or site-specific cancers when analyzed singly. Presence of any pathogens or presence of any late-colonizing pathogens was not associated with total or site-specific cancer.
(more…)
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