The blog of Xeno, a slightly mad scientist
Periodontitis is a risk factor for heart disease. Now a team of researchers has shown that a periodontal pathogen causes changes in gene expression that boost inflammation and atherosclerosis in aortic smooth muscle cells. The research is published ahead of print in Infection and Immunity, a journal of the American Society for Microbiology.
The circumstantial evidence that led to this study was ample. The periodontal pathogen, Porphyromonas gingivalis, has also been found in coronary artery plaques of heart attack patients. And in two species of animal models, P. gingivalis has been shown to cause and accelerate formation of coronary and aortic atherosclerosis. The investigators, led by Torbjörn Bengtsson of the Department of Clinical Medicine, School of Health Sciences, Örebro University, Örebro, Sweden, showed how this happens.
They began by culturing human aortic smooth muscle cells, and infecting them with P. gingivalis. They found that gingipains, virulence factors produced by P. gingivalis, boost expression of the pro-inflammatory angiopoietin 2, while dampening expression of the anti-inflammatory angiopoietin 1 in the smooth muscle cells, with the net effect of increasing inflammation. Inflammation is strongly implicated in atherosclerosis.
“Although unstimulated [aortic smooth muscle cells] produce angiopoietin 2 at a low level, stimulation with wild-type P. gingivalis dramatically increases the gene expression of angiopoietin 2 in [aortic smooth muscle cells],” the investigators wrote.
“Angiopoietin 2 directly increases the migration of aortic smooth muscle cells,” said first author Boxi Zhang, a PhD student in Bengtsson’s laboratory. “The migration of smooth muscle cells is involved in the pathogenesis of atherosclerosis.”
As with ginginpains, tumor necrosis factor (TNF), a human-produced inflammatory cytokine and cardiovascular risk factor, also induces and promotes atherosclerosis via the two angiopoietins. However, their research showed that ginginpains operate independently from TNF, said Bengtsson.
“Our research clarifies the mechanism behind the association of periodontitis and cardiovascular disease,” said Zhang. “Our aim is to find biomarkers that can help us diagnose and treat both diseases.”
To protect your heart health, you should get any gum disease treated immediately. Here’s more you should know about this pathogen:
It is found in the oral cavity, where it is implicated in certain forms of periodontal disease, as well as the upper gastrointestinal tract, respiratory tract, and in the colon. It has also been isolated from women with bacterial vaginosis. Collagen degradation observed in chronic periodontal disease results in part from the collagenase enzymes of this species. It has been shown in an in vitro study that P. gingivalis can invade human gingival fibroblasts and can survive in them in the presence of considerable concentrations of antibiotics.P. gingivalis also invades gingival epithelial cells in high numbers, in which cases both bacteria and epithelial cells survive for extended periods of time. High levels of specific antibodies can be detected in patients harboring P. gingivalis.
In addition, P. gingivalis has been linked to rheumatoid arthritis. It contains the enzyme peptidyl-arginine deiminase, which is involved in citrullination. Patients with rheumatoid arthritis have an increased incidence of periodontal disease and antibodies against the bacterium are significantly more common in these patients.
P. gingivalis is a “red” bacterium and a “keystone” bacterium in the onset of chronic adult periodontitis. Though it is found in low abundance in the oral cavity, it causes a microbial shift of the oral cavity, allowing for uncontrolled growth of the commensal microbial community. This leads to periodontitis through the disruption of the host tissue homeostasis and adaptive immune response. After using laser capture microdissection plus qRT-PCR to detect P. gingivalis in human biopsies, colocalization of P. gingivalis with CD4+ T cells was observed. However, the infection mechanism of T cells by P. gingivalis remains unknown.
P. gingivalis has been associated with increasing the virulence of other commensal bacterium in both in vivo and in vitro experiments. P. gingivalis outer membrane vesicles were found to be necessary for the invasion of epithelial cells of Tannerella forsythia.P. gingivalis short fimbriae were found to be necessary for coculture biofilm formation with Streptococcus gordonii Interproximal and horizontal alveolar bone loss in mouse models are seen in coinfections involving P. gingivalis and Treponema denticola. The role of P. gingivalis as a community activist in periodontitis is seen in specific pathogen-free mouse models of periodontal infections. In these models, P. gingivalis inoculation causes significant bone loss, which is a significant characteristic of the disease. In contrast, germ free mice inoculated with a P. gingivalis monoinfection causes no bone loss, indicating P. gingivalis alone cannot induce periodontitis 
Right. How do you kill the little bastards? Hydrogen Peroxide? Apparantly not:
Porphyromonas gingivalis is one of the major anaerobic pathogens associated with periodontal diseases in man. Like other anaerobic microorganisms colonising the gingival sulcus and periodontal pocket, it must withstand the deleterious effects of molecular oxygen and its metabolites such as superoxide and hydrogen peroxide generated by neutrophils . Whilst P. gingivalis possesses a superoxide dismutase [3,4] which is an important antioxidant defence mechanism, converting O2− to H2O2, it is reported not to possess either catalase or peroxidase enzymes to further degrade H2O2.
P. gingivalis and other black-pigmenting anaerobes have a growth requirement for iron protoporphyrin IX which they accumulate into their pigment. The haem pigment of P. gingivalis is composed of μ-oxo bis(protoporphyrinato) iron(III), (Fe(III)PPIX)2O .
Porphyromonas gingivalis, an anaerobic oral pathogen implicated in adult periodontitis, can exist in an environment of oxidative stress. To evaluate its adaptation to this environment, we have assessed the response of P. gingivalis W83 to varying levels and durations of hydrogen peroxide (H(2)O(2))-induced stress. When P. gingivalis was initially exposed to a subinhibitory concentration of H(2)O(2) (0.1 mM), an adaptive response to higher concentrations could be induced. Transcriptome analysis demonstrated that oxidative stress can modulate several functional classes of genes depending on the severity and duration of the exposure. A 10 min exposure to H(2)O(2) revealed increased expression of genes involved in DNA damage and repair, while after 15 min, genes involved in protein fate, protein folding and stabilization were upregulated. Approximately 9 and 2.8% of the P. gingivalis genome displayed altered expression in response to H(2)O(2) exposure at 10 and 15 min, respectively. Substantially more genes were upregulated (109 at 10 min; 47 at 15 min) than downregulated (76 at 10 min; 11 at 15 min) by twofold or higher in response to H(2)O(2) exposure. The majority of these modulated genes were hypothetical or of unknown function. One of those genes (pg1372) with DNA-binding properties that was upregulated during prolonged oxidative stress was inactivated by allelic exchange mutagenesis. The isogenic mutant P. gingivalis FLL363 (pg1372 : : ermF) showed increased sensitivity to H(2)O(2) compared with the parent strain. Collectively, our data indicate the adaptive ability of P. gingivalis to oxidative stress and further underscore the complex nature of its resistance strategy under those conditions.
How about tea tree oil? Yes, 0.0521% to 2.5% for the tea tree oil solution killed Porphyromonas gingivalis in one study:
The essential oil of Melaleuca alternifolia (tea tree oil) exhibits antimicrobial activity against a wide range of Gram-positive and Gram-negative bacteria, yeasts and fungi. In this study the bacteriostatic and bacteriocidal/fungicidal activity of a tea tree oil solution, of a new tea tree oil (Tebodont) and the respective placebo-gel, of a chlorhexidindigluconate-solution and of PlakOut was tested in vitro against ten different oral microorganisms. Minimum inhibitory concentrations were in the range from 0.0293% to 1.25% for the tea tree oil solution and from 0.0082% to 1.25% for the tea tree oil gel. The values for minimum bacteriocidal/fungicidal concentrations were in the range from 0.0521% to 2.5% for the tea tree oil solution and from <0.0098% to 3.33% for the tea tree oil gel. The most susceptible microorganisms were Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, and Porphyromonas gingivalis, whereas Streptococcus mutans and Prevotella intermedia were the least susceptible ones. Both for the chlorhexidindigluconate solution and for PlakOut the values for the minimal inhibitory concentration and for the minimal cidal concentration were between <0.0002% and 0.0125%.
Antimicrobial effects of tea tree oil (Melaleuca alternifolia) on oral microorganisms [Antimikrobielle Wirkung von Teebaumöl (Melaleuca alternifolia) auf orale Mikroorganismen.]. Available from: Link . [accessed Sep 13, 2015].
So get some tea tree oil mouth wash and save your heart. Be careful with that stuff, though. It gave me the jitters last time I used it.
Tea tree oil is LIKELY UNSAFE when taken by mouth. Don’t take tea tree oil by mouth. As a general rule never take undiluted essential oils by mouth due to the possibility of serious side effects. Taking tree tea oil by mouth has caused confusion, inability to walk, unsteadiness, rash, and coma.
Tea tree oil is POSSIBLY SAFE for most people when put on the skin, but it can cause skin irritation and swelling. In people with acne, it can sometimes cause skin dryness, itching, stinging, burning, and redness.
If it is likely unsafe in the mouth (or do they mean don’t swallow it?) then why is there tea tree oil mouth wash? Don’t swallow it and rinse well if you do use it. I think it will help if you have gum disease:
A topically applied tea tree oil gel was evaluated in a double-blind placebo-controlled study involving 49 people with severe chronic gingivitis. They were told to brush twice a day and were assessed after 4 and 8 weeks. The group that brushed with tea tree oil had a significant reduction in the degree of gingivitis and bleeding.
How about a combination punch? Blue light, curcumin, erythrosine and hydrogen peroixde.
Recently, photodynamic therapy (PDT) has been introduced as a new modality in oral bacterial decontamination. Current research aims to evaluate the effect of photodynamic killing of visible blue light in the presence of hydrogen peroxide, curcumin and erythrosine as potential oral photosensitizers on Porphyromonas gingivalis associated with periodontal bone loss and Fusobacterium nucleatum associated with soft tissue inflammation.
Standard suspension of P. gingivalis and F. nucleatum were exposed to Light Emitting Diode (LED) (440-480 nm) in combination with erythrosine (22 µm), curcumin (60 µM) and hydrogen peroxide (0.3 mM) for 5 min. Bacterial samples from each treatment groups (radiation-only group, photosensitizer-only group and blue light-activated photosensitizer group) were subcultured onto the surface of agar plates. Survival of these bacteria was determined by counting the number of colony forming units (CFU) after incubation.
RESULTS for antibacterial assays on P. gingivalis confirmed that curcumin, Hydrogen peroxide and erythrosine alone exerted a moderate bactericidal effect which enhanced noticeably in conjugation with visible light. The survival rate of P. gingivalis reached zero present when the suspension exposed to blue light-activated curcumin and hydrogen peroxide for 2 min. Besides, curcumin exerted a remarkable antibacterial activity against F. nucleatum in comparison with erythrosine and hydrogen peroxide (P=0.00). Furthermore, the bactericidal effect of visible light alone on P. gingivalis as black-pigmented bacteria was significant.
Our result suggested that visible blue light in the presence of erythrosine, curcumin and hydrogen peroxide would be consider as a potential approach of PDT to kill the main gramnegative periodontal pathogens. From a clinical standpoint, this regimen could be established as an additional minimally invasive antibacterial treatment of plaque induced periodontal pathologies.
Cool. I’m going to rinse with curcumin and hydrogen peroxide tonight and check out a 440-480 nm LED. What is erythrosine? A red food coloring. A 1990 study concluded that “chronic erythrosine ingestion may promote thyroid tumor formation in rats via chronic stimulation of the thyroid by TSH.”
I’ll skip that for now. Tonight I tried a rinse with Desert Essence tea tree oil mouth wash, Swanson Ultra Theracurmin, Concentrated Colloidal Curcumin, and Essential Oxygen Organic Brushing Rinse. I also ordered a Zoomable Scalable LED Flashlight Waterproof Flashlight 460-470nm Blue light Cree Tactical Torch Glim Lantern (Blue light High Power Flashlight). I have some gum irritation, some bone loss and some heart and lung issues over the past month, so even before I get a periodontal check up, I’m starting with the self treatment.