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This study is noteworthy and relevant to humans (it was done on mice) because it may explain why so many people taking antibiotics get frequent viruses or seem more susceptible to infections. Once bacteria (both good and bad) are killed by antibiotics, then the community becomes unbalanced (dysbiosis), so that viruses may gain a foothold and a viral infection develops. In a healthy microbial community all sorts of microbes can be found, even ones we typically consider pathogenic, but the whole community keeps them in balance. One can say that "depletion of commensal microbiota also affects antiviral immunity".

The study researchers said that the study findings were relevant to humans: that oral antibiotics could result in increased susceptibility to sexually transmitted infections, as well as other infectious viruses. Note: commensal microbes or commensalism is a the living together of two organisms (different species) in a relationship that is beneficial to one and has no effect on the other. Dysbiosis is microbial imbalance, the microbial community being "out of whack". From Science Daily:

Antibiotics may increase susceptibility to sexually transmitted infections

Commensal microbiota, populations of bacteria that inhabit the tissues of larger organisms, often have complex relationships with their hosts. Researchers have been aware for some time that commensal microbiota play a role in antiviral immunity by producing immune inductive signals that trigger inflammasome responses, among other things.

However, the role of dysbiosis on antiviral immunity hasn't been studied. Dysbiosis describes the loss of bacterial diversity within a microbiome, and the direct role that commensal microbiota play in antiviral immunity suggests that such loss would facilitate viral infections. Recently, a collaborative of Korean and Japanese scientists conducted a study into the effects of antibiotic-induced dysbiosis on antiviral immunity, and have published their results in the Proceedings of the National Academy of Sciences.

The researchers investigated the mechanisms of commensal microbial immunity on the genital mucosa by treating mice with antibiotics for four weeks and then exposing them to HSV-2. A control group received placebo. They report that the antibiotics caused dysbiosis within the vaginal microbiota, and resulted in a dramatic increase in innate immune response—specifically, they noted increases in an alarmin called IL-33, which blocked effector T cells from migrating into the vaginal tissues and secreting antiviral cytokines.

Antibiotic-treated mice succumbed to HSV-2 infection dramatically faster than control mice. They exhibited more severe pathology and all mice treated with antibiotics prior to viral exposure died within 11 days of infection. "Taking these data together, we find that depletion of commensal bacteria results in a severe defect in antiviral protection following mucosal HSV-2 infection," the researchers write.

By analyzing stool and vaginal washes from both groups of mice, they determined that antibiotic treatment induced an imbalance in the microbial composition of the vaginal mucosa. Further, they were able to determine that no single species of bacteria was responsible for the antiviral immunity effects of the commensal microbiome; rather, it was the imbalance of the microbiotic population that accounted for the effects.

 

The human mouth hosts a variety of microbes, some taking up residence on the mouth lining (blue) within days after birth. Credit: Martin Oeggerli (National Geographic)

I posted about this amazing research while it was still ongoing (Jan. 16, 2015), but now a study has been published. The small well-done pilot study looked at the microbiome (microbial communities) and microbial differences between different groups of infants during the first 30 days of life. They found significant differences in the bacteria of C-section infants (not exposed to their mother's vaginal fluid in the birth canal) compared to C-section infants who were swabbed with a gauze pad right after birth with their mother's vaginal fluids. They found that the microbiota (community of microbes) is partially restored in the swabbed C-section infants and more similar to that of vaginally delivered infants (who were exposed to the maternal bacteria naturally in the birth canal). They found that the procedure restored some bacteria, such as Lactobacillus and Bacteroides, which were nearly absent in the skin and anal samples of non-swabbed C-section babies.

In the C-section group, four mothers who were free of infections that might harm the babies, incubated a sterile gauze in their vaginas for one hour before the operation (C-section). Then, within two minutes of birth, the babies were swabbed with the gauze first over their mouths, then their faces, and then the rest of their bodies. These results are important because it is thought that microbiome differences (depending on method of birth) are long-lasting (with higher incidence of some health problems later in life with C-sections), and because the baby's early microbiome helps educate the baby's developing immune system.

Rob Knight (a leading microbiologist and one of the researchers) pointed out that the study "provides the proof-of-concept that microbiome modification early in life is possible." Now we need to see if these microbial differences persist over time and if it makes a health difference. From Science Daily:

Vaginal microbes can be partially restored to c-section babies

In a small pilot study, researchers at University of California, San Diego School of Medicine and Icahn School of Medicine at Mount Sinai determined that a simple swab to transfer vaginal microbes from a mother to her C-section-delivered newborn can alter the baby's microbial makeup (microbiome) in a way that more closely resembles the microbiome of a vaginally delivered baby. 

Babies delivered by C-section differ from babies delivered vaginally in the makeup of the microbes that live in and on their bodies. These early microbiomes help educate the baby's developing immune system. Previous research suggests a link between C-section delivery and increased subsequent risk of obesity, asthma, allergies, atopic disease and other immune deficiencies. Many of these diseases have also been linked to the microbiome, though the role a newborn's microbiome plays in current or long-term health is not yet well-understood....Other research suggests that microbiome differences between vaginal and C-section babies can persist for years."

In the study, the researchers collected samples from 18 infants and their mothers, including seven born vaginally and 11 delivered by scheduled C-section. Of the C-section-delivered babies, four were exposed to their mothers' vaginal fluids at birth as part of this study. To do this, sterile gauze was incubated in the mothers' vaginas for one hour before the C-section. Within two minutes of their birth, the babies delivered by C-section were swabbed with the gauze starting with the mouth, then the face and the rest of the body.

Six times over the first month after birth, the researchers collected a total of 1,519 anal, oral and skin samples from the mothers and infants. Knight's team then used a gene sequencing technique to map the types and relative quantities of bacterial species present at each body site.

Here's what they found: the microbiomes of the four C-section-delivered infants exposed to vaginal fluids more closely resembled those of vaginally delivered infants than unexposed C-section-delivered infants, though the difference was more distinct in their oral and skin samples than in their anal samples. This partial microbial restoration could be due to the fact that the infants received only one surface application of maternal vaginal fluids, Knight said.

Yet the oral and skin microbiome differences between C-section-delivered infants who received the microbial transfer and those who did not was still noticeable one month after birth. The results were not due to diet differences, as all of the infants received breast milk either exclusively or supplemented with formula during the first month of life. In addition, consistent with previous studies, the babies' microbiome profiles did not correlate with the amount of breast milk they received.

"The present work is a pilot study -- we need substantially more children and a longer follow-up period to connect the procedure to health effects," said Knight...."This study points the way to how we would do that, and provides the proof-of-concept that microbiome modification early in life is possible. In fact, we already have more than 10,000 additional samples collected as part of this study that still await analysis."

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It's now 3 years being free of chronic sinusitis and off all antibiotics! Three amazing years since I started using easy do-it-yourself sinusitis treatments containing the probiotic (beneficial bacteria) Lactobacillus sakei. My sinuses feel great! And yes, it still feels miraculous.

After reading the original ground-breaking research on sinusitis done by Abreu et al (2012), it led to finding and trying L. sakei as a sinusitis treatment. Of course, there is an entire community of microbes that live in healthy sinuses (the sinus microbiome), but L. sakei seems to be a key one for sinus health.

I just updated the post The One Probiotic That Treats Sinusitis (originally posted January 2015) using my family's experiences (lots of self-experimentation!) and all the information that people have sent me. The post has a list of brands and products with L. sakei, as well as information about some other promising bacteria. Thank you so much! [For latest see: The Best Probiotic For Sinus Infections]

Thank you all who have written to me  - whether publicly or privately. Please keep writing and tell me what has worked or hasn't worked for you as a sinusitis treatment. If you find another bacteria or microbe or product that works for you - please let me know. It all adds to the sinusitis treatment knowledge base. I will keep posting updates. 

(NOTE: I wrote our background story - Sinusitis Treatment Story back in December 2013, and there is also a  Sinusitis Treatment Summary page with the various treatment methods. One can also click on SINUSITIS under CATEGORIES to see more posts, such as "Probiotics and Sinusitis" - a discussion by one of the original sinusitis researchers about what she thinks is going on in sinus microbiomes and what is needed.)  

This confirms what researchers such as Dr. Martin Blaser (in his book Missing Microbes) and others (such as Drs. Sonnenburg and Sonnenburg) have been saying about antibiotic use in infants and children: that there are negative effects to the gut microbiome from antibiotic use in early childhood, and the more frequent the use, the greater the negative effects. It is because the use of antibiotics  in early childhood "disrupts the microbiome".

Penicillins appear to be less disruptive, but macrolides (e.g., Clarithromycin, azithromycin) much more disruptive - the researchers found that the gut microbiota recovered within 6–12 months after a penicillin course, but did not fully recover from a macrolide course even after 2 years . Antibiotics can be life-saving, but they absolutely should not be used casually because there are hidden costs (such as microbiome changes). From Medical Xpress:

Antibiotic use in early life disrupt normal gut microbiota development

The use of antibiotics in early childhood interferes with normal development of the intestinal microbiota, shows research conducted at the University of Helsinki. Particularly the broad-spectrum macrolide antibiotics, commonly used to treat respiratory tract infections, have adverse effects. Macrolides appear also to contribute to the development of antibiotic-resistant strains of bacteria.  ...continue reading "Childhood Antibiotic Use Disrupts Gut Microbiome"

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Once again, two opposing views about beards have been in the news - that they harbor all sorts of nasty disease-causing bacteria vs they are hygienic. An earlier May 5, 2015 post was about the question of whether bearded men have more bacteria on their faces than clean shaven ones. I cited a 2014 study found that they don't, and that we are all covered with bacteria, all sorts of bacteria, and this is normal.

Now another study has looked at the issue of hospital workers with and without beards and whether they carry infectious bacteria. Researchers swabbed the faces (center of the cheek and the skin of the upper lip under the nostrils) of both clean shaven individuals and individuals with facial hair (beards) that worked in two hospitals (they all had direct contact with patients) and looked at the bacteria present. They especially looked for the presence of the bacteria Staphylococcus aureus, which surprisingly was found more in the clean-shaven men.

Also to their surprise, it was more of the clean shaven men who carried the pathogenic bacteria Methicillin-resistant Staphylococcus aureus (also known as MRSA). For those bacterial groups most closely associated with hospital acquired infections, such as Klebsiella species, Pseudomonas species, Enterobacter species., and Acinetobacter species, prevalence was low in both groups, and less than 2% for each group.

For other, less harmful bacteria, researchers found that bearded employees harbored no more bacteria than their clean-shaven colleagues. In summary: The researchers say that "results suggest that male hospital workers with facial hair do not harbour more potentially concerning bacteria than clean-shaven workers, and that in some instances, clean-shaven individuals are significantly more likely to be colonized with potential nosocomial pathogens". (NOTE: nosocomial means a disease originating or acquired in a hospital.)

And why is that? According to the study, one explanation is "microtrauma to the skin," which occurs during shaving and results in abrasions, which could support bacterial colonisation and growth of bacteria on the clean-shaven men. However, some other researchers have a different hypothesis — that beards themselves actually fight infection.

This stems from an experiment carried out by Dr. Michael Mosley who recently swabbed the beards of a variety of men and sent the samples to Dr. Adam Roberts, a microbiologist at University College London. Roberts grew more than 100 different bacteria from the beard samples, but found that in a few of the petri dishes a microbe was killing the other bacteria -  a bacteria called Staphylococcus epidermidis, and which they believe has antibiotic properties.

From the Journal of Hospital Infection: Bacterial ecology of hospital workers’ facial hair: a cross-sectional study

Summary: It is unknown whether healthcare workers' facial hair harbours nosocomial pathogens. We compared facial bacterial colonization rates among 408 male healthcare workers with and without facial hair. Workers with facial hair were less likely to be colonized with Staphylococcus aureus (41.2% vs 52.6%, P = 0.02) and meticillin-resistant coagulase-negative staphylococci (2.0% vs 7.0%, P = 0.01). Colonization rates with Gram-negative organisms were low for all healthcare workers, and Gram-negative colonization rates did not differ by facial hair type. Overall, colonization is similar in male healthcare workers with and without facial hair; however, certain bacterial species were more prevalent in workers without facial hair.

[Excerpts from Discussion]:Several studies to date have demonstrated that physician white coats and neck ties can act as significant sources of nosocomial bacteria. Our study suggests that facial hair does not increase the overall risk of bacterial colonization compared to clean-shaven control subjects. Indeed, clean-shaven control subjects exhibited higher rates of colonization with certain bacterial species. This finding may be explained by microtrauma to the skin during shaving resulting in abrasions, which may support bacterial colonization and proliferation. This may be akin to the enhanced risk of surgical site infections in patients shaved with razors prior to surgery. Further, our results are consistent with prior evidence pertaining to bacterial colonization on the hands and nares of HCWs (Health care workers).

A recent study using mice, and following them for 4 generations, has implications for Americans who typically eat a low-fiber diet (average of 15 grams daily). Note that current dietary guidelines recommend that women should eat around 25 grams and men 38 grams daily of fiber. The researchers found that low-fiber diets not only deplete the complex microbial ecosystems residing in the gut, but can cause an irreversible loss of diversity within those ecosystems in as few as three or four generations.

This is because fiber feeds the millions of microbes in the gut - and so a fiber-rich diet can nourish a wide variety of gut microbes, but a low-fiber diet can only sustain a narrower community. As the generations went by, the rodents’ guts became progressively less diverse, as more and more species were extinguished. If the fourth-generation mice switched to high-fiber meals, some of the missing microbes rebounded, but most did not. It took a fecal transplant (mice style) to get back the missing microbes. From Science Daily:

Low-fiber diet may cause irreversible depletion of gut bacteria over generations

A study by Stanford University School of Medicine investigators raises concerns that the lower-fiber diets typical in industrialized societies may produce internal deficiencies that get passed along to future generations. The study, conducted in mice, indicates that low-fiber diets not only deplete the complex microbial ecosystems residing in every mammalian gut, but can cause an irreversible loss of diversity within those ecosystems in as few as three or four generations.

Once an entire population has experienced the extinction of key bacterial species, simply "eating right" may no longer be enough to restore these lost species to the guts of individuals in that population, the study suggests. Those of us who live in advanced industrial societies may already be heading down that path.

The following article is interesting because it describes how microbes are high up in the sky riding air currents and winds to circle the earth, and eventually drop down somewhere. This is one way diseases can be spread from one part of the world to another. And the study looking at how antibiotic resistant bacteria are spread in the air from cattle feedlots has implications for how antibiotic resistance is spread. From Smithsonian:

Living Bacteria Are Riding Earth's Air Currents

Considering the prevailing winds, David J. Smith figured the air samples collected atop a dormant volcano in Oregon would be full of DNA signatures from dead microorganisms from Asia and the Pacific Ocean. He didn’t expect anything could survive the journey through the harsh upper atmosphere to the research station at the Mount Bachelor Observatory, at an elevation of 9,000 feet.

But when his team got to the lab with the samples, taken from two large dust plumes in the spring of 2011, they discovered a thriving bunch of hitchhikers. More than 27 percent of the bacterial samples and more than 47 percent of the fungal samples were still alive. Ultimately, the team detected about 2,100 species of microbes, including a type of Archea that had only previously been isolated off the coast of Japan. “In my mind, that was the smoking gun,“ Smith says. Asia, as he likes to say, had sneezed on North America.

 Microbes have been found in the skies since Darwin collected windswept dust aboard the H.M.S. Beagle 1,000 miles west of Africa in the 1830s. But technologies for DNA analysis, high-altitude collection and atmospheric modeling are giving scientists a new look at crowded life high above Earth. For instance, recent research suggests that microbes are hidden players in the atmosphere, making clouds, causing rain, spreading diseases between continents and maybe even changing climates.

"I regard the atmosphere as a highway, in the most literal sense of the term," Smith says. "It enables the exchange of microorganisms between ecosystems thousands of miles apart, and to me that’s a more profound ecological consequence we still have not fully wrapped our heads around."

Airborne microbes potentially have huge impacts on our planet. Some scientists attribute a 2001 foot-and-mouth outbreak in Britain to a giant storm in north Africa that carried dust and possibly spores of the animal disease thousands of miles north only a week before the first reported cases. Bluetongue virus, which infects domestic and wild animals, was once present only in Africa. But it's found now in Great Britain, likely the result of the prevailing winds.

In west Texas, researchers from Texas Tech University collected air samples upwind and downwind of ten cattle feedlots. Antibiotic resistant microbes were 4,000 percent more prevalent in the downwind samples. .... What's clear is there are far more viable microbes in far more inhospitable places than scientists expected.

New research that found that microbial communities vary between the sinuses in a person with chronic sinusitis. This is a result that many sinusitis sufferers already suspect based on their sinusitis symptoms. The researchers also found that bacterial communities in the sinuses vary between people with chronic sinusitis. It is frustrating though for me to read study after study where the researchers focus on describing the types of bacteria found in chronic sinusitis sufferers (and then just saying that the sinus microbiomes or community of microbes vary from person to person) rather than studies comparing the sinus microbiomes (bacteria and other microbes, such as fungi) between healthy individuals and sinusitis sufferers.

Since research finds that sinusitis sufferers have altered sinus microbiomes, then what would be really helpful now is finding more beneficial or keystone species (besides Lactobacillus sakei) that are needed for healthy sinus microbiomes. This would be an important step towards then adding (perhaps using a nasal spray) these missing microbes to the sinus microbiome. From Frontiers in Microbiology:

Bacterial communities vary between sinuses in chronic rhinosinusitis patients

ABSTRACT: Chronic rhinosinusitis (CRS) is a common and potentially debilitating disease characterized by inflammation of the sinus mucosa for longer than 12 weeks. Bacterial colonization of the sinuses and its role in the pathogenesis of this disease is an ongoing area of research. Recent advances in culture-independent molecular techniques for bacterial identification have the potential to provide a more accurate and complete assessment of the sinus microbiome, however there is little concordance in results between studies, possibly due to differences in the sampling location and techniques. This study aimed to determine whether the microbial communities from one sinus could be considered representative of all sinuses, and examine differences between two commonly used methods for sample collection, swabs and tissue biopsies. High-throughput DNA sequencing of the bacterial 16S rRNA gene was applied to both swab and tissue samples from multiple sinuses of 19 patients undergoing surgery for treatment of CRS. Results from swabs and tissue biopsies showed a high degree of similarity, indicating that swabbing is sufficient to recover the microbial community from the sinuses. Microbial communities from different sinuses within individual patients differed to varying degrees, demonstrating that it is possible for distinct microbiomes to exist simultaneously in different sinuses of the same patient. The sequencing results correlated well with culture-based pathogen identification conducted in parallel, although the culturing missed many species detected by sequencing. This finding has implications for future research into the sinus microbiome, which should take this heterogeneity into account by sampling patients from more than one sinus. It may also be of clinical importance, as determination of antibiotic sensitivities using culture of a swab from a single sinus could miss relevant pathogens that are localized to another sinus.

CRS can be a debilitating condition that is recalcitrant to treatment. Bacterial colonization of the sinuses is likely to play an important role in the pathogenesis and perpetuation of the disease; however different studies have yielded contrasting results with respect to which bacterial taxa are characteristic of the disease (ref). We observed bacterial communities dominated by different taxa in CRS patients; for example some have sinuses colonized primarily with Haemophilus, while others are dominated by Corynebacterium and Staphylococcus, or Pseudomonas. Some patients’ sinuses contain anaerobic bacteria such as Anaerococcus, Finegoldia, and Peptoniphilus, while these were absent from others. Indeed, our results have shown, for the first time, that it is possible for a patient to simultaneously have different bacterial communities in different sinuses, pointing to distinct, localized microbiomes within the same patient. Understanding this variation in the sinus microbiome could prove critical to the appropriate selection of treatments for CRS in the future.

The weighted unifrac distances between samples within patients (Figure 1) demonstrate that at least some CRS patients have substantial variation of bacterial communities between sinuses, although it is significantly smaller than the variation observed between different individuals. While this variation was related to abundance rather than the presence or absence of dominant community members, some of these variations were large: for example Corynebacterium sequences dominating the right sinuses of patient 003 (60.7 and 41.7% of all sequences), while the left sinuses had much smaller abundances (9.8 and 6.2%) and were dominated by the anaerobic bacteria Anaerococcus, Finegoldia  and Peptinophillus.

Could the bacteria described in this research be another probiotic or beneficial bacteria (besides Lactobacillus sakei) that helps protect against sinusitis? New research found that the harmless bacteria Corynebacterium accolens is "overrepresented" in children free of Streptococcus pneumoniae (pneumococcus) -  which commonly colonizes in children's noses (and that can live harmlessly as part of a healthy microbiome), but it is also an important infectious agent. Streptococcus pneumoniae is a major cause of pneumonia, septicemia, meningitis, otitis media (ear infections), and sinusitis in children and adults worldwide.

The researchers did an analysis on the microbes in the nasal passages of children and found that the nasopharyngeal (nostrils) microbiome was different in children with and without pneumococcal nasopharyngeal colonization. This revealed that Corynebacterium species and Dolosigranulum were "overrepresented" in children negative for pneumococcal colonization, whereas Streptococcus was "overrepresented" in children positive for Streptococcus  pneumoniae colonization.

The researchers found that higher numbers of  Corynebacterium accolens cells deter and limit S. pneumoniae nostril colonization, which might partly explain why children without S. pneumoniae colonization have higher levels of nasal Corynebacterium species. The researchers write that "there is direct antagonism" between Corynebacterium spp. and S. pneumoniae in the human nose. How do children get this beneficial bacteria? Interestingly, at 6 weeks of age, Corynebacterium species. and Dolosigranulum species are also "overrepresented" in the nasopharyngeal microbiota of breastfed infants compared to formula-fed infants. From Science Daily:

Good bacteria might help prevent middle ear infections, pneumonia

A new study is helping to shed more light on the important connections among the diverse bacteria in our microbiome. According to research published in mBio, scientists at Forsyth, led by Dr. Katherine P. Lemon, along with their collaborator at Vanderbilt University, have demonstrated that a harmless bacterium found in the nose and on skin may negatively impact the growth of a pathogen that commonly causes middle ear infections in children and pneumonia in children and older adults.

This study provides the first evidence that Corynebacterium accolens, a harmless bacterial species that commonly colonizes the nose, can help inhibit Streptococcus pneumoniae (S. pneumoniae) -- a major cause of pneumonia, meningitis, middle ear infection and sinusitis. According to the World Health Organization, S. pneumoniae leads to more than 1 million deaths each year, primarily in young children in developing countries. Although most people that host S. pneumoniae do not develop these infections, colonization greatly increases the risk of, and is a perquisite for, infection and transmission.

The study, titled, "Corynebacterium accolens (C. accolens) Releases Antipneumococcal Free Fatty Acids from Human Nostril and Skin Surface Triacylglycerols," is published on January 5, 2016 in mBio. In this study, first-author Dr. Lindsey Bomar and her colleagues show that C. accolens are overrepresented in the noses of children that are not colonized by S. pneumoniae, which is commonly found in children's noses and can cause infection. In laboratory research, the team further found that C. accolens modifies its local habitat in a manner that inhibits the growth of S. pneumoniae by releasing antibacterial free fatty acids from representative host skin surface triacylglycerols. The team went on to identify the C. accolens enzyme needed for this. These results pave the way for potential future research to determine whether C. accolens might have role as a beneficial bacterium that could be used to control pathogen colonization.

Image result for teeth, wikipedia Research found that postmenopausal women with periodontal disease (gum disease) were more likely to develop breast cancer than women who did not have the chronic inflammatory disease. And it's a bigger risk among those who currently smoke or quit smoking within the last 20 years. The interesting part is the fact that periodontal disease is a bacterial disease and that it results in inflammation. An earlier post discussed research that found that the human breast microbiome (microbial community) and specifically the bacteria, is different in healthy breasts (in the breast tissue) as compared to cancerous breasts. From Science Daily:

Periodontal disease associated with increased breast cancer risk in postmenopausal women

Postmenopausal women with periodontal disease were more likely to develop breast cancer than women who did not have the chronic inflammatory disease. A history of smoking significantly affected the women's risk, researchers report. Periodontal disease is a common condition that has been associated with heart disease, stroke, and diabetes. Previous research has found links between periodontal disease and oral, esophageal, head and neck, pancreatic, and lung cancers, so the researchers wanted to see if there was any relationship with breast cancer.

Jo L. Freudenheim, PhD, and colleagues monitored 73,737 postmenopausal women enrolled in the Women's Health Initiative Observational Study, none of whom had previous breast cancer. Periodontal disease was reported in 26.1 percent of the women. Because prior studies have shown that the effects of periodontal disease vary depending on whether a person smokes, researchers examined the associations stratified by smoking status.

After a mean follow-up time of 6.7 years, 2,124 women were diagnosed with breast cancer. The researchers found that among all women, the risk of breast cancer was 14 percent higher in women who had periodontal disease.

Among women who had quit smoking within the past 20 years, those with periodontal disease had a 36 percent higher risk of breast cancer. Women who were smoking at the time of this study had a 32 percent higher risk if they had periodontal disease, but the association was not statistically significant. Those who had never smoked and had quit more than 20 years ago had a 6 percent and 8 percent increased risk, respectively, if they had periodontal disease.

"We know that the bacteria in the mouths of current and former smokers who quit recently are different from those in the mouths of non-smokers," Freudenheim explained. One possible explanation for the link between periodontal disease and breast cancer is that those bacteria enter the body's circulation and ultimately affect breast tissue. However, further studies are needed to establish a causal link, Freudenheim said.