Older adults are at risk for both impaired oral health and
malnutrition, according to a study by Rutgers University researchers.
The study, recently published in the Journal of Aging Research and
Clinical Practice, analyzed the health records of 107 community-dwelling
senior citizens treated at the Rutgers School of Dental Medicine clinic
between 2015 to 2016.
The results showed that more than 25 percent of the patients had
malnutrition or were at risk for malnutrition. The researchers saw a
trend in which patients with 10 to 19 teeth were more likely to be at
risk for malnutrition. Those patients classified as having malnutrition
had higher rates of weight loss, ate less and more frequently reported
that they suffered with dementia and/or depression and severe illnesses
than those who had a normal nutrition status.
"The mouth is the entry way for food and fluid intake," said lead
author Rena Zelig, director of the Master of Science in Clinical
Nutrition Program at Rutgers School of Health Professions. "If its
integrity is impaired, the functional ability of an individual to
consume an adequate diet may be adversely impacted."
Although further studies need to examine the relationships between
tooth loss and malnutrition risk, Zelig said the findings show that
dental clinics are ideal locations to perform nutritional status
screenings as they can identify patients who may not regularly visit a
primary care provider and who may be at risk for malnutrition.
"Clinicians also can provide patients with referrals to Registered
Dietitians and community assistance programs such as Meals on Wheels to
prevent further decline in nutritional status," she said.
This was the first part of a mixed-methods grant to research the
associations between tooth loss and nutritional status in older adults.
The second part of the grant built on these results and qualitatively
studied the eating experience and eating-related quality of life of
community-dwelling older adults using qualitative interviews.
The study sets the stage for further research to examine the
relationships between tooth loss and malnutrition risk and the impact of
tooth loss on the eating experience and eating-related quality of life.
Scared, ashamed, happy or proud - how do children feel when they
lose their first baby tooth? An interdisciplinary research group at the
University of Zurich has now found that children's feelings are
predominantly positive. The study also reveals that previous visits to
the dentist's as well as parental background and level of education
affect how children experience the loss of their first tooth.
Deciduous teeth, more commonly known as milk or baby teeth, are the
first set of teeth that develop in children. These teeth usually fall
out and are replaced by permanent teeth. Children generally lose their
first baby tooth when they're about six years old: The tooth comes loose
and eventually falls out, leaving a gap which is then permanently
filled by its replacement tooth. This gradual process is probably one of
the first biological changes to their own bodies that children
experience consciously. The emotions that accompany this milestone are
extremely varied, ranging from joy at having finally joined the world of
grown-ups to fear about the loss of a body part.
Parents report positive reactions
An interdisciplinary team of dental researchers and developmental
and health psychologists at the University of Zurich, in cooperation
with the City of Zurich's School Dental Services, has now examined the
feelings that children experience when they lose their first baby tooth,
and which factors are at play. The scientists surveyed parents of
children who had already lost at least one of their milk teeth. Of the
nearly 1,300 responses received for the study, around 80 percent of
parents reported positive feelings, while only 20 percent told of
negative emotions. Raphael Patcas, first author of the study, is happy
with the findings: "The fact that four out of five children experience
the loss of a baby tooth as something positive is reassuring, for
parents and dentists alike."
The longer it's loose, the better the feelings
The researchers found that previous visits to dentists played a role
when it comes to children's feelings. Children whose previous visits
were cavity-related and thus perhaps associated with shame or guilt
experienced fewer positive emotions when they later lost their first
baby tooth. If, however, previous dental appointments were the result of
an accident, and thus an abrupt, unexpected and painful event, then the
loss of the first milk tooth was more likely to be associated with
positive emotions. According to dental researcher Raphael Patcas, one
possible explanation for this is that baby teeth loosen gradually before
falling out - a process that, unlike an accident, unfolds slowly and
predictably. This is also supported by the fact that children who
experience the loosening of their tooth over an extended period of time
tend to have more positive feelings: The longer the preparation and
waiting time, the greater the relief and pride when the tooth finally
falls out.
Parental education and background matter
Moreover, the study also found that sociodemographic factors are
related to children's feelings: For example, children were more likely
to have positive feelings such as pride or joy if the parents had a
higher level of education and came from non-Western countries. The
researchers indicate that cultural differences could be at play here:
These include education style and norms that parents pass on to their
children, as well as transitioning rituals that accompany the loss of
the first baby tooth.
"Our findings suggest that children deliberately process previous
experiences concerning their teeth and integrate them in their emotional
development," says Moritz Daum, UZH professor of developmental
psychology. This finding is important for dentists and parents alike:
"Especially where cavities are concerned, it's worth communicating with
children prudently", says Daum. "This way, emotions in connection with
teeth and dentists can be put on the most positive trajectory possible."
Researchers
at Queen Mary University of London have produced a new orthodontic
bracket bonding adhesive that protects the tooth surfaces around the
brackets from decay. This decay is often referred to as white spot
lesions which affects, according to a 2015 meta-analysis, nearly 70 per
cent of people fitted with orthodontic braces*.
The problem areas
are around the edges of the retaining brackets where plaque
accumulates. Because of the wires and brackets it is difficult to keep
the teeth clean. This results in many patients ending up with straight
teeth after orthodontics but with blotchy marks that can affect their
willingness to smile and reduce their self-confidence. This
discolouration takes many months or even years to disappear.
The
new bioactive bonding adhesive differs from the currently used materials
by continuously releasing fluoride, calcium and phosphate to form
fluorapatite. Fluorapatite will remineralise adjacent tooth surfaces and
also reduce plaque formation around the orthodontic bracket, reducing
the risk of initial decay seen as a chalky surface on the tooth enamel.
Professor Robert Hill at Queen Mary University of London said: “This
is a significant breakthrough which will benefit all those wearing
orthodontic braces” explained. The research we undertook is an extension
of the technology we developed with BioMin Technologies when developing
BioMin F toothpaste and this adhesive prevents the development of
unsightly white spot lesions around the brackets.”
Braces are
very popular, with more than 200,000 children and adults in England and
Wales starting orthodontic treatment last year. They allow the wearer to
have an attractive, confident smile, bite correctly, eat more
comfortably, and to care for their teeth and gums more effectively. In
the USA, over four million people are wearing braces, of which 25
percent are adults.
Professor Robert Hill added: “This
new special adhesive includes a much lower sodium content than that
used in BioMin F toothpastes so it reacts, rather than dissolves. Our
latest research shows the adhesive forms protective fluorapatite - the
fluoride analog of tooth mineral – around the brackets. We hope to see
the first commercially available product within two years.” The research is published in the journal Dental Materials.
People with high blood pressure
taking medication for their condition are more likely to benefit from the
therapy if they have good oral health, according to new research in the
American Heart Association's journal Hypertension.
Findings of the analysis, based on a review of medical and dental exam
records of more than 3,600 people with high blood pressure, reveal that those
with healthier gums have lower blood pressure and responded better to blood
pressure-lowering medications, compared with individuals who have gum disease,
a condition known as periodontitis. Specifically, people with periodontal
disease were 20 percent less likely to reach healthy blood pressure ranges,
compared with patients in good oral health.
Considering the findings, the researchers say patients with periodontal
disease may warrant closer blood pressure monitoring, while those diagnosed
with hypertension, or persistently elevated blood pressure, might benefit from
a referral to a dentist.
"Physicians should pay close attention to patients' oral health,
particularly those receiving treatment for hypertension, and urge those with
signs of periodontal disease to seek dental care," Pietropaoli said.
"Likewise, dental health professionals should be aware that oral health is
indispensable to overall physiological health, including cardiovascular
status," said study lead investigator Davide Pietropaoli, D.D.S., Ph.D.,
of the University of L'Aquila in Italy.
The target blood pressure range for people with hypertension is less than
130/80 mmHg according to the latest recommendations from the American Heart
Association/American College of Cardiology. In the study, patients with severe
periodontitis had systolic pressure that was, on average, 3 mmHg higher than
those with good oral health. Systolic pressure, the upper number in a blood
pressure reading, indicates the pressure of blood against the walls of the
arteries.
While seemingly small, the 3mmHg difference is similar to the
reduction in blood pressure that can be achieved by reducing salt intake by 6
grams per day (equal to a teaspoon of salt, or 2.4 grams of sodium), the
researchers said. The presence of periodontal disease widened the gap even farther, up to 7
mmHg, among people with untreated hypertension, the study found. Blood-pressure
medication narrowed the gap, down to 3 mmHg, but did not completely eliminate
it, suggesting that periodontal disease may interfere with the effectiveness of
blood pressure therapy. "Patients with high blood pressure and the clinicians who care for them
should be aware that good oral health may be just as important in controlling
the condition as are several lifestyle interventions known to help control
blood pressure, such as a low-salt diet, regular exercise and weight
control," Pietropaoli said.
While the study was not designed to clarify exactly how periodontal disease
interferes with blood pressure treatment, the researchers say their results are
consistent with previous research that links low-grade oral inflammation with
blood vessel damage and cardiovascular risk.
Hypertension is estimated to affect up to 40 percent of people over age 25
worldwide.
Untreated or poorly controlled hypertension can lead to heart attacks,
strokes and heart failure, as well as kidney disease. Hypertension is estimated
to claim 7.5 million lives worldwide.
Red, swollen, tender gums or gums that bleed with brushing and flossing are
tell-tale signs of inflammation and periodontal disease. So are teeth that look
longer than before, a sign of receding gums, and teeth that are loose or
separating from the gum line.
Microbiome-triggered Th17 cells switch from protective to destructive; may be potential treatment targets
NIH/National Institute of Dental and Craniofacial Research
IMAGE: A new study led by NIDCR clinical
investigator Dr. Niki Moutsopoulos suggests that periodontal disease is
driven by Th17 immune cells, which are triggered by an unhealthy
bacterial community.
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Credit: National Institute of Dental and Craniofacial Research, NIH
An unhealthy population of microbes in the mouth triggers
specialized immune cells that inflame and destroy tissues, leading to
the type of bone loss associated with a severe form of gum disease,
according to a new study in mice and humans. The research, led by
scientists from the National Institute of Dental and Craniofacial
Research (NIDCR) at the National Institutes of Health and the University
of Pennsylvania School of Dental Medicine, Philadelphia, could have
implications for new treatment approaches for the condition. The
findings appear online Oct. 17, 2018, in Science Translational Medicine.
Periodontal disease is a common disorder that affects nearly half of
American adults over age 30, and 70 percent of adults 65 and older. In
those affected, bacteria trigger inflammation of the tissues that
surround the teeth, which can lead to loss of bone and teeth in an
advanced stage of the disease called periodontitis.
"We've known for years that microbes stimulate inflammation.
Removing bacteria by tooth-brushing and dental care controls
inflammation, but not permanently, suggesting there are other factors at
play," said study senior author Niki Moutsopoulos, D.D.S., Ph.D., a
clinical investigator at NIDCR. "Our results suggest that immune cells
known as T helper 17 cells are drivers of this process, providing the
link between oral bacteria and inflammation."
Moutsopoulos and colleagues observed that T helper (Th) 17 cells
were much more prevalent in the gum tissue of humans with periodontitis
than in the gums of their healthy counterparts, and that the amount of
Th17 cells correlated with disease severity.
Th17 cells normally live in so-called barrier sites--such as the
mouth, skin, and digestive tract--where germs make first contact with
the body. Th17 cells are known to protect against oral thrush, a fungal
infection of the mouth, but they are also linked to inflammatory
diseases such as psoriasis and colitis, suggesting that they play dual
roles in health and disease.
To better understand this dynamic, the NIDCR scientists teamed up
with an NIDCR-funded research group led by study senior author George
Hajishengallis, D.D.S., Ph.D., at the University of Pennsylvania School
of Dental Medicine and colleagues from NIH's National Institute of
Allergy and Infectious Diseases (NIAID) and National Cancer Institute
(NCI).
The scientists found that similar to humans, more Th17 cells
accumulated in the gums of mice with periodontitis compared to healthy
mice, which served as a control group.
To see if the oral microbiome might be the trigger for Th17 cell
accumulation, the researchers placed mice on a broad-spectrum antibiotic
cocktail. They found that eliminating oral microbes prevented expansion
of Th17 cells in the gums of mice with periodontitis while leaving
other immune cells unaffected, suggesting an unhealthy bacterial
population triggers Th17 cell accumulation.
Next, the group wanted to know if blocking Th17 cells could lessen
periodontal disease. When the scientists genetically engineered mice to
lack Th17 cells, or gave the animals a small-molecule drug that prevents
Th17 cell development, they saw similar outcomes: reduced bone loss
from periodontitis. RNA analysis showed the Th17-blocking drug led to
reduced expression of genes involved in inflammation, tissue
destruction, and bone loss, suggesting that Th17 cells may mediate these
processes in periodontitis.
Finally, the researchers studied a group of 35 patients at the NIH
Clinical Center with a gene defect causing them to lack Th17 cells. The
scientists reasoned that if Th17 cells are as important to periodontitis
as the animal studies suggested, not having Th17 cells should protect
against gum disease. This is indeed what the group found--the patients
were less susceptible to the condition and had less inflammation and
bone loss compared to age- and gender-matched volunteers.
"Our clinical observations point to the relevance of our animal
studies to humans and provide further evidence that Th17 cells are
drivers of periodontitis," said NIDCR researcher Nicolas Dutzan, Ph.D.,
first author of the paper.
"These results provide key insights into the mechanisms that
underlie development of periodontal disease," said NIDCR Director Martha
J. Somerman, D.D.S., Ph.D. "Importantly, they also offer compelling
evidence for therapeutic targeting of specific cells, which might
eventually help us provide better treatment and more relief to patients
with this common disease."
T cells help fight off infection, but they can go overboard. A new
study led by researchers at the University of Pennsylvania School of
Dental Medicine and the National Institutes of Health (NIH) shows that a
subset of T cells contributes to the problematic inflammation and bone
loss that is associated with periodontitis, a severe form of gum
disease.
The research, conducted with the help of animal models and a group
of human patients with a rare genetic mutation, point to a new target
for treating periodontitis, as well as other diseases involving the
inappropriate response of this group of T cells, known as Th17 cells.
These include autoimmune conditions such as rheumatoid arthritis and
multiple sclerosis. The work appears in Science Translational Medicine.
"I think this work leaves no doubt that these cells are important
mediators of periodontitis," says George Hajishengallis, the Thomas W.
Evans Centennial Professor in the Department of Microbiology at Penn
Dental Medicine. "The translational aspect of our studies is pinpointing
a new approach to blocking the tissue destruction we see in
periodontitis, by inhibiting Th17 development."
Hajishengallis collaborated on the work with Niki M. Moutsopoulos of
the NIH's National Institute for Dental and Craniofacial Research, with
whom he has made previous insights into the molecular drivers of
periodontitis.
T cells are broadly considered to fall into two categories: helper T
cells, which aid in orchestrating the immune system's response to
threats, and cytotoxic T cells, which take a lead role in carrying out
an attack. Until about 13 years ago, helper cells were further divided
into two groups: Th1 or Th2 cells. Then a new subset, Th17 cells, was
identified, and researchers quickly realized Th17 cells played a role in
certain human diseases. By 2008, Hajishengallis and other researchers
began to suspect that these cells may be implicated in periodontitis.
More recent studies have found that people with chronic periodontitis
have an unusually high number of Th17 cells in their gum tissue, but
these investigations hadn't uncovered the particular role of these cells
in the condition or whether they were required for the development of
periodontitis.
In the current work, the researchers looked at gum tissue from
patients with chronic periodontitis and confirmed that they had higher
numbers of Th17 cells compared to healthy controls, with the numbers
correlating with the severity of disease. In parallel, they observed
that mice in which periodontitis was induced, Th17 cell numbers, along
with the IL-17 signaling molecule which they produce, increased with the
onset of gum disease. This increase in Th17 cell numbers, the
researchers found, was the result of local proliferation rather than
recruitment from nearby lymph nodes.
To interrogate possible triggers of the local expansion of Th17
cells, the team decided to see how changes in the community of microbes
in the gum tissue, the gingival microbiome, affected the accumulation of
Th17 cells. In the mouse model of disease, animals were treated with
broad- or narrow-spectrum antibiotics. Only those antibiotics which
lowered the numbers of Th17 cells were capable of suppressing the
disease, again implicating these cells in disease.
To definitively link the cells to the condition, however, the
researchers took advantage of a mouse model missing a key protein
required for Th17 cell development, as well as a population of human
patients with a mutation in the corresponding gene, Stat3, who are
monitored at the NIH. In both cases, they found that the Stat3 mutation,
which dramatically cut the number of Th17 cells present in the gum
tissue, also protected against the bone loss seen in chronic
periodontitis. While people with this Stat3 mutation have other
problems, gum disease is not one of them.
"Here we have a unique patient population with the same defect we
checked in the mice, and they are similarly not susceptible to the same
disease," Hajishengallis says. "This type of rigorous evidence is not
easy to come by in medical science."
Though antibiotics could serve to protect against the disease, the
side effects of taking such drugs, which can kill both beneficial and
disease-causing microbes throughout the body, are too significant to
recommend the treatment for broad use. But employing a small-molecule
that inhibits Th17 cell development gave the researchers a similar
effect, reducing Th17 cell accumulation and associated periodontal bone
loss in mice.
"There is no antibiotic that is that targeted, that specific,"
Hajishengallis says. Such an inhibitor offers promise as a periodontal
therapy and perhaps as a target for treating other diseases in which
Th17 play a destructive role.
IMAGE: Top row: The discoloration of enamel
exposed to cigarette smoke. Middle row: Minimal discoloration of enamel
exposed to the aerosol from a Tobacco Heating Product. Bottom row:
Minimal discoloration of...
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Credit: British American Tobacco
A study by scientists at British American Tobacco has shown that
e-cigarettes and tobacco heating products cause significantly less
staining to teeth than conventional cigarettes.
For the first time at BAT, scientists assessed and compared a novel
e-cigarette (EC), a tobacco heating product (THP) and a conventional
cigarette for their impact on teeth enamel staining. The results are
published today in the American Journal of Dentistry.
While cigarette smoke caused significant enamel discoloration,
vapour from the EC and aerosol from the THP caused only minimal staining
(see Figure 1).
These next generation products (NGPs) do not involve combustion; the
vapour and aerosol they produce are less complex and contain
significantly lower levels of certain toxicants compared to cigarette
smoke.
It is well known that smoking cigarettes causes stains on teeth that
cannot easily be removed by regular brushing, but little is known about
such effects from NGPs. So scientists at BAT conducted in vitro teeth
staining studies to compare the effect of an EC, BAT's THP glo, and a
reference cigarette (3R4F).
Tests were carried out on enamel blocks cut from bovine incisors. To
mimic conditions in the mouth, the enamel blocks were first incubated
with saliva to allow the formation of a pellicle layer, a protective
protein film that normally forms on teeth. The enamel blocks were
exposed to the particulate matter (isolated from the smoke/vapour) for
14 days and then whole smoke/vapour (equivalent to one pack of
cigarettes per day) for 5 days.
The enamel samples were assessed before, during and after treatment;
colour readings were determined by an independent laboratory using an
established method involving a commercially available spectrophotometer
and trained scientists.
Discoloration of enamel blocks exposed to cigarette smoke was
apparent in as little as one day and continued to increase as the
concentration of cigarette smoke increased. In contrast, exposure to
vapour from the EC or THP resulted in little or no colour change that
was comparable to the untreated controls.
"Many studies have postulated that it is the tar in cigarette smoke
that stains teeth. We now have a method where we can rapidly assess in
the laboratory the level of enamel discoloration by cigarette smoke and
vapour from our ECs and THPs," explains Annette Dalrymple, a senior
scientist at BAT R&D.
"The data generated from this study clearly shows that the EC and
THP assessed caused minimal discoloration--very promising for consumers
of our NGPs. However, further studies are required to understand the
long-term effect on teeth staining and oral health when smokers switch
to using NGPs."
Long-term exposure to periodontal disease bacteria causes
inflammation and degeneration of brain neurons in mice that is similar
to the effects of Alzheimer's disease in humans, according to a new
study from researchers at the University of Illinois at Chicago.
The findings, which are published in PLOS ONE, suggest that
periodontal disease, a common but preventable gum infection, may be an
initiator of Alzheimer's, which currently has no treatment or cure.
"Other studies have demonstrated a close association between
periodontitis and cognitive impairment, but this is the first study to
show that exposure to the periodontal bacteria results in the formation
of senile plaques that accelerate the development of neuropathology
found in Alzheimer's patients," said Dr. Keiko Watanabe, professor of
periodontics at the UIC College of Dentistry and corresponding author on
the study.
"This was a big surprise," Watanabe said. "We did not expect that
the periodontal pathogen would have this much influence on the brain, or
that the effects would so thoroughly resemble Alzheimer's disease."
To study the impact of the bacteria on brain health, the Watanabe
and her colleagues -- including Dr. Vladimir Ilievski, UIC research
assistant professor and co-author on the paper -- established chronic
periodontitis, which is characterized by soft tissue damage and bone
loss in the oral cavity, in 10 wild-type mice. Another 10 mice served as
the control group. After 22 weeks of repeated oral application of the
bacteria to the study group, the researchers studied the brain tissue of
the mice and compared brain health.
The researchers found that the mice chronically exposed to the
bacteria had significantly higher amounts of accumulated amyloid beta --
a senile plaque found in the brain tissue of Alzheimer's patients. The
study group also had more brain inflammation and fewer intact neurons
due to degeneration.
These findings were further supported by amyloid beta protein
analysis, and RNA analysis that showed greater expression of genes
associated with inflammation and degeneration in the study group. DNA
from the periodontal bacteria was also found in the brain tissue of mice
in the study group, and a bacterial protein was observed inside their
neurons.
"Our data not only demonstrate the movement of bacteria from the
mouth to the brain, but also that chronic infection leads to neural
effects similar to Alzheimer's," Watanabe said.
The researchers say these findings are powerful in part because they
used a wild-type mouse model; most model systems used to study
Alzheimer's rely on transgenic mice, which have been genetically altered
to more strongly express genes associated with the senile plaque and
enable Alzheimer's development.
"Using a wild-type mouse model added strength to our study because
these mice were not primed to develop the disease, and use of this model
gives additional weight to our findings that periodontal bacteria may
kick-start the development of the Alzheimer's," Watanabe said.
The researchers say that understanding causality and risk factors
for the development of Alzheimer's is critical to the development of
treatments, particularly when it comes to sporadic, or late-onset
disease, which constitutes more than 95 percent of cases and has largely
unknown causes and mechanisms.
While the findings are significant for the scientific community, Watanabe said there are lessons for everyone.
"Oral hygiene is an important predictor of disease, including
diseases that happen outside the mouth," she said. "People can do so
much for their personal health by taking oral health seriously."
The composition of oral
microbiota -- the collection of microorganisms, including beneficial
bacteria, residing in the mouth -- in two-year-old children may predict
their weight gain, according to a new study of over 226 children and
their mothers.
Credit: Penn State
Weight gain trajectories in early
childhood are related to the composition of oral bacteria of
two-year-old children, suggesting that this understudied aspect of a
child's microbiota -- the collection of microorganisms, including
beneficial bacteria, residing in the mouth -- could serve as an early
indicator for childhood obesity. A study describing the results appears
September 19 in the journal Scientific Reports.
"One in three children in the United States is overweight or obese,"
said Kateryna Makova, Pentz Professor of Biology and senior author of
the paper. "If we can find early indicators of obesity in young
children, we can help parents and physicians take preventive measures."
The study is part of a larger project with researchers and clinicians
at the Penn State Milton S. Hershey Medical Center called INSIGHT, led
by Ian Paul, professor of pediatrics at the Medical Center, and Leann
Birch, professor of foods and nutrition at the University of Georgia.
The INSIGHT trial includes nearly 300 children and tests whether a
responsive parenting intervention during a child's early life can
prevent the development of obesity. It is also designed to identify
biological and social risk factors for obesity.
"In this study, we show that a child's oral microbiota at two years
of age is related to their weight gain over their first two years after
birth," said Makova.
The human digestive tract is filled with a diverse array of
microorganisms, including beneficial bacteria, that help ensure proper
digestion and support the immune system. This "microbiota" shifts as a
person's diet changes and can vary greatly among individuals. Variation
in gut microbiota has been linked to obesity in some adults and
adolescents, but the potential relationship between oral microbiota and
weight gain in children had not been explored prior to this study.
"The oral microbiota is usually studied in relation to periodontal
disease, and periodontal disease has in some cases been linked to
obesity," said Sarah Craig, a postdoctoral scholar in biology at Penn
State and first author of the paper. "Here, we explored any potential
direct associations between the oral microbiota and child weight gain.
Rather than simply noting whether a child was overweight at the age of
two, we used growth curves from their first two years after birth, which
provides a more complete picture of how the child is growing. This
approach is highly innovative for a study of this kind, and gives
greater statistical power to detect relationships."
Among 226 children from central Pennsylvania, the oral microbiota of
those with rapid infant weight gain -- a strong risk factor for
childhood obesity -- was less diverse, meaning it contained fewer groups
of bacteria. These children also had a higher ratio of Firmicutes to
Bacteroidetes, two of the most common bacteria groups found in the human
microbiota.
"A healthy person usually has a lot of different bacteria within
their gut microbiota," said Craig. "This high diversity helps protect
against inflammation or harmful bacteria and is important for the
stability of digestion in the face of changes to diet or environment.
There's also a certain balance of these two common bacteria groups,
Firmicutes and Bacteroidetes, that tends to work best under normal
healthy conditions, and disruptions to that balance could lead to
dysregulation in digestion."
Lower diversity and higher Firmicutes to Bacteroidetes (F:B) ratio in
gut microbiota are sometimes observed as a characteristic of adults and
adolescents with obesity. However, the researchers did not see a
relationship of weight gain with either of these measures in gut
microbiota of two-year-olds, suggesting that the gut microbiota may not
be completely established at two years of age and may still be
undergoing many changes.
"There are usually dramatic changes to an individual's microbiota as
they develop during early childhood," said Makova. "Our results suggest
that signatures of obesity may be established earlier in oral microbiota
than in gut microbiota. If we can confirm this in other groups of
children outside of Pennsylvania, we may be able to develop a test of
oral microbiota that could be used in clinical care to identify children
who are at risk for developing obesity. This is particularly exciting
because oral samples are easier to obtain than those from the gut, which
require fecal samples."
Interestingly, weight gain in children was also related to diversity
of their mother's oral microbiota. This could reflect a genetic
predisposition of the mother and child to having a similar microbiota,
or the mother and child having a similar diet and environment.
"It could be a simple explanation like a shared diet or genetics, but
it might also be related to obesity," said Makova. "We don't know for
sure yet, but if there is an oral microbiome signature linked to the
dynamics of weight gain in early childhood, there is a particular
urgency to understand it. Now we are using additional techniques to look
at specific species of bacteria -- rather than larger taxonomic groups
of bacteria -- in both the mothers and children to see whether specific
bacteria species influence weight gain and the risk of obesity."
