ECD III - Boehm (online) - Nutrition Science 062416

Nutrition Science For Dentistry
Tobias K. Boehm

Why do we care?
Out in the ocean, seafarers have long known a dreadful disease that befalls those who don’t eat well.
Hear Antonio Pigafetta, who travelled with Magellan on his voyage across the globe in the 15th
century,
describe the particular horror that befell his fellow men while out in the middle of the Pacific Ocean:
“We had been three months and twenty days without taking refreshment of any kind. We ate
biscuit which was no longer biscuit, but powder with handfuls of maggots because these
creatures had eaten the good part. It smelled strongly of rat urine. We drank water that was
yellow and putrefied for many days, and we ate certain cowhides which were placed over the
main yard so that the yard should not break the shrouds, hardened by sun, rain and wind. We
left the hides in the seas for four or five days…Many times we ate sawdust. Rats were sold for
half a ducat each, when we could get them.
But above all other calamities this was the worst: in some men the gums grew over the teeth,
both lowers and uppers, so that they could not eat in any way and thus they died of this
sickness. Nineteen men died and also the Patagonian giant and an Indian from the land of Brazil.
Twenty-five or thirty men became sick, some in the arms, in the legs or other places, so that few
remained healthy.
By the grace of God I had no sickness.”
(Translated excerpt from “Il Primo Viaggio Intorno Al Mondo di Antonio Pigafetta” , edited by C.
Manfroni 1928)
This is one of the early accounts of how poor nutrition resulted in deadly oral disease, and subsequent
generations of seafarers in the age of sail feared this condition more than most other disasters, as it was
bound to happen on any long distance voyage. It took well into the 19th
century to understand the role
of food in preventing malnutrition states like scurvy, and to develop techniques to that preserved
perishable foods at sea.
Today, it is rare to see such severe forms of malnutrition in developed countries, but you may find a
surprising number of patients who have subtle forms of malnutrition or who may be at risk for becoming
malnourished.
Therefore, let’s review the role of nutrients in the human body, learn to identify patients at risk for
malnutrition and explore different approaches for nutritional counseling.

Scientific underpinnings of Nutritional Science
Since we will be talking about scientific evidence, let’s review some key scientific terms before we get
started. Much of the evidence we present here is based of clinical research.
The simplest and weakest evidence for many nutrition-oral health relationships are based on case
reports where someone describes an unusual disease brought on by poor nutrition. The report on
malnutrition causing oral disease on Magellan’s voyage can also be seen as a case report. If the report
describes several patients who have signs and symptoms associated with malnutrition, we have a little
more evidence in the form of a case series.
Now, since case reports and case series may just document coincidence in rare cases, scientists conduct
a variety of studies to discover consistent associations of oral disease and nutrition. For nutrition, most
studies are cross-sectional in nature, where a large group of subjects is tested for presence of oral
disease. The same group is also assessed for their nutritional status, and correlations between having a
certain nutrient in their diet and oral health are made.
STRENGTH OF EVIDENCE
Expert opinion, CE
Systematic
review
Randomized
Clinical Trial
Cohort studies
Case-Control studies
Cross-sectional studies
Case reports & series
Animal studies & Benchtop experiments
A
B
C
D
Levels of Evidence (modified from the Oxford Centre for Evidence-based Medicine)
Figure 1: Levels of Evidence (modified from the Oxford Centre for Evidence-based
Medicine)

Since any associations seen in cross-sectional studies may only be coincidence created by another factor
that actually causes oral disease, other study designs are needed. For example, in cohort studies, groups
of subjects that have different nutritional status are followed over a time period to see if one group
develops more oral disease than the other. More proactively, and most likely to imply a cause-effect
relationship are randomized clinical trials, which are very rare for nutrition-oral health relationship
research. In a randomized clinical trial, subjects would be allocated to randomized groups that have
similar characteristics, and one group would receive a certain nutrient while the other group gets
minimal nutrient levels in their diet. Any associations seen here would likely indicate that a nutrient is
indeed responsible for prevention of oral disease.
Clinical research can also consist of reviewing past research, and attempting to mathematically combine
separate research studies into a single study. This is done in a process called meta-analysis, and
essentially indicated if research findings from comparable studies agree with each other. For nutritional
science and oral health, there are not many studies of this kind.
Lastly, there is also basic research, which mostly aims to uncover the underlying mechanisms of clinical
associations. This either involves benchtop research, or animal research, and there are a number of
studies using oral disease models in rats for the study of nutrition effects on oral health.
Here, we will grade available evidence using a scheme similar to that proposed by the Oxford Centre for
Evidence-based Medicine (Figure 1).
The strongest level of evidence, graded as “A”, is given for any findings that have been confirmed by
multiple well-controlled clinical trials and summarized in systematic reviews and meta-analyses.
The next highest level of evidence, graded as “B”, is evidence produced by a well controlled randomized
clinical trial, or if not ethical or feasible to do a clinical trial, evidence from well controlled cohort
studies. These types of experimental designs are the only clinical studies that can demonstrate a likely
cause and effect relationship between a nutritional component and oral health.
We assigned a grade of “C” to cross-sectional studies and well-matched case-control studies as they
produce evidence showing an association between nutrition and oral health. It is more likely with these
retrospective studies that associations could be coincidental, and that findings gained from these
studies may not be predictive for your patients.
Case reports and series were given a “D” grade as they might show interesting cases and drive
hypothesis generation, but most likely are not predictive for your patient’s diagnosis and treatment.
Basic research reports are not given a level of evidence since they may provide mechanisms of nutrition
deficiencies causing disease, but usually are not directly applicable to patient care as rats and cell
cultures may behave differently from complete human beings.
Expert opinion, textbooks and continuing education is also not graded as they often provide correct
information, but usually are not peer-reviewed, and may be skewed by personal values and preferences.

Since quality of the information and usefulness can vary widely, I advise you to critically evaluate these
types of literature individually.
Since many studies on nutrition and oral health are cross-sectional and cohort studies, there are some
statistical terms we need to review.
Often these studies aim to find out if a group of patients with a nutritional characteristic has a lesser or
greater chance of contracting a disease or poor treatment outcome. For each group, the chance of
adverse events can be expressed in terms of risk or odds. Risk is essentially the percentage of patients in
a group that gets a disease or experiences a poor outcome, and is expressed as a number ranging from
zero to one. Likewise, odd ratios are also expressed zero to one, but it represents a ratio of the number
of patients who get a disease over the number of patients who do not get the disease. For instance, if in
a group of one hundred obese patients half of these patients experience worsening of their gum
condition within a year, the risk of worsening gum condition is 0.5, but the odds is 1 since these patients
were as likely to get worsening of their gums than experiencing no further worsening of their gums. As
you can see, the odds are always higher than the risk of an event, but for events happening at very low
frequency, odds and risk values become very similar.
Since the goal of most studies is to find out if a group of patients has a higher change of getting a
disease compared to another group, they usually calculate the risk or odds values for each group and
form ratios of these. A risk ratio is nothing more than the ratio of risk of disease in one group over the
risk of disease in another group, and it is the same with odds ratios. It tends to be easier to understand
risk ratios as they indicate how much more likely a group is getting a disease. If we use the previous
example, and assume that another group of one hundred patients experienced worsening of disease in
twenty-five patients, we know that the risk of disease worsening in non-obese patients is 0.25. As you
remember, the risk of obese patients getting worse disease was 0.5, and you can clearly see that in this
example, obese patients were twice as likely to experience disease worsening as the risk ratio of 0.5
over 0.25 equals 2.
Odds ratios are more difficult to comprehend and they tend to magnify differences. Using the previous
example, the odds of disease worsening in non-obese patients was 25 over 75, or 1/3. As the odds of
disease worsening in obese patients was 1, the odds ratio now is 3 and obese patients have three times
higher odds of getting disease worsening. For most people, this sounds worse than the risk ratio, and
shows how odds ratios magnify differences. Generally, most researchers would find an odds ratio of
equal or less than two not to be an important finding.
In either case, it would be nice to know how likely it is that an observed risk or odds applies to other
groups of patients similar to the one studied. This is where confidence intervals are important. Based on
the number of patients studied, and assuming that research findings will tend to cluster around a certain
value in a normally distributed fashion, it is possible to calculate confidence intervals for risks, odds and
their respective ratios. In essence, a confidence interval typically tells you that you would observe these
numbers 95% of the time if you would repeat the study over and over again, and that most likely you
would observe similar values in your own patients. Provided that results do follow this mathematical

model, and mostly they do, confidence intervals become smaller with increasing subject numbers, and
studies with large samples tend to be more predictive for your patients.
You will hear or see the term “statistically significant” or “significantly different”. This means that there
is a high chance that observed differences are truly different, and usually this is indicated with a p-value.
If a p-value is listed as less then 0.05, that means that were is less than a 5% chance that a reported
difference is just a fluke finding, and that most likely the results of this study apply to other, similar
patients. Determining “statistical significance” is done with statistical testing, and implies that
distribution of research results match the mathematical models that underscore these statistical tests.
For confidence intervals, a simple test of statistical significance is to see if confidence intervals of risk
ratios or odds ratios overlap. If they do not, there is a high chance that groups have different risks.
One task, however, that statistical significance testing does not perform is to determine clinical
significance. You have to determine that by judging if a reported difference in risk or odds is large
enough to observe clinically, and if it merits changing your clinical practice.
Two other terms you will hear in this course are prevalence and incidence, both of which are measures
of risk for a population of subjects. Prevalence is a measure of how likely a given subject in a population
has a condition or disease, and is simply calculated by the dividing the number of subjects with that
condition over the total number of subjects in a given population.
Incidence is similar to prevalence, but it also includes a temporal component, and it represents the
likelihood of a subject of a given population experiencing a disease or condition within a certain time
span. An example would be the number of flu cases in California between November 2013 and March
2014.
Now that we have reviewed some basic scientific terminology, let us look at nutrition. We will start with
reviewing key nutrients and possible malnutrition states, identify patients at risk for malnutrition and
come up with some strategies of changing nutritional habits to improve oral health.

Macronutrients
When it comes to nutrition, most people will ask, how much do
I need to eat of a certain nutrient to stay healthy? This can be
difficult to answer as different sources will differ on
recommended amounts, and the question on key nutrients can
be obscured by vast quantities of information available.
Although not free of controversy, for this presentation I used
the U.S. Department of Agriculture’s Current Dietary Guidelines
for Americans published in 2015 for recommended amounts of
key nutrients (see Dietary Guidelines for Americans 2015-2020,
8th
edition at
http://health.gov/dietaryguidelines/2015/guidelines/ ) .
Generally, these recommendations are accepted as nutritional
guidelines for healthy adults and have good scientific support.
The guidelines are still current until the next version will be
published in 2020, as guidelines usually get updated every five
years.
Generally, the guidelines use the following terminology for
recommended amounts:
The recommended dietary allowance (RDA) is the
recommended average amount of a given nutrient that will be
sufficient for 97-98% of healthy individuals at a given age and
gender to meet nutrition needs. Essentially, this is the daily
amount of a nutrient that a healthy individual needs to
consume in order to stay healthy.
Dietary Reference Intake (DRI) is a new term that replaces the
recommended dietary allowance (RDA) term, and expands it by
including other estimates such as
The adequate intake (AI), which is an estimated average intake of a nutrient as observed in experimental
studies of healthy subjects. The adequate intake is usually reported when a recommended dietary
allowance cannot be determined.
It also includes the tolerable upper intake level (UL), which is the average highest daily level of a nutrient
you can consume while likely having no risk to your health.
LEARNING
OBJECTIVES
- RECALL TYPES OF DIETARY
CARBOHYDRATES
- RECALL PURPOSE OF
CARBOHYDRATES IN DIET
- RECALL RELATIONSHIP OF
OBESITY AND PERIODONTAL
DISEASE
- RECALL RELATIONSHIP OF
CARBOHYDRATES AND
CARIES
- ASSESS A PATIENT'S ORAL
HEALTH RISK POSED BY A
PATIENT'S DIET
- RECALL ESSENTIAL AMINO
ACIDS
- RECALL PURPOSE OF
PROTEINS IN DIET
- RECALL DISEASES CAUSED
BY SEVERE PROTEIN
DEFICIENCY
- RECALL PURPOSES OF LIPIDS
IN DIET
- RECALL PURPOSES OF
ESSENTIAL FATTY ACIDS
IDENTIFY BENEFITS AND
RISKS OF CHOLESTEROL,
TRANS-FATTY ACIDS
- ASSESS THE LEVEL OF
EVIDENCE LINKING DIETARY
LIPIDS WITH PERIODONTAL
DISEASE

Before we delve into nutrients and how many miligrams of X you ought to have in your diet, it is
worthwhile to think of why we eat anyway?
Sure, eating can be a source of comfort, pleasure, or can have social functions like a wedding banquet or
a family dinner. But ultimately, we eat to live. Living requires energy, as energy is needed to maintain
orderly processes and structures of life. Every living being requires energy to maintain its cells, to grow,
move about and to store for leaner times.
For this reason, there is a base level of energy needed depending on age and size of the body, with
younger individuals needing more energy for growth, and larger individuals needing more energy. Since
men tend to be larger than women, men also have higher energy needs. (see FDA estimated calorie
needs at http://health.gov/dietaryguidelines/2015/guidelines/appendix-2/#table-a2-1-estimated-
calorie-needs-per-day-by-age-sex-and-physic)
In addition to that basal energy requirement, energy needs increase with increasing amount of physical
activity.
If more energy is created than consumed, energy is stored for future use as glycogen or fat, as a
safeguard against times when there is less food available than required.
Carbohydrates
The primary source for energy is carbohydrates, compounds of carbon, hydrogen and oxygen, arranged
in usually six-member rings of carbon atoms and one oxygen molecule, linked to other rings with oxygen
molecules and hydroxide side chains. Most plants store energy obtained from photosynthesis in the
form of starches, which are long carbohydrate polymers, while in animals the primary carbohydrate
used for energy is glycogen, a large branched carbohydrate polymer. Humans have domesticated wild
grasses for increased grain sizes, and utilize these grains such as wheat, rice and corn as primary source
of carbohydrates. Humans digest these long carbohydrate polymers using salivary enzymes such as
maltose into simpler carbohydrate oligomers and monomers such as maltose and glucose.
Since carbohydrates are vital to life, it is probably the reason why the tongue has taste receptors for
simple carbohydrates on the tip of the tongue in order to find carbohydrate-containing foods. It is
probably also the reason why sweet flavor is generally desirable for humans.
Carbohydrates are largely broken down to the basic 6-carbon sugar glucose, which is largely
metabolized using glycolytic and citric acid cycle into ATP, the body’s basic energy unit, carbon dioxide
and water. If carbohydrate intake exceeds energy needs, glucose will get converted into glycerin, fatty
acids and triglycerides, a.k.a. fat by the liver and stored in adipocytes.
Another use of carbohydrates is a source of precursor multiple carbon units for amino acids and other
molecules synthesized in the body. Glucose units also are extensively incorporated into very large

Figure 2. Fiber intake is related to periodontal status (Staudte et al.
2012). The amount of dietary fiber intake was assessed in 80 patients
with varying levels of periodontal disease, and those patients
categorized as “Periodontitis” and “Control” based on plaque levels,
gingival bleeding and pocket depth. The average fiber intake in both
groups was significantly different (p<0.05).
proteoglycan and glycoproteins that make up the water-retaining and space-maintaining ground
substance proteins of cartilage and connective tissue such as chondroitin and dermatan sulfate.
The RDA of carbohydrates is about 130 grams per day for adults, which equals to just about 5 slices of
bread. Obviously, carbohydrates are found in grains, and grain-based products such as bread and pasta.
Digestible carbohydrates are also found in any fruit, starchy vegetables such as peas and potatoes, milk,
and of course refined sugars, sweets and honey.
Apart from carbohydrates that can be digested by humans, indigestible carbohydrates such as cellulose
are known as dietary fiber. Far from being useless, some amount of dietary fibers is thought to be
important for promoting GI movement and provide moisture retention in stool. Dietary fibers such as
oat bran can also retain cholesterol and prevent high serum cholesterol levels.
In a case-control study by
Dr. Staudte and others
(Figure 2, Quintessence
International 2012; 43:907-
916) of 80 patients, it was
noticed that patients with
periodontal disease had
significantly lower fiber
intake than periodontally
healthy controls. A
drawback of this study is
that “periodontitis” was
merely defined as presence
of pockets greater than 3.5
mm at more than four
teeth, while the healthy
group had to have pockets
equal or less than 2 mm and
no bleeding on probing. This
study suggests that a diet
higher in fiber may be
associated with periodontal
health, but it is unclear if the healthy patients tended to have a healthier lifestyle in general as there
were no smokers in the healthy group compared to the “periodontitis” group.
A deficiency is carbohydrates is rare, but is said to result in loss of energy, being listless, emaciation and
wasting of muscle tissue as muscle protein is metabolized to meet energy needs. Carbohydrate excess in

Figure 3: Israel Kamakawiwo’ole. 450-lb musician
known for his rendition of “Over the rainbow”. Died
of a heart attack and multiple complications from
obesity at age 37.
Table 1: Obesity Classification based on BMI
absence of physical activity will lead to obesity, and by extension of obesity as a risk factor, increase the
risk of type 2 diabetes mellitus, stroke and myocardial infarct. Orally, obesity is associated with
periodontal disease, and excess intake of digestible carbohydrates without proper oral hygiene will
increase the risk of caries.
As mentioned before, obesity is a risk factor
for type 2 diabetes mellitus, coronary heart
disease, hypertension, stroke and myocardial
infarcts. Obesity is also associated with some
cancers of the GI tract, and premature death
as illustrated by musician Israel
Kamakawiwo’ole.
A common screening tool for obesity is the
body mass index (BMI): In order to figure out
a BMI, take a patients weight in kilograms,
and divide it twice by the patient’s height in
meters. If the BMI is greater or equal to 30,
than the patient might be obese. Of course,
this is just a crude screening tool, as well-
built athletes also tend to be considered
“obese” by the BMI. Further observations
and tests such as chest/waist ratio, skin fold
tests and immersion tests are used to arrive at a clinical diagnosis of obesity.
Since obesity is a risk
factor for many chronic
diseases that are costly to
treat, public health
researchers have noticed
with worry that obesity
prevalence in the United
States has been steadily increasing. In California, currently more than 20% of adults are considered
obese (Centers for Disease Control. MMWR 2010; 59:1-5 (early release))
At Western University of Health Science’s Dental Center 13% out of 2,300 patients seen for
comprehensive care were visibly obese, and these obese patients were 1.4 times more likely to have
chronic periodontitis as defined by 1999 International Workshop Definitions. Obese patients also have
more severe periodontal disease than non-obese patients in this clinic. (Figure 4)
What could explain this finding? Mealey and others (2006, Figure 5) proposed a mechanism in their
review of obesity, diabetes and periodontal disease relationships.
We know that periodontal disease is an inflammatory disease triggered by infection of the gingiva.

During the course of this inflammatory process, cells such as neutrophils, fibroblasts and macrophages
release cytokines such as Interleukin-1, Interleukin-6 and Tumor necrosis factor alpha. All of these
cytokines serve to recruit and activate additional immune cells, so that the infection can be contained in
the periodontal tissues. However, as we know, these cells are not successful in eliminating these
bacteria, and the
infection and
inflammatory
process persists.
These inflammatory
mediators, however,
do not stay in in the
periodontium, but
leak into the blood
stream, and get
carried off to other
parts of the body.
Now, one might
think that the
amount of cytokines
released is a trivial
amount since it just
involves a bit of
gingiva next to teeth. However, in a patient with severe periodontal disease, the area of inflammation
has been estimated by Hujoel and Listgarten in 2001 to be 8-20 square centimeters large. 20 Square
centimeters is about the size of your forehead, and so this area of inflammation can be very significant!
Figure 4. Periodontal Disease is more severe in Obese Patients at the Western U Dental Center
1886 Patients were examined between 2010 and 2013 and their periodontal disease diagnosed by
clinical attachment loss. Patients were then categorized according as “visibly obese” if waist width
exceeded chest width, or as “not apparent” if waist to chest ratio appears to be close to unity.
Visibly Obese
Gingivitis
Mild CP
Moderate CP
Severe CP
Health
Obesity not apparent
Figure 5. Mechanism on how obesity influences periodontal disease according
to Mealey BL et al. 2006

The amounts of inflammatory mediators is also significant enough that they can be detected in
meaningful amounts in your serum, and that periodontal disease treatment significantly reduces total
body inflammatory mediators, as shown by d’Aiuto and others in 2004, as well as in a number of other
studies.
We also know now that adipose tissue also uses Interleukin-1, Tumor-necrosis factor alpha, and
Interleukin-6 to regulate fat storage, and the more adipose tissue you have, the higher your systemic
levels of these cytokines are.
So you see that periodontal inflammation and large amounts of body fat can increase your total level of
inflammatory mediators in your body.
Once in the blood stream, tissue does not discriminate where these mediators come from, and the
increased level of mediators will then recruit and activate immune cells throughout the body, enhancing
inflammation throughout the body.
And of course, some of these inflammatory mediators get carried back to the periodontal tissues,
enhancing local inflammation and resulting in even more inflammatory mediators.
Now, inflammatory mediators such as Interleukin 1 and Interleukin 6 also counteract normal insulin
action, preventing uptake of glucose into tissues, presumably so that there is more glucose available for
immune cell function.
Therefore, you increase blood glucose and blood lipids, as the liver will release more glucose and
synthesizes lipids from the higher serum levels of glucose.
Having higher glucose levels in serum also will increase the risk of glucose undergoing a Schiff base
reaction with blood vessel wall proteins, forming advanced glycation end products. These modified
proteins are detected by macrophages throughout the body, and will stimulate these to create more
inflammation and mediators everywhere, including periodontal tissues.
The increased lipid levels are also available to grow more adipose tissue, and increased amounts of lipids
in the blood also increase the potential of these becoming oxidized. These oxidized lipids can damage
blood vessel walls, leading to activation of more immune cells. Ultimately, this proposed mechanism
could explain why obese patients have more periodontal disease, and have a higher risk for developing
type 2 diabetes mellitus, atherosclerosis, hypertension, heart attacks and strokes.
What is the relationship of obesity to periodontitis?
Overall, we can say that there is excellent evidence that periodontitis and obesity are associated, as
summarized in a systematic review by Caffesse and Weston in 2010. Numerous rat studies on obesity,
inflammation and diabetes provide a plausible mechanism as explained before. The only weakness in
our evidence is that there appears to be no study that shows that weight loss reduces periodontal
disease, or that periodontal disease treatment helps with weight loss.

We know however from a cohort study performed by Zuza and others in 2011, that obesity does not
seem to reduce the chance of success for non-surgical treatment of periodontal disease. This at least is
better than tobacco use, which is known to reduce success in periodontal disease treatment.
Since bariatric surgery, also known as “lap band” surgery, is increasingly used to treat obesity, it may be
important to know that in a case series by Moravec and Boyd it was found that bariatric surgery may
adversely affect oral health. Patients who had this type of surgery experienced more gastric reflux,
which could erode teeth, and also developed nutritional deficiencies due to lack of appropriate
counseling and diet change.
When it comes to implants, we do not know of any research that evaluated the effect of obesity on
implants.
What is the relationship between carbohydrates and caries?
We know that caries is associated with an infection of tooth surfaces by acidogenic, meaning acid-
producing, and aciduric, meaning acid-tolerating, bacteria.
It is still not quite clear what causes the onset of caries, but according to Dr. Marsh, caries is the result of
an ecological catastrophe, where changes in the oral environment such as increased presence of
fermentable sugars favors growth of bacteria that are able to ferment these. With time, bacteria that
can ferment sugars will displace bacteria that are protective for the tooth surface, and maintain a new
environment of permanently low pH that favors enamel dissolution and development of clinical caries.
The oral dysbiosis concept proposed by Darveau and Hajishengallis may also apply here as the bacteria
associated with caries are also capable of maintaining their new environment by producing acids and
extracellular matrix which keeps the acid from dissipating.
The classic bacterium associated with caries development is Streptococcus mutans type bacteria, which
are a collection of closely related oral, beta-hemolytic, gram-positive, facultative cocci. They all use
sucrose as a primary energy source, and produce a sticky extracellular matrix composed of glucans using
an enzyme called glucosyltransferase. They also produce lactic acid as a major metabolic byproduct,
which dissolves enamel and causes clinical caries, and along with bacteriocins they produce prevent
growth of other, more protective streptococci.
Xylitol has been shown to inhibit growth of these bacteria by Assev and others in 1983, and it is possible
to prevent caries by patients chewing xylitol containing gum or candy.
While Streptococcus mutans is a prime suspect in caries development, there are many other bacteria
capable of causing caries. Lactobacillus acidophilus, also found in yogurt, produces lactic acid as well and
can survive low pH. It is thought that Lactobacillus may be associated with established caries. Also, other
streptococcal species are also capable of creating caries, especially in animals with teeth other than
humans.

What are cariogenic foods and how can you counsel patients on this topic?
We know that development of caries essentially depends on the balance between fermentable
carbohydrates favoring low pH development and dissolution of teeth, and saliva stimulation and
presence of calcium and fluoride ions in the food, which both favor high pH values and enamel
mineralization.
So depending on the sugar content of the food, and its ability to stimulate saliva or release calcium salts,
food can range from cariogenic, increasing the risk of caries, to preventive, inhibiting development of
caries.
Cariogenic potential also depends on other factors besides overall carbohydrate content. In order to be
cariogenic, the carbohydrates must be able to be broken down to sucrose, glucose or fructose by human
or bacterial enzymes. Therefore, it is mainly foods containing a lot of amylose (starch), sucrose, glucose
or fructose that are considered cariogenic, which means foods such as bread, pasta, rice, candy, cakes,
fruit juices and soda.
In addition, cariogenic potential increases if the food is sticky and does not easily clear from between
teeth, as shown in the Vipeholm studies where chewy candy was given to institutionalized children, who
developed higher rates of caries. Foods that fall into this category are pretzels, potato chips, taffy, sugar-
containing gum, pasta, bread, potatoes, cookies, cakes and similar foods.
Cariogenic potential also increases if cariogenic foods are consumed on a frequent basis, as shown in the
Vipeholm and Michigan studies. This explains why caries risk increases significantly if you sip on juice or
soda throughout the day, but your risk is lower if you restrict cariogenic foods to meal times followed by
oral hygiene.
Therefore, if you have a patient who consumes a lot of sticky, cariogenic foods such as taffy, pretzels,
pasta, white rice, bread, potato chips or chocolate, you will have to watch for caries development. The
same is true for patients who habitually will sip on sodas, fruit juice, sweetened coffee or tea, or hold
hard candy in their mouth. This is also true for children who are fed juice unsupervised in a sippy cup or
nursing bottle.
If you have a patient who experiences more than a few active lesions of caries, you should consider
overconsumption of cariogenic foods as a cause. If the patient is found to overconsume cariogenic
foods, consider the following strategies to limit cariogenic potential instead of simply telling the patient
to quit eating sugary foods:
Try limiting cariogenic foods to the main meal times, in order to decrease frequency of cariogenic food
intake and allow remineralization of tooth surfaces in between meals.
Replace cariogenic snacks with Xylitol-containing gum or candy, or use these products after eating
cariogenic foods to stimulate saliva flow and inhibit bacterial growth. However, advise patients to be
cautious as overconsumption of xylitol can lead to bloating, stomach upset and diarrhea.

Another strategy is to follow cariogenic foods with a drink of water to rinse out sticky foods between
teeth.
Since the pH drops and demineralizes enamel after eating cariogenic foods, tell patients to wait with
brushing and flossing for 30 minutes after eating sugary foods, or rinse out the mouth with water
containing baking soda to neutralize bacterial acids.
You may also suggest replacing cariogenic snacks with foods that favor tooth mineralization:
Vegetables such as carrot, celery sticks, broccoli florets and beans are a nutritious and satisfying
alternative, stimulating salivary flow and food clearance from teeth.
Cheeses are an excellent caries-preventing snack as they provide calcium minerals for remineralization
of tooth surfaces. However, it is important to watch for fat intake as some cheeses can contain a lot of
saturated fats. On the other hand, low-fat varieties might have added carbohydrate content to make
them feel smooth in the mouth, and some carbohydrates might be cariogenic. The best cheese snacks
might be string cheese sticks, or strongly flavored hard cheeses such as Parmesan or feta cheese where
small amounts are quite satisfying.
Nuts are also a good satisfying snack that supplies energy. However, nuts may be contraindicated in a
patient with brittle teeth or fragile restorations.
For some patients, a good alternative to a solid snack is a glass of skim milk, tea without sugar or water,
either plain or flavored with sugar-free additives. As added benefit, green and black tea contain fluoride,
but can also stain teeth.
What is the level of evidence behind all these recommendations?
Given the focus of dentistry on caries, what is the level of science behind nutrition recommendation?
On one hand, it is a very well researched field, and we know from several long term cohort studies such
as the Michigan, Vipeholm, Newcastle/Northumberland studies that caries is associated with increased
frequency, amount and stickiness of consumed cariogenic foods. We also have decades of benchtop
research demonstrating mechanisms of caries on bacterial cultures, extracted teeth, dentin disks and in
various animals.
However, we still do not know conclusively if caries can be reduced by reducing sucrose intake, as a
systematic review by Stillman-Lowe and others in 2005 failed to produce conclusive evidence.
So, it is a good idea to look into a patient’s diet as a possible etiology of current caries experience.
However, reduction of cariogenic foods alone may not be enough to reduce a patient’s caries
experience. In a patient with significant amounts of caries you should also consider evaluating quantity
of saliva, pH and buffering capacity of saliva; amounts of cariogenic bacteria; mucogingival, restorative
and anatomic factors favoring plaque retention; occlusal function; parafunctional habits and medical
history to investigate causes of caries in these patients.

For management of patients with high risk or incidence of caries, you should consider caries
management by risk assessment techniques as developed by University of California at San Francisco,
also known as CAMBRA. A course in CAMBRA methodology is currently available for free on the
California Dental Association’s website at www.cda.org.
Proteins and Amino Acids
The next important macronutrient is proteins or amino acids. Proteins are digested in your duodenum
into amino acids for absorption in the small intestine. Humans use twenty two amino acids for synthesis
of proteins, which could be either structural such as collagens found in bone, periodontal ligament or
teeth, or have other functions such as enzymes, antimicrobial peptides or antibodies.
As an alternative energy source to glucose, amino acids can be metabolized to yield energy, although at
lower efficiency.
For humans, there are nine essential amino acids that the human body cannot synthesize in sufficient
quantities on its own, and that are needed in the diet to maintain health. These are histidine, leucine,
isoleucine, lysine, methionine, phenylalanine, threonine and valine. Tryptophan is also considered an
essential amino acid since the body can only synthetize limited amounts of it from phenylalanine.
The RDA of protein is 0.6 of protein per kg bodyweight. So, for a dental student weighing 150 lb, the
average protein requirement for the day is only a little less than a two-ounce filet mignon, which is likely
less than the smallest steaks served at any restaurant.
To put this in context, the US Department of Agriculture estimated that in 2000, the average American
ate 195 pounds of meat in the year, or about 8 ½ ounces per day. This is also the reason why total
protein deficiency and deficiencies of specific amino acids are quite rare.
During famines, protein deficiency may manifest itself in a severe form
called Kwashiorkor disease (Figure 6), producing muscle wasting and
bloated abdomen from increased fluid retention in the peritoneal
cavity, and the condition is eventually fatal. More commonly, protein
deficiency will result in stunted growth and development of children,
and poor wound healing and risk of infections. Since wound healing is
impaired and resistance to infections lowered, periodontal disease
may become severe in patients with protein deficiency, and
necrotizing periodontal diseases culminating in Noma or facial
gangrene can develop.
Protein deficiency to this extreme is unlikely encountered in a
common dental office, as proteins are widely available in meats, dairy,
legume such as kidney beans, eggs and to a lesser degree in most
other foods.
Figure 6. A 3-4 year old boy
suffering from Kwashiorkor
(J.E. Armstrong)

Lipids
The third important macronutrient is fat. According to USDA guidelines, fats should make up 25-35% of
caloric intake, which sounds like a lot, but actually is easily achievable given the high calorie content of
fat. The USDA recommends eliminating solid fats as much as possible, aiming for a level of less than
10% of caloric intake, or about ½ ounce per day. Most fats consumed should be in the form of liquid oils,
or a little less than one ounce per day.
Lipids get digested as they get emulsified into small droplets by bile liquid and absorbed in the small
intestine, producing chylomicrons that are further processed by the liver into packages of Very low
density lipoprotein (VLDL) and low density lipoprotein (LDL) for further consumption in body tissues.
Fats are mostly needed as energy source and for energy storage, but are also important part of organs
and form a protective, insulating layer around vital organs. Fats are also used for absorption of fat-
soluble vitamins, and serve as major component of cell membranes and cell organelles. Important
hormones and immune mediators such as androgens and prostaglandins are synthetized from certain
fats.
There are two essential fatty acids needed in human diet, both of them unsaturated cis-fatty acids found
in plant oils and certain animals.
One is linoleic acid, with an adequate intake level of about 12-17 grams per day, and mostly found in
vegetable oils such as safflower, grape seed, corn and to a much lesser degree, olive oil.
The other essential fatty acid is either alpha linolenic acid (ALA), Eicosapentaenoic acid (EPA) or
Docosapentaenoic acid (DPA), which can be interchangeably converted by the body. The adequate
intake level is about 1.1 to 1.6 grams per day for ALA, and they are found in cold water marine fish oil,
kiwifruit or flax seeds.
Both essential fatty acids are needed as precursors for arachidonic acid, an important precursor for a
variety of messenger molecules such as prostaglandins. Linolenic acid (ALA) and related acids are called
n-3 fatty acids, and converted slower to arachidonic acid, which supposedly results in an anti-
inflammatory effect as prostaglandin synthesis is slowed down.
The reason the USDA is emphasizing using predominantly oils as a fat source is that liquid oils contain
unsaturated fatty acids including essential fatty acids, whereas solid fats are made of saturated fatty
acids that are solid at room temperature. Solid fats can also be generated by hydrogenating vegetable
oils, which converts unsaturated fatty acids into saturated fatty acids by adding hydrogen atoms to
double-bonded carbons.
Since this process involves heat, it can also produce what is called trans-fats such as elaidic acid. Trans-
fats develop when naturally occurring oils are heated, which causes the cis-configuration double bonds
to be transformed into trans-forms.

Trans-fats are desirable from a food manufacturing point as they are cheap, have higher melting points
than normal vegetable oils, and make products containing trans-fats chewier, moister, softer and more
stable while being stored.
Unfortunately, trans-fats are not easily metabolized, and increased intake of trans-fats has been
associated with higher LDL, triglyceride levels (Katan MB et al. 1995); increased systemic inflammation
(Mozaffarian D et al. 2004); higher risk of cardiovascular disease and diabetes (Ascherio A et al. 1999;
Salmeron J et al. 2001).
Therefore, since about the mid-2000s, use and consumption of trans-fat containing foods has been
discouraged.
Cholesterol received a bad name in the 1990s when the relationship of heart disease and high
cholesterol levels became publicized. However, small amounts of cholesterol less than 300 mg per day
are needed as cholesterol forms a vital part of cell membrane, where it stabilizes the cell membrane,
preventing cell death.
It is found in any animal products as all animal cells contain cholesterol, but it is especially common in
egg yolk, liver and shellfish.
What is the relationship between lipid intake and periodontal disease?
Interestingly, in a Chinese study by Shi D and others (2006), patients with aggressive periodontitis and
chronic periodontitis had significantly higher levels of serum cholesterol than those who had gingivitis or
periodontal health.
A year later, a randomized clinical trial by Oz SG and others (2007) demonstrated in fifty patients that
serum LDL and cholesterol significantly decreased in three months if subjects had non-surgical
periodontal treatment.
Judging from several mice experiments, small clinical trials and larger cross-sectional studies, it seems
that intake of unsaturated fatty acids may be beneficial for periodontal disease. Bendyk A and others
(2009) noted that in experimental periodontitis mouse model, omega-3 fatty acid supplementation in
the mice’s diet was associated with less bone loss. There are also similar Japanese studies on rats
confirming this observation.
In humans, Naqvi AZ and others (2010) analyzed data from the 1999 to 2004 National Health and
Nutrition Examination Survery (NHANES), and found that adults who had higher dietary levels of n-3
fatty acids had less periodontitis. Similarly, a diet with low n-3 fatty acid content was associated with
higher levels of periodontitis in a survey of older Japanese (Iwasaki M et al. 2001).
Interestingly, Rosenstein ED and others (PLFA journal 2003; 68(3):213-8) conducted a small clinical trial
where they treated small groups of patients with scaling and root planing and different fatty acid diet
supplements. The found that borage oil, a plant oil rich in n-6 fatty acids showed significant reduction in
inflammation and pocket depths (about ½ mm) compared to patients who took placebos or other types

of oils in 3 months. (Table 2) It was also interesting to see that fish oil, a source of n-3 fatty acids, and
shown to be associated with less periodontal disease in the Japanese study mentioned before had no
effect. Findings from this study were confirmed by another study by Deore and others in 2014, with
similar methodology and similar results.
Table 2. Dietary fatty acid supplementation influenced periodontal
treatment outcomes
Adult patients received fatty acid supplements for 12 weeks after
scaling and root planning, and periodontal parameters were
measured before and after this time period.

Micronutrients - Vitamins
As important as the macronutrients in your diet are
micronutrients such as vitamins, as their name suggests “vita”,
Latin for life.
Fat-soluble Vitamins
Vitamins can be classified as either fat-soluble or water-soluble.
The vitamins A, D, E and K are fat-soluble.
Vitamin A
The dietary reference intake for vitamin A is 900 micrograms or
3000 international units for men and 700 micrograms for
women. Vitamin A has two important functions. One is a role in
cell differentiation and maturation, for example during tooth
development. The other important function is its role as
precursor to retinal pigment, where it is essential for night
vision. Vitamin A can be consumed in two varieties in a diet.
One is as retinoids, a group of closely related chemicals found
in animal fats and especially fish oil. The other variety is plant-
derived carotenoids which your body can convert into retinoids
as needed. As the name suggests, carotenoids are found in
carrots, but also in many other darkly colored leafy vegetables
or red/orange colored vegetables such as cantalopes and bell
peppers. Unlike retinoids, carotenoids are not toxic, and can
serve as anti-oxidant.
As Vitamin A is essential for retinal pigments, deficiency will
result in blindness. It also leads to impaired brain function, and
development abnormalties.
As hinted at before, retinoids are toxic at high doses, and a
retinoid overdose will result in dry mouth, loss of hair and headaches. Vitamin A toxicity may also
produce gingival erosions, ulceration, bleeding, tissue swelling and dekeratinization of gingiva.
There is no known relationship of vitamin A levels and periodontal disease, but since Vitamin A supports
cell differentiation case reports of Vitamin A improving drug induced overgrowth (Norris JF & Cunlifee
WJ 1987), lichen planus (Piatelli A et al. 2007) and leukoplakia (Epstein JB & Gorski M 1999) seem
plausible.
LEARNING
OBJECTIVES
- RECALL FAT SOLUBLE
VITAMINS
- RECALL CONSEQUENCES OF
DEFICIENCIES IN FAT-
SOLUBLE VITAMINS
- RECALL SOURCES OF FAT-
SOLUBLE VITAMINS
- RECALLCONTRIBUTIONS OF
FAT-SOLUBLE VITAMINS TO
ORAL HEALTH
- RECALLDEFICIENCY STATES
CAUSED BY B-VITAMIN
DEFICIENCIES
- RECALL SOURCES OF B-
COMPLEX VITAMINS
- RECALL GENERAL ROLE OF
B-COMPLEX VITAMINS
- RECALL RELATIONSHIPS OF
B-COMPLEX VITAMINS WITH
PERIODONTAL DISEASE
- RECALL FUNCTIONS OF
VITAMIN C
- RECALL DEFICIENCY STATES
CAUSED BY VITAMIN C
DEFICIENCY
- ASSESS THE LEVEL OF
EVIDENCE LINKING VITAMIN
C WITH PERIODONTAL
DISEASE

Vitamin D
Vitamin D is another fat soluble vitamin, and the metabolically active form is calciferol or vitamin D2.
The dietary reference intake level is 15 micrograms per day or 600 international units, and the main role
of vitamin D is calcium metabolism. It promoted calcium uptake from the intestines, maintains adequate
calcium serum levels and promotes bone turnover and calcification.
Main dietary sources are fortified milk and cod liver oil, but in sunny climates, fair-skinned humans make
sufficient vitamin D in skin tissue if exposed 15 minutes a day to sun light.
Vitamin D deficiency will result in either osteomalacia in adults or Rickets in children. In children, where
bone still develops, Vitamin D deficiency will result in deformed bones as mineralization is delayed,
creating bowed legs and deformed chest cavities, known as rachitic chest. In adults, growth is complete,
but vitamin D will impair bone turnover and adaptation to mechanic stress, resulting in increased risk of
fractures and bone pain.
Overdoses of vitamin D will result in too high serum calcium levels, which will produce abdominal
cramps and vomiting, as well as cardiac arrhythmia, confusion, and ultimately death.
If there is a chronic, but slight overdose of vitamin D, there is an increased risk of kidney stones.
Unlike Vitamin A, Vitamin D may play a role in periodontal disease given its role in bone metabolism.
Dietrich and others found in NHANES data a positive association of high Vitamin D levels and periodontal
health (Dietrich et al. 2004, 2005), while Bogess and others found low levels of Vitamin D associated
with periodontal disease in pregnant women (2010).

Interestingly, Bashutski
and others (Figure 7, J
Dent Res 2011;
90(8):1007-12) performed
a clinical trial with
patients who either had
low serum Vitamin D
levels or high levels. For
these patients they
performed flap surgery for
pocket reduction and
noted that patients with
sufficient serum Vitamin D
levels had consistently
lower pocket depths after
surgery and greater
attachment gain
compared to patients with
Vitamin D insufficiency.
So, it might be useful to
supplement patients
undergoing periodontal
surgery with Vitamin D if
Vitamin D levels are
suspected to be low.
Figure 7. Vitamin D improves outcomes after periodontal pocket reduction
surgery in Vitamin D – deficient patients.
Periodontal disease parameters in the months following flap surgery on
Vitamin D-deficient patients who either received placebo or Vitamin D
containing supplements.

Vitamin E
Vitamin E is a group of 8 lipid-soluble chemicals called tocopherols, and their main function is to be
scavenger molecules that prevent oxidative damage to cell membranes.
The dietary reference intake is 15 milligram, and it can be found in nuts, seeds and whole grains, as well
as spinach.
Vitamin E deficiency is rare, but it may produce ataxia, meaning the inability to walk, and peripheral
neuropathy.
There is no toxicity syndrome, but there have been case reports of patients who took mega doses of
vitamin E and having bleeding complications. Through some mechanism, vitamin E seems to interfere
with clotting mechanisms (Dowd D & Zheng ZB 1995).
The relationship of Vitamin E and periodontal disease is unclear, since a study showed a slight
association of serum Vitamin E to attachment loss (Iwasaki M et al. 2012), but other studies did not
show a relationship or improved treatment outcome with vitamin E deficiency (Carvalhorde S et al.
2013; Slade EW Jr et al. 1976; Cohen RE et al. 1991)
Vitamin K
The last fat-soluble vitamin, Vitamin K, is an important cofactor for enzymatic carboxylation of glutamic
acid residues. As such it is required for synthesis clotting factors II, VII, IX and X, and it is also required
for bone proteins suchas osteonectin and bone-matrix gla proteins.
The dietary reference intake is 120 microgram for men, and 90 microgram for women, and it is mainly
found in dark green leafy vegetables such as spinach, romaine lettuce and broccoli. Intestinal bacteria
also produce a significant amount of vitamin K.
As you would expect, vitamin K deficiency results in a hypocoagulative state similar to that induced by
Coumadin or Warfarin, and reduced bone mineral density.
Vitamin K toxicity is rare, but can occur in infants who received vitamin K injections after birth and who
get vitamin K-supplemented formula after birth. Similarly, patients who receive regular injections of
Vitamin K might get this condition. In this case, jaundice develops from hemolytic anemia, producing too
much bilirubin that discolors the skin.
There is no known effect of Vitamin K on periodontal disease.

Water-soluble Vitamins
The water-soluble vitamins are either part of the B complex or vitamin C. As water-soluble vitamins,
they all have fairly low toxicity as the body tends to excrete excess vitamins in urine. However, because
of the same property, water soluble vitamins usually are not stored in the body, and deficiency states
are more common. All vitamin B complex vitamins are associated with some metabolic function. The
term vitamin contains “amin” since many B complex vitamins contain carbon-nitrogen bonds like the
chemical class of amines.
Vitamin B 1 (Thiamine)
Thiamine is typical of the vitamin B complex that it contains these chemical structures and is involved in
metabolism and energy production. The dietary reference intake is 1.1 to 1.2 milligram per day, and it is
found in a variety of foods ranging from fortified breakfast cereal to meats and orange juice.
Alcoholics or patients with gastric bypass surgery and inadequate dietary counseling may experience
Beriberi deficiency. Beriberi disease got its name from a Sinhalese word meaning “extreme weakness”,
and may date back to times when unfortified white rice was a staple food and meat rare, causing
thiamine deficiency. There are two varieties of this disease: One is dry beriberi, where there is a gradual
degeneration of peripheral nerves and muscles in legs and arms, causing weakness and eventual
inability to support oneself. The more acute version of the disease, wet beriberi, there is edema as a
result of cardiac insufficiency. Onset of symptoms can be quite fast within a week or so of a diet lacking
thiamine, but recovery depends on the type of symptoms encountered. Cardiac symptoms tend to
improve quickly with thiamine supplementation, whereas nerves take much longer to recover, of if
severe, will never recover.
In alcoholics, thiamine deficiency may also be associated with Wernicke-Korsakoff Syndrome that
produces slowing of conscious movement, nystagmus, ataxia, and eventually loss of consciousness and
death. In some, it can also cause mental confusion, dysphonia, meaning blurred and unintelligent
speech, and confabulation, or the making up of events and stories.

Vitamin B complex may be associated with periodontal health as some B-vitamins were associated with
longer retained teeth in elderly Japanese (Yoshihara A et al. 2005), and a small randomized clinical trial
by Neiva and others (Table 3, Journal of Periodontics 2005) with patients undergoing pocket reduction
surgery showed s a small improvement in attachment level if the patients had taken vitamin b complex
supplements. Best improvement was observed with deep pockets, where almost an additional
millimeter of attachment gain was observed.
Vitamin B 2 (Riboflavin)
Riboflavin, or Vitamin B2, functions as electron recipient during energy production, and is needed 1.3
milligrams per day. It can be found in milk, fortified breakfast cereals and any animal products.
There is no known deficiency state or toxic state, or any effect known on periodontal health. It has been
suggested in some textbooks that riboflavin deficiency may result in glossitis, angular cheilosis and
stomatitis, but I could not find any case reports supporting this statement.
Vitamin B 3 (Niacin)
Niacin, or Vitamin B 3, is involved in a multitude of metabolic processes, and plays a role in fat and
energy metabolism. The dietary reference intake value is 14 to 16 milligrams per day, and again found in
fortified breakfast cereal. It is also found in a variety of other foods such as beets, yeast, organ meat,
fish, seeds and nuts. The body can also synthesize small amounts from tryptophan, as the similar
chemical structure suggests.
As with thiamine, the main risk factor from deficiency in this country is alcohol abuse. Niacin deficiency
results in a condition called Pellagra (Figure 8), which produces the following signs, referred to as the “4
Ds”, in the sequence they occur with increasing severity of the niacin deficiency: Dermatitis, Diarrhea,
Dementia and Death.
Table 3: Vitamin B complex supplementation improves outcome after periodontal flap surgery
(Neiva BL et al. 2005)
Parameter Group Baseline 90 days 180 days Change
PD Vit-B 3.98+-0.57 2.47+-0.16 2.41+-0.23 -1.57+-0.34
Placebo 4.32+-0.56 2.50+-0.30 2.82+-0.35 -1.50+-0.21
CAL Vit-B 4.03+-0.94 3.86+-0.80 3.62+-0.82 +0.41+-0.12*
Placebo 4.07+-1.14 4.33+-1.22 4.59+-1.39 -0.52+-0.23
Both groups significantly improved after periodontal flap surgery; however the group receiving
Vitamin B supplementation had significant gain of attachment compared to the placebo group.

Uncommon for water-soluble vitamins, niacin exhibits some
toxicity at doses of 0.7 to 1.6 grams, which is only attainable by
ingesting niacin supplements. As niacin has cholesterol lowering
properties, some patients used it as a “natural” anti-cholesterol
drug, and ended up with toxicity, mostly involving a flushed and
itchy skin. At extreme doses, it can induce nausea and liver
damage.
Vitamin B 4 (Choline)
Choline was once called vitamin B4, but is not essential.
The daily reference intake for choline is about 550 milligrams per
day, and as part of phosphatidylcholine it is an important structural component of cell membranes.
Phosphatidylcholine, which is the major component of lecithin, is also part of an important membrane
lipid cell signaling system performing numerous tasks. It also plays an important role in transmission of
nerve impulses, methyl transfers, lipid transport and metabolism.
Choline is found in fatty foods such as milk, egg, liver and peanuts.
Choline deficiency is rare in healthy humans since normal diet usually contains some choline, and the
majority of needed choline can be synthesized in the body. In patients unable to eat, choline deficiency
may appear and cause fatty liver and hyperlipidemia, demonstrating its role in lipid metabolism.
The upper intake limit appears to be about 3.5 milligrams per day, and there is no known effect on
periodontal disease.
Vitamin B 5 (Pantothenic Acid)
Vitamin B5, or much more commonly called Pantothenic acid, is a component of co enzyme A, and thus
responsible for synthesis and breakdown of fats, cholesterol, steroid hormones, acetylcholine and
melatonin. Co-enzyme A is also involved in maintaining the citric acid cycle for energy production.
The dietary reference intake value is 5 milligram per day in adults, and it is found in many foods.
As it is found in many foods, deficiency is rare, possibly producing paresthesia and dysesthesia in feet.
There is no known toxicity syndrome. In a cross-sectional study of older Japanese, persons with low
levels of pantothenic acid had more periodontal disease (Yoshihara A et al. 2005)
Figure 8. Sharply Delineated
dermatitis on sun-exposed skin (from
Robbins & Coltran Pathologic Basis of
Disease, 7th
edition)

Vitamin B 6
Vitamin B6 is a group of similar chemicals involved in many metabolic reactions ranging from nucleic
acid synthesis to amino acid synthesis and lipid metabolism. The dietary reference intake is 1.7 milligram
per day, and again it can be found in many foods such as nuts, fortified breakfast cereal, fish and
poultry, bananas and spinach.
Vitamin B6 deficiency is rare, but may result in seizures. On the other hand, Vitamin B6 also has nervous
system toxicity at very high doses in excess of 200 milligram per day.
Again, as with several other B complex vitamins, vitamin B6 deficiency may be associated with
periodontal disease. (Yoshihara A et al. 2005)
Vitamin B 7 (Biotin)
Biotin, or rarely called vitamin B7, is needed for carboxylase enzymes to function. It also is needed for
energy storage and production, leucine metabolism, metabolism of odd chain fatty acids and
biotinylation of histones where it controls DNA transcription and replication
The dietary reference intake value is small at 30 microgram per day, and it is found in many foods. Gut
bacteria may also synthetize it.
Since it is found in many foods, deficiency is rare, but it is speculated to involve hair loss, a scaly red rash
and various neurologic symptoms such as hallucination and paresthesia.
There is no known toxic level, and no association with periodontal disease.
Vitamin B 8 (Inositol)
Inositol, or Vitamin B8, is not known to have deficiency or toxic states, and some users take grams of
this substance for support against anxiety disorders. It is widely found in foods and there is no known
periodontal or oral health effect of this vitamin.
Vitamin B 9 (Folic acid, Folate)
Folic acid, or folacin and rarely called vitamin b9, is required for thymidine synthesis and amino acid
metabolism. The dietary reference intake is 400 micrograms per day, and it can be found in fortified
cereals, poultry, fish, spinach, beans and many other foods.
Since folic acid is quickly destroyed by heat, cooked food contains low levels of folic acid. In adults,
severe folic acid deficiency will result in megaloblastic anemia. Folic acid is critical in early neuronal
development, and is given to pregnant women to prevent neural tube defects such as spina bifida.

There is no known toxicity.
Folic acid may be protective for periodontal disease, as Dr. Yu YH and others (2007) noticed in NHANES
data that adults with low levels of serum folate will have higher levels of periodontitis. Similarly, Staudte
and others (2012) noted that for a small sample of German individuals.
Interestingly, two small randomized clinical trials demonstrated that folic acid supplementation reduced
phenytoin- induced overgrowth in children (Arya R et al. 2011; Brown RS et al. 1991)
Vitamin B 10 & B 11
Vitamin b10, which is more widely known as para-amino benzoic acid, and vitamin b11, which is salicylic
acid, are not recognized as vitamins by the USDA, but used as dietary supplements as shown here. There
is no known need or toxicity, but some alternative medicine sources suggest these being useful for a
variety of conditions. Salicylic acid is related to acetylsalicylic acid, or aspirin, and also has similar effects
on pain, fever and platelets. 6% Salicylic acid is most commonly used in cosmetic and anti-dandruff
products as it exfoliates skin and kills skin bacteria. It is also used as food preservative in small amounts.
Dietary supplement sites list salicylic acid as not having toxic effects, but that is incorrect as high doses
of salicylic acid in excess of 150 mg/kg cause metabolic acidosis.
Vitamin B 12 (Cyanocobalamin)
Vitamin B12 or cyanocobalamin is involved in one carbon unit transfers, and essential to regenerate folic
acid during thymidine synthesis. The daily recommended intake is 2.4 microgram per day for adults,
with older adults needing more.
It is only found in animal sources, and is the one supplement that vegans must take in order to avoid
megaloblastic anemia.
During pernicious anemia, Vitamin B12 uptake is impaired as the cells making intrinsic factor required
for Vitamin B12 uptake are destroyed during an autoimmune reaction. As consequence, Vitamin B12
deficiency is the result, which leads to development of megaloblastic anemia, and it may also produce
numbness, ataxia and death depending on the severity of the condition. The is no known toxicity and no
known effect on periodontal disease
Vitamin C (Ascorbic acid)
Vitamin C is ascorbic acid, and its main function is to help hydroxylation of proline and lysine for collagen
synthesis. It also is an energy source for neutrophils and macrophages, and is found in vegetables and
fruits such as citrus fruits.

Deficiency is rare, but possible with a diet poor in fresh vegetables and fruits. The classic deficiency
syndrome of vitamin C is scurvy, which produces muscle weakness, lethargy, diffuse tissue bleeding and
bruises, painful and swollen joints, gingivitis and loosening of teeth. Rebound scurvy can happen in
patients who regularly take large doses of vitamin C and suddenly stop taking it.
Vitamin C insufficiency might also be associated with unusually severe periodontitis.
Toxicity is expected at a level greater than 1 gram a day, and probably results in kidney stones.
Surprisingly, the evidence linking vitamin c to periodontal health is quite weak, as all studies only show
small differences and are limited to either animal studies or cross-sectional studies. (Nishida et al. 2000;
Tomofuji et al. 2006; Iwasaki M et al. 2012; Staudte H et al. 2012)
There is no compelling evidence at this point that vitamin c mega doses improve immune function.

Micronutrients – Electrolytes and Others
Besides vitamins, there are a number of minerals that are
essential to life. Some minerals are needed in large quantities,
whereas some other minerals are needed only in trace
amounts.
Sodium
Sodium ion is the most common positively charged ion in
extracellular fluid, and is a key electrolyte involved in fluid
retention and nerve conduction. The optimum intake is 0.5 to
2.4 grams per day, depending on perspiration, but the average
intake for most adults is higher than that. Sodium ions are
found in any food, but of course concentrated in salt, canned
vegetables and other processed foods.
Deficiency is rare, but can happen as a result of dehydration or
excessive water consumption, diarrhea or vomiting, and
produces a medical emergency called hyponatremia. Major
electrolyte imbalances such as hyponatremia usually start with
headaches, progresses to confusion, seizures and ultimately
death.
There is no known toxic syndrome, but excess intake of sodium
ions has been associated with hypertension.
There is no known effect on periodontal disease, also warm salt
water rinses can help healing after surgery.
Potassium
Potassium ion is the most common positively charged ion inside
of cells, and has similar functions like sodium, but INSIDE cells.
Potassium levels are associated with decreased blood pressure
and stroke risk.
There is no recommended amount, but is estimated that 1.6 to 3.5 gram per day is adequate. Potassium
ions are found in most foods, but particularly in foods such as oranges, prunes, bananas, strawberries,
watermelons, mushrooms, leafy vegetables and most types of meat.
Potassium deficiency is rare, but can be caused by loop diuretics. Hypokalemia is another medical
emergency, manifesting itself with muscle cramps, confusion, cardiac arrhythmia and death.
LEARNING
OBJECTIVES
- RECALL FUNCTIONS OF
MAJOR ELECTROLYTES
RECALL DEFICIENCY AND
TOXIC STATES OF MAJOR
ELECTROLYTES
- RECALLEVIDENCE LINKING
ELECTROLYTES WITH
PERIODONTAL DISEASE
- RECALL ROLE OF SULFUR
AND PHOSPHOROUS
- RECALL ROLE OF IRON IN
METABOLISM
- RECALL ROLE OF ZINC IN
METABOLISM AND
DEFICIENCIES
- RECALL HALIDE
DEFICIENCIES AND SOURCES
OF THESE IONS
- RECALL OPTIMUM WATER
FLUORIDATION LEVEL
- RECALL THE ROLE OF
SELENIDE, COPPER,
CHROMIUM, MANGANESE
AND MOLYBDENUM IONS IN
METABOLISM
- RECALL TRACE MINERALS
THAT MAY HAVE A
BENEFICIAL EFFECT ON
PERIODONTAL DISEASE

Toxicity is rare, but excess serum potassium can happen as result of extensive tissue damage or
Addisons disease, in which case nausea, bradycardia or cardiac arrhythmia could result from this
condition.
There is no known effect on periodontal disease.
Magnesium
Magnesium is the second most common positive ion inside cells, and it is involved in energy transfers
and enzyme function. Dietary reference intake is 420 mg, and it is found in many foods.
Hypomagnesemia can occur in alcoholics and frequently in ICU patients, with more than half possibly
affected. Hypomagnesemia will result in cardiac arrhythmia, disorientation, combativeness, psychosis,
ataxia, vertigo and ultimately death.
The role of magnesium in heart physiology is exemplified by the fact that a severe, life-threatening form
of polymorphic ventricular tachycardia called “torsade de pointes” can sometimes be reversed with an
infusion of a large amount of magnesium salts.
Hypermagnesemia is rare, and usually caused by renal failure, lithium therapy or Addison disease. The
consequences of hypermagnesemia are muscle weakness, loss of tendon reflexes and bradycardia.
There several cross-sectional studies of small patient populations that shown an association of
magnesium with periodontal health (Meisel et al. 2005; Tanaka K et al. 2006; Staudte H et al. 2012)
Calcium
Calcium ion is the primary positive ion of hard tissue mineralization, and involved in muscle contraction.
The dietary reference intake is 1.3 grams/day, and it can be found in dairy, calcium-enriched foods,
canned fish and various vegetables such as soybeans and collard greens.
As with all electrolytes, calcium deficiency can be life threatening if severe, and calcium insufficiency is a
risk for osteoporosis.
It is important to know that calcium supplements and dairy products can interfere with absorption of
many drugs such as tetracyclines, vitamins and ciprofloxacin. Excess intake of calcium can result in
nausea and constipation.
As calcium is related to bone metabolism, several studies have investigated a possible role in
periodontal disease. Unfortunately, the evidence is inconclusive, as an older study Uhrborn E and
Jacobson L (1984) did not show any effect of calcium supplementation. Newer studies do seem to show
an association between calcium and periodontal health, however the evidence is quite weak. (Krall et al.
2001; Miley et al. 2009; Adegboye AR et al. 2012)

The highest level of evidence of a role for Vitamin
D and calcium supplementation is a moderately
sized cohort study of about 120 patients, half of
which take Vitamin D and calcium supplements
and the other does not. In that study, Garcia and
others noted during 1 year of periodontal
maintenance that subjects who took Vitamin D and
Calcium supplements consistently had better
clinical characteristics to begin with, and had
slightly better periodontal maintenance outcome
throughout the study (Figure 9). It is unclear
though if the subjects taking these supplements
also had better eating and hygiene habits overall.
Chloride
Chloride is the major negative ion
counterbalancing potassium and hydrogen ion, and
is important for nerve and muscle function. The
Bohr effect in erythrocytes regulating hemoglobin
oxygen binding also depends on chloride ions.
Chloride ions are found in all foods, and there is no
known deficiency in adults or role in periodontal
disease.
Phosphorus
Phosphorous as phosphate and related ions are important for nucleic acid synthesis, but also as pH
buffer and for energy transfers. Phosphate ions are the major counterbalancing ions to calcium in hard
tissues, and the dietary reference intake value is 700 milligram per day.
There is no known deficiency, toxicity or role in periodontal disease.
Sulfur
Unlike the previous minerals, sulfur is found in both organic and inorganic molecules. It is part of
cysteine and methionine amino acids, and at the active sites of co-enzymes such as co-Acetyl and
Figure 9. Patients attachment levels tend to be
better if patients take Vitamin D and Calcium
supplements.
Patients received periodontal therapy and
maintenance for 1 year. Mean attachment level
was always significantly better in patients who
used Calcium/Vitamin D supplements (light blue)
compared to patients who did not (purple)

glutathione. It also is a major negatively charged ion attached to heparin and chondroitin. There is no
known deficiency syndrome or role in periodontal disease.
Patients may have allergies to sulfites or sulfonamides.
Iron
Iron has two oxidative states, with ferrous iron being the preferred ion. Ferric ion is toxic to cells. The
dietary reference intake value is 18 milligram per day for adults, and iron plays an important function in
oxygen transport in hemoglobin, and redox reactions. Red meat and red grapes are an good sources of
iron.
Iron deficiency will produce hypochromic anemia, whereas iron overdose will cause liver cirrhosis. There
is no known role in periodontal disease.
Zinc
Zinc ions are cofactors for more than fifty enzymes, and the dietary reference intake is 11 miligram/day
for adults. Zinc ions are found in most foods, and it is thought that zinc deficiency produces impaired
wound healing, mild anemia and short stature.
Given its role in wound healing, there was some interest in studying a relationship between zinc and
periodontal disease. Unfortunately, some studies show a positive association between zinc and
periodontal health (Orbak R et al. 2007; Willershausen B et al. 2011) while others don’t. (Freeland JH, et
al. 1976; Tanaka H et al. 2006)
Iodide
The only role of iodide ions is to be part of thyroid hormones, which control the rate of metabolism. The
dietary reference intake is 150 micrograms per day, and iodized salt or ocean fish are good sources for
iodine. Strangely enough, deficiency and overdose will induce goiter formation, enlargement of the
thyroid gland. There is no known role of iodine in periodontal disease.
Fluoride
Fluoride ions are needed in small amounts to support tissue mineralization, and the adequate intake
level is estimated to be 0.03 to 0.05 milligram per kilogram. Fluoride naturally occurs in sardines, grapes
and green or black teas, and can also be obtained through drinking fluoridated water, or using
fluoridated salt or infant formula.

Fluoride deficiency increases the risk of caries and osteoporosis, while levels greater than 5 mg per
kilogram will induce toxic reactions such as nausea, vomiting, diarrhea, abdominal pain and paresthesia.
As an added note, stannous fluoride has antibacterial properties.
The optimum water fluoridation level is 0.7 to 1.2 parts per million, with fluoridation levels decreasing
for hotter climates to counteract increased water consumption.
The environmental protection agency has set a maximum level of 4.0 mg/L or 4.0 parts per million for
drinking water, and it estimates that undesirable side effects such as dental fluorosis happen at levels of
2.0 parts per million and above.
Selenium
Selenium, or to be precise, selenide ions, is another micronutrient that is toxic at high amounts, but
required at low amounts. The dietary reference intake value is 55 micrograms per day for adults, and
selenide is required to maintain the glutathione peroxidase system, which protect cell and cellular
organelle membranes from oxidative damage. It is thought that a deficiency in selenide lowers
resistance to various types of stress, which the reason why some individuals take supplements
containing selenide. To this date, there is no known role in periodontal disease.
Copper
Copper, or to be precise, cuprous ion, is essential to maintaining iron ions in their biologically useful
form as ferrous ion. It is also an essential component of superoxide dismutase, which is an enzyme that
quickly inactivates superoxide radicals. The dietary reference intake is 900 micrograms each day for
adults.
Copper deficiency is rare, but may cause neutropenia and impaired bone calcification. Given the role of
copper in iron metabolism, it could also result in hypochromic anemia similar to that caused by iron
deficiency.
There are two ways in which copper toxicity can be seen. One form is the acquired form, where intake
of too much copper causes toxicity. Intake of several grams of copper salt will cause fatal hemolytic
anemia, but the more common form is a slow, chronic form of copper poisoning caused by drinking
acidic beverages or milk from copper containers. In this case, gastroenteritis will develop and early onset
liver cirrhosis.
Another possible way of copper toxicity develops as consequence of a genetic defect that causes copper
accumulation in liver and nervous tissue. In Wilson’s disease, this genetic defect causes hepatitis and
gradual deterioration of nerve function. Another sign of this disease might be a yellow discoloring of the
iris-sclera interface called Kayser-Fleischer rings.

Interestingly, Freeland and others (1976) found that out of all micronutrients, copper was the only
micronutrient with a positive correlation to periodontal disease severity, meaning that patients with
higher serum copper levels also had more periodontal disease.
Manganese
Manganese ions are needed at 2.3 milligrams per day, and they are important cofactors for a variety of
enzymes. They also play a role in bone structure development. There is no known deficiency, and
toxicity is usually associated with jobs involving manganese handling, where it can cause neurologic
symptoms similar to Wilson or Parkinson disease.
Molybdenum
Regarding deficiency, toxicity and periodontal effects, Molybdenum ions are similar to Manganese. The
dietary reference intake value is 45 micrograms per day, and is an important enzyme cofactor for
enzymes metabolizing xanthine, sulfites and aldehydes.
Chromium
Although chromium ions can be extremely toxic, the body needs a miniscule amount of chromium for
normal sugar and fat metabolism, and chromium deficiency can lead to a diabetes-like state. Clinically
more important, many medications can result in chromium insufficiency, and chromium supplements
can enhance effect of beta-blockers, corticosteroids, insulin, nicotinic acid and NSAIDs. The dietary
reference intake is 35 micrograms per day, and chromium is enriched in foods like yeast, liver, cheese
and whole grains.
Co-enzyme Q10
Co-enzyme Q10 is a popular supplement, but there is no recommended value as most human tissues
synthesize sufficient amounts of it for normal life and meats and vegetable oils contain co-enzyme Q10.
In a cohort of subjects in Denmark, the average daily intake was about 3 to 5 milligrams per day.
Co-enzyme Q10 is an important redox partner in mitochondria, and as a good redox partner, it is also a
good antioxidant. It also plays a role in acidification lysosomes, allowing breakdown of ingested material
by cells.

There is no known deficiency or toxicity, but coenzyme Q10 supplementation can decrease the
effectiveness of Warfarin or Coumadin.
There is no known effect on periodontal disease. Given its potential as antioxidant, different researchers
tried applying it topically to gingival tissues during non-surgical therapy to see if it reduces inflammation.
Unfortunately, there are no conclusive results as there either was no effect at all, or only a slight
decrease in inflammation (Hanioka T et al 1994; Hans M et al. 2012)
Lipoic Acid & L-Carnitine
Another set of popular antioxidants are lipoic acid and L-carnitine. As with coenzyme Q10, the human
body synthesizes these in sufficient amounts, and there is no known deficiency syndrome for either one.
A recent animal study showed that a combination of lipoic acid and vitamin C seemed to reduce bone
resorption somewhat in an experimental rat periodontitis model.
For L-carnitine, there is no known role in periodontal disease.
Micronutrients and Periodontics
So, in general the evidence for using dietary supplements to help with periodontal disease treatment is
rather poor (Figure 10). The best evidence we have seen is for Vitamin B complex, Vitamin D, Calcium
Zinc and Omega-3 fatty acids supplements, where small to moderate improvements in healing were
observed in a randomized clinical trial after flap surgery. However, the studies vary widely in quality, and
overall results needs to be used with caution.
Despite the historical association of Vitamin C and scurvy, we did not find any strong evidence for a role
of Vitamin C in treatment of common periodontal diseases.

LEVEL OF EVIDENCE: MICRONUTRIENT &
PERIDONTITIS PREVENTION/TREATMENT B-C
Systematic
review
Randomized
Clinical Trial
Cohort studies
Case-Control studies
Cross-sectional studies
Case reports & series
Animal studies & Benchtop experiments
Rat studies: Omega-3 FA, Vitamin C, D, E, Calcium
Omega-3/PUFA Vitamin D, Calcium
Vitamin C
Vitamin B1,B3, B5, B6
combination
Magnesium, Copper
Zinc
LEVEL OF EVIDENCE: MICRONUTRIENT &
PERIDONTITIS PREVENTION/TREATMENT B-C
Rat studies: Omega-3 FA, Vitamin C, D, E, Calcium
Figure 10. Evidence grade for the use of micronutrients to prevent periodontal disease or
enhance periodontal treatment

Dietary Counseling for Oral Health
Now that we have reviewed necessary nutrients, how does this
translate into a healthy diet that supports systemic and oral
health?
Risky Eating and Identifying Patients at Risk for
Malnutrition
We know that nutritional deficiencies and excesses can lead to
frank disease, and that even subtle nutritional insufficiencies
may result in suboptimal tissue functions such as impaired
immunity. If tissues are not functioning properly, you will have
signs and symptoms of disease, and that has been recognized
widely by many cultures and across the ages, even though it
may have lacked scientific rationale.
As there are many ways of achieving minimal nutritional
requirements while satisfying individual and cultural tastes,
there are many ways and ideas of healthy eating.
Recommendations of dietary intake values in this presentation
stem from the U.S. Department of Agriculture’s best scientific
attempt of coming up with nutrition amounts, which also has
been popularized by different food pyramids published over the last decades.
People also look for nutritional guidance to communities that have historically achieved longevity with
low rates of chronic diseases. Examples of these would be the Mediterranean diet with a focus on
unsaturated fatty oils, citrus, vegetables and lean protein sources such as fish and aged cheeses.
Another example is the diet practiced by Okinawans, again with a focus on vegetables and fish as a lean
source of protein.
Partly of ethical, but also physical and spiritual health reasons, vegetarian diets derived from European
and Indian cuisines have attracted a large following, again with a focus on vegetables and non-meat
based sources of protein.
Beyond these there are countless other diets and fads that people follow, in search of good nutritional
advice.
Now, the goal of a dentist is not write new nutrition guide books, or to prescribe a certain diet. You are
not being trained to be registered, licensed dietitians. However, your have three roles when it comes to
nutrition. First, your task is to spot dental patients who also might have nutritional deficiencies, and
refer them to a physician for further evaluation and referral to a dietitian. This is similar to instances
where you identify undiagnosed medical conditions and refer patients for further medical evaluation.
LEARNING
OBJECTIVES
- RECALL CHARACTERISTICS
OF A HEALTHY DIET
- IDENTIFY ROADBLOCKS
THAT PREVENT HEALTHY
EATING GIVEN A CASE
- IDENTIFY PATIENTS AT RISK
FOR MALNUTRITION GIVEN
A CASE
- IDENTIFY SIGNS OF
MALNUTRITION
- DIFFERENTIATE BETWEEN
FOOD DIARIES AND
QUESTIONAIRES
- RECOGNIZE WHEN TO REFER
TO A PHYSICIAN / DIETITIAN
GIVEN A CASE ADVISE A
PATIENT ON NUTRITION FOR
ORAL HEALTH

The second role you have as a dentist is to identify patients where their oral condition is caused or
worsened by nutritional habits, and counsel them on nutrition in order to treat their oral condition. This
is similar to a patient who smokes and who complaints about discolored teeth, where you might provide
tobacco cessation counseling. Lastly, as a health care professional you should promote a healthy lifestyle
that reduces the risk of disease. For that reason you should exemplify and advise patient on healthy
living, and that includes maintaining a healthy diet.
So, what constitutes a healthy diet? In general, healthy diets feature the following characteristics: First,
caloric intake is appropriate for the individual activity level. So you would not recommend a diet
restricted to 500 calories to a construction worker lifting heavy loads all day.
Second, healthy diets tend to include a variety of foods. The all-you-can-eat bacon diet probably is not
that good for you, and probably as bad the all you have is broccoli diet.
Third, healthy diets tend to contain a large proportion of plant-derived foods, which supply most
essential fatty acids, vitamins, caloric value and volume.
Fourth, healthy diets often contain a small amount of lean meat, eggs or fish for a good supply of
essential amino acids and certain vitamins. It is possible to eliminate meat from a diet if one wishes to
do so, but you most likely will have to supplement your diet with various types of dairy, or intelligent
combinations of various beans, grains and vitamin supplements.
Lastly, healthy diets contain little added sugars, salt, alcohol, trans-fats and saturated fats.
As you can see, a healthy diet is not so much about eliminating foods from your diet, but changing the
proportions of your diet.
But why is eating right hard to do?
Typical road blocks to a healthy diet include the following:
Not enough time – the best, healthiest meal is the one you cook fresh for yourself as you are in charge
of the ingredients, and since it is freshly made, it is more likely to contain sensitive nutrients. But making
your own meals can take time, and not everyone can cook. Therefore, the temptation is eating out or
going through the drive-thru, where meals are often pre-cooked, and where meals are loaded with salt
and fat to entice your ancient hunger for calories.
Expense – making your own food may be more expensive as it involves utensils and buying groceries.
Also, high quality foods such as lean meat, certain dairy products and fresh fruit can be pricey depending
where you live. However, in the long run it is cheaper as you eliminate the cost of someone preparing
your food, and unprocessed foods cost less per pound.
Lack of access – in many neighbor hoods there may not be a grocer who has fresh vegetables or meats.

Habit/culture can also work against you. If your culture developed a cuisine that was meant to ensure
survival of individuals working hard out in the fields, but your lifestyle now is that of an office drone
working your finger muscles as main activity, your diet will turn you into a 500 lb bag of lard in no time.
Poverty can prevent you from eating healthy in more than one way. Of course, if you have no money
you cannot buy the food you want. You tend to live in a poorer area where groceries are scarce, and
there won’t be a farmers market selling the freshest organic carrot. You may not have a car, or a car that
only sporadically runs, and you cannot get to a place that sells food. You may not have a kitchen or
utensils to make food since you cannot afford a place that has these things. You may be sicker than
other people which limits your energy to seek out food and prepare it. In any way, being poor sucks in
more way than one, and eating right is not your greatest worry, but survival is.
Not knowing much will also hold you back, as it may feed into poverty, and it may prevent you from
realizing that living of TV dinners may not be that good for you.
Lastly, recreational drugs may suppress your urge to feed yourself, but may also trigger eating binges, or
supply your body with empty calories through alcohol. Either way, you are not going to get the foods
you need.
You can distill these roadblocks into warning signs that a patient in a dental office may be at risk for
malnutrition. From the medical history, the following might warrant further consideration:
= Significant chronic medical conditions putting the patient in a American Society of Anesthesiology Risk
Category greater than two: The reason for this if you have a severe chronic medical condition, you may
be too tired to seek out and prepare your own food.
= Recent unexplained weight gain/loss. This indicates an imbalance of caloric intake versus metabolic
need. It simply may indicate a change in lifestyle, and nutrition has not kept up with, or it might also
indicate onset of an undiagnosed medical condition such as diabetes , or even cancer.
= Pregnant adolescents: Pregnant women experience an increased need of nutrients to support the
developing fetus, but adolescents may suppress their hunger in order to hide a potentially unwanted
pregnancy.
= Disability. As explained before, disability may limit your ability to seek out food due to lack of money,
transportation or energy.
= Alcohol and drug abuse as mentioned before.
= History of increased frequency of colds/infections. Often the immune system is weakened through
nutritional deficiencies, causing more frequent infections.
You may also see the following signs and symptoms that may suggest nutritional deficiency during the
evaluation of a patient:

If a patient complains that their dental condition prevents them from eating, malnutrition is likely.
Unusually severe periodontal disease may also be linked to nutritional deficiency, especially if the
disease is in proportionate to plaque levels, lacks obvious systemic and local etiologic factors, and does
not favor any particular area.
Lingual tooth erosions that cannot be explained other than being caused by eating disorders may also
suggest a higher risk of malnutrition.
Unkempt appearance may indicate an inability to care for oneself, including an inability to feed oneself.
Poverty in the form that a patient has no money for simple, inexpensive dental procedures may also
indicate money for food is tight.
Transportation issues for dental appointments may also indicate a lack of transportation to food
sources.
And lastly, nutrition should be
considered in cases of
unexpectedly poor healing.
There are a couple formal
screening tools one can use.
Posner BM and others (Figure
11, 1993) published this
screening tool that is intended
for older adults who live
independently. Depending on
how many “yes” answers you
get, the higher the risk.
Figure 11. Posner’s Nutrition Screening Initiative Checklist

For patients in nursing homes or those who are incapacitated, Rubenstein Z et al. 2001and others also
published this assessment that relies more on signs than symptoms of nutrition (Figure 12). A low score
here points to malnutrition.
On the other side of the spectrum, malnutrition is a concern in adolescents. For this purpose, another
tool checks for risky nutritional habits (California Department of Public Health Nutritional Risk Screening
Tool, 2000; see Figure 13).
Figure 12. Mini-nutritional assessment short form (MNA-SF, by Rubenstein Z et al. 2001)
If the screening score is less than 12 points, malnutrition should be considered.
Figure 13. The CA DoPH Nutritional Risk Screening Tool (2000)

Analyzing a Patient’s Diet & Suggesting Changes
So you identified a patient at risk for malnutrition. How do you find out what their nutritional challenge
is?
If you suspect an eating disorder based on dental findings or using one of the screening tools, don’t
waste time and refer to a medical provider for further referral. Taking care of these things is outside of
your scope of practice, and insurance will not cover a dietitian unless prescribed by a physician.
If you identify a “moderate risk” patient using the screening tools, you should educate the patient about
nutrition, oral health and overall health, and consider investigating the issue further with diaries or
questionnaires, and see if you can suggest changes in their diet. Depending on severity, you still may
want to refer the patient to a physician if there are any systemic signs of malnutrition
If the patient is low risk, encourage maintaining current habits and provide information to the patient as
you see fit and your patient requests it.
There are two ways of checking a patient’s diet. One is by the use of diary where the patient keeps a
detailed record of all foods, snacks and drinks, recording time and amounts. For homemade or specialty
foods, patients may have to count ingredients. If it is processed food or fast food by a major chain,
recording the brand and name of the meal can allow you looking up nutrition information.
Have the patient do this for 3 to 7 days, and you have a highly diagnostic tool that may also educate the
patient on nutritional changes he or she has.
Unlike the prospective diary, questionnaires are retrospective, and can be be obtained preprinted from
places like the California Department of Public Health, where the patient just checks of what they eat.
This is easily interpreted using the USDA food pyramid, but the patient may not remember everything
they ate.
Once you obtain this data, you now analyze it and recommend changes if needed
If the patient has a high snacking frequency, you either get a high caries risk with starchy, sticky, sugary
foods and an added obesity risk if foods are fatty, starchy or sugary.
If the patient drinks a lot of acidic beverages like soda, there is a caries and tooth erosion risk
Excess meat, fat, sweets, cereal intake may lead to obesity risk and the associated risks of obesity such
as type 2 diabetes mellitus, cardiovascular disease and periodontal disease.
Vitamin deficiencies are likely if the fruit/vegetable count is low, and poor wound healing and
exaggerated periodontal disease may happen during therapy.
Low dairy count may increase osteoporosis risk unless there is calcium supplementation or other foods
containing calcium such as tofu. With osteoporosis, there is also an increased risk of periodontal
attachment loss.

Low meat/poultry/fish count may indicate a risk for protein and iron deficiency, which could lead to
poor wound healing.
Once you identify risk areas, you best present this in a motivational interview technique (Figure 14,
Miller and Rollnick 2012). Essentially in this process, you go through four stages: Engaging, Focusing,
Evoking and Planning. Engaging a patient is critical as in this step you establish trust and a working
relationship with a patient as further counseling steps will not be successful without it. Often than not,
the engaging step will already have occurred prior to nutritional counseling during the initial dental visit.
The next step, focusing, may also have been accomplished already in some patients, as now the
question becomes what goals the patient has, and if your goals differ from that of the patient. The
important aspect is that it should feel at this point that you and your patient can work together to
achieve your patient’s goals such as “better teeth”, “healthier gums”, “better healing” or “better
appearance”. In a third step, you should find out what motivates the patient to change, and if there is
any intrinsic factor that a patient possesses which could drive change. In this evoking step, you need to
be careful not to lecture a patient about diet, or to pull a patient into accepting any diet changes.
Change has to come from the patient and not from you. In the last step, you want to facilitate a
patient’s own plan for nutritional change by offering needed information and support. In this planning
stage, you have to be careful not to prescribe changes, and you should step back to allow a patient to
come up with his or her own solutions. This is important as diet changes are much more likely to happen
if there is an intrinsic motivator. In contrast, you trying to badger patients into accepting nutrition
changes likely will cause a reaction, and you are more likely to lose this patient as the door for change
slams shut.
Figure 14. Analysis and Motivational Interviewing
1. Identify malnourished patients and refer to physician for physical
evaluation and referral to dietitian
2. Gather Information on Food Intake and Activity Level for about 5 days
a. Diary (Prospective)
b. Questionnaire (Retrospective)
3. Review Food Intake
a. Meets minimum levels of macro & micronutrients?
b. Adequate calorie intake; Appropriate for activity level?
c. Diabetes/Cardiovascular disease risk
d. Caries risk
4. Motivational Interviewing:
a. Engaging
b. Focusing
c. Evoking
d. Planning

References:
Adegboye AR et al. (2012) Intake of dairy products in relation to periodontitis in older Danish adults.
Nutrients 4:1219-29
Akman S et al. (2013) Therapeutic effects of alpha lipoic acid and vitamin C on alveolar bone resorption
after experimental periodontitis in rats: a biochemical, histochemical, and stereologic study J Perio
84:666-74
Arya R et al. Folic acid supplementation prevents phenytoin-induced gingival overgrowth in children.
Neurology 76:1338-43
Asherio A et al. (1999) trans Fatty acids and coronary heart disease. N Engl J Med 340:1994-8
Assev S et al. Further studies on the growth inhibition of some oral bacteria by xylitol. Acta Pathol
Microbiol Immunol Scand B 91:261-5
Bahutski JD et al. (2011) The Impact of Vitamin D Status on Periodontal Surgery Outcomes. J Dent Res
90:1007-12
Bendyk A et al. (2009). Effect of dietary omega-3 polyunsaturated fatty acids on experimental
periodontitis in the mouse. J Periodontal Res: 44:211-6
Boggess KA et al. (2010). Vitamin D status and periodontal disease among pregnant women. J Perio
82:195-200
BM Posner et al. (1993). Nutrition and Health Risks in the Elderly: The Nutrition Screening Initiative. Am J
Public Health 83: 972-978
Brown RS et al. (1991). The administration of folic acid to institutionalized epileptic adults with
phenytoin-induced gingival hyperplasia. A double blind randomized placebo-controlled parallel study.
Oral Surg Oral Med Oral Path 71:565-8
Burt BA et al. (1988). The Effects on Sugars Intake and Frequency of Ingestion on Dental Caries
Increment in a Three-Year Longitudinal Study. J Dent Res 67:1422-29
Carvalho Rde S (2013). Vitamin E does not prevent bone loss and induced anxiety in rats with ligature-
induced periodontitis. Arch Oral Biol 58:50-8
Chaffee BW & Weston SJ (2010). Association between chronic periodontal disease and obesity: A
systemic Review and Meta-analysis. J Perio 81:1708-24
Cohen RE et al. (1991) Effect of vitamin E gel, placebo gel and chlorhexidine on periodontal disease. Clin
Prev Dent 13:20-4
Darveau RP et al. (2012). Porphyromonas gingivalis as a potential community activist for disease. J Dent
Res 91:816-20

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