You Are What You Eat: Nutrition and Periodontal Health

Crest

+ Oral-B

at dentalcare.com

Course Author(s): Maria L. Geisinger, DDS, MS

CE Credits: 2 hours

Intended Audience: Dentists, Dental Hygienists, Dental

Assistants, Dental Students, Dental Hygiene Students, Dental

Assisting Students

Date Course Online: Aug 3, 2023

Last Revision Date: NA

Course Expiration Date: Aug 2, 2026

Cost: Free

Method: Self-instructional

AGD Subject Code(s): 150, 490

Online Course: www.dentalcare.com/en-us/ce-courses/ce664

Disclaimer: Participants must always be aware of the hazards of using limited knowledge in integrating new techniques or procedures into their

practice. Only sound evidence-based dentistry should be used in patient therapy.

Conflict of Interest Disclosure Statement

• Dr. Geisinger reports no conflicts of interest associated with this course. She has no relevant

financial relationships to disclose.

Introduction – You Are What You Eat: Nutrition and Periodontal Health

This course seeks to review the association between micronutrient levels and periodontitis and

the underlying physiologic mechanisms of interaction between micronutrient consumption and

periodontal health or disease.

You Are What You Eat: Nutrition and

Periodontal Health

Continuing Education

Brought to you by

Crest

+ Oral-B

at dentalcare.com

Course Contents

• Overview

• Learning Objectives

• Introduction

• Systemic Inammation and Periodontal

Disease

• Nutritional Components and their Relation

to Periodontal Health and Disease

• Macronutrients

• Micronutrients

• Nutritional Counseling in the Dental Practice

• Summary

• Course Test

• References / Additional Resources

• About the Authors

Overview

Periodontitis is a chronic inflammatory disease

caused by oral microorganisms, characterized

by the loss of structures supporting the

teeth, i.e., periodontal ligament, cementum,

and alveolar bone. In the United States, the

prevalence of periodontitis among adults over

30 years of age is approximately 42% and

causes significant impact on overall and oral

quality of life.

While periodontitis is initiated

by the microorganisms and their byproducts in

dental plaque biofilm, its disease progression

is mediated by the individual host immune-

inflammatory response.

As such, periodontal

disease progression may be influenced by

many systemic and environmental risk factors,

including smoking, diabetes mellitus, alcohol

consumption, psychosocial stress, and/or sex

hormonal levels. In addition to these systemic

influences, recent findings suggest that

periodontitis is also influenced by local and/

or serum/plasma micronutrient levels. These

levels are dependent upon dietary, lifestyle

factors, and/or nutrigenetic characteristics.

The old adage,“you are what you eat“

relates to periodontal health as well.

Eating a balanced diet is critical to overall

health and an imbalance, deficit, or

overconsumption of dietary components can

lead to severe systemic and oral diseases.

Both macronutrients (protein, fats, and

carbohydrates) and micronutrients can impact

cell function, host cell immunity, and biofilm

formation and maturation. Findings suggest

that dietary consumption may influence

periodontal health and that deficiencies of both

macro- and micronutrients may play a role

in the onset or exacerbation of periodontal

diseases. This course seeks to review the

association between micronutrient levels and

periodontitis and their underlying physiologic

mechanisms.

Learning Objectives

Upon completion of this course, the dental

professional should be able to:

• Discuss the role of inflammation in

periodontal disease.

• Recognize nutrient requirements for optimal

oral health.

• Understand the connection between diet/

nutrition and periodontal health.

• Assess the effects of both macro- and

micronutrient imbalance on periodontal

health status.

• Recognize the potential role of dietary

modification in periodontal therapy.

• Identify and utilize tools to counsel

and motivate patients to seek dietary

modifications.

Introduction

Dietary consumption and overall nutrition have

been associated with the development of many

health conditions, including cardiovascular

diseases, diabetes mellitus, and cancer.

Diet has been defined as the habitual eating

patterns of an individual, whereas nutrition

refers to the science of food intake and

biological processes involved in consumption

and utilization of nutrients.

4,5

Nutrients can

be categorized into macronutrients (proteins,

carbohydrates, lipids), micronutrients (minerals,

vitamins), and water.

Overall caloric intake

as well as macronutrient consumption have

been associated with oral and overall health

status.

3,5

Further, approximately 10% of the

US population is thought to have at least one

clinically significant nutritional deficiency.

The most common deficiencies identified in

US individuals include: Vitamin B, Iron, and

Vitamin D.

It is also well-established that oral

health status can impact the types of foods that

individuals consume. Compromised oral health

is associated with a marked decrease in whole

food consumption and an increase in processed

food consumption.

Such changes in diet have

Crest

+ Oral-B

at dentalcare.com

the potential to impact both oral and systemic

health. Given the impact of diet and on overall

health and oral health, oral healthcare providers

should strive to understand the interaction

between nutritional intake and periodontal

health.

Systemic Inflammation and Periodontal

Disease

Periodontal diseases are both infectious and

inflammatory diseases of the supporting

structures around the teeth: the gingiva,

periodontal ligament, alveolar bone, and

cementum.

2,9,10

The two most common forms

of periodontal disease are gingivitis and

periodontitis.

Gingivitis is a non-specific

inflammatory reaction to the accumulation of

dysbiotic bacterial biofilm.

All individuals are

susceptible to developing gingivitis after oral

hygiene procedures are stopped. Gingivitis is

also a necessary precursor to periodontitis and,

ultimately, a loss of hard and soft tissues around

the teeth.

Removal of biofilm and local etiologic

factors results in the reversal of gingivitis

symptoms and resolution of local and systemic

levels of inflammatory markers is associated

with reestablishment of gingival health.

11-13

Periodontitis is initiated by dysbiotic biofilm

accumulation in a susceptible host and

this biofilm dysbiosis triggers an immune-

inflammatory response that then leads to the

destruction of hard and soft tissues supporting

the teeth.

14-15

Periodontal disease progression

is generally slow to moderate. Average

clinical progression of periodontal disease

is approximately 0.1mm of attachment loss

and 0.2 teeth lost annually.

In longitudinal

investigations, groups with the fastest

and slowest disease progression differed

considerably with regard to demographics and

underlying health conditions.

In an updated

classification system from the American

Academy of Periodontology (AAP) and European

Federation of Periodontology (EFP), individuals

with periodontitis are classified with a Stage and

Grade, which are meant to capture both the

current state of disease severity and distribution

and risk of future disease progression based

upon the history of diease progression and

patient-level risk factors.

15,17

Periodontitis Stages

I-IV are assigned based upon patients’ current

clinical presentation of periodontitis, including

attachment loss, alveolar bone levels, and

tooth loss, and the Stage may be modified by

case complexity and need for multidisciplinary

care.

15,17

In order to describe the risk of future

disease progression, Periodontitis Grades A-C

are determined based upon individualized

patient risk factors (i.e. smoking status and

glycemic control) and direct and/or indirect

evidence of disease progression, including the

calculation of alveolar bone loss/age.

15,17

The

prevalence of periodontitis has been estimated

to be over 42% of U.S. adults over 30 years of

age.

Of those individuals, 7.8% were found to

have severe periodontitis.

Severe periodontitis

was also most prevalent among US adults

65 years or older, Mexican Americans, non-

Hispanic blacks, and current heavy (>10

cigarettes daily) smokers.

Among US adults,

periodontitis prevalence is nearly 4-fold greater

than that of diabetes mellitus

and over 6-fold

greater than that of coronary artery disease,

making it extremely common within the

population. Periodontal disease progression

and destruction of both hard and soft tissues

occurs through host-mediated inflammatory

pathways,

which may vary based upon

genetic and environmental risk factors,

potentially including nutritional factors.

2,20-23

It should also be noted that a number of

systemic diseases that are influenced by diet

and nutritional intake, including diabetes

mellitus, cardiovascular disease, and obesity

have been associated with periodontal disease

development or progression.

24-26

The process of periodontal tissue destruction

is mediated by pro-inflammatory cytokines

and mediators such as interleukin-1ß (IL-1ß),

interleukin-6 (IL-6), tumor necrosis factor-α

(TNF-α), prostaglandin E2 (PGE2), receptor

activator of nuclear factor kappa B ligand

(RANKL), and matrix metalloproteinases

(MMPs).

2,9,10

These pro-inflammatory

mediators drive the activation of osteoclastic

functions and lead to alveolar bone loss. The

heterogeneity of the immune-inflammatory

response among individuals can influence

disease susceptibility and severity.

Additionally,

periodontal disease severity is correlated to

increased levels of pro-inflammatory mediators

systemically.

27-30

Because dietary intake can

Crest

+ Oral-B

at dentalcare.com

Macronutrients

Macronutrients required for optimal human

processes include protein, carbohydrates, and

lipids. Current recommendations allow for more

flexibility based upon individualized dietary

needs and suggest that adults consume 45% to

65% of their total calories from carbohydrates,

20% to 35% from fat, and 10% to 35% from

protein.

37,38

Protein is the most common non-

water substance in the body, making up 50% of

dry weight of humans.

31,32

In the periodontium,

proteins are present as structural proteins, such

as collagen, and enzymes.

31,32

When proteins

are consumed, they are subsequently broken

down into the component amino acids.

31,32

Overall, 22 amino acids are required for protein

synthesis and nine are considered essential

amino acids (i.e. histidine, isoleucine, leucine,

lysine, methionine, phenylalanine, threonine,

tryptophan, and valine).

31,32

Major dietary

sources for dietary protein are milk, meat,

eggs, and legumes.

31,32

Carbohydrates are used

primarily as a source of energy and also aid

in fat metabolism.

31,32

In periodontal tissues,

carbohydrates are found as glycoproteins

and glycosaminoglycans, which are required

for the synthesis of the ground substances of

connective tissues such as chondroitin, keratin,

make a significant impact on systemic levels

of inflammation, nutrition has the potential to

influence the progression of periodontitis.

Nutritional Components and their

Relation to Periodontal Health and

Disease

It is well-established that carbohydrate

substrate and cariogenic bacteria are the

causative agents for dental caries. The

role of diet and nutritional consumption

on periodontal health are less well-

defined. Nutrients are generally classified

as macronutrients or micronutrients and

delineated by the amount consumed in a

typical diet.

31,32

Macronutrients are consumed

in gram quantities and include protein,

carbohydrates, and lipids.

31,32

Conversely,

micronutrients are required in the diet in

milligram or even microgram quantities and

include vitamins and minerals.

31,32

Humans also

require adequate consumption of water for

health and optimal functioning.

31,32

A variety

of nutrients have been identified as having a

major impact on periodontal health.

33-36

will discuss the impacts of macronutrients and

select micronutrients on periodontal health

and disease (Figure 1).

Figure 1. Macronutrients in common foods.

Crest

+ Oral-B

at dentalcare.com

Analysis of the National Health and

Nutrition Examination Survey (NHANES) data

demonstrated a positive association between

low fat intake (<23.2% of total caloric intake)

and periodontal disease progression.

However, the nature of the fat consumed is

also a significant consideration for the impact

on periodontal health.

A diet high in anti-

inflammatory omega-3 fatty acids and/or with

a favorable omega-3 to omega-6 fatty acid

ratio has been demonstrated to promote

periodontal health.

43,44,52

Conversely, high

dietary consumption of saturated fatty acids or

an unfavorable omega-3 to omega-6 fatty acid

ratios can promote increased inflammation

and a progression of the inflammatory process

in periodontal disease.

43,44,52,53

Micronutrients

Micronutrients consist of vitamins, minerals

and trace elements. While micronutrients do

not have energy value, they are essential for

many biological processes including those that

promote periodontal health and/or disease.

Figure 2 summarizes micronutrients associated

with oral health.

Vitamin A Complex

Beta-carotene, the naturally occurring pigment

responsible for red, orange, and yellow colors

in many fruits and vegetables, is a precursor

to vitamin A, also known as retinol. Beta-

carotene can act as a scavenging antioxidant

to destroy free radicals and may also promote

increased integrity of epithelial cells and

cell-to-cell attachments.

Considering the

antioxidant function of beta-carotene, it has

been studied to determine the association

between periodontitis and beta-carotene

with findings suggesting that increased

beta-carotene consumption was associated

with decreased periodontitis prevalence.

Further, beta carotene has been associated

with improved healing in nonsmokers after

nonsurgical therapy, including greater

reductions in probing depth.

These findings

suggest that consumption of beta-carotene

may improve antioxidant capacity and may

significantly improve periodontal health.

Beta-

carotene deficiency is also associated with

increased periodontitis prevalence and gingival

bleeding.

dermatan sulfates.

31,32

Glucose is also required

for erythrocyte and neurological functioning.

31,32

Lipids provide energy, energy storage, and

thermal insulation.

31,32

Humans require two

essential fatty acids: linoleic and linolenic

acid.

31,32

Fats are also required for the absorption

of fat-soluable vitamins (i.e. Vitamins A, D, E, and

K).

31,32

When used for energy, 1 gram of protein

or carbohydrates provide 4 kilocalories (kcal) of

energy whereas 1 gram of lipid provides 9kcal of

energy.

31,32

An overall excess in calorie consumption

can result in several adverse outcomes,

including insulin resistance, excess glucose

production, and increased adiposity.

39,40

When

caloric intake exceeds overall energy needs,

metabolic pathways are activated to induce

insulin metabolism and lipoprotein synthesis

in the liver and, ultimately, increases in free

fatty acids and a decrease in lipolysis, which—

when sustained—can result in increased

adiposity.

As adipose tissue deposits increase,

a concomitant increase in pro-inflammatory

cytokine production and, further, an increase in

the production in reactive oxygen species (ROS)

and markers of systemic inflammation, like

C-reactive protein.

High levels of carbohydrate consumption

(defined as > 45% of total caloric intake) have

been associated with an increased periodontal

disease prevalence and increased gingival

inflammation.

41-43

Gingival inflammation and

risk of periodontal disease progression was

also reduced when carbohydrate consumption

was restricted.

It is also important to note

that refined carbohydrates (e.g. sugars) and

other carbohydrates (fiber and sugar alcohols)

have divergent effects on periodontal health.

Excessive consumption of refined carbohydrates

promote increased microbial dysbiosis and,

thus, periodontal disease progression.

44,45

Free

sugars also act on cells in the periodontal

ligament inducing apoptosis and decreasing

proliferation.

Conversely, fiber and sugar

alcohols (e.g. xylitol) may have a protective

effect on the periodontium.

42,47-49

Xylitol has been

shown to demonstrate an antimicrobial effect

on periodontal pathogens like Porphrymonas

gingivalis (P.g.) and Aggregatibacter

actinomycetemcomitans (A.a.).

47-49

Crest

+ Oral-B

at dentalcare.com

Vitamin C/Ascorbic acid

Vitamin C has long been known to be

associated with gingival health. This

association between vitamin C and oral health

was first described in the scientific literature

in what has been called the first randomized

controlled trial.

This study identified a lack

of vitamin C consumption as the causative

deficiency for scurvy in British sailors.

Scurvy, which is now known to be extreme

vitamin C deficiency, was a frequent ailment

amongst sailors who lacked access to vitamin

C-containing foods during long voyages at

sea. Due to scurvy’s association with severe

gingival bleeding and tooth mobility, vitamin C

deficiency has been postulated to play a role in

gingivitis. A well-balanced nutrient-rich 7-day

diet that omitted vitamin C, resulted in no

changes in plaque index or probing depths but

increased bleeding on probing was noted.

has been established that vitamin C enhances

collagen synthesis and protects against

tissue damage by scavenging reactive oxygen

species (ROS).

Studies have demonstrated

an inverse relationship between periodontal

disease prevalence and serum vitamin C

concentrations and this relationship is more

pronounced in individuals with more severe

forms of periodontal disease and in never-

smokers.

Additionally, consumption of whole

food sources of vitamin C (e.g., grapefruit) for

two weeks in vitamin C deficient individuals

resulted in increased plasma vitamin C levels

and improved sulcular bleeding scores.

Vitamin C may also blunt the cytotoxic

effects of Porphyromonas gingivalis on human

gingival fibroblasts in vitro.

59-61

These findings

suggest that dietary vitamin C consumption

may play an important role in promoting

improved periodontal health and outcomes of

periodontal therapy.

Vitamin E

Vitamin E (tocopherol) is a fat-soluble vitamin

that has been identified as a key extracellular

antioxidant and has been suggested to

improve periodontal treatment outcomes.

Dietary sources include: poultry, meat, fish,

nuts, seeds, and cereal grains.

Serum

levels of saturated vitamin E, are negatively

associated with clinical signs of periodontal

disease including: probing depths and overall

assessment of periodontal disease severity.

Dietary supplementation with vitamin E results

Figure 2. Micronutrient sources and recommended daily intake.

Crest

+ Oral-B

at dentalcare.com

vitamin D in regulation of plasma calcium and

phosphorus levels for bone metabolism has

long been established, it is also essential for

cell development, neuromuscular functions,

and inflammatory system modulation.

Vitamin D has also been found to inhibit pro-

inflammatory cytokines and T-lymphocyte

proliferation.

Vitamin D is unique among the

vitamins discussed in this course in that rather

than naturally occurring in dietary sources,

sunlight exposure is the most common source

of vitamin D.

Vitamin D and Vit-D Receptor

complex interact with receptor activator

of nuclear factor Kappa-B ligand (RANKL)

expression and downregulate osteoprotegerin

(OPG), thereby increasing differentiation and

activation of osteoclasts and consequently

bone resorption.

When vitamin D levels

become low, parathyroid hormone indirectly

stimulates bone resorption in order to increase

vitamin D levels, so increased vitamin D intake

may reduce bone resorption.

Despite its

role in mineral absorption and metabolism,

equivocal study results have not established a

definitive association between dietary vitamin

D deficiency and periodontal health and/

or post-treatment periodontal healing in the

general population.

Local administration,

however, of vitamin D has demonstrated

enhanced bone turnover in clinical scenarios.

For example, dental implants coated with

vitamin D3 have demonstrated enhanced

osseointegration

and intraperitoneal

injections of vitamin D3 have been shown to

accelerate orthodontic tooth movement.

70,71

It should be noted that co-supplementation

of calcium and vitamin D has demonstrated a

positive effect on the outcomes of periodontal

therapy

and in two studies of dietary

consumpution in a Danish population, higher

intake of dairy products high in calcium and

vitamin D has been associated with decreaed

periodontal disease severity.

73,74

Minerals and Trace Elements

Balanced levels of minerals and trace elements

are essential for optimal host immune

responses and may preventing progression

of chronic conditions such as periodontitis.

32,55

Iron (Fe++) is the most abundant essential trace

element with many functions in the human

in a reduction of bleeding upon probing and

periodontal inflammation.

After nonsurgical

periodontal therapy, increased dietary

intake of vitamins A, B, C, E combined with

with omega-3-fatty acid intake resulted in

improved healing in nonsmokers but not in

smokers when compared to those who did

not take supplements.

These preliminary

findings may indicate a role for vitamin E

supplementation during the periodontal

treatment to enhance periodontal outcomes,

particularly in some patient populations.

Vitamin B Complex

The vitamin B complex refers to eight water-

soluble vitamins, which together perform

functions essential to the body including

cell metabolism, repair, and proliferation.

These vitamins include thiamine (B1),

riboflavin (B2), niacin (B3) pantothenic

acid (B5), pyridoxine (B6), biotin (B7 or B8),

folate (B9), and cobalamin (B12).

Vitamin

B complex deficiencies demonstrate a

range of symptoms from dermatititis to

paresthesia and include oral manifestations

such as angular cheilitis and glossitis.

Vitamins in the B complex may also play

a role in periodontal disease progression

and severity. B2, B3, B6, B12 deficiencies

have been linked to hemorrhagic gingivitis

and periodontitis.

These vitamins support

healthy immune functions by strengthening

epithelial barriers and cellular and

humoral immune responses.

Vitamin B

complex supplementation is associated

with statistically significantly higher mean

clinical attachment gain at shallow and

deep periodontal pockets after periodontal

therapy.

While heterogeneity exists in clinical

investigations, the direct effect of these

micronutrients may be influenced by other

factors like age and smoking status, which

can obscure results.

Additional research to

assess the role of the Vitamin B-complex and

periodontal health is needed.

Vitamin D and Calcium

Vitamin D is required for a number of

essential functions of the human body,

including it role in the enhanced resorption

of minerals including calcium, magnesium,

iron, phosphate and zinc.

While the role of

Crest

+ Oral-B

at dentalcare.com

Eating Assessment for Participants (short

version) (REAP-S) can be utilized chairside

to assess a patients’ nutritional intake and

may be particularly informative in assessing

the overall impact of macronutrients on

oral health (Figure 3).

80,81

More targeted

assessments and/or laboratory testing may

be recommended in patients with other

signs of micronutrient deficiencies or in high

risk individuals (e.g., Stage IV or Grade C

patients). Further, dietary recommendations

that include the consumption of more

whole food nutritional sources and less

processed foods can postiviely impact

appropriate consumption of macronutrients

and micronutrients. The current findings

also suggest that a diet that includes lower

proportions of refined carbohydrates,

including more carbohydrates from whole

food sources and fiber, higher levels of

omega-3 fatty acids, high in casein and whey

proteins, and an inclusion of foods with

antioxidant properties may promote more

optimal periodontal health.

Summary

Healthy dietary habits, including avoiding

a caloric surplus, may be beneficial to

oral and systemic health. Further, specific

macronutrients and micronutrients may

enhance periodontal health and healing.

Periodontal diseases are microbially-induced

diseases that are propagated by host-

mediated inflammation that results in disease

progression and loss of periodontal tissues.

The interaction between nutritional intake and

the overall host inflammatory state may allow

for improved outcomes with modification

of dietary intake. In some instances,

dietary changes and/or vitamin or mineral

supplementation may improve outcomes for

patients with periodontal diseases.

body and is found primarily in blood.

Iron

is also required for the synthesis of enzymes

and plays a role in the innate and adaptive

immune responses.

32,75

The recommended daily

allowance for iron varies with age and sex with

highest levels recommended for women of

reproductive age.

While direct evidence linking

iron deficiencies to periodontitis development

is scant, inflammation from periodontitis may

result in increased pro-inflammatory cytokines,

which then may suppress erythropoiesis in

bone marrow and lead to periodontal disease

progression.

32,76

Other essential trace minerals, including

selenium (Se), magnesium (Mg), zinc (Zn),

and copper (Cu), have antioxidant enzymes

that can aid in neutralizing ROS and prevent

tissue damage. They also play important roles

in regulating immune function and wound

healing.

In particularly vulnerable patient

populations, adequate levels of these minerals

may be crtically important. For example,

zinc has been identified as a potential factor

in preventing diabetes-related periodontal

disease progression.

78,79

Therefore, achieving

ideal levels of these micronutrient minerals

may be a critical component in periodontal

care.

Nutritional Counseling in the Dental

Practice

Dental healthcare professionals have long

established that nutritional counseling for

caries prevention is a critical part of our

preventative mission. However, emerging

data suggest that the role of nutrition in the

development, disease progression, and healing

potential after periodontal therapy may be

significant and should be considered in a

dietary analysis to develop a risk assessment

for all oral diseases. Tools such as the Rapid

Crest

+ Oral-B

at dentalcare.com

Figure 3. REAPS (Rapid Eating Assessment for Participants – shortened version)80,81 version)

80,81

Crest

+ Oral-B

at dentalcare.com

Course Test Preview

To receive Continuing Education credit for this course, you must complete the online test. Please

go to: www.dentalcare.com/en-us/ce-courses/ce664/test

1. Approximately _______ of U.S. adults over 30 years old suffer from periodontal disease.

A. 24%

B. 38%

C. 42%

D. 65%

2. It is estimated that approximately _______ of the US population has at least one clinically

significant nutritional deficiency.

A. 1%

B. 5%

C. 10%

D. 50%

3. In longitudinal studies the average tooth loss due to periodontal disease is approximately

____ teeth lost annually.

A. 0.2

B. 0.5

C. 1.0

D. 2.0

4. All of the following are pro-inflammatory cytokines involved in periodontal tissue

destruction EXCEPT one, which is the exception?

A. interleukin-1ß (IL-1ß)

B. interleukin-6 (IL-6)

C. tumor necrosis factor-α (TNF-α)

D. interleukin-4 (IL-4)

5. Consider the following two statements:

Nutrients are generally classified as macronutrients or micronutrients and delineated by

the amount consumed in a typical diet.

Micronutrients are required in the diet in gram quantities and include vitamins and

minerals.

A. Both statements are true

B. The first statement is true, the second statement is false

C. The first statement is false, the second statement is true

D. Both statements are false

6. All of the following are macronutrients EXCEPT one, which is the exception?

A. Proteins

B. Carbohydrates

C. Water

D. Lipids

Crest

+ Oral-B

at dentalcare.com

7. Protein is the most common non-water substance in the body, making up ________ of dry

weight of humans.

A. 20%

B. 35%

C. 50%

D. 75%

8. How many amino acids are considered essential?

A. Six

B. Nine

C. Fifteen

D. Twenty-two

9. When used for energy, 1 gram of protein or carbohydrates provide 4kcal of energy

whereas 1 gram of lipid provides _______ kcal of energy.

A. 5

B. 7

C. 9

D. 12

10. Which sugar alcohol has been shown to demonstrate an antimicrobial effect on

periodontal pathogens like Porphrymonas gingivalis (P.g.) and Aggregatibacter

actinomycetemcomitans (A.a.)?

A. Xylitol

B. Sorbitol

C. Erythritol

D. Mannitol

11. Which of the following lipids has been associated with improved periodontal health?

A. Omega-3 fatty acids

B. Omega-6 fatty acids

C. Monounsaturated fatty acids

D. Saturated fatty acids

12. When vitamin C is omitted from an otherwise well-balanced diet for 7 days, which of the

following results?

A. Decreased plaque index

B. Increased probing depths

C. Increased tooth mobility

D. Increased bleeding on probing

Crest

+ Oral-B

at dentalcare.com

13. Consider the following two statements:

Serum levels of saturated vitamin E, are associated with increased clinical signs of

periodontal disease including: probing depths and overall assessment of periodontal

disease severity.

Dietary supplementation with vitamin E results in more bleeding upon probing and

periodontal inflammation.

A. Both statements are true

B. The first statement is true, the second statement is false

C. The first statement is false, the second statement is true

D. Both statements are false

14. After periodontal therapy, supplementation with vitamin B complex results in _________

mean clinical attachment gain at shallow and deep periodontal pockets.

A. Greater

B. No difference in

C. Less

D. Inconsistent

15. Consider the following two statements:

Dental implants coated with vitamin D3 have demonstrated enhanced osseointegration.

Interperitoneal injections of vitamin D3 have been shown to accelerate orthodontic

tooth movement.

A. Both statements are true

B. The first statement is true, the second statement is false

C. The first statement is false, the second statement is true

D. Both statements are false

16. Which of the following trace elements is the most common in the human body?

A. Zinc

B. Iron

C. Selenium

D. Copper

17. Which of the following is a nutritional assessment tooth that can be used chairside in the

dental office?

A. Quick Intake Patient Review (QIPR)

B. Rapid Eating Assessment for Participants (short version) (REAP-S)

C. Nutritional Intake Measure for Dentistry (NIMD)

D. Dietary Intake Evaluation Tool (DIET)

Crest

+ Oral-B

at dentalcare.com

18. Consider the following two statements:

Nutritional assessment allows dental healthcare professionals to make targeted

recommendations for patients to promote oral and systemic wellness.

For patients at a high risk of periodontitis (e.g., Stage III or IV and/or Grade C

Periodontitis) or who present with signs of micronutrient deficiencies, advanced

laboratory testing may be warranted.

A. Both statements are true

B. The first statement is true, the second statement is false

C. The first statement is false, the second statement is true

D. Both statements are false

19. Current evidence suggests that all of the following nutritional recommendations could

have a positive influence on periodontal health EXCEPT one, which is the exception?

A. Limit refined carbohydrates

B. High casein and whey protein intake

C. Inclusion of foods with antioxidant properties

D. Higher omega-6 fatty acid intake

Crest

+ Oral-B

at dentalcare.com

References

1. Eke PI, Thornton-Evans GO, Wei L, et al. Periodontitis in US Adults: National Health and

Nutrition Examination Survey 2009-2014, J Am Dent Assoc. 2018;149(7):576-588.e6.

2. Kornman KS, Page RC, Tonetti MS. The host response to the microbial challenge in

periodontitis: assembling the players. Periodontol 2000. 1997 Jun;14:33-53.

3. Martin-Hadmas RM, Martin SA, Romonti A, Marginean CO. The effect of dietary intake

and nutritional status on anthropometric development and systemic inflammation: An

observational study. Int J Environ Res Pub Health 2021;18(11):5635.

4. Raindi D. Nutrition and Periodontal Disease. Dent Update 2016;43:66-68, 71-62.

5. Hujoel PP, Lingström P. Nutrition, dental caries and periodontal disease: a narrative review. J

Clin Periodontol 2017;44(Suppl 18):S79-s84.

6. US Department of Health and Human Services. US Department of Agriculture. 2015–2020

dietary guidelines for Americans. Skyhorse Publishing Inc., 2017. Accessed June 19, 2023.

7. US Centers for Disease Control and Prevention. Second national report on biochemical

indicators of diet and nutrition in the US population 2012. Atlanta (GA), National Center for

Environmental Health, 2012. Accessed June 19, 2023.

8. Gondivkar SH, Gadbail AR, Gondivkar RS, Sarode SC, Sarode GS, Patil S, Awan KH Nutrition and

Oral Health Disease-a-Month; 2019; 65(6): 147-154.

9. Flemmig TF. Periodontitis. Ann Periodontol 1999; 4: 32-37.

10. Page RC and Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of

current work. Lab Invest 1976; 33: 235-249.

11. Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health and gingival disease and

conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of

the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and

Conditions. J Periodontol 2018; 89(Suppl 1): S74-S84.

12. Chapple ILC, Van der Weijden F, Doerfer C, et al. Primary prevention of periodontitis:

managing gingivitis. Proceedings of the 11th European Workshop on Periodontology. J Clin

Periodontol 2015; 42(Spec Iss 16): S71-S76.

13. Mombelli A. Microbial colonization of the periodontal pocket and its significance for

periodontal therapy. Periodontol 2000. 2018 Feb;76(1):85-96. doi: 10.1111/prd.12147. Epub

2017 Nov 30.

14. AAP Glossary of Terms. Periodontitis. Accessed June 19, 2023.

15. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2

of the 2017 Workshop on the Classification of Periodontal and Peri-Implant Diseases and

Conditions. J Periodontol 2018; 89(Suppl 1): S173-S182.

16. Needleman I, Garcia R, Gkranias N, et al. Mean annual attachment, bone level, and tooth loss:

A systematic review. J Periodontol 2018; 89(Suppl): S120-S139.

17. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: Framework

and proposal of a new classification and case definition. J Periodontol 2018; 89(Suppl 1):

S159-S172.

18. Centers for Disease Control and Prevention (CDC). National Diabetes Statistics Report 2020.

Estimates of Diabetes and its Burden in the United States. Accessed June 19, 2023.

19. Centers for Disease Control and Prevention (CDC). Heart Disease Facts. Accessed June 19,

2023.

20. Löe H, Anerud A, Boysen H, Smith M. The natural history of periodontal disease in man. The

rate of periodontal destruction before 40 years of age. J Periodontol 1978; 49: 607-620.

21. Michalowicz BS, Aeppli DP, Kuba RK, et al., A twin study of genetic variation in proportional

radiographic alveolar bone height. J Dent Res 1991; 70: 1431-1435.

22. Michalowicz BS, Aeppli DP, Virag JG et al. Periodontal findings in adult twins. J Periodontol

1991; 62: 293-299.

23. Kornman K, Crane A, Wang H. The interleukine-1 genotype as a severity factor in adult

periodontal disease. J Clin Periodontol 1997; 24: 72-77.

Crest

+ Oral-B

at dentalcare.com

24. Preshaw PM, Alba AL, Herrera D, et al. Periodontitis and diabetes: A two-way relationship.

Diabetologica 2012; 10: 257-265.

25. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and cardiovascular

disease. Periodontol 2000 2013; 61:160-176.

26. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular

disease. J Periodontol 1996; 67:1123-1137.

27. Winning, L., Linden, G. Periodontitis and systemic disease. BDJ Team 2, 15163 (2015).

28. Loos BG. Systeic markers of inflammation in periodontitis. J Periodontol 2005; 76: 2106-2115.

29. Noack B, Genco RJ, Tevisan M, Grossi S, Zambon JJ, De Nardin E. Periodontal infections

contribute to elevated C-reactive protein level. J Periodontol 2005; 76: 2075-2084.

30. Loos BG, Craandiij J, Hoek FJ, Weterhin-van Dillen PME, van der Velden W. C-reactive protein

and other markers of systemic inflammation in relation to cardiovascular diseases are

elevated in periodontitis. J Periodontol 2000; 71: 1528-1534.

31. Schifferle RE. Nutrition and periodontal disease. Dent Clin N Am 2005; 49:595-610.

32. Najeeb S, Zafar MS, Khurshid Z, Zohaib S, Almas K. The role of nutrition in periodontal health:

An update. Nutrients 2016; 8:530 doi:10.3390/nu8090530

33. Ritchie CS, Kinane DF. Nutrition, inflammation and periodontal disease. Nutrition 2003;

19:475.

34. Dodington DW, Fritz PC, Sullivan PJ, Ward WE. Higher intakes of fruits and vegetables, beta-

carotine, Vitamin C, α-tocopherol, EPA, and DHA are positively associated with periodontal

healing after nonsurgical periodontal therapy in nonsmokers and smokers. J Nutr 2015;

145:2512-2519.

35. Antonoglou G, Knuuttila M, Niemela O, et al., Low serum level of 1,25(OH)2D is associated

with chronic periodontitis. J Periodontal Res 2015; 50:274-280.

36. Hujoel PP, Lingstrom P. Nutrition, dental caries and periodontal disease: a narrative review. J

Clin Periodontol 2017;44(Suppl 18):S79-S84.

37. Ryan-Harshman M, Aldoori W. New dietary reference intakes for macronutrients and fibre.

Can Fam Physician. 2006;52(2):177-179.

38. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for energy,

carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids. Washington, DC:

National Academy Press; 2002.

39. Raindi D. Nutrition and periodontal disease. Dent Update 2016;43:66-68.

40. Chapple IL. Potential mechanisms underpinning the nutritional modulation of periodontal

inflammation. J Am Dent Assoc 2009;140:178-184.

41. Feinman RD, Pogozelski WK, Astrup A, et al. Dietary carbohydrate restriction as the first

approach in diabetes management: Critical review and evidence base. Nutrition 2015; 31:1-

13.

42. Lula ECO, Ribeiro CCC, Hugo FN, Alves CMC, Silva AAm. Added sugars and periodontal

diseases in young adults: An analysis of NHANES III Am J Clin Nutr 2014; 11:1182-1187.

43. Woebler JP, Bremer K, Vach K, Konig D, Hellwig E, Ratka-Kruger P, Al-Ahmad A, Tennert C. An

oral health optimized diet can reduce gingival and periodontal inflammation in humansA

randomized controlled pilot study. BMC Oral Health 2017; 17.

44. Bosma-den Boer MM, VanWetten ML, Pruimboom L. Chronic inflammatory diseases are

stimulated by current lifestyle: How diet, stress levels, and medication prevent our body

from recovering. Nutr Metab 2012;9:32.

45. Adler CJ, Dobney K, Weyrich LS, et al. Sequencing ancient calcified dental plaque shows

changes in oral microbiota with dietary shifts of the Neolithic and industrial revolutions. Nat

Genet 2013; 45:450-455.

46. Liu J, Jiang Y, Mao J, Gu B, Liu H, Fang B. High levels of glucose induces a dose-dependent

apoptosis in human periodontal ligament fibroblasts by activating caspase-3 signaling

pathway. Appl Biochem Biotechnol 2013; 170:1458-1471.

Crest

+ Oral-B

at dentalcare.com

47. Park E, Na HS, Kim SM, Wallet S, Cha S, Chung J. Xylitol, an anticaries agent, exhibits

potentent inhibition of inflammatory responses in THP-1 derived macrophages infected with

porphyromonas gingivalis J Periodontol 2014; 85, e212-223.

48. Keukenmeester RS, Slot DE, Rosema NAM, Van Loveren C, Van der Weijden GA. Effects of

sugar-free chewing gum sweetened with Xylitol or Malitol on the development of gingivitis

and plaque: A randomized clinical trial. Int J Dent Hyg 2014; 12: 238-244.

49. Kim S, Park MH, Song YR, Na HS, Chung J. Aggregatibacter Actinomycetemcomitans-induced

AIM2 inflammasome activation is suppressed by Xylitol in Differentiated THP-1 Macrophages.

J Periodontol 2016; 87: e116-e126.

50. Forouhi NG, Krauss RM, Taubes G, Willett W. Dietary fat and cardiometabolic health:

evidence controversies, and consensus for guidance. BMJ 2018; 361:k2139.

51. Hamasaki T, Kitamura M, Kawashita Y, Ando Y, Saito T. Periodontal disease and percentage

of calories from fat using national data. J Periodont Res 2017; 52: 114-121.

52. Varela-Lopez A, Giampieri F, Bullon P, Battino M, Quiles JL. The role of lipids in the onset,

progression, and treatment of periodontal disease. A systematic review of studies in

humans. Int J Mol Sci 2016; 17, 1202.

53. Milward MR, Chapple I. The role of diet in periodontal disease Clin Dent Health 2013; 52:18-

21.

54. Martinon P, Fraticelli L, Giboreau A, Dussart C, Bourgeois D, Carrouel F. Nutrition as a key

modifiable factor for periodontitis and main chronic diseases. J Clin Med 2021; 10:197.

55. Gaur S, Agnihotri R. Trace mineral micronutrients and chronic periodontitis—a review. Biol

Trace Elem Res. 2017;176(2):225-38.

56. Dodington DW, Fritz PC, Sullivan PJ, Ward WE. Higher intakes of fruits and vegetables,

β-carotene, vitamin C, α-tocopherol, EPA, and DHA are positively associated with periodontal

healing after nonsurgical periodontal therapy in nonsmokers but not in smokers. J Nutr.

2015;145(11):2512-9.

57. Lind J. A treatise of the scurvy. In three parts. Containing an inquiry into the nature, causes,

and cure, of that disease. Together with a critical and chronological view of what has been

published on the subject. 1753. Edinburgh. Printed by Sands, Murray, and Cochran for A

Kincaid and A Donaldson.

58. Leggott PJ, Robertson PB, Rothman DL, Murray PA, Jacob RA. The effect of controlled ascorbic

acid depletion and supplementation on periodontal health. J Periodontol. 1986;57(8):480-5.

59. Haffajee AD, Socransky SS, Patel MR, Song X. Microbial complexes in subgingival plaque. J

Clin Periodontol. 1998;25(2):134-44.

60. Staudte H, Sigusch BW, Glockmann E. Grapefruit consumption improves vitamin C status in

periodontitis patients. Br Dent J. 2005;199(4):213-7.

61. Staudte H, Güntsch A, Völpel A, Sigusch BW. Vitamin C attenuates the cytotoxic effects of

Porphyromonas gingivalis on human gingival fibroblasts. Arch Oral Biol. 2010;55(1):40-5.

62. Varela-López A, Navarro-Hortal MD, Giampieri F, Bullón P, Battino M, Quiles JL. Nutraceuticals

in periodontal health: a systematic review on the role of vitamins in periodontal health

maintenance. Molecules. 2018;23(5):1226.

63. Garcia-Closas R, Berenguer A, Tormo MH, et al. Dietary sources of vitamin C, vitamin E, and

specific carotenoids in Spain. Br J Nutr 2004; 91:1005-1011.

64. Zong, G.; Scott, A.E.; Griffiths, H.R.; Zock, P.L.; Dietrich, T.; Newson, R.S. Serum alpha-

tocopherol has a nonlinear inverse association with periodontitis among US adults. J Nutr.

2015;145(5):893–899.

65. Willershausen B, Ross A, Försch M, Willershausen I, Mohaupt P, Callaway A. The influence of

micronutrients on oral and general health. Eur J Med Res. 2011;16(11):514.

66. Maggini S, Wintergerst ES, Beveridge S, Hornig DH. Selected vitamins and trace elements

support immune function by strengthening epithelial barriers and cellular and humoral

immune responses. Br J Nutr. 2007;98(S1):S29-35.

67. Neiva RF, Al-Shammari K, Nociti Jr FH, Soehren S, Wang HL. Effects of vitamin-B complex

Crest

+ Oral-B

at dentalcare.com

supplementation on periodontal wound healing. J Periodontol. 2005;76(7):1084-91.

68. Hennig BJ, Parkhill JM, Chapple IL, Heasman PA, Taylor JJ. Association of a vitamin D

receptor gene polymorphism with localized early-onset periodontal diseases. J Periodontol.

1999;70(9):1032–8.

69. Javed F, Malmstrom H, Kellesarian SV, Al-Kheraif AA, Vohra F, Romanos FE. Efficacy of Vitamin

D3 supplemetation on osseointegration of implants. Implant Dent 2016; 25:281-287.

70. Kawakami M, Takano-Yamamoto T. Local injection of 1,25-dihydroxyvitamin D3 enhanced

bone formation for tooth stabilization after experimental tooth movement in rats. J Bone

Miner Metab 2004; 22:541-546.

71. Kale S, Kocadereli I, Atilla P, Asan E. Comparison of the effects of

1,25-dihydroxycholecalciferol and prostaglandin E2 on orthodontic tooth movement. Am J

Orthod Dentofac Orthop 2004; 125:607-614.

72. Garcia MN, Hildebolt CF, Miley DD, et al. One-year effects of vitamin D and calcium

supplemnetiaon on chronic periodontitis. J Periodontol 2011; 82:25-32.

73. Adegboye AR, Christensen LB, Holm-Pedersen P, Avlund K, Coucher BJ, Heitmann BL. Intake

of dairy products in relation to periodontitis in older Danish adults. Nutrients. 2012; 4:1219-

1229.

74. Adegboye AR, Boucher BJ, Kongstad J, Fiehn N, Christensen LB, Heitmann BL.Calcium, vitamin

D, casein, and whey protein intakes and periodontitis among Danish adults Public Health

Nutr 2016; 19: 503-510.

75. Hou J,Yamada S, Kajikawa T, et al. Iron plays a key role in the cytodifferentiation of human

periodontal ligament cells. J Periodontal Res. 2014;49(2):260-267.

76. Gokhale SR, Sumanth S, Padhye AM. Evaluation of blood parameters in patients with chronic

periodontitis for signs of anemia. J Periodontol. 2010;81(8):1202-6.

77. Apon A, Kamble P. Role of trace minerals in periodontal health: a review. Clin Trials Degener

Dis. 2019;4(2):30.

78. Pushparani DS. Serum zinc and β D glucuronidase enzyme level in Type 2 diabetes mellitus

with periodontitis. Curr Diabetes Rev 2015; 11.

79. Pushparanis D. Zinc and type 2 diabetes mellitus with periodontitis—a systematic review.

Curr Diabetes Rev 2014; 20:397-401.

80. Segal-Isaacson CJ, Wylie-Rosett J, Gans KM. Validation of a short dietary assessment

questionnaire: the Rapid Eating and Activity Assessment for Particpants short version

(REAP-S). Diabetes Educ 2004; 30:774,776,778.

81. US Department of Agriculture (USDA) SNAP-Ed Connection. Accessed June 19, 2023.

Additional Resources

• No Additional Resources

Crest

+ Oral-B

at dentalcare.com

About the Authors

Maria L. Geisinger, DDS, MS

Mia L. Geisinger, DDS, MS is a Professor and Director of Advanced Education

in Periodontology in the Department of Periodontology in the University of

Alabama at Birmingham (UAB) School of Dentistry. Dr. Geisinger received

her BS in Biology from Duke University, her DDS from Columbia University

School of Dental Medicine, and her MS and Certificate in Periodontology

and Implantology from the University of Texas Health Science Center at San

Antonio. Dr. Geisinger is a Diplomate in the American Board of Periodontology

and a Fellow in the International Team for Implantology. She has served as

the President of the American Academy of Periodontology Foundation, as the

Chair of the American Dental Association’s Council on Scientific Affairs, and on multiple national

and regional organized dentistry committees. She currently serves as the AAP’s Vice President,

as a Board member for the ADA Science and Research Institute, and on numerous AAP, AADOCR

and ADA committees and task forces. She has authored over 75 peer-reviewed publications and

serves on the editorial and advisory boards of several publications. Her research interests include

periodontal and systemic disease interaction, implant dentistry in the periodontally compromised

dentition, and novel treatment strategies for oral soft and hard tissue regeneration. She lectures

nationally and internationally on topics in periodontology and oral healthcare.

Email: [email protected]