Integrating Preventive Oral Health Measures Into HealthCare Practice

A Discussion of Oral Disease

Department of Health and Family Services, Division of Public Health

Funded by : • The Federal Maternal and Child Health Block Grant• Health Resources Services Administration

Thank you to: • Nevada State Health Division Oral Health Initiatives for

their cooperation and many resources • Nancy Rublee, RDH, CDHC CDHC Price County Oral Health Coordinator

Presented by:Wisconsin Regional Oral Health Consultants

Maternal Oral Health

Discuss the incidence, prevalence, etiology and socio-cultural factors of oral disease

Review growth, development, and function of teeth Describe oral disease processes (caries and

periodontal) Review physiologic changes during pregnancy Review the effect of oral diseases on pregnancy Explain maternal oral health risk assessments Describe oral disease prevention and health promotion

strategies

GROWTH AND DEVELOPMENT

Development of Tooth Buds• The primary teeth begin to form around the 4th

week in utero.• Mineralization begins around the fourth month of

fetal development.• The permanent teeth begin to form around the sixth

month in utero.

Sequence of Eruption

Eruption usually occurs symmetrically in each arch. Mandibular (lower) teeth generally precede the

maxillary (upper) teeth. Sequence of eruption is more important than the

timing. Premature babies and children with special health care

needs may have a delayed eruption pattern.

Eruption Patterns

Function of Healthy Teeth

Chewing and eating Speech Smiling Self-esteem Loss of function contributes to health problems,

speech impediments and loss of self-esteem

Dental CariesIncidence and Prevalence

Among 5- to 17-year-olds, dental caries is more than 5 times as common as a reported history of asthma and 7 times as common as hay fever.

Despite progress in reducing dental caries, individuals in families living below the poverty level experience more dental decay that those who are economically better off.

In addition to poverty level, the proportion of teeth affected by dental caries also varies by age and race/ethnicity.

Oral Health in America: A report of the Surgeon General, May 2000

Anatomy of a Tooth

Enamel Dentin Cementoenamel junction Cementum Vascular supply Nerve Soft tissue Periodontal ligament

Dental Caries Process

Host -Tooth

Agent - Bacteria

Environment - pH

Time - Frequency

Dental Caries: Multifactorial

Agent(bacteria)

Host(teeth)

Environment(diet)

Time•Early Infection

with Strep Mutans•Harmful

Food Behaviors

•Enamel Developmental Defects•Lack of Fluoride

•Poor Oral Hygiene•Access to Oral Health Services

(frequency)

Dental Caries Process: Etiology

Host:– Susceptible teeth– Crown (covered with enamel)– Pits and fissures (sealants)– Smooth surface– Root surface is not covered by

enamel

Dental Caries Process: Etiology

Agent– Mutans Streptococci (ms),– Lactobacilli (deep dentinal lesions)– Mutans Strep colonization occurs after the

eruption of primary teeth– Transmission – The earlier the colonization of mutans strep the

greater the risk

Dental Caries Process: Etiology

Environment• Mutans Streptococci utilize mono and

disaccharides (glucose, fructose & sucrose) during glycolosis

• Results in acid byproduct which lowers the pH • Bacteria attach to the tooth forming a plaque.• Sugar consumed as a snack between meals is

associated with a marked increase in caries.

Dental Caries Process: Etiology

Time

– Length of time

– Frequency

Recurring Dental Decay

•White spot lesionDecay

Super Eruption

Dental Caries Along the Gum Line

Dental Caries

Maternal Dental Caries Risk Assessment Checklist

See Training Manual

Tab 1

Maternal Dental Caries Risk Assessment

Physiologic Changes During Pregnancy that Affect Oral Health

Hormonal effects (mainly estrogen) may:– Increase tooth mobility– Cause Xerostomia (dry mouth) or Ptyalism

(excessive saliva)

Clinical signs of pregnancy gingivitis are:– Inflammation– Hemorrhage– Edema

Generalized Acute Marginal Gingivitis

Inflammation Plaque

Physiologic Changes During Pregnancy that Affect Oral Health

Esophageal reflux and vomitus may cause tooth erosion

Pregnancy granuloma (pregnancy tumor)

Pregnancy Granuloma

Pregnancy Granuloma

Effect of Oral Diseases on Pregnancy

Preterm, low birth weight (LBW) linked to periodontal disease

Studies: • Offenbacher et al. 1998

– Prostaglandin is an inflammatory mediator associated with labor and the inflammatory process.

– Found PGE2 significantly higher in gingival crevicular fluids of women who give birth preterm.

Studies

• Jeffcoat et al. 2001• Jeffcoat et al. 2003

Women who receive periodontal root planing and scaling are less likely to give birth prematurely.

Periodontal DiseasesIncidence and Prevalence

Among adults aged 35-44, 48 percent have gingivitis.

22 percent have destructive gum disease. Tobacco use increases the risk of periodontal

disease.

Oral Health 2000: Facts and Figures, U.S. Department ofHealth and Human Services, May 2000.

Periodontal Diseases

Gingivitis: is limited to the gingival tissues

Periodontitis: infects the periodontal ligament and the underlying bone.

Periodontal Disease: Etiology

1. Microbial Challenge

Environmental and Acquired Risk Factors

2. Host Immuno-Inflammatory

Response

3. Connective Tissueand Bone Metabolism

4. Clinical Signs of Disease

Initiation andProgression

Innate (Genetic) Risk Factors

Metalloproteins MMP’s

Antibody/PMN’s Cytokines/Prostanoids

Antigens,Lipopolysaccharide

Reprinted with permission from The Compendium of Continuing Education in Dentistry. Williams RC. Periodontal Disease: The Emergence of a New Paradigm. Compend Contin Educ Dent. 1998;19(Special Issue):4-10.

Periodontal Disease: Etiology

Microbial Challenge:– Actinobacillus actinomycetemcomitans– Porphyromonas gingivalis– Bacteroides forsythus– T. Denticola– Significantly higher quantities are found in the

mouths of women who gave birth preterm.

Host Immuno-inflammatory Response

Allows bacteria to gain access to connective tissue and blood vessels

PGE2, IL-1 and TNF released during the inflammatory process mediates bone resorption

MMP’s degrade collagenous connective tissue Leads to connective tissue destruction, bone

metabolism and signs of disease

Periodontal Disease and Heart Disease

Elevated C-reactive protein (CRP) levels increase the risk for cardiovascular disease.

Periodontal disease causes oral bacterial byproducts to enter the bloodstream and triggers the liver to make proteins such as CRP.

"Periodontal disease needs to be considered as a major contributor to increased levels of CRP by the medical community," said Dr. Steven Offenbacher.

Periodontal disease and body mass index are jointly associated with increased levels of CRP in healthy adults.

Gingivitis

Healthy Gingiva

Pink healthy tissue

Inflamed Gingiva

Red, edematous tissue

Healthy Gingiva

Pink, healthy tissue

Plaque and Calculus (tartar)

Plaque and Calculus

Plaque and Calculus

Post Oral Prophylaxis

Periodontitis: Medical Risk Relationship

Diabetes– Poorly controlled or diabetics of long duration are at

greater risk.– Accumulation of deposits known as “AGE’s” may

interfere with transport across the vessel wall, prolonging inflammation.

– Well-controlled diabetics receiving regular maintenance care are no more likely to develop periodontitis than non-diabetics.

Women's Oral Health and Periodontal Disease

Menopause and Osteoporosis

Human Immunodeficiency Virus Infection

Cardiovascular Disease

Pregnancy

Maternal Periodontal Disease Risk Assessment Checklist

See Training ManualTab 1 Maternal Periodontal Disease Risk

Assessment

Periodontal Disease: Risk Factors

Innate Risk Factors– Race– Gender– Genetic Info./Inheritance– Congenital Abnormalities– Phagocyte dysfunction– Down’s Syndrome– Papillon-Lefevre Syndrome– Ehlers-Danlos Syndrome

Acquired/Environmental Risk Factors

Risk Factors continued

•Poor Oral Hygiene

•Age

•Medications

•Tobacco/Smoking

•Stress

•Acquired Immune Defects

•Acquired Endocrine Disease

•Acquired Inflammatory Disease

•Nutritional Deficiencies

Basic Screening Survey (BSS)

• Standardized screening• Developed by the Association of State and

Territorial Dental Directors• Adults, School-Aged and Preschool Children• Used across the country in public health for data

collection• Used for Wisconsin’s Make Your Smile Count

Data Collection and Seal a Smile programs

Adult Basic Screening Form

See Training Manual: TAB 1

DEPARTMENT OF HEALTH AND FAMILY SERVICES Division of Public Health DPH 0310 (06/04)

STATE OF WISCONSIN

ADULT ORAL HEALTH SCREENING

Participation is voluntary, information collected on this form will be used for tracking treatment, and services provided to the patient and will be used only for this purpose. See instructions below. Date of Screening (mm/dd/yyyy)

Site Initials - Screener

PARTICIPATION INFORMATION Identification Number

Birth Date (mm/dd/yyyy) Age

Gender 1=Male 2= Female

Race and Ethnicity 1= White 2= African American 3= Hispanic/Latino(a) 4= Asian

5= American Indian/Alaska Native 6= Native Hawaiian/Pacific Islander 7= Multiracial 9=Unknown

Edentulous 0=No natural teeth 1=At least on natural tooth

Untreated Caries 0=No untreated cavities 1=Untreated cavities

Periodontal Disease Risk Factors or Signs of Inflammation Present 0=No risk factors or signs of inflammation 1=Periodontal risk factors or signs of inflammation present

Treatment Urgency 0=No obvious problem 1=Early dental care 2=Urgent care

Comments

Gums appear red and puffy

1

0

1

1 1

1

Adult Screening Form

1. Edentulous

2. Untreated Caries

3. Treatment Urgency

4. Periodontal Disease Risk Factors or Signs of Inflammation Present

Adult Screening Form

Natural Teeth

0=No natural teeth

1=Has natural teeth

Code 1: Has Natural Teeth

2. Untreated Caries

0=No untreated caries

1=untreated caries present

Code 1: Untreated Caries

Code1: Untreated Caries

Code 0: No untreated caries present (staining)

Staining verses Caries

GUIDELINE - area considered carious when at least 1/2 mm of enamel is lost (a hole is present)

WHEN IN DOUBT - Be conservative and use a lower classification

Code 0: No untreated caries (What else do you see?)

3. Treatment Urgency

Code 2: Urgent or emergency need for dental care (within 24 hours)– pain or infection, swelling or soft tissue ulceration of

more than 2 weeks duration– overriding accompanying signs (multiple decay)

Code 1: Early dental care is needed (within several weeks)

Code 0: No obvious problems (next regular checkup)

Code 1: Untreated Caries Present

Code 2: UrgentPeriodontal or Gingival Abscess

Code 2: Urgent Treatment Need

Code 1: Early Treatment Need

Code 0: No Obvious Problems

Prevention Strategies for Periodontal Disease

The goal is to prevent gingival inflammation andincrease or maintain the resistance of the host.

Assess risk Promote optimum oral hygiene Improve nutritional status Promote smoking cessation

Maternal Prevention Strategies

Fluoride – Assess fluoride sources– Low-dose frequent exposure to topical fluorides will

increase the resistance of the host Dental sealants Promote optimal oral hygiene Assess nutrition status

– Soda consumption

Xylitol – Research

Xylitol is a natural sugar substitute in a group of pentitol compounds containing five hydroxyl groups know as sugar alcohols.

Recent research demonstrates xylitol has anticariogenic properties.

Xylitol has been used in the United States as a sweetener in food since the 1960’s.

Xylitol

According to recent studies xylitol accumulates intracellularly in S. mutans. This inhibits the bacteria’s growth. In addition, the bacteria appears less adherent to tooth surfaces.

Trahan L, Xylitol: a review of its action on mutans streptococci and dental plaque--its clinical significance. INT Dent J 45:77-92, 1995.

Maternal use of xylitol alters the oral environment by limiting the ability of bacteria to adhere to the tooth and produce acid. Journal of Dental Research 81(6):380-386, 2002

Xylitol / Chlorhexidine

Certain studies indicate that xylitol gum in combination with other dental therapies is associated with the arrest of carious lesions.

Lynch H, Milgrom P. Xylitol and dental caries: an overview for clinicians: J Calif Dent Assoc. 2003 Mar;31(3):205-9.

Chlorhexidine rinses for two weeks followed by daily use of xylitol gum led to major reductions in S.mutans.

Hildebrandt GH, Sparks BS, Maintaining mutans streptococci suppression with xylitol chewing gum. J Am Dent Assoc 131(7):909-16,2000.

Thank You

Questions?