Integrating Preventive Oral Health Measures Into HealthCare Practice
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Integrating Preventive Oral Health Measures Into HealthCare Practice A Discussion of Oral Disease Department of Health and Family Services, Division of Public Health Presented by: Wisconsin Regional Oral Health Consultants Funded by : The Federal Maternal and Child Health Block Grant
Integrating Preventive Oral Health Measures Into HealthCare Practice

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Slide 1

Integrating Preventive Oral Health Measures Into HealthCare Practice

A Discussion of Oral Disease

Department of Health and

Family Services, Division of Public Health

Slide 2

Presented by:

Wisconsin Regional Oral Health Consultants

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

Slide 3

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

Slide 4

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.

Slide 5

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.

Slide 6

Eruption Patterns

Slide 7

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

Slide 8

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

Slide 9

Anatomy of a Tooth

  • Enamel

  • Dentin

  • Cementoenamel junction

  • Cementum

  • Vascular supply

  • Nerve

  • Soft tissue

  • Periodontal ligament

Slide 10

Dental Caries Process

  • Host -Tooth

  • Agent - Bacteria

  • Environment - pH

  • Time - Frequency

Slide 11

Dental Caries: Multifactorial

  • Enamel Developmental Defects

  • Lack of Fluoride

  • Early Infection

  • with Strep Mutans

  • Harmful

  • Food Behaviors

Agent

(bacteria)

Time

(frequency)

Host

(teeth)

Environment

(diet)

  • Poor Oral Hygiene

  • Access to Oral Health Services

Slide 12

Dental Caries Process: Etiology

  • Host:

    • Susceptible teeth

    • Crown (covered with enamel)

    • Pits and fissures (sealants)

    • Smooth surface

    • Root surface is not covered by enamel

Slide 13

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

Slide 14

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.

Slide 15

Dental Caries Process: Etiology

  • Time

    • Length of time

    • Frequency

Slide 16

Recurring Dental Decay

  • White spot lesion

Decay

Slide 17

Super Eruption

Slide 18

Dental Caries Along the Gum Line

Slide 19

Dental Caries

Slide 20

Maternal Dental Caries Risk Assessment Checklist

See Training Manual

Tab 1

Maternal Dental Caries Risk Assessment

Slide 21

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

Slide 22

Generalized Acute Marginal Gingivitis

Plaque

Inflammation

Slide 23

Physiologic Changes During Pregnancy that Affect Oral Health

  • Esophageal reflux and vomitus may cause tooth erosion

  • Pregnancy granuloma (pregnancy tumor)

Slide 24

Pregnancy Granuloma

Slide 25

Pregnancy Granuloma

Slide 26

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.

Slide 27

Studies

  • Jeffcoat et al. 2001

  • Jeffcoat et al. 2003

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

Slide 28

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 of

    Health and Human Services, May 2000.

Slide 29

Periodontal Diseases

  • Gingivitis: is limited to the gingival tissues

  • Periodontitis: infects the periodontal ligament and the underlying bone.

Slide 30

Periodontal Disease: Etiology

Environmental and Acquired Risk Factors

Antigens,Lipopolysaccharide

1. Microbial

Challenge

2. Host Immuno-

Inflammatory

Response

3. Connective Tissue

and Bone Metabolism

4. Clinical Signs

of Disease

Initiation and

Progression

Cytokines/Prostanoids

Antibody/PMN’s

Metalloproteins MMP’s

Innate (Genetic) Risk Factors

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.

Slide 31

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.

Slide 32

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

Slide 33

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.

Slide 34

Gingivitis

Slide 35

Healthy Gingiva

Pink healthy tissue

Slide 36

Inflamed Gingiva

Red, edematous tissue

Slide 37

Healthy Gingiva

Pink, healthy tissue

Slide 38

Plaque and Calculus (tartar)

Slide 39

Plaque and Calculus

Slide 40

Plaque and Calculus

Slide 41

Post Oral Prophylaxis

Slide 42

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.

Slide 43

Women's Oral Health and Periodontal Disease

  • Menopause and Osteoporosis

  • Human Immunodeficiency Virus Infection

  • Cardiovascular Disease

  • Pregnancy

Slide 44

Maternal Periodontal Disease Risk Assessment Checklist

See Training Manual

Tab 1

Maternal Periodontal Disease Risk Assessment

Slide 45

Innate Risk Factors

Race

Gender

Genetic Info./Inheritance

Congenital Abnormalities

Phagocyte dysfunction

Down’s Syndrome

Papillon-Lefevre Syndrome

Ehlers-Danlos Syndrome

Periodontal Disease: Risk Factors

Slide 46

Risk Factors continued

Acquired/Environmental Risk Factors

  • Poor Oral Hygiene

  • Age

  • Medications

  • Tobacco/Smoking

  • Stress

  • Acquired Immune Defects

  • Acquired Endocrine Disease

  • Acquired Inflammatory Disease

  • Nutritional Deficiencies

Slide 47

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

Slide 48

Adult Basic Screening Form

See Training Manual:

TAB 1

Slide 49

Adult Screening Form

1

1

1

0

1

1

Slide 50

Adult Screening Form

1. Edentulous

2. Untreated Caries

3. Treatment Urgency

4. Periodontal Disease Risk Factors or Signs

of Inflammation Present

Slide 51

Natural Teeth

  • 0=No natural teeth

  • 1=Has natural teeth

Slide 52

Code 1: Has Natural Teeth

Slide 53

2. Untreated Caries

  • 0=No untreated caries

  • 1=untreated caries present

Slide 54

Code 1: Untreated Caries

Slide 55

Code1: Untreated Caries

Slide 56

Code 0: No untreated caries present (staining)

Slide 57

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

Slide 58

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

Slide 59

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)

Slide 60

Code 1: Untreated Caries Present

Slide 61

Code 2: UrgentPeriodontal or Gingival Abscess

Slide 62

Code 2: Urgent Treatment Need

Slide 63

Code 1: Early Treatment Need

Slide 64

Code 0: No Obvious Problems

Slide 65

Prevention Strategies for Periodontal Disease

The goal is to prevent gingival inflammation and

increase or maintain the resistance of the host.

  • Assess risk

  • Promote optimum oral hygiene

  • Improve nutritional status

  • Promote smoking cessation

Slide 66

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

Slide 67

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.

Slide 68

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

Slide 69

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.

Slide 70

Thank You

Questions?


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