maternal oral health powerpoint presentation
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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
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
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