1 / 70

Integrating Preventive Oral Health Measures Into HealthCare Practice

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

Download Presentation

Integrating Preventive Oral Health Measures Into HealthCare Practice

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.


Presentation Transcript

  1. Integrating Preventive Oral Health Measures Into HealthCare Practice A Discussion of Oral Disease Department of Health and Family Services, Division of Public Health

  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

  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

  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.

  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.

  6. Eruption Patterns

  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

  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

  9. Anatomy of a Tooth • Enamel • Dentin • Cementoenamel junction • Cementum • Vascular supply • Nerve • Soft tissue • Periodontal ligament

  10. Dental Caries Process • Host -Tooth • Agent - Bacteria • Environment - pH • Time - Frequency

  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

  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

  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

  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.

  15. Dental Caries Process: Etiology • Time • Length of time • Frequency

  16. Recurring Dental Decay • White spot lesion Decay

  17. Super Eruption

  18. Dental Caries Along the Gum Line

  19. Dental Caries

  20. Maternal Dental Caries Risk Assessment Checklist See Training Manual Tab 1 Maternal Dental Caries Risk Assessment

  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

  22. Generalized Acute Marginal Gingivitis Plaque Inflammation

  23. Physiologic Changes During Pregnancy that Affect Oral Health • Esophageal reflux and vomitus may cause tooth erosion • Pregnancy granuloma (pregnancy tumor)

  24. Pregnancy Granuloma

  25. Pregnancy Granuloma

  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.

  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.

  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.

  29. Periodontal Diseases • Gingivitis: is limited to the gingival tissues • Periodontitis: infects the periodontal ligament and the underlying bone.

  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.

  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.

  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

  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.

  34. Gingivitis

  35. Healthy Gingiva Pink healthy tissue

  36. Inflamed Gingiva Red, edematous tissue

  37. Healthy Gingiva Pink, healthy tissue

  38. Plaque and Calculus (tartar)

  39. Plaque and Calculus

  40. Plaque and Calculus

  41. Post Oral Prophylaxis

  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.

  43. Women's Oral Health and Periodontal Disease • Menopause and Osteoporosis • Human Immunodeficiency Virus Infection • Cardiovascular Disease • Pregnancy

  44. Maternal Periodontal Disease Risk Assessment Checklist See Training Manual Tab 1 Maternal Periodontal Disease Risk Assessment

  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

  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

  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

  48. Adult Basic Screening Form See Training Manual: TAB 1

  49. Adult Screening Form 1 1 1 0 1 1

  50. Adult Screening Form 1. Edentulous 2. Untreated Caries 3. Treatment Urgency 4. Periodontal Disease Risk Factors or Signs of Inflammation Present

More Related