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Healing Dental Caries: The Minimal Intervention Approach Edmond R. Hewlett. D.D.S. Maintenance & Sustainabililty …of esthetic treatments …of oral health bbb Young, et al. J Calif Dent Assoc Oct. 2007 Young, et al. J Calif Dent Assoc Oct. 2007 Caries: The New Paradigm MEDICAL management of caries Treatment of dental caries as a disease Caries: Terminology “Caries” – from the Latin for ‘rot’ or ‘rotten’ DENTAL CARIES is a disease • PEOPLE have caries • TEETH have carious lesions Caries: Terminology “Caries” – from the Latin for ‘rot’ or ‘rotten’ DENTAL CARIES is a disease • A rotten tooth = a carious tooth • An area of rot = a carious lesion Caries: A Brief History Ancient societies • little/no enamel caries • some root caries • associated with gum recession/bone loss • progressed slowly Caries: A Brief History Ancient societies • little/no enamel caries • some root caries • associated with gum recession/bone loss • progressed slowly Caries: A Brief History The Caries Epidemic • Europe and U.S. in 1700’s • REFINED SUCROSE! • RAPID progression • Began in tooth ENAMEL • Cause was a mystery Caries: A Brief History The Caries Epidemic • Cause was a mystery! Caries: A Brief History Treatment of Caries • 3 historical phases Caries: A Brief History Phase 1 (1700’s-early 1900’s) • Caries = GANGRENE of the teeth Diagnosis = Pain Treatment: • amputation (extraction) • local debridement • fillings? Caries: A Brief History Phase 2 (early 1900’s-1970’s) • Refined filling technology • Fillings preferred over extractions • Cavity shapes driven by filling material properties INVASIVE G.V. Black Caries: A Brief History Phase 2 (early 1900’s-1970’s) • Refined filling technology • Fillings preferred over extractions • Cavity shapes driven by filling material properties INVASIVE Caries: A Brief History Phase 2 (early 1900’s-1970’s) Diagnosis = DETECTION • the earlier, the better • visual, sharp explorer, radiograph Etiology • acid-producing bacteria Prevention • plaque removal and diet Caries: A Brief History Phase 2 (early 1900’s-1970’s) Standard of Care = RESTORATION Phase 3: The Present… Caries: Our Present Understanding Caries is NOT gangrene Caries is a complex DISEASE Caries: Our Present Understanding 1. Caries is a bacterial disease • S. mutans, lactobacilli, A. viscosus • S. sobrinus • acidogenic, acid tolerant Bacteria in dentinal tubules Liquefaction of dentin caused by fusion of bacterial accumulations Caries: Our Present Understanding 2. Caries is dependant on dietary sucrose • affects thickness and chemistry of plaque Caries: Our Present Understanding 3. Caries is driven by the frequency of eating • deminremin balance Caries: Our Present Understanding 4. Caries is modified by fluoride • harder tooth structure • inhibits acid production by bacteria Caries: Our Present Understanding 4. Caries is modified by fluoride, calcium, and phosphate • harder tooth structure • inhibits acid production by bacteria Caries: Our Present Understanding 5. Caries is modified by saliva • buffering • deminremin balance • low flow = HIGH risk! Caries Management by Risk Assessment (CAMBRA) Educators Scientists Administrators Organized Dentistry Third-Parties February, 2003 March, 2003 October, 2007 November, 2007 Caries Management by Risk Assessment The Caries Imbalance Demineralization & Remineralization (Image Courtesy of Dr. Steve Steinberg) (Image Courtesy of Dr. Steve Steinberg) (Image Courtesy of Dr. Steve Steinberg) (Image Courtesy of Dr. Steve Steinberg) Caries Management by Risk Assessment 1. Caries is a bacterial disease Change the microflora topical chlorhexidine and topical fluoride Caries Management by Risk Assessment 2. Caries is dependant on dietary sucrose Reduce dietary sucrose Add Xylitol Xylitol Acts directly on bacteria Sugar alcohol Gets substituted for fructose in bacterial metabolism cycle • No acid production • Acidogenic bacteria die • Environmental shift favoring nonpathogenic bacteria • New biofilm is not as harmful Xylitol Works synergistically with other remin therapies Caries in young children – whole family should use xylitol to combat the INFECTION 6-10 g/day (6-10 servings of gum) Caries Management by Risk Assessment 3. Caries is driven by the frequency of eating Decrease the frequency of eating Caries Management by Risk Assessment 4. Caries is modified by fluoride, calcium, and phosphate Add fluoride, calcium, & phosphate Caries Management by Risk Assessment 5. Caries is modified by saliva Increase salivary flow • • mechanical stimulation/vigorous chewing changing drugs which reduce flow Caries Management by Risk Assessment Assessment Determine Risk Status • Low • Medium • High • Extreme Caries Management by Risk Assessment Clinical Protocol (specific for risk status) • • • • • • • • • Frequency of radiographs Frequency of caries recall exams Saliva test (flow rate, bacterial culture) Antimicrobials (chlorhexidine, xylitol) Behavior Modifications Fluoride (OTC, Rx, varnish) Calcium/Phosphate Sealants Restorations Caries Management by Risk Assessment Monitor • Are the non-invasive interventions working? • Adjust risk status and clinical protocol accordingly Caries Risk Assessment Form Disease Indicators Risk Factors Protective Factors Saliva Deficiency Causes Medication Side Effects Stress Dehydration Salivary Gland Dysfunction Disease Hormonal Imbalance Smoking Signs Difficulty Eating or Swallowing Tongue Sticking to the Roof of your Mouth/Cheeks Sticking to Teeth Changes in Taste Inadequate Denture Retention Increased Rate of Decay Soft Tissue trauma Saliva Testing Saliva Testing Saliva-Check® (GC America) 10 minute test • Salivary Production • Salivary Consistency • Resting Saliva pH • Stimulated Saliva Flow • Stimulated Saliva pH • Saliva Buffering Capacity Saliva Check® (GC America) When? New Patient Diagnostic Tool treatment planning Prior to extensive treatment determine cause of problems focus future management • • • Prior to Ortho procedures Risk assessment Monitor patients Saliva Testing CRT®buffer (Ivoclar) 5 minute test • Buffering capacity only Treatment: Xerostomia increased water intake (spray bottles) change medications saliva substitutes • Biotene® and Oral Balance® Lubricating gel intraorally • KY Jelly • GC Dry Mouth Gel Vaseline or Lansinoh cream on lips Treatment: Xerostomia toothpastes without additives (e.g., Biotene®) DO NOT USE lemon & glycerine swabs/toothettes (turns to alchohol) DO NOT USE alcohol containing mouthwashes Treatment: Xerostomia ACP Products Enamel Care (Arm & Hammer) Enamel Pro (Premier) Nite White ACP (Discus) Aegis products (Bosworth) • P&F sealant, C&B cement, ortho adhesive Best for pts. w/mild remin probs and high motivation Amorphous Calcium Phosphate stabilized by Casein Phosphopeptides CPP-ACP CPP-ACP 1946 - anticariogenic properties of milk were due to casein, calcium and phosphate 1981, Australia – Prof Eric Reynolds et al. at University of Melbourne: milk, milk concentrates, powders and cheeses have anticariogenic activity in animals and in situ caries models CPP-ACP 1980s-90s Casein Phosphopeptides (CPP) are responsible for the tooth-protective activity CPP can bind calcium and phosphate and keep them in a soluble, amorphous state CPP-ACP Amorphous Calcium Phosphate Free & available to be incorporated into the tooth structure CPP provides SUBSTANTIVITY to ACP CPP-ACP ACP is available for over 3 to 4 HOURS CPP-ACP in plaque CPP-ACP CPP-ACP 1980s-90s: •normally, calcium + phosphate = insoluble calcium phosphate crystals (Enamelon) •in the presence of CPP, calcium and phosphate stay in a form that can actually penetrate into the tooth enamel, work synergistically with fluoride and repair demineralized areas CPP-ACP 1990s: •patents on CPP-ACP and licensed exclusively to Recaldent P/L first sold in Japan, Australia, Europe and later in USA (Bonlac Bioscience International PTY LTD - Pfizer) CPP-ACPs 1990s-2000s – Australia and Japan GC licensed for distribution of Tooth Mousse™ via dental practices (prescription not needed in Australia) 2004 – USA MI Paste™ (GC) distribution via dental practices MI Paste Application Apply pea-size amount on finger MI Paste Indications High caries risk Infants & Children Expectant Mothers Orthodontics Prof.. L Walsh MI Paste Indications Whitening sensitivity Root exposure Chemotherapy, radiation MI Paste Plus - with Fluoride •CPP-ACP: 10% •NaF: 900 ppm* •ph: 7.2 (OTC toothpaste: 1000 ppm*) WHY ADD FLUORIDE? CPP-ACP Plus Fluoride exhibits superior anti-caries effect than Fluoride alone Designed for Patients at high risk for dental caries and dental erosion MI Paste PlusTM 5:3:1... 5/Calcium - 3/Phosphate – 1/Fluoride Prof L Walsh, GC Asia Prof L Walsh, GC Asia Prof L Walsh, GC Asia Prof L Walsh, GC Asia Incipient caries, no cavitation 6 weeks MI Paste 2 x daily Sept 2005 Nov 2005 Glass Ionomer Sealant Ultimate protection for newly- and partially-erupted molars! Resin Sealants + - Durability & Seal Partial Eruption Tech. Sensitive Static No available Fl, Ca or Phosphate - Inhibits Enamel Maturation vs. + + + + GI Sealants Durability Partial Eruption Moisture-Friendly Dynamic Fl, Ca & Phosphate are available + Enhances Enamel Maturation Minimally-Invasive Smile Enhancement Management of White Spot Lesions Image Courtesy of Dr. Steve Steinberg White Spot Carious Lesions BEFORE AFTER White Spot Carious Lesions BEFORE AFTER Mild Fluorosis Moderate Fluorosis Severe Fluorosis Enamel Hypomineralization Enamel Hypomineralization BEFORE AFTER Enamel Hypomineralization BEFORE AFTER White Spot Lesions Arrested lesion: • Check saliva • Remove sealed skin Acid etch for 60 sec Scrub with pumice and rubber cup Repeat until no more shiny surface Apply MI Paste “Oral Health Improving for Most Americans, But Tooth Decay Among Preschool Children on the Rise” -CDC news release April 30, 2007 To learn more… …visit the websites: • CDA Foundation • WCMID • Biotene • GC America • Recaldent Thank You!
