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 1700s 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 (1700s-early 1900s)

Caries = GANGRENE of the teeth

Diagnosis = Pain Treatment:

amputation (extraction) local debridement fillings?

Caries: A Brief History

Phase 2 (early 1900s-1970s)

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 1900s-1970s)

Refined filling technology Fillings preferred over extractions Cavity shapes driven by filling material properties

INVASIVE

Caries: A Brief History

Phase 2 (early 1900s-1970s) 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 1900s-1970s) 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

demin remin 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 demin remin 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

Signs

Medication Side Effects Stress Dehydration Salivary Gland Dysfunction Disease Hormonal Imbalance Smoking

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 Prior to extensive treatment

determine cause of problems focus future management treatment planning

Prior to Ortho procedures Risk assessment Monitor patients

Saliva Testing

CRTbuffer (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 ACP is available for over 3 to 4 HOURS

CPP-ACP

CPP-ACP in plaque

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

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
Prof.. L Walsh

High caries risk Infants & Children Expectant Mothers Orthodontics

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!