Caries management symposium

Caries risk assessment

When Presenter 17 November 2018 Laurie Walsh

Where Copyright Disclaimer © 2018 Laurie Walsh Business School University of Sydney Darlington NSW 2006 This work is copyright to Laurie Walsh

No part of this work may be reproduced except with More information the written permission of the copyright holder/s. Continuing Education in Dentistry Level 7, 2 Chalmers Street Surry Hills, NSW 2010 Phone: 02 9351 8348 Fax: 02 9351 8310 dental.ce@sydney.edu.au

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Caries risk assessmentLaurence J. Walsh AO

© 2018

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Not a simple task• Not one, but multiple pathogens

• Complex aetiology, with episodic progression

• Holistic assessment includes• Past disease history

• Site factors (tooth and oral cavity, plaque dysbiosis, salivary defence, lesion distribution)

• Patient biological factors (genetics, medical Hx)

• Lifestyle factors, family environment food selection

• SES, social disadvantage, community F

Mutans Streps.

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•Disease occurs in micro-bursts

•Caries risk can change suddenly

•Caries risk is never zero, only low

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Caries risk assessment & Mx approaches

•Malmo, Sweden• Cariogram (Douglas Bratthall,

U Malmo)

• California, USA• CAMBRA (John Featherstone

UCSF)

• USA AAPD• CAT (Caries Assessment Tool)

• Europe• ICDAS / ICCMS (Nigel Pitts,

Dundee); Dundee Caries Risk Assessment Model (DCRAM)

• Australia• CMS Caries Management

System (Evans and Dennison: USyd)

• TLM Traffic Light Matrix (H Ngo & LJW: Adl & UQ)

• STEM (UQ)

Mount GJ and Hume WR (Eds). Preservation and restoration of teeth, 2nd edition. 2005

Mike Williams (GC) 2001

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Walsh LJ. Internat Dent 2008

International Dentistry 2008;3 (1):34-48.

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Brostek AM, Walsh LJ. Minimal intervention dentistry in general practice. Oral Health and Dental Management 2014;13(2):285-294. ; Walsh LJ. Minimal intervention management of the older patient. British Dental Journal. 2017; 223(3):151-161.

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FIXED ORTHO PATIENT SJOGREN’S SYNDROME PATIENT

Bratthall D, Petersson GH. Cariogram – a multifactorial risk assessment model for amultifactorial disease. Community Dent Oral Epidemiol 2005;33: 256-264

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AAPD C.A.T.

American Academy of PediatricDentistry. Guideline on caries risk assessment and management for infants, children, and adolescents. Pediatr Dent 2010;32:101–108

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• Each instrument has been found to have limitations, particularly in the prediction of the high risk individual residing in a low caries community.

• Most studies conclude that past caries experience is still the most reliable predictor of future caries experience in children and that a clinician’s intuition or ‘gut feeling’ is often more accurate than current diagnostic technologies.

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How good are we at assessing risk accurately?

Nobody is perfect ! Low sensitivity, high specificity: as with caries Dx

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How to do better - Look beyond the teeth

PERSON

ORALCAVITY

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Patterns of past disease• Poulsen S, Horowitz HS. An evaluation of a

hierarchical method of describing the pattern of dental caries attack. Community Dent Oral Epidemiol. 1974;2(1):7-11.

Rapid breakdown of the dentition: the last survivors?

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Site distribution is informative of:

• Plaque dysbiosis in local micro-environments

• Substrate access

• Oxygen tension

• Salivary defence

• Shear force of fluids

• Effects of appliances and prostheses

Missed disease according to the methods used and the threshold applied

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Diagnostic performance of existing methods varies widely

Traditional methods often have high specificity but low sensitivity and miss early forms of the disease

More sensitive methods find greater prevalence of disease (Fluorescence, DiFOTI, ECM, OCT, etc)

DMF index vs. ICDAS/ICCMS

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Is the lesion active?

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Patient lifestyle risk factors• Fermentable CHO

• Between meals

• Consistency and retentiveness

• Acid exposure frequency

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How reliable are traditional diet charts?

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How pathogenic is the dental plaque biofilm?

• MS as a keystone pathogens (GTF role)

• Multiple other species involved

• Ecological change: Acidic pH provides selective pressure; causes biofilm dysbiosis and reduced diversity

• Co-aggregation of MS with Candida albicans

Walsh 2006

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Multiple bacteria

as well as fungi

• Mannoproteins (mannans) in the outer cell wall of Candida will bind to S. mutans in the presence of sucrose.

• GftB enzyme secreted by S mutans, synthesizes glue-like polymers (glucans).

• Candida promotes this process, resulting in a sticky biofilm that allows yeast to adhere to teeth and bind to S mutans.

• Hwang et al. PLoS Pathog. 2017 Jun 15;13(6):e1006407.

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Walsh 2007

International Dentistry 2006;1(3):4-13.

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Plaque pathogenicity varies by site

Walsh 2007

MAXILLARY LABIAL

MANDUBULAR LABIAL

Plaque pathogenicity can be changed

BASELINE

AFTER Tx 2 WEEKS

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Red = Rose BengalBlue = Acid Fast GreenSubstrate = sucrose

Tabatatee et al. 2016

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Before and after TMP for 4 weeks

Tabatatee et al. 2016

Is there value in plaque analysis?

• The addition of plaque microbiological testing to ICDAS caries scoring system seemed to significantly enhance the statistical power of the final predictive model for caries risk for preschool children at the d(3) level of lesion detection after four years. This had a sensitivity of 65% and specificity of 69%.

• Macritchie HM, Longbottom C, Robertson M, et al. Development of the Dundee Caries Risk Assessment Model (DCRAM) – risk model development using a novel application of CHAID analysis. Community Dent Oral Epidemiol 2012;40:37–45.

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Salivary properties and their influence

International Dentistry 2007;2(3):16-30

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Walsh 2001

Reduced salivary defence

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Walsh 2005

The wheel of misfortune: Plaque pathogenic features versus salivary defence

The modulating role of lifestyle factors

Putting all the pieces together !!

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