Op Exam 1 Combined

Cariology

Study of dental caries and cariogenesis

Is caries all cavity?

No — non-cavitated lesions exist

Tooth worm theory

Old belief that a worm gnawed the tooth → caries thought infectious and transmissible

Keyes triad (1963)

Tooth (host) + bacteria + sugar substrate, with TIME in the center

What did the Keyes triad leave out?

The drop in pH (acid) that causes demineralization — the new paradigm

Does the Keyes triad still hold?

Yes

Infectious/transmissible era treatment

Chemicals or excision by drilling

Current caries paradigm

Ecological and non-communicable chronic disease — not transmissible, not infectious

Does caries pass between two touching teeth?

No — not patient to patient or tooth to tooth

Definition of dental caries

A BIOFILM-MEDIATED, DIET-MODULATED process that can lead to an IMBALANCE in the cycle of DEMINERALIZATION and REMINERALIZATION causing LOCALIZED DESTRUCTION of tooth structure

Biofilm mediated

Microscopic communities of bacteria in a slimy matrix (plaque) — gives bacteria a home

Diet modulated

With sugars (degradable carbohydrates), bacteria make acid and lower pH — frequency of exposure is critical

Extended low pH =

Microbiome in DYSBIOSIS

When does demineralization start winning?

When pH drops below the CRITICAL pH

Imbalance on the seesaw

De- and remineralization always occur; caries when demineralization wins

What drives remineralization?

Fluoride (including water fluoride), saliva, Ca²⁺/PO₄³⁻

Seesaw: disease indicators

White spot lesions; restorations < 3 years; enamel lesions; caries/dentin

Seesaw: risk factors

Pathogenic bacteria; absence of saliva; destructive lifestyle habits

Seesaw: protective factors

Saliva and sealants; antibacterials; fluoride/Ca²⁺/PO₄³⁻; effective lifestyle habits; risk-based reassessment

Risk factors share one thing:

They lower pH (low saliva/xerostomia, frequent sugar, poor hygiene)

Why is saliva protective?

It neutralizes acid (low flow/xerostomia raises risk)

Coffee with milk and sugar vs coffee alone

Sipping with sugar = frequent low pH (higher risk); coffee alone lowers pH less

Truck driver sipping soda all night

High caries risk at the PATIENT level

Rotated tooth that can't be cleaned

High caries risk at the TOOTH level

Tooth death spiral

Small filling → bigger filling → 1-, 2-, 3-surface → crown → root canal → extraction → implant

Why does the death spiral happen?

The DISEASE (risk) is never addressed — only lesions are drilled and restored

CariesCare International (CCI)

Practitioner-oriented guidelines, skeleton of the module (Martignon, Br Dent J 2019)

CariesCare 4-D in order

Determine, Detect, Decide, Do

Which D starts the cycle?

DETERMINE (risk) — not Detect

Four aims of CariesCare

Prevent new caries; prevent progression; preserve tooth structure; manage caries risk

1st D: Determine

Determine patient-level (and tooth-level) caries risk

2nd D: Detect

Detect and assess caries: staging (severity) and grading (activity)

3rd D: Decide

Personalized care plan at patient and tooth level

4th D: Do

Prevention and management of cavitated and non-cavitated lesions; then cycle restarts

Why is CariesCare a cycle?

Risk and disease are dynamic — reassess and keep lowering risk (risk-based recall interval)

Center of the 4-D gear diagram

Improving health outcomes

Patient-level Decide example

Truck driver sips ice water instead of soda

Tooth-level Decide example

Class I or II filling if the lesion demands it

Why classify caries? (slide 3)

Validated criteria for practitioners (caries control/management) and for researchers/public health planners (effects/need for interventions)

Classification is also a mode of…

Communication (e.g., 'caries in the distal pit of #2, deep, active')

Staging vs grading

Staging = severity (depth). Grading = activity (progressing or not)

Three criteria for classifying caries

Location, severity, activity (+ primary vs around restoration)

Only two classification systems you're responsible for

ICDAS and ADA CCS

Classification used at TUSDM

ADA Caries Classification System (ADA CCS)

ICDAS year and basis

based on SEVERITY (not activity); used worldwide

Coronal caries sites

Pit and fissure; proximal; smooth surface

Pit and fissure caries

Occlusal surface; easiest to see visually

Smooth surface caries location

Facial or lingual, most often near the gingival line (biofilm)

Proximal caries: where and how found

Just below the contact area; bitewing radiograph (not directly visible)

Primary caries

Caries with no existing restoration

CARS

Caries around restorations and sealants (older term: secondary caries)

Why not say 'secondary caries'?

Misnomer: you can't tell if it's a second primary lesion or truly secondary; sealants included

Three detection tools in the TUSDM clinic

Visual, bitewing radiographs, fiber-optic transillumination (FOTI)

Visual exam requirements

Clean (prophy/remove biofilm), dry, good light, loupes; mirror, reflected light, air-water syringe

Why 'bitewing'?

Its angle opens up the contacts

Three ways to look at severity

Histologically, visually, radiographically

Before a visual caries exam

Remove biofilm and dry the surface (5 seconds)

ONE exception to drying the tooth

ICDAS 4 (dentin shadow) is best seen slightly WET

ADA CCS ↔ ICDAS merge

Sound = 0; Initial = 1, 2; Moderate = 3, 4; Advanced = 5, 6

ADA CCS chart colors

Sound green/white; Initial yellow; Moderate orange; Advanced red

ICDAS 0

Sound: no change in enamel translucency after 5 s air drying

Non-carious enamel defects (opacity, hypoplasia, fluorosis, DI) are coded…

SOUND (ICDAS 0) — may still need restoration

Hypoplasia (ICDAS slide definition)

Reduced localized thickness of enamel, no dentin exposed

ICDAS 1

• First visual change in enamel: nothing when wet

• white/brown opacity after 5 s drying

• limited to pit/fissure

• outer 50% of enamel

ICDAS 1 histology

Outer 50% of enamel

ICDAS 2

• Distinct visual change visible even when WET

• inner 50% of enamel to outer 1/3 of dentin

• no cavitation

ICDAS 2 histology

Inner 50% of enamel to outer 1/3 of dentin

ICDAS 1 vs 2 key question

'Can you see the white spot when it's wet, or only after you dry it?' Only after drying = 1; when wet = 2

ICDAS 3

• Localized enamel breakdown (microcavitation) with NO visible dentin and NO shadow

• middle 1/3 of dentin histologically

Microcavitation means…

Cavity just in enamel — you will not see dentin

ICDAS 4

Underlying dark shadow (grey/blue/brown) from dentin through apparently intact enamel, with or without breakdown; seen best WET; middle 1/3 dentin

ICDAS 5

Distinct cavity with visible dentin; inner 1/3 of dentin, close to pulp

ICDAS 6

Extensive distinct cavity with visible dentin (deep and wide); inner 1/3 of dentin

What separates Advanced from Moderate?

Visible dentin in a cavity (ICDAS 5–6)

ICDAS 3 vs 4

3: enamel microcavity, no shadow. 4: dentin shadow through intact enamel

Slide 28 arrow lesion answer

ICDAS 2, Initial — enamel change, no dentin shadow, no microcavitation

Radiographic: Sound

No change

Radiographic: Initial

up to outer 1/3 of dentin

Radiographic: Moderate

D2 — middle 1/3 of dentin

Radiographic: Advanced

D3 — inner 1/3 of dentin

Moderate

• shadowing + microcavitation

Advanced

• dentin clearly visible (root lesion)

Initial

• white chalky changes around grooves

Lecture 2 summary points

Classification is key to detecting, diagnosing, managing; consider caries in context of risk; tooth level: location, primary/secondary, severity, activity; ADA CCS used at TUSDM

Who gets root caries?

• Elderly with gingival recession/exposed roots

• decreased motor skills

• less saliva

• xerostomia drugs

• systemic conditions

Why is root caries increasing?

Life expectancy up — people keep teeth longer

Tooth-level root caries factors

• Recession from poor OH and attachment loss

• irregular root surface

• wide interproximal spaces protect biofilm

Where does root caries start?

Directly in DENTIN, after thin cementum is removed (e.g., traumatic brushing)

Critical pH: enamel vs dentin

Enamel 5.5; dentin 6.5

Why does root caries spread fast?

Higher critical pH, tubules, thin cementum, specific microbiota

Consequences of root caries

Sensitivity, pain, chewing difficulty → pulp inflammation, infection, tooth loss, poor nutrition/QOL

4 reasons root caries is alarming

Rapid progression; often asymptomatic; closer to pulp; harder to restore (saliva, bleeding)

Active root caries

Yellowish/slightly brown, undefined borders, soft/leathery, visible biofilm → restore

Inactive/arrested root caries

Dark brown/black, defined borders, smooth, bright, hard → monitor; restore only for esthetics

What arrests root caries?

Protective factors: better brushing, more fluoride, body reactions

Instrument to probe a suspected lesion

Rounded WHO probe (not explorer — avoids cavitating it)

CARS definition (Lecture 3)

Lesion at margins of existing restorations — just another primary lesion near a restoration/sealant

Procedural causes of CARS

Wrong matrix/wedge use, defective material placement, wrong adhesive/light-curing (marginal gaps)

Disease-level cause of CARS

Only the lesion was treated, not the patient's disease — risk stays high

CARS key statistic

8× more frequent than primary lesions in adults (esp. >50); greatest reason for restoration failure