1037DOH - Oral Cariology

cariology for dental hygiene (week 4 onwards)

what is the definition of dental caries?

• localised, progressively destructive tooth disease that starts at the external surface (usually enamel) with apparent dissolution of the inorganic components by organic acids that are produced by the enzymatic action of masses of microorganisms (in bacterial plaque) on carbohydrates

key components of the definition of dental caries

• bacteria required to produce disease

• bacteria use metabolise-refined carbs

• when metabolism anaerobic, acids are produced

• acids dissolve inorganic phase of teeth

dental caries aren’t just holes in teeth. the process of bacteria fermenting foods to produce _____ and dissolving tooth mineral

acids

what are some of the acids produced by bacteria?

• lactic

• acetic

• formic

• propionic acids

dental caries is a ________ _________ disease

• transmissible bacterial disease

describe the transmission of bacteria causing dental caries from mother to child

• bacteria transferred to babies from mothers or caregivers in very early life

• colonisation of soft tissues possible before tooth eruption

• teeth erupt, cariogenic bacteria colonise surface, establish dental plaque

• cycle of destruction begins if plaque accumulates

4 factors according to the Jordan diagram to have dental caries

(BSST)

• biofilm/plaque presence

• susceptible tooth surface

• sugars (food for bacteria)

• time (to allow acid to demineralise the tooth)

• these factors without any protective factors or with multiple risk factors will result in dental caries

list some of the primary modifying factors (main influence)

• tooth anatomy

• fluoride use

• saliva

• biofilm pH and composition

• diet

• oral hygiene

• meds

• genetic factors

• immune system

list some secondary modifying factors (these modify the primary modifying factors)

• socioeconomic status

• education

• lifestyle

• environment

• age

• ethnic group

• occupation

acidogenic vs aciduric bacteria

• genic) produce acid

• uric) live in an acidic environment

the normal protection for caries on the tooth surface is regular _____ ________ ______

mechanical biofilm removal (toothbrushing and interdental cleaning)

factors on the tooth surface that influence caries position (yk like where the caries are more present on the tooth surface)

• pits/fissures

• below contact points

• cervical area of tooth

• developmental defects (grooves etc, encourages plaque accumulation and makes it harder to clean

• poor restorations (if ledges/edges, encourages plaque accumulation, inc. risk of caries developing between margin of restoration and tooth)

• iatrogenic damage (areas the dentist damaged lol)

• areas of hypomineralisation (less mineralisation, so more susceptible to damage)

mineral content ____ in different areas of teeth. substitution of ______ in tooth structure for ______ increases susceptibility of an acid attack (solubility)

• varies

• carbonate

• phosphate

fluoride applied during which two moments reduces solubility (susceptibility to acid attacks)?

• systemically before eruption

• topically after eruption

how does biofilm start and how does it evolve?

• highly organised sequence of events

• starts as initial pellicle of enzymes, glycoproteins and immunoglobulins

• turns into complex colonies of many bacteria (strep and actinomyces species)

• aciduric bacteria tend to arise later because the environment they need to live in arises later too

higher maternal salivary levels of bacteria leads to higher WHAT in the child

• salivary levels of bacteria

4 steps of plaque formation on tooth surface

1. acquired pellicle formation

2. initial adhesion of bacteria on pellicle surface

3. co-aggregation (more bacteria of different types, extracellular polysaccharides come that form the visible portion of plaque)

4. maturation and diffusion (gets thicker, saliva prevented to getting to tooth surface and areas where bulk of acid is produced)

diet and dental caries - you need a _______ substrate within the diet. what other factors do you need to consider? in the absence of the above substrate, what happens?

• need a fermentable substrate

• factors:

  • amount

  • frequency

  • how consumed (held in the mouth for how long, when consumed (with or after meal?)

  • formulation (boiled sweet vs fluid vs sticky)

  • temperature (enzymatic reaction to produce acid (metabolic process) so its rate is temp dependent, colder = slower, therefore less cariogenic than something hot)

• in the absence of a fermentable carbohydrate, caries don’t develop

elaborate on the primary modifying factors:

• tooth anatomy

• saliva

• biofilm pH

• biofilm composition

tooth anatomy

• sites that are more difficult to clean

saliva

• flow rate, buffering capacity

• natural defence against caries

biofilm pH

• directly related to thickness and amount/frequency of sugar consumed

composition

• depends on bacterial flora

• how long undisturbed

• and presence of sugars

• all these influence the development of extracellular polysaccharides (what you see clinically)

elaborate on the primary modifying factors of:

• fluoride use

• oral hygiene

fluoride use

• decreases solubility of dental hard tissue when incorporated into enamel

• antibacterial effect

oral hygiene

• acid production requires anaerobic metabolism

• needs good thickness of plaque (anaerobic respiration so it can do this)

• regular removal necessary

elaborate on the primary modifying factors of:

• immune system (affects…)

• genetic factors (affects…)

• meds/radiotherapy

immune system

• affects the number and type of microorganisms in the mouth

genetic factors

• can affect the structure of teeth and salivary function

meds/radiotherapy

• many medications (incl. side effects) reduce salivary flow

• previous radiotherapy around head and neck can damage salivary glands

• xerostomia can be part of medical syndromes

elaborate on the secondary modifying factors of:

• socioeconomic status

• age

socioeconomic status

• increasing evidence caries are more prevalent in more socio-economically deprived families

  • diet (greater reliance on processed foods)

  • oral hygiene (irregular dentist visits, or not having a toothbrush)

  • self-motivation (unemployed, feeling devalued etc)

age

• teeth more susceptible to caries shortly after eruption (before absorbing fluoride)

• old age - medication that could cause xerostomia etc, intercurrent disease

initial mineral loss affects the ________ tissue

• subsurface

describe the state of the outer and inner surfaces of a tooth during an early carious lesion

• outer surface is intact

• layer below the surface is demineralised

• thus possible to reverse this in this stage

list the caries classification by site

class 1

• pits/fissures of occlusal 1/3 of molars/premolars

• occlusal 2/3 of molars/premolars

• linguals of anterior teeth

class 2

• proximal surface of molars and premolars

• just below contact point

class 3

• proximal surfaces of central/lateral incisors

• canines (not incisal angles)

• just below contact point

class 4

• proximal including incisal angles of anterior teeth

class 5

• gingival 1/3 of facial/lingual surfaces of all teeth

• below max convexity and just above ging. margin

class 6

• cusp tip of molars/premolars + canines

• naturally cleansed areas so caries here is super bad

what is common about classes 1-5 of the caries classification sites? what about class 6?

• 1-5) all these areas are where plaque stagnation occurs as they’re not self-cleansing

• 6) normally self-cleansing so caries here indicates high caries risk (eg cusp tip caries)

what are:

• primary caries?

• recurrent (secondary) caries?

• residual caries?

primary caries

• new lesion on unrestored surfaces

secondary (recurrent) caries

• adjacent to a restoration (margin)

residual caries

• caries left under a restoration (intentionally or unintentionally)

• dentist has left some caries while treating it

• cannot be seen clinically and usually seen in a radiograph

what is pathogenesis?

• biological mechanism that leads to a diseased state

• can also be used to describe origin + development of disease

  • whether acute (quick onset), chronic (slow onset) or recurrent

what is the extended ecological plaque theory (EEPT)?

• composition of the plaque is important

• plaque adapts

  • as it matures, the species that inhabit the plaque change

• if pH is habitually acidic, plaque favours aciduric and acidogenic bacteria

  • find it easier to inhabit the plaque

the tooth surface is unique as its not protected by ____-______ _______

• self-shedding mechanisms

things like new skin, nails, hair, etc

describe the tooth habitats for cariogenic biofilm (plaque)

• pellicle ideal surface for bacterial colonisation

• undisturbed plaque rapidly builds - produce an anaerobic environment

• important to break chain early - frequent tooth cleaning (early plaque might not contribute much to caries but mature plaque much more likely to)

note about plaque

(it isnt necessarily…. but its an accumulation of…)

• it isnt necessarily food debris - could be found in patients who don’t clean often

• plaque is accumulation of extracellular polysaccharides that are produced by bacteria (product of metabolising sugars)

list 4 key components of the dental caries definition

• bacteria required to produce disease

• bacteria metabolise sugars

• when metabolism is anaerobic, acids are produced

• acids dissolve inorganic phase of the teeth (enamel)

list the first 3 steps of demineralisation

1. bacteria metabolise fermentable carbohydrates (organic acids which diffuse into the tooth structure through water between crystals)

2. acid reaches susceptible site on crystal surface, calcium and phosphate dissolve into aqueous phase between crystals

3. occurs at atomic level long before it’s visible with magnification

____________ is a natural repair process for subsurface non-cavitated carious lesions

• remineralisation

explain remineralisation

• calcium and phosphate ions diffuse into tooth structure

• attaches to and rebuilds crystal remnants (doesn’t build new ones)

  • recreate not repair

• primarily saliva-sourced and some from topical sources

• fluoride aids remineralisation process

  • absorbed into tooth structure

  • fluorapatite

• need the surface layer to be intact for this to work!

once absorbed into the crystal surface, fluoride attracts _______ and ______ ions attracted to calcium

• calcium

• phosphate

fluoride is a negatively charged ion and calcium is a positively charged ion, then the calcium attracts phosphate

role of saliva in caries

• acts as a buffer

  • neutralise extreme pH fluctuation

• calcium and phosphate in saliva inhibit dissolution (promote remineralisation)

• has antibacterial components (enzymes etc)

  • effect depends on flow rate, buffering capacity (how much, how good at neutralising acids, how long tooth bathed in it) fluoride availability and time

why is saliva nature’s anticaries agent?

• bacterial clearance

  • when you swallow you swallow the flora too which die in the stomach

• direct antibacterial activity

  • assorted enzymes produced

• buffers

• remineralisation

how much saliva do adults produce?

• around 1-1.5 litres per day

when is salivary flushing most effective?

during mastication/stimulation of flow

(as theres a greater amount of saliva produced)

is saliva part of the immune system? why or why not?

• not part of the immune system

• saliva holds no memory (no specific response to certain agents)

• non specific so washes away bacteria equally

describe what salivary enzyme amylase does (action and effect)

• breaks down sucrose, depriving bacteria of its energy source

describe the action and effect of lactoperoxidase

• action) catalyses H2O2 mediated oxidation

• effect) bactericidal. suppresses biofilm formation

describe the action and effect of lysozymes

• action) lyses cells by attacking cell walls

• effect) bactericidal. suppresses biofilm formation

describe the action and effect of lipases

• action) breaks down triglycerides

• effect) free fatty acids inhibit attachment and growth of some bacteria

describe the action and effect of lactoferrin

• action) binds free iron

• effect) inhibits growth of some iron-dependent microbes

describe the action and effect of secretory immunoglobulin (predominantly IgA)

• action) agglutination of bacteria inhibits bacterial enzymes

• effect) reduced numbers in saliva and inhibits growth

describe the action and effect of glycoproteins (mucins)

• action) agglutination of bacteria

• effect) reduces numbers in saliva by precipitation

_______ capacity has a major impact on caries (along with flow rate). why?

• buffering

• reduces the potential for acid production

• encourages return to neutral pH when sugar intake stops

generally speaking, where do caries commonly appear on teeth?

• in sites that are difficult to clean

unless there is a significant risk factor to produce dental caries, how long (generally) does it take to form caries?

• months or years

what do remineralised enamel lesions look like?

• intact

• smooth white

• black or brown (trapped organic material)

• contour is still same but structure not fulllly restored ykwim

describe the progression of an enamel lesion

• surface breakdown

• surface becomes rough and plaque retentive

• easily damaged by probing, soft/easily disturbed

• further progess leads to cavitation

• colour can vary but usually light

  
  

describe the histological appearance of an enamel lesion

• widest near surface

• tapers toward dentino-enamel junction

• caries can reach dentin without cavitation

describe progression of an enamel lesion (caries) in pits and fissures

• often appears as if there are 2 lesions on opposing surfaces

• same triangular shape

• deepest in the middle

the cavitated lesions become ______ _______ which means it is an ideal environment for ________ and favours ________ progression.

• plaque retentive

• biofilm

• caries

describe a lesion at the dentino-enamel junction

• may precede cavitation

• defence reactions in pulp

  • reparative dentin (dentin tries to wall itself from the bacteria invasion - cant renew surface but dentin can be made more impervious so more is put down)

  • sclerosis of tubules (part of reparative is put inside the tubules to make it sclerotic)

  • tertiary dentin in pulp (within pulp, reduces size of pulp chamber to make it further from the bacteria)

• still asymptomatic (if precedes cavitation then can be remineralised)

describe the spread of caries at the dentino-enamel junction

• spreads laterally (mushroom shaped) along the path of least resistance

• if early, can remineralise (especially if no enamel cavitation)

• so dentin is compromised but enamel isnt. dentin acts as a cushion for enamel so when its compromised the brittle enamel breaks off (collapses)

• cavitation is delayed where theres high fluoride (fluorapatite is stronger than hydroxyapatite)

• still asymptomatic (but may be sensitive)

describe sensitivity, reversible and irreversible pulpitis

SENSITIVITY

• sharp pain

• seconds

• seen in things like sensodyne adverts

• hot/cold causes fluid to move to the dentinal tubules and pulp underneath still normal so the stim. disappears

REVERSIBLE

• seconds to minutes

• cold more than hot

• pulp becomes inflamed and responds more to stimuli

IRREVERSIBLE

• minutes to hours

• spontaneous

• hot worse than cold

• worse lying down

infected vs affected dentin

• infected: damaged beyond repair

  • colonised by bacteria

• affected: can be saved

  • typically demin. but structure still intact so can remin.

describe dentinal caries - infected dentin

• infected dentin - most superficial part of the lesion

• softened/demineralised infected with bacteria

• collagen denatured

• cannot remineralise

• appears as soft necrotic tissue - comes off in layers

• stains with caries detection dye

if you remove the ________ dentin, you reach the ________ dentin

• infected

• affected

describe affected dentin

• softened/demineralised and not infected with bacteria

• collagen cross-linking remains (structure)

• template for remin.

• comes off in chips quite easily

• doesn’t stain

• may be varying shades of colour

why are pulp caries painful?

• the pulp tries to extend with the inflammation like get bigger but bc its enclosed in hard tissue it cant so it elicits a pain response (pulp necrosis)

• can be destructive - cuts of blood supply and dies

while the pulp is still alive and can respond, it produces a number of _____ _______ against caries

defence mechanisms

describe the 4 pulp complex reparative response against caries

1. reparative dentin

2. sclerotic dentin

   • tubules filled with mineral crystals

   • called whitlockite (different structure to hydroxy.)

   • appears glassy

3. tertiary dentin

   • different than secondary dentin (normal aging)

   • this one is in response to a bad (noxious) stimulus

   • structure varies according to rate of deposition

   • reactionary dentin - mild stim

   • reparative - stronger stim

4. pulp inflammation

   • brings with it (along with blood flow) resources to fight infection

types of progression of caries

• slow progression

• rapidly progressing lesion + rampant caries

• arrested caries

describe a slowly progressing lesion

• takes around 18 months to do

• unsupported enamel collapses eventually

• wide open cavity

• cleansable sometimes

• saliva bathed sometimes

• darker and less active

describe arrested caries

• stopped progressing and are inactive

• usually self cleaning

• no food impaction

• hard and glossy

• dark brown/black in colour

• mainly buccal/lingual

• interproximal adjacent to extracted teeth (molars)

define root surface caries

• primary caries on an exposed root surface (often after gingival recession)

• penetrates dentin more easily (no enamel barrier over the surface)

  • cementum is softer (less minerals)

• pathological process is the same as primary enamel caries

key differences between enamel and root caries

THINK! colour, minerals, extents of lesion, time

• initial lesions are minimal (no colour change)

  • reduced surface hardness/texture

  • different than enamel where it appears as white spot lesions

• lower mineral content in dentin/cementum

  • therefore collagen matrix rapidly exposed (demineralisation)

  • collagen susceptible to physical damage (esp in early stages of demin)

  • structure maintained if hydrated

  • collagen matrix easily remineralised

• enamel not involved

  • may be undermined as lesion progresses

• difficult to define extent of lesion

  • still has affected and infected zones tho (margins less easy to identify)

• darkens with time

  • result of bacterial activity

  • also result of collagen matrix uptaking dyes from food

critical pH of enamel and dentin

• enamel: 5.5

• dentin 6.2-6.7

root caries progresses at _x the rate of enamel caries

2

risk factors are conditions that…

• increase risk of developing disease

• modifiable or non-modifiable (changed or can’t be changed)

risk factors for root caries

• gingival recession

• poor oral hygiene

• cariogenic diet

• presence of multiple restorations/missing teeth

• existing caries

• xerostomic medications

• compromised salivary flow rate/buffering capacity

explain gingival recession risk factor for root caries (more common in and happens when you have previous what?)

• exposed root surface required

• more common in old age

• previous periodontal disease

explain poor oral hygiene risk factor for root caries

• biofilm is a necessary component

• impaired dexterity as you age

  • medical compromise (cant floss/brush etc)

• complexity

  • multiple restorations - can be more difficult to clean (eg under bridge harder than natural teeth)

  • gingival recession

explain cariogenic diet risk factor for root caries

• same as primary enamel caries

• elderly less inclined to cook

  • ready meals have more sugar

• elderly more prone to snacking - boredom

• dry mouth can lead to sweet sucking

• presence of multiple restorations/missing teeth

• increases difficulty of cleaning

  • FPDs (fixed partial denture)

  • RPDs (removable partial denture)

explain existing caries risk factor for root caries

• caries risk is a factor for caries

• having caries means you have the right conditions to harbour more

• part of risk assessment

explain xerostomic medications AND compromised salivary flow rate/buffering capacity risk factors for root caries

XM

• most of most prescribed meds cause dry mouth

• nearly half of meds taken by institutionalised elderly cause xerostomia

• 70% of institutionalised elderly take at least 1 med that causes xerostomia

SFL/BC

• saliva flow and buffering may decrease with age although unclear how

management of root caries

(i’m lad urp)

1. improve salivary flow and buffering

2. modulate cariogenic biofilm

3. limit cariogenic food/drinks

4. attempt to remineralise lesions

5. discuss meds with GP

6. use of ETB/water irrigation (if poor manual dexterity)

7. restorations that release fluoride (glass ionomer types)

8. patient education (patient based preventive measures)

rampant/rapidly progressing caries

• rampant caries

• presence of extensive and multiple cavitated and active caries lesions in the same person

  • baby bottle caries

    • bottle feeding

  • radiation therapy caries

    • radiotherapy of head and neck

  • meth-mouth caries

    • misuse of meth (but can occur w. other stuff too)

definition of rampant caries

• suddenly appearing, widespread, rapidly burrowing caries resulting in early pulp involvement

• can affect teeth (or surfaces) regarded as immune to ordinary decay (class 3 and 6)

• more than 10 lesions

causes of rampant caries (XTREME)

• extremes of diet

• extreme compromise of salivary function

  • drug/radiation induced xerostomia

• increased virulence of strep mutans

bottle caries (early childhood caries)

• caused by excessive feeding bottle use

  • particularly at night

  • prolonged contact

  • bottles used as pacifiers

    • pacifiers coated in sugary solutions

risk factors for early childhood caries

• evolving immune system and bacterial microbiota

• hypoplastic defects (newly erupted teeth)

• breast/bottle diet

• more prevalent among children from low-income families

  • parents seek restorative (not preventive) treatment, lack of motivation and knowledge of prevention

radiation therapy caries

• results from radiation to major salivary glands, not to individual teeth

• challenging bc of increasing treatment costs and higher risk of osteoradionecrosis

• xerostomia + diet changes may influence development

• resin composites with fluoride application seems to be ideal management approach

radiation related caries continued

• hyposalivation + xerostomia caused by salivary gland damage are indirect effects mostly associated with RRC

• loss of salivary buffer capacity lowers oral pH

  • biofilm accumulation

  • shift to a more cariogenic oral microbiota mainly composed of lactobacillus sp. and strep mutans

  • difficulties in performing adequate oral hygiene practices

    • trismus, pain and oral mucositis

diet changes with radiation related caries

• highly cariogenic food

  • softer

  • carb rich

  • combat weight loss

    • poor eating dysphagia, pain and oral/oropharangeal mucositis

    • shift to sweet foods

      • last taste to disappear during treatment

meth-mouth caries

(reduces?

how it looks?

users more likely to have?)

• meth reduces salivary flow and buffering capacity

• teeth are blackened, stained and falling apart

• meth users are more likely to have untreated decay, missing/filled teeth and caries compared to non-users

meth mouth pt caries description

• long-acting

• dehydration (low saliva)

• hyperactivity (bad lifestyle, so no oral hygiene)

• increase intake of carbonated beverages (dry mouth)

• poor OH

methadone caries

• opioid used to manage opioid addiction

• frequently given as suspension high in sugar

• presents as:

  • rampant caries

  • periodontal disease

  • xerostomia

  • poor OH

• hypoglycaemia

  • frequent sugar ingestion

dental management of methadone/meth caries

• oral hygiene

• diet

• other preventive methods

• treatment

  • many illicit drug users are dental phobic

when thinking about the impact of the pattern of sugar consumption, what do you need to consider (as it affects the balance of demineralisation and remineralisation?)

1. amount of sugar consumed

2. type of sugar consumed

   • can it be washed away? sticky? takes time to dissolve in the mouth?

3. frequency of sugar consumption

what is the importance of the critical pH?

• altering pH alters the saturation point of things

• the critical pH means the saliva and plaque fluid cease to be saturated with calcium and phosphate, and the hydroxyapatite in the dental enamel can now dissolve

what factors lower the plaque pH?

• acid production (by acidogenic bacteria)

• food source available for the bacteria

what factors raise the plaque pH?

• saliva flow

• fluids in the mouth (above neutral and no sugar in them) - wash away acid

what did Stephan do?

(they didnt give me a last name lol)

• first measured plaque pH and published it in 1944

• did seminal work on plaque pH (pattern of sugar intake on dental caries)

• stephan’s curve!

flip over for visualiser of stephan’s curve