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 in immediate proximity to the tooth by the enzymatic action of masses of microorganisms (in the bacterial plaque) on carbohydrates

key components of the definition of dental caries

• bacteria required to produce disease

• bacteria use metabolise-refined carbs

• when metabolism in 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 ________ _________ _______

• 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

• 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

• saliva

• biofilm pH and composition

• fluoride use

• diet

• oral hygiene

• immune system

• genetic factors

• meds

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 and fissures

• below contact points

• cervical area of the tooth

• developmental defects (grooves, hypomineralised areas, 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 tissue)

• iatrogenic damage (areas the dentist damaged lol

• areas of hypomineralisation (less mineralisation of enamel 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)?

• topically after eruption

• systemically before eruption

how does biofilm start and how does it evolve?

• starts as initial pellicle of enzymes, glycoproteins and immunoglobulins

• highly organised sequence of events

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

• produces changing microflora based on thickness of plaque

• 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 (adhesion of bacteria on pellicle surface)

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

• genetic factors

• 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 ofL

• 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

• cuspids (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 ant/pos teeth

• below max convexity and just above ging. margin

class 6

• cusp tip of molars/premolars + cuspids

• 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

• highly organised series of events

• 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 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 some 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 hydrogen peroxide 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 - 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.

• softer than normal - but 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 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)