Caries (2) Flashcards
Define Caries:
Infectious microbiologic disease of the teeth that
results in localized dissolution and destruction of the calcified tissues.
caries is formed due to the acid
Epidemiology:
- Sex, race, geography
- Diet
- Hygiene
- Socioeconomics status
- Age
Incidence 4-8 years
Immature enamel
Incidence 11-18 years
more sugar/ more hygiene
Incidence more 55 years
Gingival retraction
Distribution
- Bilateral and symmetric often on both sides on the same tooth
- Teeth
- Surfaces
What are the most affected teeth?
- molars
- premolars
- incisors and canines
(most affected the molars and premolars)
Which surfaces are affected?
- occlusal 40-45%
- proximal 40-45%
- buccal and lingual 10%
Pathogenesis:
- microbes (plaque)
- substrate (diet)
- Host (individual characteristics, tooth surface)
- time
Whats the keyes triad?
- Microflora
- tooth
- diet
- tooth decay
When do we have a problem?
If those 3 things are not in the balance, we get caries
Whats the process of caries?
ph reduces, the acid produces caries in the mouth
On what does caries depend on?
It depends if we use fluoride toothpaste and how much fluoride the patient has
What are the primary cariogenic factors?
- Microorganism
- Diet
- Saliva
What do the microorganisms include?
- biofilm composition
- activity
What does the diet include?
- number exposures to sugar per day
- number of acidic exposures per day
What does the saliva include?
- consistency of unstimulated saliva
- ph of unstimulated saliva
- buffering capacity of stimulated saliva
What are secondary modifying factors?
- Past and present of dental status
- Past and present medical condition
- Accordance with advice on oral hygiene and diet • Lifestyle
- Socioeconomic status
Multifactorial disease
- Microbes (plaque)
- Substrate (Diet)
- Host (individual characteristics)
- Time
Biofilm
microbial community adhered to a substrate trough an extracellular polymeric matrix.
(in the plaque we have many types of bacterials, but not always it produces caries)
Bacterial dental plaque
Microbial community on the tooth’s surface in the form of a biofilm. Determinants in their composition: nutrients, oral hygiene, retentive surfaces.
(the bacteria produces some metabolic products, that other bacterial use)
Define Caries
PH alteration, composition and metabolic activity of the biofilm
Nutritional bacterial plaque factors:
- Endogenous
- Exogenous
- Inter bacterial
Endogenous
Saliva, gingival fluid, mucous.
Exogenous:
carbohydrates from diet
- sugar fermentation > acidity in plaque
- critical value of pH= 5.5 = enamel demineralisation
Inter-bacterial
metabolism products of some bacteria are used as
nutrients by other bacteria.
Bacterial plaque. Composition:
Exogenous acquired film (covers tooth surface, allows
bacteria to adhere)
Matrix: proteins, long chain polysaccharides and lipids
Bacteria. Acidogenic bacteria
Bacteria. Acidogenic bacteria implicated:
- Streptococcus mutans (mutans streptococci)-main bacterium contributor to tooth decay related to caries start, s.sobrinus, s.salivarius: that participate actively in caries developing.
- Lactobacillus, bifidobacterium, prevotella: mainly in cavitated caries, have co-aggregation with other species: caries progression.
- Actinomyces: primary teeth and root caries in adults.
When is the biofilm formed?
right after we eat, the biofiom is fprmed which also protects the tooth, in the biofilm the biofilm does not produce caries, but if we eat all the time, the streptococcus produces caries
Diet
- Type of food
- Highly cariogenic carbs
- > 20% sugar in diet = > caries incidence
- Frequency (Stephan curve)
- Poor dietary habits
What includes the type of food?
carbohydrates (glycolysis: drop PH), physical qualities of the food (stickiness, texture and solubility)
What problem do highly cariogenic carbohydrates have?
Diet of highly cariogenic carbohydrates is easily metabolized by plaque to produce acids.
What food do contain sucrose?
Sugary food, fruit juices, fizzy drinks… high molecular weight Polysaccharid. Easy solubility, quick diffusion.
Whats the Stephens curve?
The curve on a graph, first described by Robert Stephan in 1943, showing the fall in pH below the critical level of pH 5.5, at which demineralization of enamel occurs following the intake of fermentable carbohydrates, acidic liquids, or sugar in the presence of acidogenic bacteria.
Whats the usual pH?
5,5
What happens with the pH if we have breakfast?
If we have breakfast, the pH drops
Whats the aim of the healthy Stephens curve?
in this graph, the graph is more time in the healthy zone than in the ill zone
Whats the most acidic during the day?
Coffe
What happens if we brush our teeth right after having a meal?
if we brush our teeth right after, the pH goes up faster due to the fluoride
Individual hist characteristics:
- Tooth
- Saliva
- Fluoride
- Other factors
What refers to the tooth host?
Morphology, maturation, position, composition of dental tissues (fluorapatite)
What do we understand under position?
If the tooth is rotated etc.
What do we understand under composition?
How much fluoride the tooth contains
And Saliva what do we understand?
What components does the saliva contain
What contains the saliva?
Anticariogenic power
What is Anticariogenic power?
- Mechnical removal of residues
- Buffer power
- Reduction enamel solubility
- Remineralized enamel
- Bactericidal and bacteriostatic power
Whats a buffer power?
Saliva ph= 6.75
Neutralizes plaque acids
What plaque acids does it neutralise?
– carbonic acid-bicarbonate system – Phosphate-phosphoric acid system – salivary urea – salivary proteins – Ph elevator peptide or sialin
What is reduction enamel solubility?
forms the acquired pellicle, contains fluoride, calcium and phosphate ions.
Whats remineralised enamel?
calcium, phosphorus, fluoride, salivary proteins
Bactericidal and bacteriostatic power
lisozime, lactoferrin, lactoperoxidase, phosphoproteins, IgA
Whats remineralisation?
in saliva we have calcium and phosphate ions, when they get in touch with the hydroxide
When do we have remineralisation?
Saliva + hydroxyapatite= remineralization
- Calcium/phosphate ions in supersaturated solution.
- Neutralizing buffer systems.
Wats deminerlaization?
we eat, produce acid and touch the hydroxyapatite
When do we have Demineralization?
Acids + hydroxyapatite= decalcification.
- Dissociation of phosphate groups
- Release of calcium ions
Describe the concept of demineralisation and reminerlation:
After an acid attack ph decreases: Ca and P ions are released after the HAp’s dissolution, just in a few minutes, there will be an increase in the ph due to the formation of new HAp crystals thanks to saliva and fluoride.
How does fluoride work?
– Contact with the hydroxyapatite in enamel: replaces the hydroxyl ions with
fluoride, forming fluorapatite, less soluble (OH- !F-)
> rate of remineralization
< colonization and growth of the bacterial plaque, increases resistance of enamel to acid attack.
Other host factors?
- genetic
- chronic diseases or with low immunity
- oral hygiene habits
- xerestomia
What other factor does affect the oral fluoride?
due to any drugs, when we have a patient who takes many drugs, it affects the saliva and the fludity of the saliva
so might apply fluoride
What induces Xerestomia?
- Systemic diseases: Sjögren Sd.
- Radiation therapy.
- Drugs:psychotropic drugs, cytostatic…
What factors do we include as the time?
- Chronological
- Posteruptive maturation
- Period demineralisation/ remineralisation
- Development of immunity
What do we refer as chronological?
Dental plaque accumulation
What do we refer to posteruptive maturation?
Immature enamel
What do we refer to demineralisation and reminerlaization period?
2/22 h proportion
Whats the best zone?
22 hours healthy zone, 2 hours ill zone
What are Pathological factors?
- acid producing bacteria
- sub normal saliva flow and or function
- frequent eating/ drinking of fermentable carbs
- poor oral hygiene
What are protective factors?
- sliva flow and components
- demineralisation (fluoride, calcium, phosphate)
- good oral hygiene
- strategies that maintain a healthy microbiome (probiotics, probiotics, arginine, pH modifiers, erythritol and xylitol)
- strategies that modulate a dysbiotic microbiome (silber, peptides, tin, antimicrobials)
Whats the caries balance?
The caries balance, the balance between demineralisation and demineralisation is illustrated in terms of pathologic factors (ex. those favouring demineralisation) and protective factors (ex. those favouring reminerlaization)
Types of caries regarding the depth of the lesion:
1- Enamel caries
- Dentin caries (dentin pulp complex)
- Cement caries
Enamel caries:
Macroscopically
- Opacity
- White Lesion
- Brown lesion
- Cavitation
(first we note it as the opacity, then white lesion etc.)
What alway we have to do and why?
from the surface we can only see the white lesion, if its deeper or not
we can also have caries with no cavitation, thats why its importat to take an xray
Enamel caries:
Microscopically
- Surface zone
- Body of the lesion
- Dark zone
- Translucent zone
Surface zone
20-50Um
Loss of mineral content 5-10%
Body of the lesion
– Largest portion of the lesion
– Loss of mineral content 10-15%
– Porosity 5-25%
– Selective demineralization (striae of Retzius and prism cores)
Dark zone
– Dark brown band
– Loss of mineral content 5-8%
– Porosity 2-4%
– Represents process of demineralization and remineralization
Translucent zone
– The deepest zone
– Loss of mineral content 1-5%.
– Porosity 1% (x10 normal enamel)
Dentin caries:
Macroscopically
Dentin pulp complex
- Infected dentin
- Affected dentin
Infected dentin
cavity, caseous tissue, soft texture, easy to remove.
Affected dentin
hard texture, dark color.
What 2 options do we have if the caries reaches the dentin?
- reaches on the top
2. reaches on the bottom
What dentin we do just remove?
We just remove the infected dentin, the one on the top
Dentin pulp complex active caries
Microscopically
(exam)
- Infected dentin
- Affected dentin
- Hyper mineralised dentin
- Pulp reaction
Infected dentin
- Necrotic/destruction zone
* Outer demineralized dentin zone
Affected dentin:
- Inner demineralized dentin zone
* Outer sclerotic dentine zone
Hyper mineralised dentin
• Inner sclerotic or translucent laye
Pulp reaction
- 3ry dentin Reparative dentin
* Pulp inflammation
Main character of the root surface caries?
very common, problem has a quick progession, since all the rest is close its affected but they dont fell anything
Root surface caries:
– Concave anatomic surface contours
– Roughness at the termination of the enamel –cementum
– Dentin exposure to the oral environment (gingival recession)
– U-shaped with quick progression
Classification:
- Location
- Activity
- Development stage
- Mode of appearance
- Location and size
Location
- Fissures, grooves, pits
* Free enamel surfaces: Proximal, buccal, lingual • Root
Activity
- active
- arrested
- rampant
Development stage:
- White spot- incipient caries
- Dentin affected, no cavity
- Cavity
- Pulp exposure
- Crown destruction
Mode of appearance:
- Primary
- Recurrent, secondary
- Residual
Location and size:
- Hume&Mount classification.
- Black classification (disused)
Caries classification
- based on location
- occlusal surface
- proximal surface
- root
Caries in occlusal surface:
• Located in pits, grooves and fissures
• Caries progress: – Starts in the lateral walls of the cavity (Expands laterally). – Easy access – Fluoride in early detection
Proximal caries
- Located in the most cervical and buccal part of the contact area.
- Slow progress. We could try non invasive methods depending on the patient’s diet, fluoride…
(always located most cervical and buccal)
Caries progress
In pits and fissures
it spreads in triangular pattern with base towards DEJ.
Caries process:
in proximal caries
apex towards DEJ.
When caries passes through enamel, it spreads laterally along the DEJ: cone shaped lesion with its apex towards the pulp
Whats the 1st manifestation of enamel caries?
white spot
Based on activity:
Arrested- Enamel
Enamel: - Non cariogenic activity - Remineralized affected enamel: hard and bright - and feels hard if a sharp probe is gently drawn across it.
Based on activity
Arrested- dentin
Dentin:
- Marked brown pigmentation and hard, shiny.
Based on activity:
Active- enamel
Enamel:
- White mark, chalk appearance
Based on activity.
Active- Dentin
Dentin:
- Caseous, wet, soft tissue
- Light brown/ grey or yellow
Based on activity
Active- Rampant/ Early childhood caries
- quick process
- > teeth in not common surfaces
According to the development stage:
- No cavitation
- Cavitation
- Pulp exposure
- crown destruction
According to development stage:
No cavitation
- Active enamel caries lesion (white spot- incipient caries)
- Inactive enamel caries lesion
- Lesion with involvement of the dentin without cavitation : dentin affected but intact enamel. Hidden caries
Active enamel caries lesion (white spot- incipient caries):
Opaque, rough, difficult cleaning areas, gingivitis
Inactive enamel caries lesion
– pigmented or clear spot
– Enamel surface shiny smooth and polish
According to development stage:
Cavitation
- Active caries lesion with cavity
- inactivecaries lesion with cavity
Active caries lesion with cavity:
– Clear color, soft texture
– Active withe spot in around
Inactive caries lesion with cavity:
– Dark color, hard texture
– Well limited edges, without active white spot halo.
What else can we find in the no cavitation area?
normally gingivitis in this area as well cause the patient cant clean well in this area
Whats a hidden caries?
the enamel doesnt have a cavitation, but the dentin has a caries cause its inside the root: hidden caries
Main difference of active and inactive caries:
active: softer
inactive: harder
Based on mode of appearance:
- primary caries
- Recurrent or secondary caries
- Residual caries
Primary caries:
Carious lesions on unrestored tooth surface
caries that appear on the topth surface, there is no treatment necessary
Recurrent or secondary caries:
Carious lesions that develop adjacent to an obturation.
Formed around the margins and under the obturation, usually on rough areas and margins or fractured dental tissue.
we can see caries around it
Residual caries
Remaining caries that has been left behind in a prepared cavity on which an obturation is placed.
(caries left in the cavity, left in the obturation)
Location:
site 1
pits and fissures
not only occlusal, can also be on the lateral pits
Location:
site 2
Proximal surfaces
Location:
site 3
cervical areas
Stage 0:
the earliest lesion that can be identified as the initial stages of demineralization
(we can use fluoride to demineralise it)
Stage 1:
Minimal surface cavitation with involvement of dentine just beyond treatment by mineralization
(dentin is already affected, we cant remineralise it)
Stage 2:
moderate involvement of dentine. The remaining tooth is sufficiently strong to support the restoration.
(tooth is still strong enough to remain)
Stage 3:
the lesion is enlarged beyond moderate. Remaining tooth structure is weakened to the extent that cusps or incised edges are split, or are likely to fail if left exposed to occlusal load.
(cavitation is bigger, cusps are weak)
Stage 4:
extensive caries or massive loss of tooth structure e.g. loss of a complete cusp or incisal edge has already occurred.
(cup is completely broken on edge)
Hume & Mount Classification
This classification: helps to make decisions about the treatment to establish protocols for each case:
Hume and Mount:
stage 0
A white spot lesion, stage 0: remineralized techniques
Hume and Mount:
Stage 1:
Stage 1: Minimally invasive restorative treatment
Hume and Mount:
Stage 2, 3, 4
Stage 2, 3, and 4 more complex restorative treatment
Why do we have the Hume and mount classification?
In order to know how we treat them
Diagnosis:
- Patient history (how painful etc)
- Clinical examination
- Radiographic assessment
- Nutritional analysis
- Salivary analysis
Patients history:
– Asymptomatic. – Symptomatic:
• Hyper sensitivity? • Pain?
Visual
Detection of white spot, discoloration, cavity, opacity under an evidently sound or stained pit or fissure
Visual and tactile examination
- Examination wet and dry teeth surfaces.
- Plaque-free (clean surfaces)
- Mirror and not sharped explorer!
- Sound enamel refractive index (R.I)=1,62
- Demineralized enamel
Demineralized enamel:
– > porosity
– > Water accumulation (r. i = 1,33)
– After water dry: r.i = 1,0 = opaque lesion.
What can you conclude is the tooth we and you see the white spot?
no caries
What can you conclude if it is dry and you see white spot?
caries
Visual inspection:
Low sensitivity technique –
high number of not diagnosed caries
but more specific
low number of false +.
if we have stain, does it indicate caries?
No, Stain doesn’t always indicate caries.
What diagnosis is analysed in 55% caries=
55% caries diagnosis in
sound teeth.
What do we have to analyse close to the fissure?
Opacity changes
If we have a cavitation, how is the exam tester seen?
hard or soft
If we have a shiny surface, is it an indication for caries?
if the surface is shiny around we have caries, an indication at least
Tactile:
- Explores
- Dental floss
- probe
What do we use on the occlusal surface?
explorer
What do we use interproximal and what’s the consequence?
dental floss, if it breaks caries
What does the explorer do?
if retentive area in the tooth, the probe could easily enter the space. We can evaluate softness/ hardness of walls and floors
When do we NOT use the explorer?
When cavity is not cavitated, we dont use explorer
What we shouldn’t do after exploration a caries?
if we probe a large caries and with that probe we touch an obturation, we transfer the caries
What kind of probes do we use?
we only use sharp prrobes if its cavitated, otherwise round probe
When do we use sharp probes?
if its cavitated
What consequences do sharp probes have?
- Damage the sound enamel and convert remineralized lesions in irreversible lesions.
- Microorganism transmission from carious surfaces to sound surfaces
- Risk of fracture surface of the enamel, prevents future remineralization
- Transport cariogenic bacteria from a tooth with carious lesion to a sound piece
Regarding the radiograph: when can we ONLY see caries?
Only visible when there has been enough demineralization (>40%)
Only advanced lesions are detected.
so if we see smth= warn
Whats the percentage in detecting carious lesion?
50-70% sensitivity in detecting carious lesions
- high number of false + and false – in small caries
When do we often think it might be caries?
- overlapping of proximal surfaces
- cervical burnout
With what cervical burnout is often confused?
With root caries
What do we always have to do?
- xray
- visual
Occlusal caries xray
- Occlusal caries xrays
Theanatomyoftheocclusalsurfaceofposterior teeth leaves a lot of enamel covering the dentin of the buccal and lingual cusps , which , in an X-ray helps to mask any incipient occlusal demineralization in the occlusal fissures decreasing sensitivity. - In addition, the enamel - dentin line separation is difficult to appreciate at the occlusal level when we take a bitewing, leading to false positives.
What can also be confused on the xray because its seen dark?
Enamel dentin junction
Advantages of Radiograph:
- detection of lesion development
- Identification of caries in areas of difficult acess (intraproximal and sub gingival)
- Hunden occlusal caries diagnosis and pre- eruptive caries diagnosis
- Recurrent caries
- To monitor preventive therapies and monitoring already diagnosed injuries
- Legal document
- Bitewing radiographs to improve sensitivity of detection on proximal surfaces
Detection of lesion development:
– Evaluation of the depth of the injury in relation to the pulp and the biological space.
– See changes occurring at the dentin and pulp chamber (Tertiary dentin)
Biological criteria for the removal of advanced carious lesion
- How much carious tissue should I remove?
- How do I remove it?
- Are viable microorganisms into the dentin that we leave?
- Could these microorganisms be recurrent?
We have 2 ways of cleaning:
- Leaving remnant affected carious dentin: the caries
will stop progressively once it is isolated from the oral cavity - Removing all the carious dentin
Fusayama y cols, Ogawa y cols distinguish
- infected dentin
2. affected dentin
Due to Fusayama:
infected dentin
- Denatured superficial dentin
- Can’t be remineralized
- Must be removed
(infected dentin always have to be removed=
Due to Fusayama:
Affected dentin
- Deep
- Denatured but reversible.
- Can be remineralised
- Must be kept.
(we can leave it)
How to remove carious tissue?
- Removal method
2. Acid method
Removal method
Turbine, contra angle, excavator use of caries detector dyes hardness lesions
Acidic method:
Dyes (Fusayama).
Fucsina (0,5% propilenglicol)
Red acid 1% propolinglicol
Has to be washed really well cause otherwise it could affect other lesions
What dentin is stained in theory?
disorganized
What dentin is stained due to studies?
Some studies have shown that it also stains deep intertubular dentin
Caries detector:
Maltz & cols: dyes have great affinity for:
- areas of lower concentration of minerals
- surrounding-pulp deep dentin
- high degree of porosity areas (white spot)
- Intact areas
This can lead to an excessive removal of the dental structure.
in anterior teeth staining may compromise the aesthetics
It is important to associate it with the criteria of surface hardness
When do we not use a caries detector?
As soon as we know how caries feel like
What might leave stains if we dont wash it?
anterior teeth staining
Dentin hardness:
Advantages
- Most used method.
* Removal of infected dentin
Dentin hardness
Disadvantages
- no differences between infected and affected dentin
- sharp excavator eliminates non infected dentin
What main character does the affected dentin have?
Affected dentin: 35-40% softer than normal dentin
Maltz y cols: Study in 32 patients with partial removal of caries. After 6-7 m
– Color alteration
– Hardness 80%
– Significative decrease of streptococcus and lactobacillus
