most common disease major cause of loss of teeth
TRANSCRIPT
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Dental caries
most common disease
major cause of loss of teeth
progressive bacterial damage
initiated by acid production in plaque
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Dental caries
breakdown of enamel and dentine
opening way of bacteria to infection of pulp (acute pulpitis)
spread into periapical tissue (periodontitis)
toothache
infection spreads into jaw – osteomyelitis – sepsis
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Aetiology
diet
timeflora
susceptible surface
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Dental caries is a bacterial disease
• decalcification caused by acid production by plaque bacteria
• not present in germ-free animals• Streptococcus mutans, sobrinus, salivarius,
mitior, sanguis
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Dental caries is a bacterial disease
• different ability of different bacteria to:
attach to different types of tissueferment sugars (sucrose)produce acids (S. mutans) pH<5produce different polysacharides
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Dental caries is a bacterial disease
• S.mutans stores sucrose intracellulary (metabolic reserve)
• omitting of sucrose in diet - disappearance of S. mutans
• new supply - recolonization of plaque• stagnation areas (pits, fissures, interstitially)
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Streptococcus mutans
• ability to polymerise sucrose into sticky dextran-like polysaccharides (glucans) - strongly related to cariogenicity
• plaque adheres to teeth and persists there• Lactobacilli - less cariogenic (fissure caries -
plaque formation less important); contribute to tooth destruction later, after the process has been started
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Cariogenicity of S. mutans
• produces acid• survives at the low pH (4.2)• produces glycans - matrix of the plaque• adheres to tooth surface
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Bacterial plaque
• organic matrix (polysaccharides) + bacteria• distinct entity• biofilm enables much higher concentrations
of acids than those in saliva• resistant to immunological defences• plaque visible after 12-24 hours
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Bacterial plaque
• translucent film with matt surface• staining with disclosing agent• forms rapidly and abundantly in high-sucrose diet• resists friction during chewing – removal only by
toothbrushing (persistence in pits and fissures!)• plaque minerals - calcium, phosphorus, fluorides
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Acid production in plaque
• sucrose diffusion into plaque (sweet drinks x caramel) - repeated small doses more cariogenic!
• fermentation into acids - in minutes (!)• lasts 20 min. after washing-out sugar,
returns to normal after 60 min.• lactic acid
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Acid production in plaque• sucrose rich diet - main source of plaque (sweets,
snack-bars)• western countries, reverse association between
malnutrition and carries• GB - 80% of 8YO children have caries, adults in
average only 13 healthy unfilled teeth• newly erupted teeth more susceptible - progressively
increases resistance (maturation - deposition of minerals from saliva)
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Effect of fluorides• drinking water• toothpaste• mouth rinses• tablets• fluoride incorporated into the teeth during
development• reduction of enamel solubility• favorization of mineralization• possible reduction of acid production within plaque
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Role of saliva
• complex secretion, multiple factors - buffering power (bicarbonate content)
• salivary flow - clearing of cariogenic foods• xerostomia!• immune deficiencies do not have significant
role on dental caries
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Enamel caries
• enamel - usual site of initial lesions• calcium apatite, minute organic content• barrier to bacterial attack• once enamel defence is breached - dentin
represents a poor barrier• prevention - to stop caries at the enamel
level, increasing the resistence of enamel
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Enamel caries
• crystalline lattice of Ca apatite crystals - impermeable
• organic matrix - high water contents - permeable for H+ ions
• dynamic process - alternation of de- and remineralization
• progression slower in adults, fast in children
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4 phases
• early (submicroscopic)• non-bacterial enamel crystal destruction• cavity formation• bacterial invasion of enamel
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Early lesion
• white opaque spots, chalky appearance• hard to probe• changes seen best in polarized light -
demineralization - apatite crystals become smaller
• conical in shape - apex towards dentine
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Early lesion
• 4 zones - (from inside out):• translucent z. - loss of 1% of minerals -
demineralization• dark z. - loss of 2-4% - remineralization• body of the lesion - loss of 5-25%• surface z. - lost in cavitation - very important one -
remineralized (salts from plaque or by ions escaping from deeper structures)
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Pit and fissure caries
• same changes, different shape• ring around the pit
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Cavity formation
• prisms disappear - formation of pathways large enough for bacteria to enter
• bacteria reach amelodentinal junction - spread laterally - enamel undermining
• pinhole lesion in enamel - large undelying cavity• fragmentation of enamel on the surface - clinically
obvious cavity• bacterial attack of dentine enabled
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Dentine caries• initial (non-bacterial) lesion - demineralization• invasion of bacteria - role of Lactobacilli (later on
mixed population)• dentinal tubules - ideal pathway - colonization -
spread• demineralization - proteolysis• distension of tubules - coalescence - liquefaction
foci• lateral spread
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Protective reactions of dentine and pulp under caries
• odontoblast activity• reactions are not specific (any trigger - attrition,
erosion, abrasion, restorations)• more prominent in slowly progressing caries• formation of sclerotic dentine (tubular sclerosis)• reactionary dentine - regular and
irregular(eburnoid))• vulnerability - no barrier against pulpal infection
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Root surface caries
• attack on cementum• little barrier to decalcification and infection• softening, saucer shaped defect• early involvement of dentine• cementum infected along Sharpey's fibres
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Arrested caries
• white spot can be arrested - remineralized from saliva
• dentine caries - destruction of enamel - dentine exposed to saliva
• use of fluorides and less cariogenic diet• 50% of early interproximal lesions do not
progress
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Pulpitis• most common cause of dental pain and loss of teeth
in younger persons• usually due to dentine caries• other causes: open trauma (cavity preparation!),
fracture of crown, cracked tooth syndrome, thermal or chemical irritation (protective layer under restoration!)
• untreated pulpitis ->necrosis, spread of infection through root channel - periapical inflammation (periodontitis)
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Acute pulpitis
• clinically transient sensitivity to hot or cold food
• later on - toothache becomes persistent• pain is poorly localized (felt in other teeth)• pressure on the irritated nerve• pain producing substances released by
inflammatory cells
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Acute closed pulpitis
• initially hyperemia• infiltration by inflammatory cells• localized abscess or necrosis, formation of
granulation tissue• later - diffuse inflammation of the pulp,
obliteration of blood flow - necrosis
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Chronic closed pulpitis
• mononuclear cell infiltrate• chronic abscess, wall made of granulation
tissue• pulp calcifications (dentine bridges)
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Open pulpitis
• pulp exposed• massive infection• chronic inflammation
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Chronic hyperplastic pulpitis (pulp polyp)
• pulp replaced by granulation tissue• polyp may become epithelialised by
squamous cells
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Pulp calcifications
• pulp stones - rounded masses of dentine• developmental anomalies• more common in Ehlers-Danlos syndrome• diffuse calcifications - age related,
degenerative change• no clinical symptomatology
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Acute apical periodontitis
• previous pulpitis in history• escape of exsudate into periodontal tissues -
extrudes tooth - bite falls more heavily• uncomfortable feeling - tender tooth - pain• reddening of gingiva• X-ray not too much helpful
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Acute apical periodontitis
• penetration of overlying bone - swelling of surrounding soft tissues (upper canine - eylids, face)
• swelling is due to oedema• enlargement of regional lymph nodes• complication - acute osteomyelitis,
phlegmone of soft tissues (cellulitis)
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Histology
• initial phase - dilatation of blood vessels (hyperaemia), oedema
• later - suppurative inflammation - pus• abscess formation, osteolysis, fistula
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Chronic apical periodontitis
• low grade infection• inadequately treated or silent acute infection• non-vital tooth• X-ray - "apical granuloma" - 5 mm
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Histology• chronic inflamm. infiltrate (lymphocytes, plasma
cells, macrophages) + granulation tissue• osteolysis - formation of "cavity" - radiolucency• no spontaneous healing (reservoir of infection in
root canal)• proliferation of epithelial rests of Malassez - cystic
degeneration - formation of radicular cyst• rarely formation of fistula (sinus tract to buccal
gingiva)
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Resorption of teeth• deciduous teeth - physiological process• permanent teeth - always pathological• sign of pathological process in the vicinity of the
tooth (cyst, tumor, etc.)• idiopathic resorption (pink spot) - dentine is
resorbed from within the pulp - localized process - opening of pulp cavity (infection)
• idiopathic peripheral resorption - rare, usually multiple teeth - resorption of roots near apex
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Hypercementosis• apposition of excessive amounts of cementum• causes:• ageing• periapical periodontitis• functionless and unerupted teeth (alternation of
resorption and hypercementosis)• Paget's disease (mosaic pattern)• cementoblastoma• result - concrescence, difficult extraction
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Non-carious injuries to teeth
• attrition (gritty diet - developing countries, ancient skulls) - formation of reactionary dentine
• abrasion - necks (elderly - overvigorous toothbrushing, abrasive toothbrush
• erosion - dissolution by acids (fruit juices, gastric acid)