Dental caries V. Žampachová 2 Pathologic loss of tooth structure nnon-bacterial (mechanical – abrasion, attrition; non-bacterial chemical – erosion; pathological resorption, etc.) nbacterial disease associated – dental caries nDental caries is a sugar-dependent infectious disease. n Dental caries nMultifactorial dynamic process, partialy reversible nInvolves the interaction of inborn or acquired host factors (tooth surface, saliva, acquired pellicle), diet, dental plaque (biofilm). nCaries does not occur in the absence of either plaque or dietary fermentable carbohydrates. nDental caries can be modified by protective factors. n n n Etiology n nClassic triad of essential factors necessary to development of a carious lesion. All must be present for caries to occur: bacteria, degradable carbohydrate and susceptible tooth structure. nTime factor important Dental caries - etiology nbacterial plaque biofilm ncariogenic bacteria nplaque biofilm stagnation sites nsusceptible tooth surfaces nfermentable bacterial substrate (sugar) ntime Dental caries - etiology npossible interventions at any level nreduced sugar intake navoid frequent sugar intake (snack) nstimulate sugar clearance incl. salivary flow nreduction of Str. mutans nreduction of susceptible teeth surface nfluoridation nprevention during posteruptive maturation nremineralising solutions nproper restoration, fissure sealing Multifactorial process n Disease factors nGenetic ↔ Environmental n ↕ n Biological n Social n Behavioral n Psychological Dental caries incidence nchanges in the prevalence of dental caries (↓ of deciduous t. caries, ↓ of smooth surface caries, ↑ of root caries) nchanges in the distribution and pattern of the disease in the population nimproved diagnosis of noncavitated, incipient lesions and treatment for prevention and arrest of such lesions nrestorations: repair the tooth structure, possible caries stop, but commonly limited life span Teeth and caries nTooth factors: location, morphology, composition, ultra-structure, post-eruptive age of the tooth. nTeeth have a high resistance to caries (low caries prevalence in primitive humans) nModern humans have restricted this natural resistance by modifying our diets. Structural resistance nLarger and more uniform crystals ↓ the specific surface area and reactivity (solubility). nMore closely packed crystals ↓ the space for water and diffusion pathways between crystals. nSpaces between crystals → enamel a microporous material. Water - diffusion channel for acids to attack the crystals. Posteruptive maturation nCaries susceptibility greatest immediately subsequent to eruption, tends to decrease with age. nPost-eruptive maturation process with changes in the composition of the surface enamel. nRelated to the demineralization-remineralization dynamics. n Demineralization : remineralization nDynamic equilibrium state of the enamel surface with its local oral environment (plaque fluid and saliva), constant movement of ions in and out. nDrop of the pH of plaque → the mineral phase of enamel begins to dissolve. nCritical point between 5.0 and 6.0 Demineralization : remineralization n demin-re copy copy Demineralization : remineralization nProtective factors Pathological factors n Saliva – flow + components Reduced saliva functions n Proteins, antibacterial agents Bacteria: str. mutans, lactobacilli n Fluoride, calcium, phosphate Diet: carbohydrates + frequency n ↓ ↓ n___________________________________________________ n ∆ nno caries caries Demineralization nDe/remineralization process - the more soluble carbonate-rich apatite lost, replaced by apatite lower in carbonate and higher in fluoride (if fluoride present in the oral environment). nReprecipitated crystals - larger than the original crystals, creating hypermineralized areas of enamel. nResponse of the enamel - ↓susceptibility to caries occuring with age. nThe effectiveness of fluoride in caries prevention can be largely attributed to its ability to enhance the remineralization process. n Demineralization : remineralization nDemineralization of relatively unaffected surface zone ↑ rate of the progress of the lesion. nIf the surface layer above a lesion can be „strengthened“ through fluorides or mineralizing solutions, the lesion can become arrested, and the process reversed. nIf the surface area is plaque-free, then the saliva itself, (supersaturated with calcium and phosphate) can remineralize the initial lesion as well. nThe average time from the stage of a white spot lesion to clinically detectable caries - approximately two years. nA high frequency of exposure to sucrose – acceleration of demineralization; nExposure to fluorides favors remineralization. Etiology of caries nDecalcification by bacterial acid followed by destruction of all other tooth tissues nBacteria, dental plaque nRole of carbohydrates n nNo theory is universally accepted nAcidogenic theory nProteolysis chelation theory nProteolytic theory n Acidogenic theory n nDental caries is a sugar-dependent infectious disease. n Acid produced from metabolism of carbohydrate by plaque bacteria → drop in pH at the tooth surface. n In response, calcium and phosphate ions diffuse out of enamel → demineralization. nThis process is reversed when the pH rises again. nCaries is a dynamic process characterized by episodic demineralization and remineralization occurring over time. n Predominant destruction → disintegration of the mineral component → cavitation. ž Proteolytic theory nIn addition to acid, proteolytic substances produced by plaque bacteria break down the organic portion of enamel and dentin Evolution of caries copy Proteolysis chelation theory n nBacterial attack on enamel is initiated by keratinolytic bacteria causing breakdown of enamel protein, mostly keratin nOrganic and inorganic portion of enamel undergoes demineralization by formation of calcium chelates, even at neutral pH nMucopolysaccharides may act as chelators Dental plaque n nYellowish white soft, amorphous material deposited on tooth surface nFormation nAdherent layer of mucinous material from saliva. nColonisation of this layer by diffusion of microorganisms. Production of polysaccharides - glukans nWithin 48 hrs the whole layer owergrown by microorganisms. n Dental plaque nA number of endogenous oral microorganisms in dental plaque can contribute to the caries process: nmutans streptococci (S. mutans, and S. sobrinus) nS. sanguis and salivarius, and other non-mutans species nLactobacilli species nActinomyces species nyeast nEven in a caries free mouth, 1 ml of saliva contains 10-100,000 endogenous microorganisms. Dental plaque nHeavy staining and calculus deposits exhibited on the lingual surface of the mandibular anterior teeth, along the gumline. copy copy Dental plaque (Kolenbrander, Microbiol Mol Biol Rev, 2002) dental_plaque Kolenbrander biofilm Properties of cariogenic bacteria nacidogenic nable to produce low pH (at least pH 5) to start decalcification nacidoresistant, acid production at any pH npossibility of attachment - to adhere to smooth tooth surface nproduction of adhesive/sticky insoluble polysaccharides – glukans nsurvival in the mixed bacterial ecosystem - competition Dental plaque nInitial colonization of the plaque biofilm on a tooth surface is predominately S. sanguins and S. salivarius. nShortly after initial adherence to the tooth, Streptococcus mutans a major component of the biofilm. nStreptococcus mutans highly probably the most virulent of the organisms participating in dental caries. Dental plaque nMaturation of the plaque - a shift from a predominating aerobic Gram positive cocci to anaerobic Gram negative rods. nWith progress to cavitation (particularly advancing into the dentin) lactobacilli favored in sheltered, highly acidic environment. nThe process of enamel demineralization and eventual cavitation related to bacterial succession, one organism initiating the plaque, while subsequently another organism takes over. n Dental plaque pH nThe pH of dental plaque normally close to neutrality. nAfter ingestion of a fermentable carbohydrate (sucrose, etc.) the plaque bacteria produce acids → drop in the pH level. npH levels lower than 5.5 can initiate demineralization (after a sucrose rinse, the pH value can fall to as low as 4.0). nLow pH levels→ calcium and phosphate ions begin to dissolve out of the enamel, so as long as the environment remains sufficiently acidic. Stephan curve stephfreq-2 Sugar Demineralization occurs copy Properties of bacteria nAbility to produce acid by fermentation of sugars n nAbility to polymerise sugars into long chain polysaccharides → plaque adheres firmly to the tooth surface, bacteria adhere to each other n nLactic acid (mainly), acetic acid Cariogenicity of microbes nStreptococcus mutans/sobrinus nCariogenic properties nMajor source of demineralization nHighly acidogenic nExtracellular polysaccharide n from sucrose – insoluble, + reserve energy source nAdheres to pellicle nSo do most oral streptococci nTransmisible - mother/caregiver to child nSo are all oral bacteria nMicrocolonies - localized zones of high acidity in protected sites nOcclusal pits and fissures; interproximal contacts Microbes as risk factors nNecessary, but not sufficient nHigh S. mutans levels in saliva/plaque ↑ the risk nLongitudinal studies nMost people who get new lesions will have „high“ levels BUT nMany people with „high“ levels won’t get new lesions nThe majority of oral streptococci belong to non-mutans species nS. mutans - a minority streptococcus - not a good competitor nHigh % of acidogenic non-mutans = increased risk? nLow % of acidogenic non-mutans = decreased risk? nOther species may moderate risk nVeillonella may be related to lower lactate levels Antimicrobial strategies nTargeted attacks on mutans streptococci nFundamental concept - S. mutans is the main demineralizer nCaries vaccines - results not impressive nSecretory immune system (S-IgA) is tolerant of oral microbes nTopical antibodies - results not impressive nAntimicrobial peptides combine S. mutans pheromones nBroad-spectrum attempts to eliminate/limit biofilm nAllows for the possibility of other acidogenic species nSystemic antibiotics (fungal overgrowth) nChlorhexidine rinses or varnishes (recolonization from reservoirs) nQuorum sensing inhibitors nReplacement with „probiotics“, natural or genetically engineered nAll approaches have limitations, possible risks n Plaque composition nOther than organisms: nInorganic: calcium, sodium, potassium, phosphorus nOrganic: proteins, lipids, reactive inflammatory and other cells. Dental plaque (EM) n 03big copy Growth of the plaque n nMultiplication of existing bacteria nAddition of new bacteria nAccumulation of metabolic products of bacteria nFood debris from diet n Dental plaque n Acids released from dental plaque lead to demineralization of the adjacent tooth surface, and consequently to dental caries. nSaliva unable to penetrate the build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria and remineralize the tooth surface. nCause of irritation of the gums around the teeth → possible gingivitis, periodontal disease and tooth loss. nPlaque - eventually mineralized → calculus (tartar). n DENTAL PLAQUE nInadequate removal of plaque caused a build up of calculus (dark yellow color) near the gums on almost all the teeth. copy copy Dental calculus (tartar) n nHard deposit formed on the tooth (due to mineralisation of dental plaque) nPlaque converted to calculus in 50 – 60 days n nClassification nSupragingival – coronal to gingival margin nSubgingival – below the crest of gingival margin 40 Dental Plaque and Tartar http://www.travel-dental.com/web_engl/images/preise/prophylaxe/prophylaxe1.jpg Dental Tartar Products copy Composition: n n70-90% inorganic material n 10-30% organic material v nCalculus formation can result in a number of clinical manifestations: nincluding foetor ex ore (bad breath) nreceding gums, nchronic gingival inflamation. n Calculus n nSupragingival calculus: nColour: yellowish to white, blackish nConsistency: clay-like nMaximum in upper buccal region of molar teeth, lingual and interproximal surface of lower to anterior teeth. n nSubgingival calculus: nDense brown to greyish black in colour Plaque prevention n n1. Mechanical – brushing, flossing nTeeth brush twice daily using a fluoride-based toothpaste. nTeeth floss daily, or use of an interdental cleaner. n2. Chemical – Mouth wash n3. Food intake – nCoarse, dry (Avoid 3s sweet, sticky, soft) nBalanced diet. nAvoidance of tobacco products. nLimit the number of snacks throughout the day. n4. Gingival massage n n Calculus nTreatment nScaling: n Manual n Ultrasonic scaling http://www.travel-dental.com/web_engl/images/preise/prophylaxe/prophylaxe3.jpg http://www.travel-dental.com/web_engl/images/preise/prophylaxe/prophylaxe1.jpg copy copy Host factors - teeth nGenetics (twin studies) nOcclusal morphology nPredisposing nComplexity (e.g. buccal pits) nSimplicity may be protective n nEnvironment (diet, prevention) nResistance to demineralization nReplacement ions in hydroxyapatite nFluoride, strontium - protective nSelenium - predisposing http://www.zahntechnik-online.de Genetics nGenetic factors relate to: ntooth composition and structure ntooth morphology narch form ntooth alignment nsaliva flow rate and composition noral physiology nendogenous microflora nfood preferences npersonality traits Saliva nSalivary flow rate and composition nSalivary tooth protection mechanisms: nmechanical cleansing action, ndilution and buffering plaque acids nanti-microbial properties nsource of inorganic and organic components that inhibit tooth demineralization and assist in the remineralization and repair process. n nReduction or loss of salivary function associated with dramatic increases in caries activity (rampant caries in xerostomia). Host factors - normal saliva nVariation in flow rate nHigh flow rate - protective; low (normal) flow rate - predisposing nNot considered a major risk factor by itself nVariation in salivary buffering capacity nHigh basic components - protective; not considered a major risk factor by itself nVariation in antimicrobial protein concentrations nS-IgA, peroxidase, lysozyme, lactoferrin and others nExpectation: High - protective; Low - predisposing nStudies results are inconsistent, sometimes contradictory n n Host factors - no saliva n nXerostomia due to radiation therapy or Sjogren’s syndrome nVery high S. mutans levels + rampant caries nDecay in unusual sites in multiple teeth Acquired pellicle nThe acquired pellicle - acellular, essentially bacteria-free organic film of mucopolysaccrides deposited on teeth n nCritical position between the enamel surface and the dental plaque biofilm n nThe pellicle formed mainly by selective adsorption of salivary glycoproteins and proteins with a high affinity for the enamel surface, rapid adsorption to a clean enamel surface. n nThe pellicle adheres to the enamel and acts as a diffusion barrier to protect the enamel from acid exposures of short duration, as in ingestion of acidic foods. Acquired pellicle nIf removed (by dental polishing) the pellicle requires a maturation period (7 days) before it becomes maximally protective against acids. n nThe use of abrasive toothpastes and whitening products removes the pellicle, and can have an adverse effect on exposed tooth surfaces in increasing the probability of loss of tooth enamel by demineralization. Diet nThe frequency of eating fermentable carbohydrates has been strongly associated with dental caries. n nFactors associated with diet and dental caries include the relative retentiveness of the food; the presence of protective factors in food, such as calcium, phosphate, and fluoride, and the type of carbohydrate. n nComplex carbohydrates (starches) are less cariogenic than simple carbohydrates (sucrose, glucose, and fructose). Dynamic nature of caries nThe earliest macroscopic evidence of caries of a smooth enamel surface - a small opaque white region - white spot lesion. n nIts presence - indication for a localized decrease in mineral content of the enamel, although the surface still hard when examined with a dental explorer. White spot lesion n nThe appearance of the white spot lesion in the scanning electron microscope: nsmall pits representing accentuation of prism outline as the earliest stage of enamel decay. White spot lesion - EM n 10big copy Enamel caries n n The white spot lesion: conical shape with the base towards the outer enamel surface and the apex towards the amelodentinal junction. n nCaries spreads in zones: nSurface zone nBody of the lesion nDark zone nTranslucent zone n White spot lesion n1. SURFACE ZONE Initial lesion of caries, most of the demineralization begins to occur at a subsurface level, leaving the surface zone relatively unaffected. whitespo copy copy copy Surface zone n~40 micrometer thick nrelatively normal: maximum remineralization from the inorganic components of both the plaque and saliva. Subsurface nTheory: minerals dissolved from this subsurface zone pumped toward the surface → remineralization of the surface zone by precipitation of minerals n nThe surface layer of enamel also more mineralized than the subsurface layer, possibly more resistant to acid attack. n nThe surface layer relatively unaffected, but more porous in comparison with the unaffected surface. White spot lesion n2. BODY OF THE LESION nThe largest portion of carious enamel in the white spot lesion. nLoss of ~ 1/4 of its original mineral content. whitespo copy copy Body of the lesion nPore volume of 5-25% nApatite crystals larger than the normal enamel. nEffort for the remineralization, but by the further attack → further dissolution of the mineral nThe zone of maximum demineralization. White spot lesion n3. DARK ZONE nPorous zone + n mineral loss of about 6%. n whitespo copy copy Dark zone nPore volume 2-4% nSome pores larger, some smaller than in the translucent zone suggesting that some remineralization has occurred. nIn rapidly advancing lesion narrow dark zone. nPreviously liberated salts redeposited here White spot lesion n4. TRANSLUCENT ZONE nThe advancing front of the enamel lesion. More porous than the sound enamel but less porous than the dark zone. whitespo copy copy Translucent zone Zone of intial demineralization nPore volume 1% nPores larger than in the normal enamel. n↓ magnesium and carbonate content in comparison to normal enamel n Zones of enamel caries CAIR09AZ copy n The five stages of caries development1,2 1. Collins WJN, et al. A Handbook for Dental Hygienists. 3rd edition. Oxford: Wright, 1992. 2. Clarkson BH, et al. Caries Res 1991;25:166-173. 3. Collapse of surface layer to form cavity Irreversible lesion Possible formation of apical abscess Reversible lesion 1. Initial subsurface demineralization Initial subsurface demineralization Extension of demineralized zone towards dentine Collapse of surface layer to form cavity Extension of caries lesion into dentine Extension of caries into pulp 1 2 3 4 5 ToothMontage3 Enamel caries nBegins as discrete lesions in the enamel of specific sites (reservoirs) n Occlusal pits and fissures of Interproximal contacts n molars and premolars between adjacent teeth n n n n n n n n n n n n n n n / Enamel caries n nThe initial lesion is visible as a white spot, due to demineralization of the prisms in a sub-surface layer, with the surface enamel remaining more mineralized. nWith continued acid attack the surface changes from being smooth to rough, and may become stained. nAs the lesion progresses, pitting and eventually cavitation occur. ž Caries progression nEven if the enamel surface clinically intact when the lesion reaches the enamel-dentin junction, acids may diffuse into the dentin via carious enamel (together with other clinical stimuli), possible dentin and pulp response. nLateral spread along the enamel-dentin junction → a broad-based lesion following the curvature of the dentinal tubules - its narrow apex approaches the pulp. nIn the dentin: a zone of sclerosis walling off the lesion from the surrounding normal dentin. nThe pulp reacts to the advancing lesion by laying down a region of reparative dentin. Caries progression nThe body of the dentinal lesion may at first be uninfected (bacteria not able to gain access until a cavitation forms in the surface enamel). n nAt this stage - if preventive measures instituted - the lesion can remain static or regress. n nAfter cavitation of the enamel lesion bacteria can penetrate into the tissue - ↑ rate of progression of the dentin lesion n nProteolytic enzymes of the bacteria destroy the organic collagenous matrix of the enamel and dentin → characteristic dental cavity. Caries progression n 09big copy Implications for radiographic diagnosis nLaboratory studies demonstrate that histologically the lesion must penetrate just into the dentin before evidence of a carious lesion is observed on a routine bite-wing radiograph n nAt this stage the lesion is observed on the radiograph as a small triangular region of radiolucency in the outer enamel. Radiograph versus histology n cariesra Clinical implications for caries diagnosis nA carious lesion which could not be detected by explorer or X-ray has already penetrated halfway through the enamel. n nA lesion which can be observed on a bite-wing radiograph has probably already advanced into the dentin (especially in the primary dentition). copy copy Demineralized enamel n 12big copy Enamel + dentin caries n nSection of enamel and early dentinal caries. Although the outer surface of the enamel looks intact, the dentinal process (arrow) has started. 13big copy Dentinal caries nDiffers from the enamel caries - a living tissue responding in a unique way nDentin with a high organic component consisting predominantly of collagen nA defense mechanism activated in the dentin caries by pulp-predentin complex. nCaries spread much faster in this zone - more porous + dentinal tubules. nBacterial strains able to release large amount of proteolytic enzymes causing damage to dentin. n n Dentinal caries nDefense reaction of the pulpodentinal complex nSclerosis nReactionary dentine formation nSealing of the dead tracts n nCarious destruction nDemineralization nProteolysis Dentinal caries http://www.st-andrews.ac.uk/~amc/research/medical.htm http://www.dent.umich.edu/research/loeschelabs Love et al. Infect. Immun. 68:1359 • Cavitation • Demineralization + proteolysis • Bacteria move down tubules • Pulpal involvement • Major damage if unchecked Can be arrested, but generally must be restored Dentinal caries n n5 bands: outside (1) nzone of necrotic dentin nzone of infected dentinal tubules nzone of transparent dentin or sclerotic dentin nzone of fatty degeneration of tubules narea of intact dentin. 15big copy Dentinal caries nzone of necrotic dentin nproteolysis, liquefaction nfoci parallel with tubules Dentinal caries nZone of bacterial invasion nacidogenic microorganisms (lactobacilli) nacidogenic and proteolytic microorganisms Infected tubules n 16big copy Bacteria in dentinal tubules n 17big copy Dentinal caries nClefting nHorizontal clefting occurs at right angles to the dentinal tubules. The process of beading, coalescence, and clefting typifies the mode of progression of dentinal caries. Dentinal caries n 21big copy Dentinal caries n 24big copy Dentinal caries nZone of demineralization ndiffusion of acids nsoftened dentin nusually direct progression into zone of bacterial invasion nmay be brownish Dentinal caries n Beading, coalescence, and clefting in severely decayed dentin. 71big copy Dentinal caries n Extension of decay process to the pulp with reparative dentin and severe pulpal inflammation. 72big copy Dentinal caries n Edge of the intensive inflammation with reparative dentin and maintenance of part of the odontoblastic layer adjacent to the uninflamed pulp. 74big copy Dentinal caries nZone of sclerosis ntranslucent zone nodontoblastic reaction with mineralization - ↑ mineral content ndead tracts – loss of odontoblasts, contain air, possible access of bacteria – sealing with hyaline calcified matter, produced by pulpal cells Advanced dentinal caries nextreme breakdown of dentin with large clefts appearing both vertically and horizontally and with bacteria proceeding down the tubules. 22big copy Root surface caries nMechanism the same as enamel caries n nBacterial enzymes break down dentin in the root tooth anatomy copy Root caries nInitial phase ngingival recession (abrasion, aging, periodontal disease) n nPhase II nbegins apically to the cemento-enamel junction nfew clinical symptoms nbrownish color, softening Root caries ncementum - primary tissue affected in the root caries nroot exposed to the oral environment as a result of the periodontal disease, followed by the bacterial colonization. nsuperficial hypermineralisation nsubsurface demineralization of the cementum and the chain of events similar in the dentine as in the crown portion. Root caries nRoot surface caries: n45% minerals (x 88% in coronal c.) nPlaque + recession related nAcid dissolves surface – contour changes nOnce collagen destroyed, remineralization not possible (x coronal c. – possible until cavitation) n n Root caries 4801350f15 illus_learnc_whatiscavity3[1] copy Pathology of caries nClassification by site of attack n pit (fissure) caries n smooth surface caries n cemental (root) caries n recurrent caries nClassification by rate of attack n acute (rampant) caries n slowly progressive, chronic caries n arrested caries Caries sites 1.Pit-and-fissure caries initially in the fissures of the teeth, but can spread into the dentine 2.Smooth-surface caries most common on interdental surfaces, but can occur on any smooth surface of the tooth 3.Root caries attack the cementum and dentine, exposed as gums recede. tooth without cavity copy Caries progression in a fissure n car-fiss copy Smooth surface enamel caries n nEnamel caries on the smooth surface: a focally brown or white spot lesion nRadiographically undetectable because of the intact surface. Smooth surface enamel caries n 05big copy Primary teeth nPrimary molars with broad, flat contact areas in contrast to the contact „points“ in the permanent dentition. nExposition of a large interproximal area of primary teeth to stagnation, favoring bacterial colonization. nPrimary enamel thickness ~one-half that of permanent enamel, the pulp chamber is relatively larger. nThe rate of progression of a lesion through primary enamel is much faster compared with an equal distance through permanent enamel. Early childhood caries Caries-ECC-3 (Douglass et al., Am Fam Physician, 2004) ECC-erupting Early childhood caries (ECC) nAlso called Baby Bottle Tooth Decay (BBTD) nAssociated with dietary carbohydrates nRisk factors nFrequent sugar consumption nFoods/fluids sweetened with fermentable carbohydrates over extended period nExposure to environmental tobacco smoke n n n n Arrested caries nEnamel nnon-cavitary lesion accessible to plaque control nremineralization nDentin nearly dentinal sclerosis (not in acute caries) nlateral spread of caries possible, undermining, removal of softened structures nleaves brown-black hypermineralized dentine n