Dental Cariology Lecture Notes PDF

Dental Cariology Dr.Doaa Alhelais  Clinical charactrestics of carious lesion The caries lesion is the product of disequilibrium between the demineralization and remineralization processes discussed previously. When the tooth surface becomes cavitated, a more retentive surface area...

Dental Cariology Dr.Doaa Alhelais  Clinical charactrestics of carious lesion The caries lesion is the product of disequilibrium between the demineralization and remineralization processes discussed previously. When the tooth surface becomes cavitated, a more retentive surface area becomes available to the biofilm community. This situation results in a rapid and progressive destruction of the tooth structure. When enamel caries penetrates to the dentinoenamel junction (DEJ), rapid lateral expansion of the caries lesion occurs because dentin is much less resistant to acid demineralization. This sheltered, highly acidic, and anaerobic environment provides an ideal niche for cariogenic bacteria.  Clinical Sites for Caries Initiation There are three distinctly different clinical sites for caries initiation with different shapes of lesion: A) Pits and fissures of enamel (most susceptible area) B) Smooth enamel surfaces that shelter cariogenic biofilm; C) The root surface imp A) Pits and fissures of enamel: Bacteria rapidly colonize the pits and fissures of newly erupted teeth. imp S. sanguis, are found in the pits and fissures of newly erupted teeth, whereas large numbers of Mutanus Streptocci usually are found in carious pits and fissures. The shape of the pits and fissures contributes to their high susceptibility to caries: The long, narrow fissure prevents adequate biofilm removal imp A) Pits and fissures of enamel: Pit-and-fissure caries expands as it penetrates into the enamel. wideexpansion The entry site may appear much smaller than the actual lesion, making clinical diagnosis difficult. A) Pits and fissures of enamel: Pit-and-fissure caries expands as it penetrates into the enamel. The entry site may appear much smaller than the actual lesion, making clinical diagnosis difficult.  Apex Base DEJ fissure towardstheroot pulp A) Pits and fissures of enamel: In cross-section, the gross appearance of a pit-and-fissure lesion is Q's A conical lesion with the base towards the DEJ. imp It is an inverted “V” with a narrow entrance and a progressively wider area of involvement closer to the DEJ. smallentry Gets bigger towards DEJ  mostsusceptiblearea proximalcontact under B) smooth enamel surfaces of near theGingiva but underproximal The smooth enamel surfaces of teeth present a less favorable site for cariogenic biofilm morel attachment. Cariogenic biofilm usually develops only on the smooth surfaces that are near the gingiva or are under proximal contacts. imp  Q Ba se Apex Largeareta narrows towards B) smooth enamel surfaces thepulp A cross-section of the enamel portion of a smooth-surface lesion shows a V-shape, with imp a wide area of origin and the apex of the V directed toward the DEJ. A conical lesion with the apex towards the DEJ.  GI be Cementumrequires bond C) Root surface caries: v difficultto restore The root surface is rougher than enamel and readily allows cariogenic biofilm formation in the absence of good oral hygiene. The cementum covering the root surface is extremely thin and provides little resistance to caries attack. Root caries lesions have less well-defined margins, tend to be U-shaped in cross- imp section, and progress more rapidly because of the lack of protection from an enamel covering.  Progression of Enamel caries The time for progression from non-cavitated enamel caries to clinical caries (cavitation) on smooth surfaces is estimated to be 18 months ± 6 months. up 12 24 butusually18months Progression of Enamel caries A more advanced lesion develops a rough surface that is softer than the unaffected, normal enamel. Softened chalky enamel that can be chipped away with an explorer is a sign of active caries. cups Demineralization can besolved by remineralization must be restored Progression of Enamel caries The supersaturation of saliva with calcium and phosphate ions with The presence of trace amounts of fluoride ions serves as the driving force for the remineralization process. Remineralized (arrested caries) lesions can be observed clinically as intact, but discolored,usually brown or black, spots. Rough These discolored, remineralized, arrested caries areas are intact and are more resistant to subsequent caries attack. They should not be restored unless they are esthetically unacceptable. be they're more resistant to cariest they're intact D) Progression of Enamel caries These discolored, remineralized, arrested caries areas are intact and are more resistant to subsequent caries attack. They should not be restored unless they are esthetically unacceptable. Classification of Dental Caries cap  1- Enamel Caries: On clean, dry teeth, the earliest evidence of caries on the smooth enamel surface of a crown is a white spot.(chalky white, opaque areas ) These lesions usually are observed on the facial and lingual surfaces of teeth. Revealed only when the tooth surface is desiccated or dried. They termed non cavitated enamel caries lesions. Demineralized These areas of enamel lose their translucency because of the extensive subsurface porosity caused by demineralization sheignored  Microscopic Features of Non cavitated Enamel s: there are 4 zones identified pre-cavitation. These are: 1.Translucent zone – the advancing edge of the lesion 2.Dark zone 3.Body of the lesion 4.Surface zone impi Microscopic Features of Non cavitated Enamel : op Leastaffected unaffected Demineralization positivezone Advancing  9 Microscopic Features of Non cavitated Enamel 1) Translucent Zone This is the advancing edge of the enamel lesion. It is only present in 50% of lesions. 2) Dark Zone HI Lies adjacent and superficial to the translucent zone. Present in up to 95% of lesions. (Called positive zone as it is always present) 3) Body of the lesion The largest part of the lesion and lies between the surface zone and dark zone. Area of greatest demineralization 4) Surface Zone This zone appears almost unaffected in the superficial layers Minimal demineralisation also REMAINS MORE HEAVILY MINERALIZED because of Ca , P and Floride.  Base DEJ 2- Dentin Caries: Apex pulp Dentin contains much less mineral and possesses microscopic tubules that provide a pathway for the ingress of bacteria and egress of mineral Once bacteria penetrate enamel, they spread laterally along DEJ and attack dentin over a wide area. Dentinal caries is V-shaped in cross-section with a wide base at the DEJ and the apex directed pulpally. Caries advances more rapidly in dentin than in enamel because dentin provides much less resistance to acid attack owing to less mineralized content. The infected lesion of dentin is helped in its course by the presence of tubules within dentin which provide an easy pathway to the bacteria. Microscopic Features of Non cavitated Dentin : Microscopic Features of Non cavitated Dentin : Three different zones have been described in carious dentin.The zones are most clearly distinguished in slowly advancing lesions. ZONE 1: NORMAL DENTIN The deepest area is normal dentin, which has tubules with odontoblastic processes that are smooth No bacteria are present in the tubules Normal Affected infected then Microscopic Features of Non cavitated Dentin : Three different zones have been described in carious dentin.The zones are most clearly distinguished in slowly advancing lesions. ZONE 2: AFFECTED DENTIN Also called inner carious dentin, affected dentin is a zone of demineralization of intertubular dentin Can be remineralizes affected dentin zone can also be subclassified to 3 subzones: (1) subtransparent dentin (2) transparent dentin VVV (3) turbid dentin. impt ZONE 3: INFECTED DENTIN Also called outer carious dentin, this is the outermost carious layer, the layer that the clinician would encounter first when opening a lesion. The infected dentin is the zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules, which are filled with bacteria Easy a imp I  How to discriminate between different dentine layers? non vital Bacteria nobacteria vital Clinical Infected Affected Sound method Visual Paler light Yellowish/ Dark brown inspection brown white Tissue Sticky/ Wet/ soft Hard hardness scratchy imp Caries Dark Red Pale red Pink disclosing dyes infected Leave affected  2- Dentin Caries: The pulp–dentin complex reacts to caries attacks by attempting to initiate remineralization and blocking off the open tubules. Three levels of dentinal reaction to caries can be recognized: (1) Reaction to a long-term, low-level acid demineralization associated with a slowly advancing lesion. (2) Reaction to a moderate-intensity attack. (3) Reaction to severe, rapidly advancing caries characterized by very high acid levels.  2- Dentin Caries: In slowly advancing caries: Dentin can react defensively (by repair) to low-intensity and moderate-intensity caries attacks as long as the pulp remains vital and has an adequate blood circulation. This repair occurs only if the tooth pulp is vital. In slowly advancing caries, a vital pulp can repair demineralized dentin by remineralization of the intertubular dentin and by apposition of peritubular dentin. cap  2- Dentin Caries: In slowly advancing caries: notremoved Dentin that has more mineral content than normal dentin is termed sclerotic dentin Sclerotic dentin is usually shiny and darker in color but feels hard to the explorer tip. The apparent function of sclerotic dentin is to wall off a lesion by blocking (sealing) the tubules. The permeability of sclerotic dentin is greatly reduced compared with normal dentin because of the decrease in the tubule lumen diameter must Double etchant time  2- Dentin Caries: More intense caries activity results in bacterial invasion of dentin. Infected dentin contains a wide variety of pathogenic materials or irritants, including high acid levels, hydrolytic enzymes, bacteria, and bacterial cellular debris. These materials can cause the degeneration and death of odontoblasts and their tubular extensions below the lesion and a mild inflammation of the pulp happen. The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation (from undifferentiated mesenchymal cells) of replacement odontoblasts (secondary odontoblasts). These cells produce reparative dentin Reparative dentin is an effective barrier to diffusion of material through the tubules and is an important step in the repair of dentin..  2- Dentin Caries: The third level of dentinal response is to severe irritation, Acute, rapidly advancing caries with high levels of acid production overpowers dentinal defenses and results in infection, abscess, and death of the pulp. microscopicfindingstzonestresponset Thank you