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Document Details

PoshAsh

Uploaded by PoshAsh

Horus University - Egypt

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dental caries dental health tooth decay

Summary

This presentation details dental caries, discussing its definition, classification, contributing factors, mechanisms of action, and pathology of enamel and dentine caries. It elaborates on the role of saliva, theories of dental caries, and microscopic views of the disease progression. Important information on various types of caries further clarifies the complex disease process.

Full Transcript

Dental Caries Definition It is a disease characterized by demineralization of inorganic part of the tooth followed by dissolution of its organic part by the action of bacteria. It is the most common dental disease world wide. Classification 1- Pits & fissu...

Dental Caries Definition It is a disease characterized by demineralization of inorganic part of the tooth followed by dissolution of its organic part by the action of bacteria. It is the most common dental disease world wide. Classification 1- Pits & fissures caries. 2-Smooth surface caries. 3- Cemental (root) caries. 4- Recurrent caries. 5-Acute (rampant) caries. 6-arrested caries. Contributing Factors 1- Susiptable tooth surface. 2- Carbohydrates. 3- Micro-organisms. 4- Dental plaque. 1- Susceptible tooth surface: a) Tooth position. b) Tooth morphology. c) Tooth structure. d) Genetic factors. e) Fluorides. Mechanisms of cariostatic effect of fluoride: 1- Reduction of apatite solubility through conversion of hydroxy-apatite to flouro- apatite crystals. 2- Enhancement of re-mineralization of the carious lesion. 3- Anti-bacterial activity. Anti-bacterial activity of fluoride: 1- Decreased lactic acid production thus the organisms become less cariogenic. 2- Decreased glucose uptake by the organisms which lead to decrease in energy reserve & metabolic activity of the organisms. 3- Decreased bacterial adhesion. 2- Carbohydrates a) Type of carbohydrates: mono, di & polysaccharides. b) Total amount of carbohydrate intake. c) Frequency of carbohydrates intake. d) Consistency of carbohydrates. 3- Micro-organisms 1- types of bacteria involved in caries: a) Acidogenic bacteria: Lactobacilli & Streptococci (Strept. Mutans). b) Proteolytic bacteria: Actinomyces, Clostridia & Pseudomonas. c) Chromogenic bacteria: Asprigillus. Essential features of cariogenic bacteria: a) Acidogenic. b) Production of low pH (Lower than 5.5). c) Aciduric. d) Have attachment mechanisms for firm adhesion to tooth surface. e) Production of abundant polysaccharides for formation of plaque matrix. 4-Dental plaque It is an adherent bacterial structure formed on tooth surfaces. It contains a large number of closely packed micro- organisms surrounded by an extracellular material of bacterial and salivary origin. It has 2 major interfaces: a) Internal one (pellicle). b) External one (plaque saliva interface) Types: 1- Sub-gingival. 2- Supra-gingival. Composition: I- Micro-organisms. II- Matrix which is formed of protein, lipids, carbohydrates, inorganic component & water. Role of plaque matrix: 1- Acting as diffusion limiting membrane retaining acid in high concentration to initiate caries. 2- Slow down the entry of buffers from saliva, thus delaying their neutralizing action. Factors affecting plaque formation: 1- Anatomy & position of tooth. 2- Presence of appliance. 3- Structure of tooth surface. 4- Friction from diet. 5- Oral hygiene procedures. 6- Composition of the diet. Mechanism of action of dental plaque: 1- Allow adhesion of bacteria & acids on the surfaces of teeth. 2- Prevent escape of acids & entry of salivary buffers. Saliva & Caries The role of saliva in caries includes: 1- Washing effect of saliva. 2- Buffering effect of saliva by phosphate & bicarbonate content. 3- Salivary antibodies ( Ig A). 4- Antibacterial substances : lysozymes, Peroxidases & lactoferrin. Theories of dental caries 1- Acidogenic theory (Miller”s chemico- parasitic theory). Most accepted one. 2- Proteolytic theory. Explains penetrating caries under restorations & caries of impacted teeth. 3- Proteolosis- chelation theory. Pathology of Enamel Caries Clinical Picture: Firstly, White chalky area. Then, Rough to the probe with staining. Later on, Cavitations will occur. Carious lesion is cone shaped. 1-In pits & fissure caries: Base toward DEJ. Apex toward surface. 2-In smooth surface caries: Base toward surface. Apex toward DEJ. Microscopic Picture: With polarized light microscope enamel caries occurs in 4 phases: 1- Initiation phase. 2- Bacterial invasion phase. 3- Destruction phase. 4- Phase of secondary enamel caries. 1- Initiation phase is divided into 4 zones: A- Translucent zone: a) Lies at advancing front of carious lesion. b) Due to initial demineralization. c) Contains pores accounting for 1-2% of enamel volume. B- Dark zone: a) lies superficial to the translucent zone. b) Due to further enamel demineralization. c) Contains micro-pores accounting for 2-4 % of enamel volume. C- Body of the lesions: a) Lies under the surface zone & constitutes the largest area of the carious lesion. b) Due to advanced demineralization. c) Contains pores accounting for 5% at the periphery & 25% at the center of the zone d) Appears translucent. D- Surface zone: This zone although not merely intact, It appears more radio-opaque & harder than deeper zones. This may be due to: Continuous re-mineralization from saliva. It Contains much fluoride. It contains much insoluble proteins. Prism-less enamel in this zone may delay diffusion of acids. 2- Phase of bacterial invasion: Bacteria begin to invade enamel when sufficient spaces are created by the action of acids. 3- Phase of destruction: In this phase, proteolytic bacteria begin to act on the organic matrix of the enamel leading to complete destruction of enamel. 4- Phase of secondary enamel caries: When acids & bacteria reach DEJ, they spread laterally along it and begin to invade enamel from beneath leading to its undermining. Pathology of Dentine caries Clinical Picture: It appears brownish & soft to the probe. It is cone shaped with the base toward DEJ & the apex toward the pulp. Microscopic Picture: I- Initial uninfected lesions: It occur before enamel cavitations & include the following zones: 1- Zone 1: zone of reactionary or reparative dentine formation. (secondary dentine) 2- Zone 2: zone of sclerotic or translucent dentine formation. (Ca. ion deposition) 3- Zone 3: zone of body of the lesion. (dead tract) II- Infected lesion: It occurs after enamel cavitations & dentinal tubules provide a pathway of bacterial invasion that occur in 2 waves: The 1st wave: pioneer bacteria consists of acidogenic bacteria that decalcify dentine leaving organic matrix intact. The 2nd wave: consists of mixed infection containing proteolytic bacteria that distort the organic matrix. Infected lesion consists of 4 zones: Zone 1: Mild pulp inflammation. Zone 2: Reparative or reactionary dentine. Zone 3: Sclerotic dentine. Zone 4: Body of the lesion. which consists of: a) Decalcified uninfected zone. b) Decalcified infected zone. c) Destruction zone. Decalcified infected zone shows: 1- Beading: lateral distension of dentinal tubules by the action of bacteria. 2- Liquefaction foci: is the coalescence of neighboring beads & lie at long axis of dentinal tubules. 3- Transverse clefts: is a liquefaction foci lie at right angle to dentinal tubules due to their existence on a lateral branch of dentinal tubules. Thank YOU

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