Dental Caries (1) BDS10004 Lecture Notes PDF

Dental caries (1) BDS10004 Date : Aims: The aim of this lecture is to detail the histopathological features of the various stages of caries of the enamel and dentin Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of early through...

Dental caries (1) BDS10004 Date : Aims: The aim of this lecture is to detail the histopathological features of the various stages of caries of the enamel and dentin Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of early through to gross caries of the enamel and dentin Definition Progressive Bacterial damage of hard tooth structure exposed to oral environment resulting in Decalcification of inorganic content Destruction of organic content Cavity formation Etiology Multifactorial disease Substrate fermentable CHO Host Susceptible tooth & saliva Caries Time Micro- organism s I. Host A. Susceptible tooth surface 1-Position of tooth:  Upper teeth are more susceptible to caries than lower [as salivary action is not present].  Posterior teeth are more susceptible to caries than anterior teeth due to presence of fissures [retention of food].  Malposed and crowded teeth and teeth related to orthodontic appliance are more susceptible to caries [because of the creation of stagnation areas]. 2. Morphology  Pits and fissures are more susceptible to caries (retention of food).  Site below lingual and buccal convexities are more susceptible to caries (stagnation areas)  Contact areas are more susceptible to caries. 3.Fluoride has a cariostatic effect  ↓demineralization [increasing enamel resistance to demineralization] as it replaces hydroxyl ions in hydroxyapatite to form less acid soluble fluoroapatite  ↑ remineralization  Inhibition of bacterial growth Fluoride inhibits bacterial enzymes and thus stop bacterial activities. 3.Fluoride Sources of fluoride:  drinking water  Tea  seafood  Therapy (Topical application) B. Role of Saliva  Salivary glycoproteins form acquired enamel pellicle [which initially protects the enamel surface from being colonized by oral bacteria]  Cleansing effect  Salivary buffers (bicarbonates) [neutralize the acidity]  Inorganic components (calcium, phosphate and fluoride) → promote remineralization  Secretory immunoglobulin A → ♦ killing of bacteria, ♦ prevent adherence to tooth surface & ♦ inhibit bacterial activity  Antibacterial components of saliva (Lysozymes, peroxides and lactoferrin) → direct anti bacterial action II. Carbohydrates 1. Why does carbohydrates cause dental caries rather than proteins and fats?  CHO → acted upon in the oral cavity  Proteins & fats →undergo little change in oral cavity 2. Do all carbohydrates cause dental caries?  Monosaccaharides (less cariogenic) its contribution in the formation of sufficient cariogenic plaque is less than sucrose.  Disaccharides most cariogenic  Polysaccharides (Less cariogenic) can't diffuse rapidly in dental plaque due to large molecular weight. can't be easily metabolized by oral bacteria. Sucrose Is the arch criminal of dental caries Role of sucrose in caries production  Low price & low molecular weight → pass easily into dental plaque Sucrose invertase hydrolysis fructose + glucose Fructokinase glycolsis glucokinase Energy + H2O + organic acids  acids will drop the pH below the critical level (pH=5.5) at which demineralization of enamel starts Pyruvic acid Lactic acid Vipeholm experiment by Gustafson in Sweden Aim: to show the effect of total amount, frequency and texture of CHO.  400 patients in a mental hospital were divided into 7 groups  DMF was measured before the experiment Vipeholm Experiment Control group groups groups Basic low CHO diet Basic low CHO diet Basic low CHO diet Sugar in solution at mealtime Sweetened bread at mealtime Toffee between meals Caramel between meals Chocolate between meals  DMF was measured after 5 years & a diagram was drawn  Observation: ↑↑ caries activity with sticky CHO (toffee & caramel between meals)  Conclusion: frequency & texture of CHO are more effective than total amount III. Micro-organisms 3 Experiments: Miller Orland 54 Orland 55 Orland’s experiments (54) They obtained germ free animals by caesarian sectioning of pregnant rats under complete aseptic conditions Rats divided into 2 groups Grow in aseptic incubators & eat completely aseptic cariogenic food No caries live in containers in air & eat nonsterile food caries Orland’s experiments (55) Further experiments were performed by the same investigators (1955) in order to determine which species of bacteria were cariogenic.  Gnotobiotes (known life-controlled flora) Gnotobiotic animals are germ free animals to which a single known strain of m.o. is introduced to its oral activity Orland’s experiments (55) Conclusion: The most potent micro-organisms responsible for caries production are Streptococcus mutans WHY? because  Acidogenic [powerful acid producer]  Aciduric [can survive at low pH]  Form intracellular polysaccharides [acting as reserve at time of CHO deficiency]  have attachment mechanism [firm adhesion to smooth tooth surface]  Form extracellular polysaccharides [mainly dextran which forms the bulk of dental plaque] Dental plaque Definition: It is a tenaciously adherent soft, nonmineralized bacterial structure formed on the tooth surface (biofilm) Clinical appearance  Early plaque formation is seen when tooth brushing is stopped for 12-24 h.  It forms more rapidly and in greatest amount with high sugar diet.  As plaque builds up it become visible by the naked eye (more seen by disclosing solution). Dental plaque Proteins Composition of dental plaque Role of plaque matrix  It contributes to ♦adhesiveness , ♦bulk ♦resistance to washing.  It acts as a diffusion limiting membrane retaining acids in high concentrations Slow down the entry of buffers from saliva, so delaying their neutralizing action Carbohy drates Lipid Inorgani c content Dental plaque Mechanism of formation of dental plaque 1 2 3 4 Acquired enamel pellicle Initial community intermediate community Mature community & dispersion It is an acellular structurless, bacteriafree film of salivary glycoproteins is formed after thorough tooth brushing 2. Initial community  Colonization phase (8)  Pioneer micro-organisms (streptococcus sanguis, oralis, mitis) →bacterial adhesion and colonization on the tooth surface begins within minutes after the pellicle is formed  Growth phase (8-48)  Rapid growth of pioneer bacteria forming colonies →  A monolayer of m.o is formed  Then further bacterial proliferation in vertical ┴ direction[perpendicular to the tooth surface]. 3. Intermediate community Ingress & proliferation of secondary invadors (S. mutans) 4. Mature community (2 weeks or older) As the Plaque matures, Filamentous organisms (actinomyces), proliferate & predominate → they are arranged // to each other & ┴ to tooth surface Distinctive bacterial aggregation known as “corn cobs” are seen by electron microscope.  Acid production in dental plaque (Stephen’s curve) Aim: is to study the change in pH of plaque after CHO intake 1. Measuring the resting pH [by putting an electrode in contact with plaque & the other electrode in the floor of the mouth] Resting pH is the pH of an individual at least 1 hour after the last meal when there is no fermentable CHO consumed 2. Patients (with different caries activities) were allowed to rinse their mouth by 25 ml 10 % glucose for 10 seconds 3. pH changes were measured frequently & a curve was plotted  Acid production in dental plaque (Stephen’s curve)  The curves show that after the glucose rinse the pH drops rapidly reaching the critical pH. (5.5) within 2-5 minutes  The pH remains under the critical level for 10-30 minutes (depending on caries activity).  Then the pH returns slowly to the resting pH  So the more time below the critical pH the more is the caries activity. caries-resistant patients cariessusceptible patients critical pH Demineralization Key points  Dental caries is a multifactorial disease  Position and morphology of teeth affects caries activity as well as host’s saliva  Sucrose is the arch criminal of dental caries  Frequency & texture of CHO affects caries activity more than total amount  Acids will drop the pH below the critical level (pH=5.5) at which demineralization of enamel starts Aims: The aim of this lecture is to detail the histopathological features of the various stages of caries of the enamel and dentin Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of early through to gross caries of the enamel and dentin Dental Caries Reading material: Students are advised to review any relevant teaching provided in the first year. In addition they are advised to read relevant sections of the following texts: Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp107-118 Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 23-44 Thank you