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118 Cards in this Set
- Front
- Back
Eukaryotic Microbes are |
Single-celled or multicellular |
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Prokaryotic microbes are |
single celle but may exist in chains or groups |
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Acellular microbes are |
nucleic acid surrounded by protein |
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What type of magnification do you need to see Eukaryotes to Bacteria to Viruses |
Low to High but 100-400 for Eukaryotes, 1000 for bacteria with oil immerision and >20000 to see viruses |
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Key differences of eukaryotes to prokaryotes |
Eukaryotes have nuclei and inner membrane bound organelles Prokaryotes only have a nucleoid. Ribosomes run free, translation can occur right away and have pilli and flagella |
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What are the major targets for anitmicrobials on prokaryotes? |
Peptidoglycan cell walls and 70s ribosomes |
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What majorly differs in composition between gram negative bacteria and gram positive bacteria? |
Gram-Negative bacteria has an outer Lipoplysaccharide layer that gets washed away by an alochol solution which makes it easy for the peptidoglycan membrane to be stained. The think peptidoglycan wall of gram positives make it difficult for the cell to be lysed. |
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What endotoxin is specific to gram negative bacteria? |
Lipopolysaccharide, LPS |
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What type of bacteria is found mostly in the oral cavity? |
The teethy have larger proportions of Gram-positive cocci and rods but older plaque, gingiva, and periodontium have elevated levels of anaerobic Gram-negative rods. Concentrations are higher than anywhere outside of the colon |
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What are two ways disease can occur? |
1. Bacteria can be pathogenic which lead to symptoms of diseas and the virulence factors are waht make the hose sick. 2. Overgrowth of a normal microflora species can weaken host defenses and lead to an opportunistic infection |
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How do bacteria create adhesion with the pellicle? |
The forces of attraction oercome the forces of repulsion. Initial adhesion occurs at the secondary minimum, 10-20nm, and is reversible. Irreversible adhesioin requires additional interactions and exist at <1nm |
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Cross-sectional studies |
Compare the microflora in health and disease |
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Prospective studies |
Look at changes in the microflora that accompny the change from health to disease |
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Common Gram-Positive Genera |
Streptococcus, Peptostreptococcus, Micrococcus, Actinomyces, Propionibacterium, Rothia, Lactobacills, Bifidobacterium, Eubacteruim, Corynecbacterium |
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The Totality of the Oral Flora |
The flora will almost certainly be more similar from site to site (within a niche) in a given individual than between identical sites in two different individuals |
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Early vs Mature Supragingival Plaque |
Early - Mainly Gram-positive, mostly cocci, mostly facultative anaerobes Mature - Increasing representation of Gram-negatives, many morphological types, facultative anaerobes and obligate anaerobes |
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Supragingival vs. Subgingival Plaque |
Supra - Mix of Gram pos and neg., mix of cocci and rods, mix of facultatives and anaerobes, more carb fermenters, firmly adherent Sub - Dominated by Gram neg, more gram neg rods and spirochetes, more obligate anaerobes, more proteolytic species, less adherent/more motile |
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What are bacteriocins? |
Toxins produced by bacteria to kill other similar competing strains |
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Biochemical or enzymatic non-specific means of plaque control |
1. Lysozyme- Break bonds in peptidoglycan, kill amphipathic sequences, induce bacteria to kill themselves, may agglutinate bacteria 2. Histatins - Mainly anti-fungal but also anti-bacterial, prevents coaggregation, inhibits bacterial prteinases 3. Peroxidase and thiocyanate - thiocyanate ion that inhibits bacterial growth and agglutinin (grouping of bacteria made easier to get rid of) 4. Lactoferrin - sequesters iron away from bacteria. Cleaved peptide is inhibitory for bacteria 5. Salivary mucins and parotid agglutinin
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Innate Immune Mechanisms non-specific means of plaque control |
1. Defensins and antimicrobial peptides 2. Neutrophils and other phagocytic cells |
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Adaptive Immunity non-specific means of plaque control |
sIgA - Most abundant isotype in saliva and agglutiantes bacteria IgG, IgM, lymphocytes - Traditional facets of immune response will operate within periodntal pockets because gingival crevicular fluid is similar to plasma |
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Dr. Willoughby D. Miller, 1880s |
Incubated Bread, Saliva and a tooth. Tooth eventually dissolved |
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What is the Non-specific plaque hypothesis? |
Concluded that caries was initiated due to the collective acidogenic properites of plaque bacteria. |
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Work of Israel J. Kligler |
Certain species stood out with respect to producing acid and surviving low pH would be likely etiolgic agents. Found that lactobacilli dominated in advanced lesions. Lactobacilli increased as the health of the tooth decreased |
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Work of J. Kilian Clark 1924 |
Isolated bacterial species from carious lesion known as Streptococcus mutans. Higher frequency than lactobacilli and formed a sticky slime layer that help adher the bacteria. |
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Name the 2 mutans streptococci that are most cariogenic |
1. S. mutans 2. Sobrins |
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Experiment by F.J. Orland in 1954 |
Gave conventional animals and germ free animals identical diets and sucrose water. Germ fre rats never developed carious lesions. Bacteria are necessary for decay |
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Dr. Robert Stephan |
Demonstrated plaque pH varies depending on diet and depending on its microbial composition. Stephan curve. |
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Unique characteristics of S. mutans |
Most cariogenic, causes smooth surface decay, produces acid at the fasat rate, forms highly adherent biofilm, levels of s mutans increased durin the transition from health to disease |
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Marsh et al. 1990s |
Ecological Plaque Hypothesis: Greater emphasis on th eglobal compostion of the plaque. An imbalance of acidogens leads to caries. A change in the homeostatic balance of the resident microflora is responsible for conditions that promote the growth of pathogens. This change in balance may be initiated by frequent eating so that the resident microflora adapts to the low pH conditions which in turn further promotes an environment conducive to gowh of S.mutans and lactobacilli |
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Host contribution to caries by |
Host matrix metalloprtoeases (MMPs) play a role in the development or severity of dental decay |
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Van Houte et al, 1991 |
Pooled samples of white spot lesions or healthy sites. S mutans levels were much higher on white spot lesions than on healthy sites. White spot lesion samples with high or low S mutans could exhibit a high rate of pH drop and pH minimum |
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Hirose et al. 1993 |
Measure salivary S. mutans and S. sobrinus levles in children. Children placed in groups based on microbiology. Sobrinus group hade higher levels of decay and increments of decayed srufaces over the 6-month period |
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Window of Infectivity of S. mutans |
19-31 months for children, mean of 26 months |
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Why is window of infectivity so Important? |
1. S. mutans colonization of tooth fissure may prime future areas for decay 2. Longer delay of S. mutans means more likely to remain caries free 3. 2nd window of infectivity may be around 6 yrs of age |
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Sucrose Independent Adhesion |
Adhesion of S. mutans is thought to be to salivary proteins that are part of the acquired enamel pellicle. Not very efficient! Mediated by AgI/II |
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Sucrose-dependent Adhesion |
Main basis for sucrose-dependent adhesion is glucan synthesis catalyzed by glucsyltransferases (GTFs). Glucans are produced from sucrosea and are what makes the S. mutans stick to surfaces. It makes it difficult to scrape off and very efficient. |
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Why is glucan effective in promoting adhesion and accumulation? |
They have the opportunity to engage in weak-force interactions in proportion to the size of the polymer. Likely that the hydroxyl groups in glucan have the opportunity for extensive hydrogen bonding and provavly divalent cation interactions that help it stick tenaciously to tooth surfaces |
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What acid is produced in majority under conditions of sugar excess or low pH conditions? |
Lactate |
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Which gene is essential for S. Mutans for it to be cariogenic? |
LDH, Lactate Dehydrogenase |
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Noorda 1988 |
Consortia of bacteria may bring about uniquie acid properties such as more acid is produced with co-culture of S. mutans and Veillonella alcalescens than when either species is produced individually |
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What are the unique aciduricity properties of S. Mutans? |
1. It ceases to grow under pH 5 but can carry out glycolysis down to pH 4 or lower 2. It can adapt to low pH |
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Maintaining Intracellular pH |
Maintained by pumping protons out of the cell which is accomplished by F-ATPase and change in membrane fatty acids that are less permeable to protons. |
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Prevalence |
Proportion with a disease in a population at a given point in time |
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Incidence |
Proportion of new cases of a diseas in a population during a given time period |
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Changing Oral Epidemiology |
Children ages 5 to 17 have seen DMFT scores drop while 2-4 have stayed steady over time |
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Children see higher rates of caries in primary teeth or permanent teeth? |
Primary tooth caries rate are higher than for permanent teeth at young ages |
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Flouride has had the best outcome on what type of tooth surfaces? |
Smooth surfaces |
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Study of 2 to 11 year olds from 1988 to 1994 and 1999 to 2004 |
Saw a general increases of dfs but it is due to a greater number of fillings seen in the primary dentition |
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What is the root caries index? |
Surfaces with root caries experience/surfaces with recession |
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Demineralization |
Loss of minerals (calcium, phosphate, carbonate) due to acidic environment |
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Remineralization |
Gain of minerals (Calcium, phosphate, carbonate) |
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What are incipient lesions? |
They are pre-carious lesions that show early signs of caries. A build up of plaque on the teeth are non cavitated but are prime sites to develop cavities/carious lesions |
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Fissure caries |
1. Begin on sides of the fissure 2. Encompass the base of the fissure secondly 3. Less enamel to transverse to reach dentin 4. Rapid spread along DEJ
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Characteristics of Arrested or Inactive Caries |
1. White/brown 2. Shiny surface |
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What is the main duty of saliva? |
Saliva saturates plaque which prevents demineralization |
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Distribution of Elements in the enamel |
Outer layers contain Flouride, Calcium and Phosphate (majority) and Inner layers contain Water and Carbonate |
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Critical pH of Enamel and Dentin |
pH 5.5 and pH 6.2 |
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What makes up the Enamel ultrastructure? |
Enamel ultrastructure is made from enamel rods which are composed of hydroxiapatite crystal. Hydroxiapatite is dissolved by the acid |
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Enamel Demineralization patterns |
thin outer layer is removed first. Moves inward to remove inter-prismaic areas. Thus when remineralization reforms outer layer, demineralized areas underneath make it hard to be discovered |
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Carious Dentinal tubule lesions |
Outer lesion of dentin occurs. Inner lesion is subdivided into turbid, transparent and subtransparent regions. and then a normal region follows. Inner region tries to protect from invasion of bacteria further from loss of apatite crystals by forming rhomboidal crystals known as whitlockite which are lower in hardness and calcium content |
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What is tertiary dentin? |
Pulp's reaction to protect against dentin bacterial invasion. Irregular dentinal tubules and mineralization |
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Selected messages for consumers: Foods to increase |
1. Make half your plate fruits and vegetables 2. Make at least half your grains whole grains 3. Switch to fat-free or low-fat (1%) milk |
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Selected messages for consumers: Foods to reduce |
1. Compare sodium in foods and choose the foods with lower numbers 2. Drink water instead of sugary drinks |
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Estimated Average Requirements (EAR) |
Amount of a nutrient that will maintain a specific biochemical or physiological funtion in half the people of a given age and sex group |
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Recommended Dietary Allowances (RDAs) |
Average daily amount of a nutrient considered adequate to meet the known nutrient needs of practically all healthy people (EAR plus 2 standard deviations) |
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Adequate Intake |
Average amount of a nutrient that appears sufficient to maintain a specified criterion |
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Tolerable Upper Intake Level (ULs) |
Maximum amount of a nutrient that appears safe for most healthy people and beyond which there is an increased risk of adverse health effects |
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Grains Group - Fiber |
Requirements are 20-40g/day Soluble - Fruits, oats and beans Insoluble - All plants Decreased CV disease, reduced constipation and risk of GI disease, and assist with weight management |
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Vegetables - Key Nutrients |
Folate - Food sources: Dark leafy greens, orange juice, wheat germ, fortified grains Deficiensy lead to neural tube defects and CV disease Excess can mask B12 deficiencies |
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100% Juice |
High energy, low nutrient Infants < 6 months of age should not have any juice 1-6 year olds 4-6 oz a day 7-12 year olds 8-12 oz a day |
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Vitamin C |
Antioxidant Smokers have lower serum levels Lower vitamin C may lead to increased perio bleeding Ascorbic acid supplements _ chewable could increase risk of enamel erosion |
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Incomplete protein |
Missing 1 or more essential amino acids; unable to support growth, maintain health |
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Limiting amino acid |
essential amino acid not present or present in insufficient quantities |
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Complementary proteins |
2 incomplete proteins missing different essential amino acids |
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Marasmus |
Protein will be used for energy at expense of protein functions Low body fat stores, ketosis, decreased growth |
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Kwashiorkor |
Inadequate protein, adeaquate energy Edema, poor immunity, fatty liver |
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Vitamin B12 |
Found only in animals Absorption requires Stomach acid and intrinsic factor A deficiency is a concern for the elderly; confusion, neuropathies |
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Iron |
Anemia is deficiency Leading cause of mental retardation and leads to behavioral problems Iron toxicity leads to cirrhosis and CV disease Heme iron is best dietary source Acid facilitates absorption |
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Vitamin D |
Adequate intake is 5ug/day 19-50 yr Regulates calcium metabolism and maintains serum calcium/phosphorous levels via regulation of absorption and bone turnover Deficiencies are rickets, osteomalacia, osteoporosis |
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Dietary fat |
Provides energy (9 kcal/g) Carrier of fat soluble vitamins Provides satiety Carries flavors, adds moisture, texture |
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Fructose |
Found most commonly as high fructose corn syrup Preferentially converted to triglycerides |
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Benefits of vegetarianism |
Healthy body weights, lower blood pressure, less CV disease, lower cancer rates |
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Concernes of vegetarianism |
Disordered eating and lack of nutrients |
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Low Carbs mechanism |
Induce ketosis: Incomplete oxidation of fatty acids in absence of carbohydrate and appetite suppression Restricted food choices and reduced energy intake
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Low Carbs bottom line |
Weight loss is due to energy restriction Low CHO allows one to achieve energy restriction Weight loss is not permanent because one must maintain energy restriction |
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Glycemic Index |
System of ranking carbohydrate containing foods Measure of how quickly dietary carbohydrates elevate serum glucose: Quick digestiona and absorption = Increased GI Fiber, protein and fat slow digestion |
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Glycemic Load |
Glycemic index x grams CHO in food volume to measure CHO quality GL adjusts for food quantity and is the glycemic effect of a given quantity |
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Significance of GI and GL |
High GL diet predictive of developing Type 2 diabetes. Low GI diet associated with decreased risk of obesity, colon cancer, breast cancer. Improve insulin sensititvity. Decreased serum lipids |
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Oral significance of GI and GL |
High GI foods, likely to be easily fermentable by oral bacteria Low GI foods, lilely to have less simple sugar (except fructose) and be less refined |
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Hopewood House |
Birth-12 years: lactovegetarian diet emphasizing whole grains, raw vegetables and minimal sugar or white flour. 12 years+ westernized diety of local community. DMFT followed trend similar to the publics. |
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Vipeholm, Sweden |
Object was to determine how caries incidence is influenced by Mealtime exposure to nonretentive sugars, mealtime exposure to retentive sugars and between meal exposures to retentive sugars. Mental hospital was split by different wards into groups. At meal time caries increased slightly whereas between mealtime, caries increased significantly |
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Turku, Finland |
Determine the effect of total substitution of fructose or xylitol for sucrose on dental caries. Sucrose and Fructose showed high caries rate |
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Animal study of germ free environment with rats |
Showed that rats who were germ free never developed caries because there were no bacteria to take advantage of the sucrose |
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Stephan Curve |
Fall in curve represents the fermentation of the bacteria. If curve falls below critical pH demineralization occurs. Coffee alone showed longer time of hovering by critical pH vs. eating egg and toast with the coffee. Same seen with delay of eating. |
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What helps prevent bacteria fermentation? |
Calcium phosphate and fat |
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Affected vs. Infected Dentin |
Affected inner dentine -few bacteria, remineralisable, vital, sensitive, useful Outer infected dentine - bacteria invasion, unmineralisable, dead withou sensation, not useful |
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Clinical Visual Examination steps |
1. Clean Teeth 2. Thoroughly Dry teeth 3. Acute visualization and magnification with adequate light 4. Probe/Explorer - Used as an adjunct to determine consistency and texture of lesion. USE GENTLE PRESSURE |
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Use transillumination for what types of caries? |
Proximal caries |
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ICDAS Classification 0 |
Sound enamel. No evidence of caries, no change after air-drying for 5 seconds. Includes Enamel hypoplasias, fluorosis, tooth wear and extrinsic and intrinsic stains |
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ICDAS Classification 1 |
First visual change in enamel. Smooth surface: Nothing seen on wet tooth, lesion visual after 5 seconds air-drying. Pit and Fissure - Lesion contained to pit and fissure. Opacity, White or Brown. |
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ICDAS Classification 2 |
Distinct Visual Change in Enamel. Smooth surface: Lesion seen when both wet and dry. Pit and fissure - Lesion extended beyond the pit/fissure. Located in inner enamel to outer 1/3 dentin |
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ICDAS Classification 3 |
Localized enamel breakdow due to caries with no visible dentin. When viewed wet may have clear darkening of dentin though enamel. After 5 seconds air-drying: carious loss of tooth structure at entrance to or within pit/fissure. Pit/fissure may appear substansitally and abnormally wider than normal but dentin is not visible in the walls or based of cavity. Lesion depth may be down into the middle 1/3 of dentin |
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ICDAS Classification 4 |
Non-cavitated surface with underlying dark shadow from dentin. UNDERLYING GREY/BLUE/BROWN SHADOW. Shadow of discoloured dentin through apparently intact enamel surface. Lesion depth is well into the dentin |
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ICDAS Classification 5 |
Disctincty Cavity with Visible Dentin. Cavitation in opaque or discoloured enamel which exposes dentin beneath. Lesion depth middle 1/3 dentin |
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ICDAS Classification 6 |
Obvious loss of tooth structure and possible reaches pulp. Cavity both deep and wide. Dentin clearly visible on walls and base. |
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Colors of active and inactive lesions |
White is the indication of active lesions. Brown is indication of inactive lesion. |
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Visual Luster as classification of avtive or inactive lesions |
Active lesion has loss of luster. Inactive lesion is shiny. |
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Visual/Tactile classification of active or inactive lesions |
Rough/surface breakdown is an indication of an active lesion. Smooth/Hard/Surface intact is indication of an inactive lesion. |
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Primary prevention |
Prevent onset of disease to reverse or arrest disease process. Examples are brushing flossing and dental sealants. |
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Secondary prevention |
To stop disease process and restore tissues. Fillings, endo, extractions, and perio surgery. |
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Tertiary Prevention |
Replace lost tissues and rehabilitate function. Examples are bridges, dentures and implants |
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Gingival index |
0 = No inflammation 1 = Redness and Inflammation no bleeding on probing 2 = Bleeding on probing 3 = Spontaneous bleeding |
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Plaque Index |
0 = No Plaque 1 = Plaque detectable 2 = Plaque from interproximal to interproximal 3 = Plaque on more than 1/2 tooth surface |
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Bass Technique |
Tooth is scraped witha an up and down motion. Scraping works best when fine unwaxed floss or fine waxed floss is used. This method is suitable only for class 1 flossers. |
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Bass Flossing Technique Step by Step |
Obtain a peice of floss 18" long, waxed or unwaxed. Wind floss around middle fingers with thumb and fore fingers available to guide the floss. Leave approx. 1/2 to 1" space between fingers. To inser, gently see-saw back and forth through contact to avoid "snapping"/trauma. Adapt floss to each interproximal surface- a c-shape. Move floss apically into sulcus and back to contact area several times- until surface is squeaky clean. Repeat procedure on adjacent surface - use care shifting floss to prevent dapage to papilla. A clean unuse portion to be used for each proximal area. |
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Dentrifice |
A substance used with a toothbrush for the purpose of cleaning the accessible surfaces of the teeth |
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Shut it down |
Lets go Home |