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test 2

Theory 1

individual assessment score purpose education, motivation, evaluation
individual assessment score uses help patient recognize problem, reveals effectiveness of present hygiene, motivates patient, evaluates the success of treatment over a period of time by comparison
clinical trial-purpose determine the effect of an agent or procedure on the prevention, progression or control of a disease
clinical trial-uses baseline data before experimental factors are introduced, measures effectiveness of specific agents for the prevention, control or treatment of oral conditions, measures effectiveness of mechanical devices for personal care
epidemiologic survey-purpose study disease characteristics of POPULATIONS
epidemiologic survey-uses shows prevalence & incidence of a condition occurring in a given population, provides baseline data to show existing dental health practices, ASSESS THE NEEDS OF A COMMUNITY, compares effects of a community program and evaluates the results
Index an expression of CLINICAL OBSERVATIONS in numeric values
descriptive categories of indices general categories, types of simple and cumulative indices
simple index measures presence or absence of a condition (plaque index that looks at plaque only-not gingiva)
cumulative index measures ALL evidence of a condition, past and present (DMFT for caries)
DMFT decay, missing, filled teeth
(Simple and cumulative) Irreversible conditions that will not change are measured (dental caries index)
(Simple and cumulative) reversible conditions that can be changed (microbial plaque-plaque index)
selection criteria of indices simple to use and calculate, minimal equipment and expense, minimal time, no patient discomfort, clear criteria, free of subjective interpretation, reproducible, validity & reliability
choosing an index based on question you are trying to answer & based on what is observed in the patient's oral cavity
types of indices screening for periodontal health (PSR): dental biofilm: biofilm, debris, calculus; gingival bleeding; gingival/periodontal; dental caries
Periodontal Screening and recording (PSR) too assess perio health, divide dentition into sextants-each tooth is examined: procedure-instrument, probe application, criteria, recording: scoring-follow up patient management, calculation examples
PSR-procedure Instrument-specially designed probe (workning tip-a ball .5mm, color coding between 3.5 & 5.5): probe application: criteria 5 codes and an * are used may include conditions: probe entire sextant unless a code 4 is identified: recording-6 box form
Scoring (PSR) follow up pt management, trtmt plan based on highest code
Dental biofilm Plaque index of Silness and Loe (PI I), Plaque control record (O'leary, Drake, & Naylor): Plaque-Free Score-Grant, Stern, Everett
Biofilm, Debris, Calculus Patient Hygiene Performance (PHP) Simplified Oral Hygiene Index (OHI-S)
Gingival Bleeding Sulcus Bleeding Index (SBI), Gingival Bleeding Index (GBI), Eastman Interdental Bleeding Index (EIBI)
Gingival/Periodontal Gingival Index (GI), Community Perio Index of Treatment Needs (CPITN)
Dental Caries Decayed, Missing, and Filled Permanent Teeth (DMFT): Decayed, Missing & Filled Permanent Tooth Surfaces (DMFS): Primary teeth indices
for plaque lower # indicates less plaque
Polishing-removal of stains esthetic, not for health reasons
extrensic stains smoking, tea, meds, etc-can be removed by scaling, ultrasonic, rubber cup-stains may be yellow, brown, gray, green, orange or black
intrinsic stains come from w/in tooth-hereditary or developmental (high fever, excessive fluoride, trauma-these events can interfere w/ development of enamel and dentin): can appear yellow, light to dark brown, gray & black-CANNOT be removed-cover w/ restoration or bleach
selective polishing omitting tooth polishing in areas where there is no stain & when tooth polishing could cause damage
enamel damage from polishing enamel is aprx 2.5 mm thick and polishing w/ pumice for 30 seconds removes aprx. 4 microns of the fluoride rich outer layer of enamel
rubber cup polishing removal of tooth stains following scaling using a SLOW-speed hand piece and prophy paste-LIGHT PRESSURE & PLENTY OF MOISTURE W/ A VERY MILD ABRASIVE
course paste always follow w/ fine paste and fluoride trtmt
Adverse Effect of polishing-teeth removes tooth structure, avoid demineralized areas, heat production irritiates pulp, course abrasives may actually roughen tooth surfaces increasing plaque retention
Adverse effect of polishing-restorations damage restorations, making them rough-AVOID IMPLANTS
Adverse effect of polishing-soft tissue irritation if the tissue is inflamed from scaling and particles become imbedded in gingival tissue and may delay healing-May need a 4-6 week apt
Adverse effect of polishing-environment aerosol production during rubber cup polishing may provide means of disease transmission-must use over gown, eyewear, mask
Adverse effect of polishing-bacteremia medical history must be recorded initially and reviewed at each apt: artificial heart valvues, history of bacteremia, congenital heart disease, cardiac transplants w/ problem in a hear valve
contraindications of polishing latex allergy, rampant caries, patients w/ resp prob, tooth sensitivity, newly erupted teeth-mineralization not completed, xerostomia disrupts protective fluoride layer, much harder to replenish w/ xerostomia
Cleaning and polishing agents abrasives selected should produce smooth tooth surfacrs but should not remove structure and surface fluoride or abrade gingival epithelium
Factors affecting abrasive action characteristics of abrasive particles, principals for application of abrasives
characteristics of abrasive particles shape-irregular w/ sharp edges produce deeper grooves and abrade faster, hardness-harder particles abrade faster, body strength-weaker particles break down into smaller sharp edge particles=more abrasive: Particle size-larger particles more abrasive
ALWAYS USE wet agent, light pressure, light intermittent touch
Fluoride Salt of hydrofluoric acid-occurs in many tissues and stored in bones and teeth
Systemic Fluoride occurs by way of the circulation to developing teeth
topical fluoride made available directly to the exposed surfaces of erupted teeth
fluoride intake systemic nutrient coming from water, supplements, and food (small amounts)-food and beverages prepared w/ fluoridated water become a source-can be ingested from dentifrices, mouthrinses and other fluoride products
fluoride-absorption gi tract: stomach and small intestine, absorb all but 5% which is excreted, absorption is reduced if taken w/ milk or food
fluoride-blood stream max blood levels occur w/in 30 min, but are still low; blood level of fluoride fluctuates w/ intake; normal plasma levels are very low
fluoride in saliva ranges from .01-.04ppm less than plasma level
fluoride distribution and retention-young child 1/2 of intake deposits in bones and teeth
fluoride distribution and retention-adult continues to accumulate in skeleton throughout life: fluoridated water allows fluoride to enter into normal bone exchange and maintenance
fluoride storage 99% stored in mineralized tissues;stored in bone (95% of body fluoride);Teeth store small amounts, highest level on tooth surface
fluoride ion stored as fluorapatite
fluoride in soft tissues may be present, LOW in breast milk
fluoride excretion kidneys-most leaves via urine, sweat glands and feces-secrete small amounts: limited amount transfer to breast milk
fluoride and tooth development pre-eruptive: mineralization and maturation stages and post-eruptive
fluoride pre-eruptive: mineralization stage deposited during enamel formation starting at DEJ, incoporated during mineralization of ALL parts of the teeth; available to the developing teething VIA THE BLOOD STREAM(surrounding tooth bud)
fluoride pre-eruptive: mineralization stage-effects of excessive fluoride may inhibit normal activity of the ameloblasts and a defective enamal matrix can form: dental fluorosis can result
Dental Fluorosis a form of hypomineralization due to excess fluoride during tooth development
Pre-eruptive: Maturation Stage: fluoride deposition continues after mineralization and before eruption-only goes to surface enamel. Fluoride taken from nutrient tissue fluids surrounding tooth crown; EXPOSURE TO FLUORIDE 2 YRS PRIOR TO ERUPTION BENEFITS MOST
Post-eruptive-fluoride after eruption and throughout life span-from water, dentifrice, rinse, etc. inhibit demineralization and enhance remineralization: fluoride on the tooth surface can inhibit the initiation and progression of dental caries
Post-eruptive-fluoride uptake is rapid on enamel surface during the first years after eruption, higher levels of fluoride equals greater uptake; drinking water that is fluoridated is now a source of topical
Tooth surface fluoride (fluoride in enamel) highest concentration of fluoride is on the surface, concentration decreases inward from enamel surface to DEJ
Tooth surface fluoride (fluoride in dentin) higher concentration than in enamel, concentration highest at pulpal surface-exchange occurs here
Tooth surface fluoride (fluoride in cementum) increased concentration in cementum with age
fluoride in tooth from most > least dentin > outer surface of enamel > inner surface of enamel > cementum
fluoride in bacterial biofilm may contain 5-50 ppm-depends on intake, supplied by saliva, crevicular fluid, diet, topicals, and possibly from demineralizing tooth surfaces
effects of fluoride in biofilm lowers metabolism of bacteria, inhibits acid production, inhibits carb metabolism, aids in remineralization, reduces cariogenic potential
Demineralization breakdown of tooth structure w/ a loss of mineral content, primarily calcium and phosphorus-caused by organic acids produced by acidogenic bacteria after metabolism of ingested fermentable carbs-a shift of equalibrium that favors demin leads to white spot
demineraliztion "white spot" first clinically detectable lesion
demineralization-progression acids pass through microchannels between enamel rods, demin occurs in the subsurface layer-eventually a spot may be seen clinically-with further demin the lesion forms into caries
remineralization the recovery of the demin process
remineralization-process saliva buffers acid and calcium and phosphorous ions, when early remin occurs the white spot will "harden and may be hypermineralized compared w/ the enamel around it
remineralization-role of fluoride fluoride inhibits demin & enhances remin; fluid in biofilm transports fluoride, & other minerals & organic acis to the tooth surface-continuous exchange of minerals between biofilm & enamel crystals-the presence of fluoride ions acts to control demin
3 basic effects of fluoride to prevent caries inhibit demin, enhance remin; inhibit bacterial activity-interferes w/ enzyme activity and inhibits enolase, an enzyme needed to metabolize carbs
fluoride-water supply adjustment optimal concentration is 0.7-1.2 : in warmer climates 0.7 & 1.2 in cooler climates
fluoride-water supply-chemicals used sources-fluorspar, cryolite and apatite, criteria for acceptance-solubility, inexpensive, readily available
water supply-compounds used dry compound of sodium fluoride and sodium silicofluoride/ solution of hydrofluorosilicic acid
effects and benefits of fluoride-appearance of teeth optimum level-white, shiny, opaque, w/o blemishes::higher level-white bands or flecks (fluorisis)
dental caries-permanent teeth 40-65% fewer caries
root caries 50% less in life long residents of fluoridated communities
dental caries-primary teeth fluoridation from birth will reduce caries by 50%
prenatal fluoride fluoride will cross placental barrier but most mineralization occurs after birth: Crowns formed fully between 3 & 11 months of age: outermost layer of enamel formed last so fluoride ingested after birth has the most influence
tooth loss is much greater in both primary and permanent teeth w/o fluoride b/c of increased dental caries which progress mor rapidly
adults-fluoride continue to benefit from fluoridated water supply
perio disease adn fluoride indirect effects, improve bone density, caries, malocclusion and tooth loss decrease-decrease in perio problem due to retained plaque which normally setlles in areas
fluoride in foods small amounts, not enough to help caries prevention
halo effect unintentional addition of fluoride (example Pepsi)
determining the need for supplements be sure no other supplement is being used; check water fluoride levels test water or ask local health depts
breast fed infant-fluoride concentration in breast milk is low, requires supplement of .25 unless child is receiving other liquids in formula or cereal made w/ fluoridated water
professional topical fluoride essential part of a total preventive program
Nuetral Sodium Fluoride pH 7.0: 2-5% fluoride; aqueous solution, gel, foam or varnish; salty-CONTRAINDICATED FOR HIGH BP- no tooth staing, stable, can be used in tray or paint onn
Acidulated Phosphate Fluoride (APF) pH of 3.5 (enhanced uptake)- 1.23 % fluoride-aqueous solution, gel or foam, nonstaining, objectionable taste-MAY CAUSE SURFACE ROUGHENING, PITTING ETCHING OF PORCELAIN AND COMPOSITES AND TITANIUM IMPLANTS-tray or paint on
Stannous Fluoride pH 2.4-2.8; 8% fluoride; available in solution, stains tooth surfaces, esp demin areas, pits, fissures, grooves, etc. unpleasant taste-seldom used
Varnish VSF safe effective, fast, easy,over 20,000 ppm but only small amount used. Used as off label not approved in US as decay preventative-MUST DRY TEETH EXCESSIVELY
fluoride general guidelines after selective polishing, pit and fissure sealants and amalgam polishing-time is 4 minutes-even if the bottle says 1 minute-complete uptake requires 4 minutes
fluoride safety wide margins of safety, can be harmful is correct dosages are not followed
fluoride: acute toxicity rapid intake of an excess over a short period of time
certainly letha dose (cld) amount likely to cause death if not treated asap- adult CLD 5-10g, child CLD 0.5-1.0 grams (both vary by size and body weight)
safely tolerated dose (STD)-1/4 of CDL adult STD- 1.25-2.5 g of sodium fluoride, child std varies by weight and age
sings and symptoms of acute toxicity begin w/in 30 mins of ingestion may persist for 24 hours; GI-nausea, vomitting, diarrhea, abd pain, ^ salivation, thirst; systemic involvement: blood (calcium binds w/ fluoride=hypocalcemia: CNS- convulsions, paresthesias; cardio and respiratory depres
emergency trtmt induce vomitting, call 911, administer milk or lime water (binds w/ fluoride) support resp and circulation
chronic toxicity-skeletal fluorosis 20 + yrs may cause osteosclerosis
chronic toxicity-dental fluorisis only occurs when fluoride was ingested during enamel development (birth to 8/9 years)
chronic toxicity-mild fluorosis white opacities on enamal surface; occuring more frequently (halo effect???)
calculations of amount of fluoride multiply the % of fluoride ion by the molecular weight conversion ratio; obtain the ratioby dividing the molecular weight by the atomic weight of fluoride
saliva-serous secretion thin, watery secretion-is composed of water and some enzymes (amylase and maltose), salts and organic ions
saliva-mucous secretion composed of mucin. mucin is a lubrication material that aids in chewing, swallowing, and digestion
saliva-mixed secretion some glands can produce both types of secretionn
Parotid gland largest, on surface of masseter muscle, produces 25% of the volume of saliva for the mouth, produces serous secretion, parotid is teh duct opening-found on the buccal mucosa adjacent to the max 2nd molar
Submandibular gland wrapped around mylohyoid muscle, 60-65% of volume of saliva, mixed secretion, duct=sublingual caruncle, extends from deep part of the gland and runs forward in the floor of the mouth to open onto a small elevation
Sublingual Gland smallest, located in anterior floor of the mouth next to the mandibular canines, produces 10% of the volume of saliva for the mouth, duct opening is submandibular duct being the major duct w/ several smaller ducts located in a line along sublingual fold
minor salivary glands smaller and have less branching, function is not to produce saliva for mixing w/ food but to secrete minor amounts of saliva onto the surface to keep the mucosa moist . Most of these glands are pure mucous and the others are mixed.
minor salivary glands-labial glands mostly mucous
minor salivary glands-buccal glands similiar to labial
minor salivary glands-palatine glands pure mucous
minor salivary glands-glossopalatine glands pure mucous
minor salivary glands-lingual glands anterior lingual glands mostly mucous: lingual glands of von Ebner-serous only; Posterior lingual glands-mucous
Functions of saliva Lubrication & protection of the oral tissues, cleaning, tasting, degestion-food breakdown(chewing), food bolus formation, swallowing
Functions of saliva Destroying oral mo's(carrier of antibodies,hormones, enzymes & provide data for diagnostic testing): Protection of diseases: antibacterial, antifungal, antiviral : regulating oral pH, maintaining integrity of teeth (remin; protect against demin): speech
saliva in a healthy patient lubes and protects oral mucosa, aids in cleaning mouth, regulates acidity, maintains integrity of dentition, destroys bacteria-saliva contains immunoglobulins IgA & IgG-proteins that have antibody activity, synthesized by lympocytes and plasma cells
Sialolith aka salivay stone-a calculus formed in a salivary duct
Mucocele Dilation of a cavity w/ acuumulated mucous secretion (on lip)
Ranula a large mucocele in the floor of the mouth, usualy caused by obstruction of the ducts of teh sublingual salivary glands and less commonly caused by the obstruction of the ducts of the submandibular salivary glands (Elizabeth)
xerostomia dryness of the mouth from a lack of normal salivary gland secretion, ranges from dry, smooth appearing, to ulcers, can obtain candidiasis, makes patient more susceptible to caries, may cause altered taste or difficulty in chewing and swallowing
xerostomia-common causes meds, rad therapy, immunological diseases-Sjogren's syndrome
management of salivary disfunctions meticulous home care, daily use of a focused custom fluoride (ACT), chlorhexidine rinses (6 months limited use)
Nutrition & saliva saliva, etc are affected by nutrients, esp Vitamin A & protein. chewing and tasting sour stimulates saliva flow, beneficial for caries control- saliva begins digestion of carbs
Nutrition & salvia & dentures full dentures can interfere w/ the process (covering)-decrease in taste sensation possibly leading to decreased interest in food=malnutrion
Saliva pH Enamel-the critical pH for enamel is 4.5-5.0 cemetum (root caries)-critical pH for cementum is 6.0-6.7
demineralization excessive loss of mineral or inorganic salts from body tissues, in dentistry breakdown of tooth structure w/ a loss of mineral content- 1ST STEP IN CARIES PROCESS
remineralization (from saliva and Fluoride) restoration of mineral elements; enhanced by fluoride. remin areas are more resistant to initiation of dental caries than in normal tooth structure. repair of enamel rod structure following acidogenesis
factors leading to demin/remin cycle saliva, plaque, tooth
saliva; pure when emitted, but when saliva from several glands mix it is termed POOLED or WHOLE saliva: mixes w/ food, oxygen, carbon dioxide, bacteria etc.
saliva flow rate-resting slow .11-.26 ml per minute depending on the gland w/ the highest flow occuring at mdi afternoon an dlowest at 4 am- during sleep flow is almost nonexistant
saliva flow rate-moderate stimulation 1-2.5 ml per minute
saliva flow rate-effected by sex-higher for men; weather; lower in warm weather; smoking-increases flow due to oral stimulation; light deprivation-decrease; standing flow greater than sitting
saliva-chemical protection tooth damage results from a drop in pH-saliva maintains a pH of 5.5-8 & minimizes drop in pH caused by plaque, increases tooth resistance to acid attack, accelerates return of pH to nrml & provides ionic envrnmnt conducive to repair of enamel after acid
saliva-chemical protection sodium bicarbinate is the main buffer; phosphates, amphoteric proteins and ureas also help
saliva-chemical protection-ions providing most protection clacium, phosphate, and fluoride; aid in preventing demin and promoting remin
saliva proteins that are bacteriostatic or bacteriocidal lysozyme, lactoferrin, lactoperoxidase, secretory immunoglobulin A (S Ig A), these 4 may help prevent demin
plaque acid responsible for demin, it is necessary to: reduce # of bacteria, reduce amount of acid produced in existing bacteria (reduce sugar), negate the effect of the produced acids-H20 content in saliva & plaque dilutes acids-
plaque accumulates fluoride at a greater rate than saliva to help provide protection or remin
tooth-enamel more mineralized than bone or dentin (98% by weight)-made up of crystals of hydroxyapatite-calcium, phosphate & hydroxal groups (which may be replaced by fluoride) w/ enough fluoride fluorhydroxyapatite crystals result
tooth-enamel once enamel is formed, it is harder to replace hydroxyls w/ fluoride=fluoridated water is more effective than topical. Organic phase of enamel is lost during demin, but organic matrix hastens demin by providing invasive channels for acid
process of demin caused by acid formed by bacteria acting on cariogenic food (esp sucrose)
white spot lesions 4 zones translucent, dark, body of lesion, surface zone-maintained while demin occurs below the surface (enamel is intact)
remin/demin constant cycle-several times per day
caries-definition-WHO localized, post-eruptive, pathological process of external origin involving softening of the hard tooth tissue & proceding to the formation of a cavity
caries-definition-Wilkins disease of the mineralized structures of the teeth characterized by demin of the hard components and dissolution of the organic matrix
development of caries 3 requirements mo's, carbs. susceptible tooth surfaces
Microorganisms (caries) S.mutans (main), Acidogenic lactobacilli-aid in progression, not origin; bacterail plaque contains acidogenic mo's: S.mutans & lactobacilli, S. nonmutans, Actionmyces, Veillonella
Carb (mainly sucrose) Cariogenic food enters plaque, acid-forming bacteria break down sugar to acid which causes demin, decrease in salivary flow & increase in carb intake promotes growth of S. mutans & lactobacilli in plaque
susceptible tooth surface (Caries) tooth w/ optimum fluoride resist caries process
contributing factors-caries Time: acid starts forming asap when sucrose from food is taken in; the pH of the plaque; Carb intake frequency (each intake lowers pH-large amounts of carb at meals less cariogenic than small frequent intakes)
contributing factors-caries pH changes less if cariogenic foods are eaten first followed by noncariogenic foods
GV Black-Class 1plaque pH lowered promptly and takes 1-2 hours to neutralize if left undisturbed, critical pH for enamel demin=4.5-5.5 and root demin is 6.0-6.7
GV Black-Class I pits or fissures
GV Black-Class II proximal surfaces of premolars & molars
GV Black-Class III proximal surfaces of anteriors-do NOT involve incisal edge
GV Black-Class IV proximal surfaces of anteriors-do include incisal edge
GV Black-Class V cervial 1/3 of facial or lingual surfaces
GV Black-Class VI incisal edges of anterior teeth and cusp tips of posterior teeth
nomenclature by surfaces simple-one tooth surface; compound-2 tooth surfaces; complex-more than 2 tooth surfaces
progression white spot, brown spot (stained white spot), incipient lesion, advanced lesion (larger, deeper, possible pulp involvement), arrested;dark yellow-black/brown, smooth & hard; rampant-numerous lesions
etiologic factors early childhood, baby bottles, breast milk etc, radiation caries
formation of caries phase I-incipient lesions, phase II untreated incipient lesion
types of caries pit and fissure- smooth surface
root surface caries aka cemental caries, cervical caries, radicular caries-effects: cementum & dentin
root surface caries-steps in formation gingival recession exposes cementum, starts near CEJ, enamel not involved unless caries extends or undermines the enamel-INVOLVES STREPTOCOCCI, LACTOBACILLUS, & ACTINOMYCES
root surface caries-clinical recognition soft, shallow, ill defined lesion, increases laterally-around the tooth, yellowish, lt brown, dark brown or black: leathery texture when explored=active lesion: arrested root caries has cavitation & discoloration but it hard to the touch
root surface caries-predisposing factors root exposure, lack of fluoride in water, xerostomia, poor home care, diet-cariogenic
recognition of caries prep-dry tooth surface-visual exam-exploratory exam-radiographic exam
visual exam-enamel caries-chalky white demin
visual exam-enamel caries-grayish white marginal ridges proximal surfaces underneath are decayed
visual exam-enamel caries-grayish-white-margins of restorations secondary caries
visual exam-enamel caries-amalgam restorations decay appears translucent in outer portion and white adjacent to amalgam
visual exam-enamel caries-open lesions yellowish-brown to dark brown
visual exam-enamel caries-discoloration less severe when caries progresses rapidly
visual exam-enamel caries-discoloration dull, flat white, opaque areas under direct light-loss of translucency
visual exam-enamel caries-discoloration dark shadow on proximal surface-transillumination
visual exam-smooth surface caries adapt side tip of explorer-hardness vs. softness, roughness vs. smoothness; continuity of surface
visual exam-pit and fissure caries do not explore obvious caries-explorer runs straight into pit or fissure; catches when caries present-softness is evident
radiographic exam occurs in conjuction w/ clinical exam-use for proximal & root caries-radiolucent areas
caries sugar+bacteria=Acid+tooth=decay
importance of primary teeth facial growth affected, hold place for permanent teeth, proper chewing and nutrition-clear speech
dentifrice a substance used w/ a toothbrush or other applicator to remove dental biofilm, materia alba, debris, & stain from teeth, tongue & gingiva for cosmetic, theraputice or preventive purposes
dentifrice-cosmetic clean and polish tooth surfaces, freshen breath
dentifrice-theraputic some non-drug substances increase the efficiency of brush in removal of plaque, debris, and stain
dentifrice-theraputic or preventive vehicle for transporting biologically active ingredients to teeth and environment
powder dentifrice difficult to find; abrasives 20-40%; detergents 1-2%: flavor 1-1.5%: sweetener 2-3%: coloring 2-3%
paste and gel dentifrice abrasives 20-40%; detergents 1-2%: flavor 1-1.5%: sweetener 2-3%: coloring 2-3%: binders 1-2%; humectants 20-40%: preservatives 2-3%; water 20-40%
theraputic dentifrice abrasives 20-40%; detergents 1-2%: flavor 1-1.5%: sweetener 2-3%: coloring 2-3%: binders 1-2%; humectants 20-40%: preservatives 2-3%; water 20-40%: therapeutic agent 1-2%
abrasive/cleaning and polishing agents purpose: abrasive-clean, polishing agent-smooth, shiny surface that resists discoloration & bacterial accumulation/retention: Criteria for use: no damage to tooth surface, high polish-prevents or delays reaccumulation of stains/deposits
abrasives used calcium carbonate; calcium pyrophosphate (tartat control); dicalcium phosphate dihydrate, dicalcium phosphate, anhydrous; insoluable sodium metophosphate, hydrated aluminum oxide; silica, silicates & dehydrated silica gels;
abrasives used-for gel dentifrices synthetic amorphous silica zerogel, synthetic amorphous complex aluminosilicate salt
detergents (foarming agents or surfactants)-Purpose lower surface tension, penetrate and loosen surface deposits and stain, emulsify debris, FOAMING ACTION PREFERRED BY CONSUMERS
detergents (foarming agents or surfactants)-criteria for use nontoxic, neutral in rxn, active in acid or alkaline media, stable, compatible w/ other ingredients, no distinctive flavor, foaming characteristics
detergents (foaming agents or surfactants)-substances used synthetic detergents-sodium lauryl sulfate USP, sodium n-lauryl sarcosinate
flavoring agents-purpose make desirable, mask flavors of other ingredients
flavoring agents-criteria for use chemically stable, compatible w/ other ingredients
flavoring agents-substances used essential oils, menthol, artificial noncariogenic sweetener
flavoring agents-sweeteners, substances used artificial & noncariogenic, sorbitol and glycerin which are huectants and xylitol
coloring agents vegetable dyes
binders-purpose prevent serparation of solid and liquid components
binders-criteria for use stable, nontoxic,compatible w/ other ingredients
binders-types used organic hydrophilic colloids, mineral colloids, natural gums, seaweed colloids, synthetic celluloses
humectants-purpose retain moisture-prevent hardening when exposed to air, stabilize preparation
humectants-criteria stable, nontoxic
humectants-substances used requires a preservative to prevent microbial growth, glycerin, sorbitol, propylene glycol
preservatives-purpose prevent bacterial growth, prolong shelf life
preservatives-substances used alcohols, benzoates, formaldehyde, dichlorinated phenols
therapeutic and cosmetic benefits of dentifrices caries prevention, sensitivity reduction, reduction of supra calc formation, reduction of gingivitis, tooth-whitening agents
factors affecting abrasiveness stiffness of toothbrush, pressure used, concentration of dentifrice; exposure of cementum/dentin
ada acceptance program-the seal 5 yr basis; first seal 1931; application for the seal is voluntary
purposes of the seal determine safety and effectiveness of a product, review ad claims, inform profession and public about safety and efficacy of products-allows fro informed decisions about pruchase and use
ADA seal only consumer products, over 400 products carry seal
info needed to apply for seal composition, objective data from testing, advertising, proof of good manufacturing practices: must reapply every 5 yrs for otc products; any changes in composition require new app
mouthrinses cosmetic, theraputic
scope quaternary ammonium compound-freshens breath
plax high sodium content, contraindicated for elevated BP
hydrogen perioxide and sodium bicarbonate mentadent, oxyfresh-no evidence of antimicrobial effects
theraputic rinses 5 categories interfere w/ attachment of bacteria to pellicle or each other: inhibit or kill specific bacteria: broad spectrum of antibacterial activity: alters the structure of metabolic activity of biofilm; enzymes break up biofilm or modify bacterial activity
theraputic rinses-general functions oxygenating-cleansing: astringent-shrink tissues: anodyne-alleviate pain: buffering-reduce acidity: deodorizing: antimicrobial
theraputic rinses-oxygenating cleansing, antimicrobial-lmtd action: ANUG & ANUP: active ingredients-hydrogen peroxide, doium perborate, urea peroxide: continued use may cause spongy gingiva, black hairy tongue, hypersensitive roots, demin of tooth surfaces
astringents shrink tissue, used during impression making: active ingredients- zinc chloride, zinc acetate, alum, tannic acid, acetic acid, citric acid: can cause tooth demin and tissue irritation
anodynes temp relieve pain: used during rad exposure, impressions: active ingredients-phenol derivatives, essential oils
buffering agents reduce oral acidity, dissolve mucinous films, give relief of soft tissue soreness: Active ingredients-sodium borate solution NF, sodium perborate NF, SODIUM BICARBONATE USP
deodorizing agents lesson possibility of halitosis from local causes, active ingredient-chlorophyll
antimicrobial agents Active ingredients: bisbiguanides (chlorhexadine)haolgens (iodine, etc) phenolic compounds (listerine) quaternary ammonium compounds (scope) herbal extract (sanguinarine-vidadent)
antimicrobial agents-purposes and uses-clinic pretreatment rinse to reduce aerosols, facilitate impression procedures, rinse and refresh mouth during rad procedures
antimicrobial agents-purposes and uses-homecare moth cleaning, post op, post nonsurgical therapy, trtmt of ANUG ANUP; dental caries prevention (fluoride rinses); cosmetic
characteristics of effective mouthrinses nontoxic, no/limited absorbtion, substantivity-ability to bind to pellicle and tooth surface and be released over time; bacterial specificity-attack most pathogenic mo's: low induced drug resistance-so it can be used over long periods of time
Therapeutic mouthrinses clhorhexidine gluconate, stannous fluoride, phenol-related essential oils, cetylpyridinium chloride (CPC)-crest pro-health
chlorhexadine most effective anti-plaque & anti-gingivitis chemotherapeutic agent available: rx only: 15% alcohol: 0.2% chlorhexidine gluconate & .12% chlorhexadine gluconate
chlorhexadine-MOA bactericidal-wide range of g+ & g- and fungi: substantivity-released slowly, prolongs bactericidal effects
chlorhexidine short term (limit 6 mos), decreases supra plaque formation & inhibits gingivitis: adjunctive therapy following surgery: control inflammation in ANUG/ANUP: supresses S. mutans
chlorhexidine-side effects brown staining (easily removed), temp loss of taste, discomfort, burning, dryness, epithelial desquamation, slight increase in supra calc formation due to accumulation of dead bacteria
phenol-related essential oils otc, contains thymol, menthol, eucalyptol, & methylsalicylate in a hydroalcohol solution 26.9% alcohol (21.6% cool mint & fresh burst): low substanivity: inhibits bacterial plaque and gingivitis; strong taste
sanguinaria extract natural anti-bacterial agent; contains zinc citrate, otc-colgate: best when Viadent paste and rinse used together: reduces plaque, gingival inflammation, and gingival bleeding
cetylpyridinium chloride (CPC) kills 99% bacteria: alcohol free, Pro-Health
self prepared mouthrinses water, isotonic sodium chloride, hypertonic sodium chloride solution, sodium bicarbonate, sodium chloride & sodium bicarb solution
Created by: jfgwinn