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Pregunta	Respuesta
Dr. G.V. Blacks classification system is for classifying what?	Cavity lesions, preparations and finished restorations, categorized according to tooth surfaces
Blacks classification system, class I is	Pits and fissures on O or B and L of posterior teeth
Blacks classification, class II	Proximal surfaces of posterior teeth
Blacks classification, class III	Proximal surfaces of anterior teeth-does not include the Incisal angle
Blacks classification, class IV	Proximal surfaces of anterior teeth including the Incisal angle
Blacks classification, class V	Cervical 1/3 of anterior and posterior teeth- facial or lingual
Blacks classification, class VI	Caries or restoration(s) on the Incisal edge of anterior teeth or cusp tip of posterior teeth
What is the etiology of gingival, periodontal disease, and caries	Combination of specific pathogens found in dental plaque
In health, what is the color of gingival tissue	Pink or coral
In health where is the papilla, what is the sulcus depth, and where is the attached gingiva tightly bound	Papilla fills embrasure space, sulcus <3mm, attached gingiva tightly bound to underlying connective tissue
What is gingivitis	Inflammation of the gingival tissue without apical migration of the junctional epithelium
What is the pathogenesis of gingivitis	The events in the development and progression of a disease, 3 stages in the development of gingival inflammation.
The initial stage of gingivitis is the first few days characterized by	Acute inflammatory response, no visible symptoms- sub clinical infection
After 4to7 days of plaque accumulation and the appearance of lesions, initial gingivitis becomes early gingivitis and may continue for 21 days or longer. It is characterized by	Increase in t-lymphocytes in CT, exudate increases and may be white or yellow, tissues are red and swollen, collagen fibers connection CT to GE are destroyed, JE is disrupted by migrating WBC
After 15to21 days, though lesions can remain unchanged for years, early gingivitis becomes established gingivitis, and is characterized by	Distinct change in WBC present, T&B lymphocytes in equal #, B's release lymphokines that accelerate tissue destruction, increase loss of collagen fibers, tissue edema, and probing depth, changes in histology of JE, visible pus, gingiva red or bluish and shiny
True or false, gingivitis is directly related to plaque accumulation in the tooth and in the sulcus, and is reversible when plaque is removed regularly. BOP is a major clinical indicator and	True
gingival hyperplaisa and hypertrophy are both a pathologic overgrowth of gingival tissue caused by	excessive reaction to bacterial plaque, medications, infections or side effects of systemic disease
gingival hyerplasia is	enlargement due to increase in number of cells (usually firm tissue)
gingival hypertrophy is	enlargement due to increase in size but not number of cells (usually edematous (soft and spongy) tissue)
steriod hormone-influenced gingivits includes hormones associated with puberty, pregnancy and birth control medications and are related to gingivitis because of	estrogen receptors in gingival tissue, enhance tissue vascularity, changes are related to the level of plaque control
periodontitis is a disease of the supporting structures of the teeth with apical migration of the junctional epithelium and is characterized by	destruction of the attachment apparatus: alveolar bone, periodontal ligament & cementum. results in deepening of the gingival sulcus to form a periodontal pocket, tooth loss may result
Chronic periodontitis is the most common form of periodontal disease, affects both adults and adolescents. It also effects males and females equally. It always preceded by ginivitis and is characterized by,	Slow rate of progression, directly related to the presence of plaque. Modified by and/or associated with systemic diseases smoking, stress, hormones, genetics, presence of calculus, and overhanging restorations .
which is more important, pocket depth or attachment loss	attachment loss
aggressive peridontitis can be localized or generalized. it has specific clinical and laboratory finding that make it distinctly different from chronic periodontitis. These clinical features include	except for the periodontitis, patients are otherwise healthy, rapid attachment loss and bone destruction, and familial disposition
localized aggressive periodontitis is called LAP and effects what area of the teeth and occurs commonly at that age	permanent 1 molars and incisors , common between puberty and later teens
Generalized Aggressive Periodontal disease is called GAP and occurs at what age	late teens to 20's and 30's
contributory risk factors of peridontal disease include sides that were previously infected, presence of calculus, and... (several things)	anatomy, trauma, occlusion, stress, genetics, race, age, gender, endocrine, and drugs
What is the genetic factor of periodontal disease found by a blood test	Interleukin 1
Which race and gender is at the highest risk for aggressive periodontal disease	African American males
Drugs that cause gingival enlargement cause an over production of ( ) which are the producers of ( )	Fibroblasts, collagen
How is calculus related to periodontal disease	Considered the most important local contributing factor, it's porous and is a reservoir for bacteria and endotoxins
Some of the anatomical factors of periodontal disease are tooth position and crowding, what are some of the others	Root morphology, furcaition involvement, and the mesial root depression on max 1st molars
what are some of the traumatic factors of periodontal disease	toothbrush trauma, gouging or scratching of the tooth surface, food impaction, chemical injury (mouthwash, aspirin, cocaine)
true of false, occlusal trauma doesn't initiate gingival or periodontal inflammation but it can increase the rate of disease progression of inflammation is already present	true
how many times more likely is a patient with a positive IL-1 gene to develop advanced PDZ	7x
True or false race is a significant factor in aggressive and chronic PDZ	false, race is not considered a significant risk factor in chronic PDZ.
How does gender play a role in PDZ	females are considered to be more susceptible but males have a greater incidence and severity. may be because females seek treatment sooner, or may be because of hormones (estrogen)
long term physical and physiological stress seems to increase susceptibility to PDZ why may this be so	may depress the immune system, less attention may be paid to POH and stress may have an effect on healing
PDZ is the 6th complication of diabetes, however well controlled diabetics have no greater risk while brittle diabetics are at a greater risk of PDZ and severe gingivitis, why may this be so	diabetes impairs wound healing and reduces ability to cope with infections
gingivits and PDZ are more severe in some patient with hormonal imbalance such as in pregnancy and during puberty. What is important about pregnancy gingivitis in relation to pregnancy	pregnancy gingivitis is not caused by pregnancy, but is instead cause by an underlying gingivitis exacerbated by pregnancy.
Menopause and Osterporosis are not considered a definitive risk factor for PDZ but how is it related	thinning of the bone, bone becomes more porous, poor POH can lead to more severe PDZ
smoking is major and significant risk factor, smokers are 2.5x more likely to develop PDZ, why	tabacco products affect subgingival flora by factoring colonization of periodontal pathogens. it also alters host immune response, and increases temp inside the sulcus which favors growth of flora
chronic alcohol abuse increases the risk for periodontitis, how does it play a role in PDZ	increased bleeding tendencies, poor POH, tendency toward malnutrition
alcohol and tobacco combined present a significant risk for the development of what	oral cancers
how does PDZ play a role in diabetes	PDZ is responsible for higher levels of blood glucose. controlled PDZ insulin requirements can often be reduced
men with PDZ (esp those under 50) are 25% more likely to develop coronary artery disease. risk is significant enough to advise proper brushing and flossing may save patient lives. How are they related	PDZ linked with an increased risk for atherosclerosis and thromboembolisms independent of other risk factors. the bateria found in PDZ is also found in the arteries of the same patients with coronary artery disease.
PDZ is linked to low birthweight (<5.5lb) or premature (<37 weeks) babies. How many times more likely are woman with PDZ vs woman without to be effected by this	7-8x
true or false, gingivitis is reversible	true
true or false PDZ is reversible	false, POH can prevent further damage but PDZ is not reversible
Caries is latin for "Rot" or "rotten" and is characterized by demineralization of mineral componentes and dissolution of the organic matrix of the tooth. is a disease of what structures of the tooth	calcified structures (enamel, dentin and cementum)
although there are strong familial ties with caries there are no genetic links. Though 94% of adult have past or present coronal caries and it is one of the most common infectious diseases in school children. How does it effect older adults?	root caries are more common, likely because older adults often have more A/L and you have to have A/L for root caries.
caries are a bacterial infection that causes tooth destruction, incidence has increased due to increased consumption of refined carbs. The bacteria are transmitted primarily through ( ), and how soon after birth are we infected with microbes	saliva, hours
there are 3 causal factors of caries, what are they	1. agent: plaque, biofilm (s.mutans, s.sobrinus, lactobacilli, actinomyces viscosus. 2. host: tooth, saliva and immune response. 3. environment: dietary fermentable carbs
what are the 4 major caries producing pathogens	streptococcus mutans, streptococcus sobrinus, lactobacillus species, actinomyces viscosus
what is special about the major caries producing pathogens	cariogenic, acidogenic (acid-producing), aciduric (acid loving) bacterium.
s. mutans and s. sobrinus play a major role in what aspect of caries	development and progressing
acidogenic lactobacilli play a role in what aspect of caries	progression
actinomyces viscosus are indicated in what type or caries	root caries
extracellular polysaccharide are complex sugars that contribute to bacterial adherence or serve as energy source for pathogens. How are s. mutans and lactobacilli involved with these	s. mutans and lactobacilli can produce acid and extracellular polysaccharides through carb metabolism. s.mutans can directly convert sucrose to simple sugars, glucose and fructose
metabolic pathways inside the cells are activated upon exposure to sucrose which results in	organic acid production, lactic acid and lactate
enamel is the hard, thin, translucent layer of calcified tissue covering the crown of the tooth, it is the most mineralized tissue in the body and is 95-98% mineral or inorganic, it contains Ca and Phosphate and is primarily composed of...	rods of carbonated hydroxyaptitie crystals seated in an organic matrix (1-25 of tooth that is organic). The pure mineral form is called hydroxyapatite
the dentin is the hard layer of the tooth under the enamel and cementum. It is hard but not as hard as enamel. it surround the pulp and its matrix of tubules extend from the DEJ to the pulp. there is not blood supply or nerves. The dentin is composed of...	70% hydroxyapatite crystals, 20% organic collagen fibers and protein and 10% water by weight
Cementum seals the root surface it also covers the root surface and the end of the dentinal tubules. It's the attachment mechanism for PDL. It's 45-50% mineral, 50-55% organic. Why is the cementum more organically composed	Cementum has to have more organic component for the PDL fibers to attach to the tooth surface. PDL fibers will not attach to dentin.
The dental pulp is the specialized CT in the center of the tooth it contains blood vessels and nerves. Damage to the pulp results in	Death of the tooth, this does not necessarily mean loss of the tooth.
saliva helps to maintain the equilibrium of the oral cavity. there are several properties to saliva. Name them	physical, chemical, and antibacterial
what are the physical properties of saliva	physically cleanses the mouth of food and debris, dilutes and removes the organic acid from microbial plaque
what are the chemical properties of saliva	contains a number of electrolytes and organic molecules that minimize decreases in pH and facilitate the repair of enamel. salivary protein sialin tends to raise salivary pH to neutral
what are the antimicrobial properties of saliva	saliva contains several protein with antibacterial properties.
secretory immunoglobulin A (S IgA) binds to the antigen, predominant immunoglobulin found in saliva, inhibits adherence of bacteria, it is mainly secreted	from minor salivary glands adjacent to the teeth
Immunoglobulin G (IgG), major immunoglobulin un blood serum, occurs in saliva in small amounts, inhibits bacterial adherence and enzyme function and spills over into saliva via gingival....	cervicular fluid
what are the three main issues associated with carbs	1. physical form, consistency and clearance time, 2. chemical composition, 3. frequency of intake
the physical form and consistency of carbs decrease the pH of saliva and can keep them low for up to 60 min after ingested (20min avg). Sticky food increase risk but the effect of "fluid" sugars should not be discounted. How long may it take for pH to return to normal.	1-2 hrs
plaque pH before eating 6.2-7.0. Lower in caries susceptible person, higher in caries resistant person. what is the critical pH for enamel demineralization and root surface demineralization	enamel demineralization is 4.5, root surface demineralization is 6.0-7.0
simple carbs like sucrose, fructose, lactose, galactose and glucose foster colonization of s. mutans and lactobacilli. increased frequency of snaking...	extends duration of acid production and exposure to acid which increases the risk of caries.
true or false, frequency is more important that quantity in tooth decay	true
a susceptible tooth + cariogenic bacteria + fermentable carbs = acid formation which leads to	demineralization, white spot lesions (incipient) and dental caries
enamel is the most mineralized structure in the body, its formed of tightly packed carbonated hydroxyapatite crystals arranged in rods. in a cross section its key-holed shaped its separated by	space filled with water and organic matrix, the spaces form pathways through which fluid diffusion can occur
the first phase of demineralization is characterized by the first clinical evidence of white spot lesions, remineralization can occur at this stage. acids diffuse between the rods and reach the deeper areas of enamel then	acids penetrate the crystals- calcium and phosphate in subsurface and dissolve to outside of tooth and into oral cavity
phase 2 of demineralization as the acid attach continues, the lesion gets larger, there is more loss of surface enamel, progression of the lesion following the general direction of the enamel in what direction does the lesion spread.	spreads at the DEJ and continues along the dental tubules
eventually the surface layer of enamel fractures or cavitates, advanced lesions can be penetrated by the explorer, at this stage a restoration is required as it is not reversible. on exploration the lesion at this point will feel	soft and sticky
remineralization can occur during phase 1, it occurs when calcium and phosphate ions redeposit into demineralization area, the process is slow and can take up to two years, continuous interchange of ions between the enamel and saliva its enhanced by	saliva because of super saturation of calcium and phosphorus
fluoride is extremely significant for remineralization, its incorporated into the inorganic parts of the enamel and bonds firmly to calcium, fluorapatite crystals less soluble than original crystals. when is the best time to apply fluoride?	immediately after tooth eruption
this affects 1% of kids by 12-24 months, 5% affected by 35 months and prevalence is as high as 80% in native american population	early childhood caries as known as baby bottle caries
ECC affects maxillary anterior teeth most commonly, while the nipple covers the mandibular teeth so they are rarely affected. what are the main causes of ECC	nursing at will, sweetened liquid in bottle or pacifier dipped in sweetened liquid, putting baby to bed with bottle.
these are the most common type of cries, includes lingual and buccal pits, begins in minute fault in enamel, closure of enamel plate is imperfect , plaque is not easily removed in these areas, prevention is fluoride and sealants, what are they	pit and fissure caries
this type of cares are on proximal surfaces of teeth and on the cervical thirds, they are	smooth surface caries
this type of caries only occurs with ginigival recession, its a soft, progressive lesson of cementum and dentin and only involved in enamel by extension, occurs in a mildly acidic environment (6.0-7.0). soft yellow in color, to light/dark brown and black, active lesion is leathery to touch	root caries
true or false, an arrested root caries looks the same as root caries but is hard to the touch	true
what are the predisposing factors for root caries	root exposure, risk increases with age, lack of fluoride (30% decrease in fluorinated area), xerostomia, poor oral hygiene, cariogenic diet
incipient caries present as white chalky (when dry) area, frank carious lesion identified by break in enamel surface or dark brown or black color change. transillumination helpful, difficult to detect proximal caries unless,	occlusal surface has been undermined.
traditionlly explorers were used for tactile sense on caries, studies indicate that bacteria may be transfected from tooth to tooth with explorer, current practice advocates	visual assessment and judicious use of explorers
what is exceptionally valuable for detecting proximal caries	radiographs
true or false, the prime clinical significance of of dental stains is cosmetic, the stain itself is not pathogenic. pathogenic problems are associated with microbial plaque and calculus, source of stain in important in determining treatment	true
extrinsic stains are	outside the tooth, generally stained plaque
intrinsic stains are	inside the tooth
exogenous stains	develop from a source outside the body, may be extrinsic or intrinsic
endogenous stains	produced within or caused by factors within the body, always intrinsic
how is the medical and dental history during the clinical exam important in identifying stains	reveal tooth development problem. fluoride history, use of tobacco, oral hygiene behaviors.
this stain is dull, yellowish discoloration of bacterial plaque, most common stain, occurs at all ages, most evident with poor POH, similar distribution as plaque, etiology is usually food pigments	yellow stain
this stain is light yellowish green to very dark green, embedded in plawu, mainly on facial surfaces but may extend to proximal, mainly on maxillary anterior teeth, frequently superimposed by materia alba composed of chromogenic bacteria and fungi, recurrence dependent on POH	green stain
this stain occur in three forms (small curved line following gingival margin on facial 1/3, smeared irregularly on facial surfaces, streaked-following grooves or lines in enamel, enamel underneath may be demineralized due to plaque retention, occurs at any age but mainly children, permanent and primary teeth	green stain
this stain may become embedded in enamel (exogenous intrinsic stain), can be caused by decomposed hemoglobin and small amounts or organ element (Ca, K, sodium) occurs with poor POH. you do not want to scale this type of stain	green stain
this stain can be caused by chlorophyll preparations, metallic dust, and drugs such a marijuana	green stain
this stain is highly retentive black or dark brown, forms along gingival margins or primary or permanent teeth, more frequent in females, does not cause oral disease, gingiva is firm with no bleeding, heavy deposits may be detected with explorer	black stain
this stain is continuous, uninterrupted fine (1mm) line, band may be wider in severe cases, follows gingival margin, appears black in base of pits and fissures, facial and lingual surfaces of anterior teeth except rarely found on facial surfaces of maxillary anterior teeth	black stain
this stain is most frequently on lingual and proximal surfaces of maxillary posterior teeth, composed of iron compounds in saliva or gingival crevicular fluid embedded in dental pellicle, plaque or plaque bacteria, stain is a ferris sulfide, tends to recur despite meticulous plaque control, found in cleans mouths with few caries	black stain
this stain is light brown to dark leathery brown or black, diffuse narrow band or wide tar-like bank, incorporated into calculus deposits, heavy deposits can become exogenous intrinsic, primarily cervical 1/3, any surface as well as pit and fissures, most frequently on L surfaces	tobacco stain
this stain is composition of tar product combustion, brown pigment from smokeless tobacco, the quality of the stain is not proportional to about of tobacco used, increased stain with poor POH, amount of plaque and calculus present for adherence	tobacco stain
other types of brown stains include brown pellicle (take on stain from food), stannous fluoride (light brown, sometimes yellow, results from formation of stannous sulfide or brown tin oxide for reaction of tin oxide in the SnF compound. foodstuffs (coffee, tea, occurs less frequently in good POH) and this causes brown staining especially on exposed root, considered a signif. med side effect	chlorhexidine
this type of stain has caries inhibiting effects, dark mahogny brown, almost black, may become hard and thick, removed by scaling, common in eastern countries, its cause from	chewing betel leaf
this stain is in the cervical 1/3 of teeth, most frequently on facial and lingual surfaces of anterior teeth, rare (red more rare than orange) caused by chromogenic bacteria	orange and red stains
copper or brass(green or bluish-green), iron(brown to greenish brown), nickel(green), cadmium(yellow or golden brown), primarily found on anterior teeth but can occur anywhere, cervical 1/3 more commonly effected. these are examples of what type of stain	metallic salts from industrial dust
how do metallic salts from industrial dust stain teeth	worker inhales dust bringing metallic substance in contact with teeth, metal gives color to plaque, may penetrate tooth and become exogenous intrinsic stain
metalic substances contained in drugs stain teeth by entering plaque and imparting color, pigment from drug might attach directly to the tooth. you can prevent it by drinking liquid through a straw or using tablets or capsules. what are examples of staining drugs	iron supplements and bismuth (pepto-bismol) cause brown or black stain
these stain develop during tooth development and are within the tooth structure	endogenous intrinsic stain
this stain has a wide range of colors from light yellow-brown to bluish-black, orange or greenish orange. it results from hemorrages in the pulp and a breakdown of blood and other elements to pulpal tissue. pigments from this penetrate the dental tubules. it is caused by	endodontically treated teeth (pulpless teeth). not all endodontically treated teeth discolor
when kids fall and hit their front teeth allowing blood to escape the pulp and leaking into the dentin. this type of stain is	endogenous intrinsic
this endogenous intrinsic stain is characterized by light green to dark yellow, or grayish brown, it may be generalized or limited to teeth that were developing during drug use. it can effect children's teeth is its taken as a child or giving to mom during pregnancy. it has an affinity for mineralized tissues such as teeth. what is it caused by	tetracyclines. amount and color or stain depends on dosage and length or time drug was used and type of tetracycline used
this endogenous intrinsic stain is caused by genetic partially or completely missing enamel, due to generalized disturbance of ameloblasts. teeth are yellowish brown or gray. this is called	amelogenesis imperfecta
this endogenous intrinsic stain is genetic, is causes teeth to appear translucent or opalescent because of opalescent dentin. vary in color from gray to brown, the dentin is abnormal because of generalized disturbance or odontoblasts this is called	dentinogenesis imperfecta
this endogenous intrinsic stain is NOT genetic it is incomplete formation of enamel due to disruption of ameloblastic activity during the apposition and mineralization stage of enamel formation. its caused by poor nutrition, protracted fever, isolated trauma during tooth development, too much systemic fluoride( fluorosis). localized or generalized. this is called	enamel hypoplasia
this endogenous intrinsic stain is characterized by white spots or flecks on the teeth, same causes as enamel hypoplasia, occurs during maturation stage of enamel development, matter of when disturbance of ameloblast take place. its called	enamel hypocalcification
this exogenous intrinsic stain is caused when metallic ions seep into the enamel/dentin, corrosion on the surface releases sulfides which stain the enamel near the margin, blackish color. it is caused by	silver amalgam
exogenous intrinsic stains can also be caused by	tobacco, green stain, most any extrinsic stain can become intrinsic over time
an abnormal accretion or concentretion composed of mineral salts that may occur in hollow organs or ducts of the body	calculus
mineralized bacterial plaque that is covered on it's external surface by adhernt, active bacteria, significant in the progression of the infections and inflammatory responses of PDZ. does not come off with brushing and flossing	dental calculus
control of what can greatly reduce the risk of PDZ	bacterial plaue and dental calculus
True or false, dental calculus does not cause periodontal infections, bacterial plaque causes periodontal infections	true
surpragingival calculus is most commonly found on L suface of the man. anterior teeth and F surfaces of max 1st and 2nd molars (near salivary ducts) and is located where on the tooth	clinical crown above the gingival margin
duct that drains the parotid gland located opposite the maxillary molars	Stensen's duct
duct that drains the parotid gland located opposite the maxillary molars	Stensen's duct
what duct drains the sublingual salivary gland	bartholians duct
what duct drains the submandibular salivary gland	whartons duct
what can be found on tooth surfaces that are non-functional, such as dentures and dental prosthesis	supragingival calculus
upramarginal, extracoronal, coronal, salivary are all other terms for	supragingical calculus
this type of calculus is located crown apical to the margonin of te gingiva as well as the exposed root surfaces of the periodontal pocket. generlized or localized, interproximal most prone to this type	subgingival calculus
submarginal or serumal are other terms for this type of calculus	subgingival
this type of calculus occurs on primary or permanent teeth, more prevalent after 30, more because of increasing accumulation vs. tendency to form to new deposits, may be related to ability to remove bacterial plaque	subgingival calculus
which type of calculus can be seen with a mirror with dehydration turns yellow or white and chalky and can be felt with tactile exam	supragingival
which type of calculus can be felt with tatile exam, can been seen on readiographs (if dense and usually in proximal areas) and can be identified by signs of gingival inflammation on gingival tissue	subgingival calculus
what percentage of calculus is organic? inorganic?	75-85% inorganic, 15-25% organic
true or false, subgin calculus doesn't develop from the direct extension of supragin even though plaque does so. subgin and supra mineralize separately, you can have one without the other	true
Ca, phosphorus, carbonate, Na, mag, K, brushite, whitlockitie, octacalcium phosphat, fluoride, 2/3 crystalline (mainly hydroxyapatite) are the composition of what	inorganic component of calculus
necrotic microorganisms, desquamated epithelial cells, salivary mucin, leukocytes, outer surface covered with live microbial plaque are the compostion of	organic component of calculus
calculus forms in three phases, what are they	pellicle formation, bacterial plaque formation/,aturation, mineralization
this stage of calculus formation forms within minutes after soft and hard deposits have been removed from tooth surface. composed of salivary mucoproteins or glycoproteins	pellicle formation
in this stage of calculus formation, plaque near the gingival margin thickens (more gram - bacteria) by day 5 filamentous and fusiform bacteria enter. colonized initially by dead epithelial cells and streptococcal microorganisms	bacterial plaque formation and maturation
during this stage of calculus formation, mineralization centers (foci) form w/in 24-74hrs, center grown large enough to touch each other, crystals form, minerals from saliva encourage supragin calculus formation	mineralization
the crystals formed during mineralization phase form in the intercellular matrix of the plaque, on the surface of the bacteria and then finally within the bacteria. these crystals form from	hydroxyapatite, octacalcium phosphate, whitlocktite, brushite
what indicates that the pellicle mineralizes	calculus-like deposits have been observed on the teeth of germ-free animal
heavy calculus formers have high salivary levels of	calcium and phosphorus
light calculus formers have higher levels of	parotid pyrophosphate
plaque mineralization is strongly influenced by POH roughness of tooth surface, individual patient. It can take anywhere from 24-48r up to 20 days to form, however the average is	12 days
arranged in layers parallel to the tooth surface, appositional layers look like growth rings on a tree trunk, calculus has a rough surface perfect for plaque accumulation, outer layer only partially calcified, covered with viable living plaque. These are examples of	physical structure of calculus
this occurs when there are restoration or surface irregularities in the cementum or enamel, more difficult to remove and difficult to determine when all calculus is removed	mechanical locking
this is typical of calculus formed on enamel and/or recently scaled and debrided tooth surfaces, easily removed	pellicle attachment
this is more difficult to remove, minerals of calculus are inter locked with the surface structure of the cementum, differentiation between calculus and cementum sometime difficult	cemental attachment
white, stained, invisible until dried, amorphous, bulky, may for bridge, moderately hard, porous, covered with plaque, POH, diet, tobacco, coronal to gingival margin, opposite salivary ducts, this all describes	supragingival calculus
dark brown, green, black, flattened, crusty, spiny ledge, veneered, islands, brittle, harder than supra, covered with black, directly related to pocket depth, age of calculus, POH, diet, tobacco, apical to gingival margin, heaviest proximal areas w or w/o supra, these all describe	subgingival calculus
true or false, calculus does not cause gingival and PDZ but is provides a surface for pathogenic microorganisms to colonize. plaque is the major etiologic factor in the development of gingival and PDZ	true
what aides in the prevention of calculus formation	POH, professional removal, anticalculus dentifrice (tartar control toothpaste)
pyrophosphates or zinc added, does not affect calculus already formed, no effect on subgin calculus formation, limited effects on supragin formation, can cause dentinal hypersensitivity, these are all attributes of	anticalculus dentifrice (tartar control toothpaste)
T or F, calculus is mineralized microbial plaque, it acts as a reservoir or haven for pathogenic microorganisms, amount of calculus does not determine the amount of PDZ, understaning the attachment mechanism of calculus is important in understanding debridement techniques	true
T or F, pathogenic microbial plaque is the main etiologic factor in the development and progression of periodontal diseases; gingivitis and periodontits	True
T or F, dental caries, gingival infections and periodontal infections are all initiated by microorganisms in microbial plaque	true
each of the type of soft depositis are separate entities, terminology is not interchangeable, these soft deposits include	acquired pellicle, microbial plaque, materia alba, food debris
what is the role of the RDH	preventive therapist, educate patients about initiation of disease and progression of disease
this is amorphous, acellular, organic, tenacious, membrane that forms over exposed tooth surfaces, restoration and calculus. its derived from salivary glycoproteins, forms within minutes of removal with toothbrush or polishing agent	acquired pellicle
salivary glycoproteins in the acquired pellicle are selectively adsorbed by the ( ) of the tooth surface and forms a highly insoluble coating over everything it covers	hydroxyapatite
there are three types of aquired pellicle, one is translucent, insoluble, not readily visible unless disclosed, thin and pale pink when stained, the 2nd can take on an extrinsic stain, the 3rd is continious with surface pellicle, embedded in tooth surface esp where tooth is demineralized. name these pellicles	unstained surface, stained surface, and subsurface pellicle
protective (provides a barrier against acids, helps prevent tooth decay), nidus for bacteria (aids in adherence of bacteria, plaque formation) attachment of calculus (one way for calculus to attach to teeth) these are all the significant factors of what	acquired pellicle
T or F microbial plaque forms in mushroom like colonies of bacteria, dental plaque is a biofilm	true
T or F, the definition of biofilm is a dense, nonmineralized, complex mass of microbial colonies in a gel-like inter microbial matrix. dental plaque adheres firmly to the acquired pellicle, calculus, fixed & removable restorations. it is the major etiologic factor in development of tooth decay.	true
this type of bacteria is non-motile, non-spore forming gram +, aerobic or facultative aerobic, occurs in pairs or short or long chains, commonly found in the mouth, some are pathogenic. S. mutans associated with dental caries and bacterial endocarditis	streptococci
this type of streptococci is pairs of cocci, often found in parasites	diplococci
this type of streptococci occurs in grape like clusters, gram +, staph infections characterized by formation of abscesses, MRSA	staphylococci
this type of bacteria is gram +, aeroboes or facultative anaerobes, spore-bearing, rod-shaped, can cause a wide variet of diseases from anthrax to TB	Bacilli
this type of bacilli are short and thick, somewhat oval in shape	coccobaccilli
this type of bacilli are large cigar shaped bacillus, anaerobic	fusiform bacilli
this type of bacilli is long, thread-like bacilli	filamentous forms
this type of bacilli is slender, social, motile, gram-, treponema denticola associated with severe periodontitis is an example	spirochetes
this type of bacilli is curved, motile, gram-	vibrio
formation of pellicle, bacteria attach to pellicle, bacterial multiplication and colonization, plaque growth and maturation, and formation of intermicrobial matrix, these are all part of the stages of	plaque formation
the first stage of plaque formation is characterized by	pellicle forms on the tooth by selective adsorption of protein components from saliva
the second stage of plaque formation is characterized by	bateria attach to the pellice, initial attachment is selective-specific bacteria adhere, innate characteristics of the bacteria and the pellicle determines what will attach to a particular pellicle
the 3rd stage of plaque formation is characterized by, microcolonies form in layers, multiply and grown, increase in size, colonies meet and coalesce (mushroom shape) first few hours mainly gram + cocci and rods and is called	bacterial multiplication and colonization
the 4th stage of plaque formation is called plaque growth and maturation and is characterized by	increase in mass size and thickness due to multiplication of bacteria and adherence of new bacteria to existing mass
the 5th stage of plaque formation is called formation of the intermicrobial matrix and is characterized by	substance for supragin plaque derived mainly from saliva, subgin plaque derived mainly from sulcular fluid and exudate, also, polysaccharides, glucans, and fructans or levans produced by some bacteria from dietary sucrose
the population in plaque density is very high, risk of developing tooth decay and/or gingivitis increases as the number of microorangisms increases what happens as plaque it ages	the population density of microogansims increases
what is the bacterial composition of a well cleaned mouth	epithelial cells and a few cocci
what is the bacterial composition of 1-2days of incomplete plaque removal	primarily cocci, s. mutans, s. sanguis and some short rods
what is the bacterial composition of 2 to 4 days of incomplete plaque removal	cocci still donimate, increasing numbers of filamentous forms (will eventually replace cocci) and slender rods on surface of cocci colonies
what is the bacterial composition of incomplete plaque formation after 4 to 7 days	increased # of filaments, mixed flora w/rods, filametous forms and fusobateria, plaque near gingival margin thickens, new plaque extending coronally
what is the bacterial composition of incomplete plaque removal after 7-14 days is	vibrios and spircohetes, # of WBCs increases, more gram- anaerobic, clinical signs of inflammation becomes evident in gingival tissue
what is the bacterial composition of incomplete plaque removal after 14-21 days	vibros, spirochetes, cocci (attach in corncob formation), filamentous forms (forms line themselves perpendicular to the tooth). gingivitis is evident
T or F subgin plaque results from the apical migration of supragin plaque	true
in the early stages of gingivitis and periodontitis supragin plaque strongly influences the accumulation and pathogenic features of subgin plaque. as the pocket deepens	subging plaque affects plaque located at the most coronal edge of the pocket
what is greater than or = to 4mm, with no bone loss, no loss of fiber, no apical migration	gingival or pseudo pockets
what is greater than or equal too 4mm, junctional epithelium has migrated, apical migration	periodontal pocket
flora of subgin plaque different that flora of supragin plaque, more anaerobic and motile organisms and predominately gram ( )	gram -
gram - bateria have a toxic outer membrane made of lipopolysaccharides (LPS) when phagocytized it causes a release of	endotoxins
this forms over the pellicle, layer of densely packed microorganisms, closest to tooth, mostly gram + cocci and rods, associated with root caries, calculus formation and root resorption	tooth attached plaque
this is loosely attached to the pocket epithelium, mainly gram - microorganisms and WBC, many virulent pathogens in this area associated with advancement of periodontal disease, microorganisms in the lay invade the underlying CT	epithelium- attached plaque
this prevents plaque or bacteria in sulcus from going into connective tissue in the periodontal ligament space, forms a biologic seal, only about 9mm long, goes around tooth, top at CEJ, bottom at root, forms like a triangle	junctional epithelium
this is between the layers of attached plaque, many motile, gram- organisms, "fluid" plaque, contains lots of WBC	unattached plaque
invasion of bacteria into underlying tissue is a significant pathogenic mechanism for the progression of a	periodontal infection
in the composition of plaque there are microogranisms in an intermicrobial matrix, composition differs from tooth to tooth and person to person, as plaque changes it ages. what portion of plaque is organic & inorganic solids? what percent is water	20% organic and inorganic solids, 80% water
what are the inorganic components of plaque	calcium, phosphorus, fluoride
carbs (produced by several types of bacteria, glucans and fructand from dietry sugar, help to hold bacteria together, energy source), proteins (supra-derived from saliva, sub- derived from gingival exudates and sulcular fluid) lipid (LPS endotoxins from gram - bacteria) these are examples of what component of plaque	organic components of plaque
On what surfaces can plaque be located	supragin (above the gingival margin) subgin (below gingival margin), gingival (on gingival tissues) pits &fissures (hard to removed) tongue(dorsal surface)
T or F, supragin plaque formation beings as gin margin esp proximal surfaces, spreads over gin 1/3 onto middle 1/3, apical proliferation	True
tooth surfaces irregularities, tooth contour (xtra or missing cusps, erosion, abrasion, over/undercontoured restorations) tooth postion (crowding, missing teeth) dental prosthesis (ortho bands, fixed or removable prosthesis) poor POH, diet/eating habits, tobacco habits, these are all examples of	factors influencing plaque accumulation
what are the ways of detecting plaque	direct vision (thin plaque, easier to see with disclosing solution. thick plaque tooth appraise dull, mat fur like) explorer or probe (may feel rough if its begun to calcify, slippery)
this plays a significant role in initiation and progression of dental decay and PDZ, all ( ) are not the same	bacterial plaque
several different theories have evolved regarding the significance of bacterial plaque, name them	non-specific plaque hypothesis, specific plaque hypothesis, host bacterial interaction theory
this theory states dental caries and PDZ result from bacterial products of the entire plaque floar, plaque is all the same, disease activity is determined by # of microorganisms and the response of the host	non-specific plaque hypothesis (1965-1975)
this theory say plaques are due to specific microorganisms, particular microorganisms must always be present in association w/specific infection, prevention or treatment procedures would be directed at those specific plaque microorganisms is	specific plaque hypothesis (1975-1985)
this theory says interation of the host with the pathogenic bacteria that contol the development and progression of PDZ, bacterial infection alone is not sufficient to result in PDZ, certain risk factors increase host susceptibility is called	host-bacterial interaction theory (current)
what are the three main categories of plaque	cariogenic (associated with caries), PDZ producing (promotes inflammatory responses) calculus or calculogenic (encourages mineralization of plaque)
bacterial plaque is the main etiologic agent in the development of	tooth decay (caries) and peirodontal disease (gingivitis and periodontitis)
this is a disease of the mineralized (inorganic) and nonmineralized (inorganic) structure of the tooth, primary cause cariogenic bacteria, diet POH, genetics	dental caries
this is inflammtion of the gingiva with no loss of attachment, bone, PDL or cementum, no apical migration of JE. Characterized by changes in color, gin form, position, surface appearnce and presence of bleeding/exudate	gingivitis
this is inflammation of the supporting structures of the teeth, progression of gingival inflammation into deeper periodontal structures, apical migration of JE. loss of PDL, alveolar bone, cementum, ging CT fiber	periodontitis
this is loosely adherent mass of bacteria and cellular debris, often on top of plaque, accumulation of living and dead bacteria, desquameted epithelial cells, disintegrating leukocytes, salivary proteins, food debris	materia alba
this is found around the cervical 1/3 & proximal embrasures of teeth, open contacts, mobility, self-cleansing action of tongue and saliva help to remove debris	food debris
this is white of grayish white, may resemble cottage cheese, can be removed with water spray or oral irrigator unlike plaque witch cannot be removed w/oral irrigation of water pik	materia alba

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	Creado por angela.dennis22 hace alrededor de 11 años