Dr. G.V. Blacks classification system is for classifying what?

Blacks classification system, class I is

Blacks classification, class II

Blacks classification, class III

Blacks classification, class IV

Blacks classification, class V

Blacks classification, class VI

What is the etiology of gingival, periodontal disease, and caries

In health, what is the color of gingival tissue

In health where is the papilla, what is the sulcus depth, and where is the attached gingiva tightly bound

What is gingivitis

What is the pathogenesis of gingivitis

The initial stage of gingivitis is the first few days characterized by

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

After 15to21 days, though lesions can remain unchanged for years, early gingivitis becomes established gingivitis, and is characterized by

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

gingival hyperplaisa and hypertrophy are both a pathologic overgrowth of gingival tissue caused by

gingival hyerplasia is

gingival hypertrophy is

steriod hormone-influenced gingivits includes hormones associated with puberty, pregnancy and birth control medications and are related to gingivitis because of

periodontitis is a disease of the supporting structures of the teeth with apical migration of the junctional epithelium and is characterized by

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,

which is more important, pocket depth or 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

localized aggressive periodontitis is called LAP and effects what area of the teeth and occurs commonly at that age

Generalized Aggressive Periodontal disease is called GAP and occurs at what age

contributory risk factors of peridontal disease include sides that were previously infected, presence of calculus, and... (several things)

What is the genetic factor of periodontal disease found by a blood test

Which race and gender is at the highest risk for aggressive periodontal disease

Drugs that cause gingival enlargement cause an over production of ( ) which are the producers of ( )

How is calculus related to periodontal disease

Some of the anatomical factors of periodontal disease are tooth position and crowding, what are some of the others

what are some of the traumatic factors of periodontal disease

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

how many times more likely is a patient with a positive IL-1 gene to develop advanced PDZ

True or false race is a significant factor in aggressive and chronic PDZ

How does gender play a role in PDZ

long term physical and physiological stress seems to increase susceptibility to PDZ why may this be so

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

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

Menopause and Osterporosis are not considered a definitive risk factor for PDZ but how is it related

smoking is major and significant risk factor, smokers are 2.5x more likely to develop PDZ, why

chronic alcohol abuse increases the risk for periodontitis, how does it play a role in PDZ

alcohol and tobacco combined present a significant risk for the development of what

how does PDZ play a role in diabetes

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 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

true or false, gingivitis is reversible

true or false PDZ is 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

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?

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

there are 3 causal factors of caries, what are they

what are the 4 major caries producing pathogens

what is special about the major caries producing pathogens

s. mutans and s. sobrinus play a major role in what aspect of caries

acidogenic lactobacilli play a role in what aspect of caries

actinomyces viscosus are indicated in what type or 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

metabolic pathways inside the cells are activated upon exposure to sucrose which results in

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...

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...

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

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

saliva helps to maintain the equilibrium of the oral cavity. there are several properties to saliva. Name them

what are the physical properties of saliva

what are the chemical properties of saliva

what are the antimicrobial properties of saliva

secretory immunoglobulin A (S IgA) binds to the antigen, predominant immunoglobulin found in saliva, inhibits adherence of bacteria, it is mainly secreted

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....

what are the three main issues associated with carbs

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.

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

simple carbs like sucrose, fructose, lactose, galactose and glucose foster colonization of s. mutans and lactobacilli. increased frequency of snaking...

true or false, frequency is more important that quantity in tooth decay

a susceptible tooth + cariogenic bacteria + fermentable carbs = acid formation which leads to

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

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

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.

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

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

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?

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

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

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

this type of cares are on proximal surfaces of teeth and on the cervical thirds, they are

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

true or false, an arrested root caries looks the same as root caries but is hard to the touch

what are the predisposing factors for root caries

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,

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

what is exceptionally valuable for detecting proximal caries

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

extrinsic stains are

intrinsic stains are

exogenous stains

endogenous stains

how is the medical and dental history during the clinical exam important in identifying stains

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

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

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

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

this stain can be caused by chlorophyll preparations, metallic dust, and drugs such a marijuana

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

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

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

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

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

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

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

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

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

how do metallic salts from industrial dust stain teeth

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

these stain develop during tooth development and are within the tooth structure

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

when kids fall and hit their front teeth allowing blood to escape the pulp and leaking into the dentin. this type of stain is

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

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

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

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

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

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

exogenous intrinsic stains can also be caused by

an abnormal accretion or concentretion composed of mineral salts that may occur in hollow organs or ducts of the body

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

control of what can greatly reduce the risk of PDZ

True or false, dental calculus does not cause periodontal infections, bacterial plaque causes periodontal infections

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

duct that drains the parotid gland located opposite the maxillary molars

duct that drains the parotid gland located opposite the maxillary molars

what duct drains the sublingual salivary gland

what duct drains the submandibular salivary gland

what can be found on tooth surfaces that are non-functional, such as dentures and dental prosthesis

upramarginal, extracoronal, coronal, salivary are all other terms for

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

submarginal or serumal are other terms for this type of calculus

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

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

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

what percentage of calculus is organic? inorganic?

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

Ca, phosphorus, carbonate, Na, mag, K, brushite, whitlockitie, octacalcium phosphat, fluoride, 2/3 crystalline (mainly hydroxyapatite) are the composition of what

necrotic microorganisms, desquamated epithelial cells, salivary mucin, leukocytes, outer surface covered with live microbial plaque are the compostion of

calculus forms in three phases, what are they

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

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

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

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

what indicates that the pellicle mineralizes

heavy calculus formers have high salivary levels of

light calculus formers have higher levels of

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

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

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

this is typical of calculus formed on enamel and/or recently scaled and debrided tooth surfaces, easily removed

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

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

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

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

what aides in the prevention of calculus formation

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

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

T or F, pathogenic microbial plaque is the main etiologic factor in the development and progression of periodontal diseases; gingivitis and periodontits

T or F, dental caries, gingival infections and periodontal infections are all initiated by microorganisms in microbial plaque

each of the type of soft depositis are separate entities, terminology is not interchangeable, these soft deposits include

what is the role of the RDH

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

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

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

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

T or F microbial plaque forms in mushroom like colonies of bacteria, dental plaque is a biofilm

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.

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

this type of streptococci is pairs of cocci, often found in parasites

this type of streptococci occurs in grape like clusters, gram +, staph infections characterized by formation of abscesses, MRSA

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

this type of bacilli are short and thick, somewhat oval in shape

this type of bacilli are large cigar shaped bacillus, anaerobic

this type of bacilli is long, thread-like bacilli

this type of bacilli is slender, social, motile, gram-, treponema denticola associated with severe periodontitis is an example

this type of bacilli is curved, motile, gram-

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

the first stage of plaque formation is characterized by

the second stage of plaque formation is characterized by

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

the 4th stage of plaque formation is called plaque growth and maturation and is characterized by

the 5th stage of plaque formation is called formation of the intermicrobial matrix and is characterized by

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

what is the bacterial composition of a well cleaned mouth

what is the bacterial composition of 1-2days of incomplete plaque removal

what is the bacterial composition of 2 to 4 days of incomplete plaque removal

what is the bacterial composition of incomplete plaque formation after 4 to 7 days

what is the bacterial composition of incomplete plaque removal after 7-14 days is

what is the bacterial composition of incomplete plaque removal after 14-21 days

T or F subgin plaque results from the apical migration of supragin plaque

in the early stages of gingivitis and periodontitis supragin plaque strongly influences the accumulation and pathogenic features of subgin plaque. as the pocket deepens

what is greater than or = to 4mm, with no bone loss, no loss of fiber, no apical migration

what is greater than or equal too 4mm, junctional epithelium has migrated, apical migration

flora of subgin plaque different that flora of supragin plaque, more anaerobic and motile organisms and predominately gram ( )

gram - bateria have a toxic outer membrane made of lipopolysaccharides (LPS) when phagocytized it causes a release of

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

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

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

this is between the layers of attached plaque, many motile, gram- organisms, "fluid" plaque, contains lots of WBC

invasion of bacteria into underlying tissue is a significant pathogenic mechanism for the progression of a

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

what are the inorganic components of plaque

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

On what surfaces can plaque be located

T or F, supragin plaque formation beings as gin margin esp proximal surfaces, spreads over gin 1/3 onto middle 1/3, apical proliferation

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

what are the ways of detecting plaque

this plays a significant role in initiation and progression of dental decay and PDZ, all ( ) are not the same

several different theories have evolved regarding the significance of bacterial plaque, name them

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

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

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

what are the three main categories of plaque

bacterial plaque is the main etiologic agent in the development of

this is a disease of the mineralized (inorganic) and nonmineralized (inorganic) structure of the tooth, primary cause cariogenic bacteria, diet POH, genetics

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

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

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

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

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