Dent 1015 Test 2

Front 1

Acquired Pellicle

Back 1

Coating on teeth that is acellular, made up of glycoproteins from saliva. Forms within minutes of being brushed off

Front 2

Characteristics of Dental Plaque

Back 2

Cellular, non-mineralized, microbial colonies grow and develop into a continuous gel-like intermicrobial matrix

Front 3

Organisms in plaque after first few hours

Back 3

Gram positive cocci and rods

Front 4

Organisms in plaque after 1-2 days

Back 4

Cocci

Front 5

Organisms in plaque after 2-4 days

Back 5

Cocci dominate, filamentous forms replace cocci, more pathogenic slender rods

Front 6

Organisms in plaque after 4-7 days

Back 6

More filamentous forms (spirilla), plaque in the gingival margin has spirochetes and vibrios. Mixed flora include fusobacteria

Front 7

Organisms in plaque after 7-14 days

Back 7

Vibrios and spirochetes, Gram negative, anaerobic, inflammation starts and WBC's increase

Front 8

Organisms in plaque after 14-21 days

Back 8

Vibrios and spirochetes are prevalent, gingivitis is evident clinically

Front 9

What occurs after 21 days of maturing plaque?

Back 9

ANUG: acute necrotizing ulcerative gingivitis

Front 10

Three Stages of Plaque

Back 10

1. Proteins attach to tooth enamel and form pellicle

2. Microorganisms colonize pellicle to form early plaque

3. Plaque organisms multiply and change as plaque ages

Front 11

Materia Alba

Back 11

Cellular, non-mineralized, soft loose mass of living and dead bacteria. Looks like cottage cheese, can be removed by vigorous brushing, flossing, and rinsing

Front 12

Food Debris

Back 12

Cellular, non-mineralized, visible in mouth

Front 13

Hard Deposits

Back 13

Cellular, composed of mineralized bacterial plaque, mineral source is saliva, occurs at any age and on primary or permanent teeth

Front 14

How do we see supragingival calculus?

Back 14

Use compressed air, it shows up chalky. Also is easier to remove

Front 15

Components of Calculus

Back 15

15-25% Organic: early cocci/rods, and water

75-90% Inorganic: Calcium, phosphorus, sodium, magnesium, potassium, etc.

Front 16

What mostly composes the inorganic matter of calculus?

Back 16

2/3 is crystalline, mainly hydroxyapatite or fluoroapatite if the person had systemic fluoride while growing up

Front 17

Why do some people form more calculus?

Back 17

Heavy formers have high levels of calcium and phosphorus (forms after 10 days). Light formers have higher levels of parotid pyrophosphate (forms after 20 days)

Front 18

What is significant about pyrophosphate?

Back 18

It is a calcification inhibitor

Front 19

Extrinsic Stains

Back 19

Occurs on external surface of tooth, can be removed by scaling or polishing

Front 20

Intrinsic Stain

Back 20

Occurs within the tooth structure, cannot be removed

Front 21

Exogenous Stain

Back 21

Develops or originates from outside the tooth, may be extrinsic or intrinsic

Front 22

Endogenous Stain

Back 22

Develops or originates from within the tooth, always intrinsic

Front 23

What compose the green stain?

What category is green stain?

Back 23

Gram positive microorganisms, chromogenic bacteria, decomposed hemoglobin

Exogenous Intrinsic Stain

Front 24

Where is green stain found and what does it lead to?

Back 24

Embedded in pellicle along gingival margin, facial cervical 1/3 of Mx Anteriors. May be streaked on grooves or lines of enamel.

Leads to demineralization of enamel and gingival bleeding

Front 25

What composes the black line stain and who does it occur in?

Back 25

Gram positive rods, cocci. Found in females with good oral hygiene with low incidence of caries or disease

Front 26

What are the characteristics of black line stain and where is it found?

Back 26

Attached to the pellicle, highly retentive, composed of tar products, found near gingival margin on lingual and proximal surfaces of maxillary posterior teeth

Front 27

What causes brown stain?

Back 27

Tobacco, stannous fluoride, tea, coffee, soy sauce, chlorohexidine, and batel leaf chewing

Front 28

Tobacco Brown Stain

Back 28

Narrow band around gingival crest , can be over the central 1/3 Can become exogenous intrinsic (penetrates the enamel). Most often in lingual surfaces, pits, and fissures

Front 29

Stannous Fluoride

Back 29

Only stain that actually affects plaque accumulation, pellicle picks it up after topical application

Front 30

Metallic Stain

Back 30

Copper, Brass, Iron, Nickel, Cadmium. Usually found on anterior teeth on the cervical third. When industrial workers inhale dust, metal stain may be exogenous intrinsic.

Front 31

Tetracycline Stain

Back 31

Systemic, antibiotics, if taken first trimester of pregnancy, it transfers through the placenta and is absorbed by the developing teeth and bones. Light green/dark green stain can occur generally or on individual teeth

Front 32

Amelogenesis Imperfecta

Back 32

Enamel is partially or completely missing due to disturbance of ameloblasts, looks yellow brown or gray brown

Front 33

Dentinogenesis Imperfecta

Back 33

Disturbance of odontoblasts, teeth appear translucent or gray

Front 34

Enamel Hypoplasia

Back 34

Ameloblastic disturbance for a short time, teeth erupts with white spots or pits

Front 35

Dental Fluorosis

Back 35

Hypoplasia caused by excessive fluoride, mottled or brown enamel. Very healthy teeth

Front 36

Other Systemic Causes of Endogenous Intrinsic Stains

Back 36

Prolonged jaundice (yellow-green)

Erythroblastosis Fetalis (green, brown, or blue)

Front 37

Other Causes of Exogenous Intrinsic Stains

Back 37

Amalgam, composite, ammoniacal silver nitrate, black carious lesion discoloration of dentin

Front 38

What are the components of the periodontium

Back 38

Gingive

Cementum

Periodontal Ligaments

Alveolar Process

Front 39

Gingiva

Back 39

Keratinized masticatory mucosa that surrounds the teeth

Front 40

Marginal Gingiva

Back 40

Closer to crown, 0.5-2 mm coronal to CEJ

Front 41

Gingival Sulcus

Back 41

Space between marginal gingiva and tooth, healthy would be 0.5-3 mm.

Front 42

Sulcular Epithelium

Back 42

Surrounds free gingiva, non-keratinized stratified squamous epithelium. Attaches gingival sulcus to tooth at junctional epithelium

Front 43

Gingival Groove

Back 43

Where marginal gingiva connects with alveolar gingiva (attached)

Front 44

Attached Gingiva

Back 44

Divided from alveolar mucosa by the mucogingival junction, covers alveolar bone and roof of mouth

Front 45

Interdental Papilla

Back 45

Space between two adjacent teeth, shape is dependent upon the space

Front 46

Col

Back 46

Non-keratinized saddle of interdental gingiva that connects the facial and lingual aspects of the papilla

Front 47

Alveolar Mucosa

Back 47

Non-keratinized epithelium, is a darker shade of red due to larger blood supply

Front 48

Gingivitis

Back 48

Bacterial endotoxins and enzymes released from Gram negative bacteria, breakdown of epithelial intercellular substances and the sulcular epithelium is ulcerated. Bleeding, edema, swelling, exudate from sulcus

Front 49

Initial Lesion

Back 49

2-4 days, WBC's in JE and sulcus, sulcus fluid is increased and fills spaces

Front 50

Early Lesion

Back 50

7-14 days, collagen fibers start to break down, fluid, lymphocytes and neutrophils infiltrate connective tissue. Early gingivitis is reversible

Front 51

Established Lesion

Back 51

Chronic inflammation, connective tissue fibers don't support

Front 52

Advanced Lesion

Back 52

Bacteria from supragingival plaque enters the sulcus, JE continues to migrate apically, alveolar bone destruction occurs, pocket forms

Front 53

Pseudopocket

Back 53

Gingival enlargement without apical migration of the JE

Front 54

Suprabony

Back 54

Base of pocket is coronal to alveolar crest

Front 55

Intrabony

Back 55

Base of pocket is apical to alveolar crest

Front 56

Perio Pocket

Back 56

JE migrates apically, attachment apparatus is involved, tooth wall is cementum (supra)

Front 57

Goals of the Hygienist

Back 57

1. Prevent initiation of gingivitis

2. Prevent progression of gingivitis to periodontitis

3. To arrest/maintain periodontal disease (not cure)

Front 58

Types of Interdental Papilla

Back 58

1. Bulbous

2. Cratered

3. Blunted

4. Festooned

Front 59

Stillman's Cleft

Back 59

Localized recession, may be V-shaped or slit-like

Front 60

Floss Cleft

Back 60

Incorrect floss positioning, v-shaped fissure in marginal gingiva

Front 61

Gingival Crevicular Fluid (GCF)

Back 61

Serum-like fluid present in pt's with inflammation. Made of plasma proteins, saliva, WBC's, lymphocytes. If it progresses, it can become purulent with bacteria, enzymes, and necrotic tissue

Front 62

What is the best indicator of damage to the periodontium?

Back 62

Attachment Loss

Front 63

How do we measure attachment loss?

Back 63

Compare distance from CEJ to the base of the sulcus, includes both pocket depth and recession

Front 64

How do we measure attached gingiva?

Back 64

Total width of the gingiva minus the depth probed

Front 65

Classes of Furcation

Back 65

1. Detect concavity of furcation, can't enter

2. Enter furcation but can't go through other side

3. Pass explorer all the way through furcation

4. Furcation is clinically visible

Front 66

Classes of Mobility

Back 66

1. Slight mobility, up to 1 mm of horizontal displacement (facial-lingual)

2. Moderate, between 1-2 mm of horizontal displacement

3. Over 2 mm of displacement or any vertical displacement

Front 67

Fremitus

Back 67

Vibration felt when palpating a tooth as patient taps teeth together

Front 68

Occlusal Trauma

Back 68

Non-inflammatory perio condition where supporting structures are damaged because of the occlusal forces acting on them

Front 69

Primary Occlusal Traumatism

Back 69

Destruction to supporting structures is caused by occlusal forces acting on normal periodontium. Bruxism, clenching, malocclusion

Front 70

Secondary Occlusal Traumatism

Back 70

Occlusal forces acting on already diseased periodontium

Front 71

Periodontal Case Type I

Back 71

Gingival Disease, REVERSIBLE

Characterized by change in color, gingival form, position, and presence of bleeding or exudate

Front 72

Periodontal Case Type II

Back 72

Early Periodontitis, slight bone loss and slight loss of connective tissue attachment

Front 73

Periodontal Case Type III

Back 73

Moderate Periodontitis, increased destruction of periodontal structures and noticeable loss of bone support, may be increased tooth mobility, may be furcation involvement

Front 74

Periodontal Case Type IV

Back 74

Advanced Periodontitis, major loss of alveolar bone, increased tooth mobility, furcation involvement

Front 75

Prepubertal Periodontitis

Back 75

Impaired Neutrophil Function, generalized or localized, gram negative anaerobic bacteria predominates

Front 76

Juvenile Periodontitis

Back 76

Usually affects permanent first molars and incisors, AAA gram negative bacteria anaerobic (actinomycetemcomitans)

Front 77

Rapidly Progressive Periodontitis

Back 77

Onset is early 20's and mid 30's, presents with severe generalized vertical and horizontal bone loss, Gram negative anaerobic bacteria, and impaired neutrophil function

Front 78

Necrotizing Ulcerative Periodontitis

Back 78

Severe and rapidly progressing disease, erythema, necrosis, severe loss of periodontal attachment

Front 79

What are three contributing factors to dental caries?

Back 79

Susceptible teeth (host)

Indigenous Flora (parasite)

Diet or substrate (environment)

Front 80

Cavitation

Back 80

Occurs when the subsurface demineralization is so extensive that the tooth structure subsurface collapses.

Front 81

What is the main offender in promoting caries?

Back 81

Sucrose because of the ability of oral bacteria to break it down and use the energy to form extracellular polysaccharide which promote plaque formation, can be later broken down to acid

Front 82

What is the primary cavity initiator?

Back 82

Streptococcus Mutans, produces acid and can exist in an acid environment

Front 83

What is a secondary cavity promoter?

Back 83

Lactobacilli, numbers only increase on tooth after decay has begun so a carious lesion may be a pre-requisite for their colonization

Front 84

What bacteria is associated with root caries?

Back 84

Athinomycoses viscosis

Front 85

How microflora influences caries development

Back 85

Microbial composition, content of buffer: calcium and phosphate, carb fermenting enzymes

Front 86

Incipient Caries

Back 86

Lesion in enamel characterized by a virtually intact surface but it has a porous surface. Appears chalky white when dried. Can be remineralized

Front 87

Recurrent Caries

Back 87

Occurs around a restoration due to leaky margins and improper cleansing

Front 88

Arrested Caries

Back 88

Cavity is open and brown stained with a hard surface, secondary dentin is usually evident. May be arrested by topical fluoride

Front 89

Acute Cavities

Back 89

Progress quickly in closed cavity, may have rapid pulp involvement in children, pain

Front 90

Class I Cavity

Back 90

Occlusal surfaces of premolars, molars

Lingual surfaces of Maxillary incisors

Occlusal 2/3 of facial and lingual surfaces of molars

Front 91

Class II Cavity

Back 91

Proximal surfaces of posterior teeth

Front 92

Class III

Back 92

Proximal surfaces of incisors and canines, not involving incisal angle

Front 93

Class IV

Back 93

Proximal surfaces of incisors and canines, including the incisal angle

Front 94

Class V

Back 94

Gingival third of facial or lingual aspects of any tooth

Front 95

Class VI

Back 95

Incisal edges anterior teeth and cusp tips of posterior teeth