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Clinical Applications I > Polishing, Gingivitis, Periodontitis > Flashcards

Polishing, Gingivitis, Periodontitis Flashcards

1
Q

what are the active ingredients in polishing materials?

A

(FAAWDA) fluoride, antimicrobials, anticalculus, whitening, desensitizing, antihalitosis

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2
Q

what are the inactive ingredients in polishing materials?

A

(HWSPAT) abrasive, humectant, water, sweetener, preservative, thickening agent

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3
Q

what is the purpose of fluoride in polishing material?

A

caries reduction

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4
Q

what is the purpose of antimicrobials in polishing material?

A

plaque reduction, reduces inflammation

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5
Q

what is the purpose of anti-calculus ingredients in polishing material?

A

reduce level of calculus growth (but does not eliminate)

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6
Q

what is the purpose of whitening agents in polishing material?

A

removes stains

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7
Q

what is the purpose of desensitizing material in polishing material?

A

reduces root sensitivity (does NOT reduce tissue sensitivity)

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8
Q

what is the purpose of antihalitosis/malodor in polishing material?

A

reduces bad breath

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9
Q

what is the purpose of abrasive in polishing material? what percentage does it make up?

A

deposit removal, 20-40%

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10
Q

what is the purpose of humectants in polishing material? what percentage does it make up?

A

retains moisture, 20-40%

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11
Q

what is the purpose of water in polishing material? what percentage does it make up?

A

solvent and helps to reach desired consistency, 20-49%

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12
Q

what is the purpose of sweetener in polishing material? what percentage does it make up?

A

taste, 2-3%

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13
Q

what is the purpose of preservative in polishing material? what percentage does it make up?

A

increase shelf life, <1%

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14
Q

what is the purpose of thickening agent in polishing material? what percentage does it make up?

A

prevent separation of ingredients, 1-2%

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15
Q

examples of anti-caries ingredients

A

sodium fluoride, sodium monofluorophosphate, stannous fluroide, xylitol

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16
Q

examples of anti-plaque/anti-gingivitis/anti-microbial ingredients

A

triclosan/copolymer, stannous fluoride, zinc citrate, baking soda, hydrogen peroxide

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17
Q

examples of anti-calculus ingredients

A

tetrapotassium pyrophosphate, tetrasodium pyrophasphate, sodium hexametaphosphate, zinc compounds

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18
Q

examples of anti-halitosis ingredients

A

essential oils, chlorine dioxide, triclosan/copolymer, stannous fluoride/sodium hexametaphosphate

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19
Q

examples of desensitizers ingredients

A

potassium citrate, potassium nitrate, potassium chloride, stannous fluoride, strontium chloride

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20
Q

________ is a defensive reaction to irritation (mechanical, bacterial) producing ______ of tissue

A

inflammation, degeneration

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21
Q

pathogenic agent that injures tissues, resulting in inflammation

A

infection

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22
Q

infection is usually accompanied by _______, but _____ may occur without ______

A

infection, inflammation, infection

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23
Q

what type of tissue is most vunerable?

A

non-keratinized tissue

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24
Q

what areas are non-keratinized tissues that are most at risk?

A

sulcular epithelium, junctional epithelium, col area

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25
events in inflammation process
1. injury 2. invasion 3. BV contract 4. BV dilate 5. WBC/plasma enter, edema 6. chemical stimulus to attract WBC 7. phagocytosis 8. pus formation
26
how many steps in the inflammation response?
8
27
why do BV initially contract?
increase blood flow so immune defenders come to site
28
why do BV dilate after initial contraction?
leukocytes can move from center of BV to wall
29
leukocytes ingest foreign particles
phagocytosis
30
cells and plasma fluid that exits
exudate
31
the whole body responds to an irritant, true or false?
true
32
body destroys irritant by
walling off irritant, neutralizing toxic products, removing necrotic debris
33
tissue destruction occurs when _______ response is greater than _____ response
inflammatory, repair
34
key phagocytic cells
polymorphonuclear leukocytes (PMNs), macrophages
35
possible end results of inflammatory response
resolution/gingival tissues back to health, continuation of disease (lead to chronic inflammation)
36
cardinal signs of inflammation
heat, redness, swelling, pain, loss of function
37
examples of vascular changes in the inflammatory response
decreased flow (d/t dilation), increased permeability, cells migrate toward walls of BV/adhere to walls/exit because of increased permeability
38
examples of cellular changes in the inflammatory response
PMNs transmigrate through BV walls to engulf infectious material via phagocytosis and secrete cytokines
39
cytokines are a mediator that recruits more _____, ______ permeability of BV wall, and causes tissue ______/___ ____.
PMNs, increases, destruction, bone loss
40
chemical changes in the inflammatory response
direct the inflammatory response, regulatory in nature
41
inflammation is a ____ by which the body tries to repair itself against infection
process
42
inflammation of the gingiva with plaque present at the gingival margin
plaque-induced gingivitis
43
incidence of plaque-induced gingivitis (men and women)
85% men, 79% women
44
where does initial inflammation occur with gingivitis?
sulcular epithelium, col epithelium
45
ulcerations of the epithelium
lesions
46
causes of gingivitis
enzymes/endotoxins of bacteria, increase in quantity/maturation of plaque, increase in gram negative anaerobic m/o
47
local risk factors for gingivitis
calculus, poor oral hygiene, food impactions, mal-positioned teeth, tooth contours, faulty dentistry
48
systemic risk factors for gingivitis
immunosuppressed, drug action, hormonal changes, heredity
49
degree of ______ = ____ of plaque + _____ makeup of plaque + ___ response
inflammation; volume, microbial, host
50
gingivitis causes bone loss, true or false?
false
51
localized gingivitis is ___% of teeth involved, or _/28 teeth
less than 30%, 8
52
generalized gingivitis is ___% of teeth involved, or _/28 teeth
greater than 30%, 9
53
severity descriptors with gingivitis
mild, moderate, advanced (acute/chronic)
54
inflammation of the gingiva and attachment apparatus; a continuation of gingivitis
periodontitis
55
clinical features of periodontitis
gingival inflammation, attachment/bone loss, periodontal pocket depth
56
inflammation results
effect of by-product of endotoxins/enzymes, m/o invade ulcerated epithelium
57
causative factors of periodontitis
bacteria and their by-products (endotoxins/enzymes)
58
pocket depth formation occurs by BOTH free gingival margin moving ____ and epithelial attachment _____
coronally, apically
59
distinguishing factors of infrabony pockets
epithelial attachment apical (beneath/under) to crest of bone, vertical bone loss
60
distinguishing factors of suprabony pockets
epithelial attachment coronal (above) to bone, horizontal bone loss
61
what are similarities between gingivitis and periodontitis?
involve inflammation of gingiva, caused by bacterial byproducts (enzymes and toxins)
62
systemic risk factors for periodontitis
hormones, diabetes, smoking, nutrition, prescription drugs
63
important protection cells
antibodies, polymorphonuclear leukocytes, macrophages
64
Treatment of gingivitis
patient education, debridement/instrumentation, Tx of localized factors (overhanging restorations, caries, etc), plaque reduction
65
Treatment of periodontitis
patient education, debridement/instrumentation (scaling and root planing [SRP]), Tx of localized factors, possible antibiotics (if severe)
66
purpose of polishing agents is to remove deposit without...
removing tooth structure, abrading gingival tissue, producing excessive heat
67
agent composed of particles hard enough to cut a softer material
abrasive
68
wearing away of a surface by friction
abrasion
69
production of smooth, glossy surface (use of finer particles)
polishing
70
item that uses an abrasive agent in removing pellicle, plaque, stain (primarily stain)
polishing agent
71
considerations in selecting a polishing agent
size (grit), shape, hardness, body strength
72
substance (gel, paste, powder) used in conjunction with a toothbrush/interdental cleaner to facilitate bacterial plaque biofilm removal
dentrifice
73
measures carried out so disease will not occur and is truly prevented
primary level of prevention
74
treatment of early disease to prevent progression of potentially irreversible condition
secondary level of prevention
75
complex and involved treatment of disease; prevent loss
tertiary level of prevention
76
therapeutic procedure to treat patients with periodontitis
scaling and root planing
77
levels of professional care
prophylaxis, debridement, scaling and root planing, maintenance therapy

Clinical Applications I (11 decks)

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