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Periodontics > Test 1 (Ch1-3) > Flashcards

Test 1 (Ch1-3) Flashcards

1
Q

What are the types of gingivitis

A 
Plaque induced
due to systemic factors
due to medications
non plaque induced
genetic origin
gingival manifestations of systemic conditions
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2
Q

What are the systemic factors of gingivitis

A

endocrine and blood dycrasias or leukemia

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3
Q

What are the endocrine factors that effect the gingiva

A

Puberty, Pregnancy, Diabetes

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4
Q

What are the medications associated with gingivitis

A

Dylantin (Phenytoin sodium)
Nifedipine (Ca blocker)
cyclosporin (sand…)

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5
Q

What non plaque bacteria can cause gingivitis

A

N. gonorrhea, T. pallidum and Streptococcal (Betta-hemolytic)

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6
Q

What viral factors are involved in gingivitis

A

Herpes 1 and 2

Varicell-zoster infections

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7
Q

What are all the non-plaque induced gingivitis?

A

Bacterial,
Viral
Fungal

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8
Q

What are the 3 fungal infections associated with gingivitis

A

Hisoplasmosis
Candidia albicans
linear gingival erythema

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9
Q

What type of gingival manifestations of systemic conditions are there

A

Muccocutaneous disorders
Allergic reactions
Traumatic Lesions
Foreign Body Reactions

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10
Q

What are the causes of mucocutaneous disorders and Allergic reactions in gingivitis

A 
Mucocutaneous disorders include 
Lichen planus
pemphigoid
erythema multiform
lupus erythematosus

Allergic Reactions
Nickel
Acrylic
toothpastes

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11
Q

Treatment of gingivitis include use of a

A

electric tooth brush, water pick, chx rinse, flossing, toothpics

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12
Q

What does gingivitis look like

A

red blunted papilla

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13
Q

What are the 5 types of Acute periodontitis

A 
Acute pericoronitis
Acute Herpetic gingivostomatitis
ANUG
Acute Periodontal Abscess
Acute Gingival Abscess
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14
Q

What is the Diagnosis of Acute periodontitis

A

S/S: pain > swelling and edema > lymphadenopathy > fever

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15
Q

What is the treatment of Acute periodontitis

A

control infection

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16
Q

How does acute periodontitis apeare

A

increased redness of soft tissues and altered contours- blunted bulbus
Increased bleeding on probing
Loss of CAL

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17
Q

Chronic Periodontitis is characterized as what

A

Localized where the % is 30%

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18
Q

How does Chronic periodontitis appear

A

Increased renew of soft tissues and altered contours, blunted/bulbus
increased bleeding on probing
loss of CAL
Increasing probing depths and CAL

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19
Q

Aggressive Periodontitis is characterized as

A

Localized Aggressive Periodontitis (Vertical bone loss)

Generalized Aggressive Periodontitis (Horizontal bone loss or jevenile.=)

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20
Q

Periodontitis as a manifestation of systemic Disease

A

Hematological - acquired neutropenia, leukemia
Genetic - familial and cyclic neutropenia, down syndrome, leukocyte adhesion deficiency syndrome, Papillon-Lefvre Syndrome, Chediak-Higashi Syndrome

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21
Q

What are the necrotizing Periodontal Diseases

A

NUG NUP

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22
Q

What is NUG

A

reversible not contagious age of onset is 15-30

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23
Q

What are the signs and symptoms of NUG

A

fetid oralis, pseudomembrane, necrosis (spirochetes), wet sticky appearance (fibrin meshwork), pain, sudden onset, spontaneous gingival bleeding, lymphadenopathy, fever.

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24
Q

how does NUG progress and what is the etology

A

anterior to posterior

stressed induced, smoking systemic diseases (AIDS,EBV)

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25
Q

What are the layers of NUG

A

Bacterial zone –> PMN rich zone –> necrosis–> spirochetes (lamina propia)

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26
Q

What cells are involved with NUG

A

PMN’s, macrophages (defect in chemotaxis or phagocytosis)

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27
Q

NUP is described as

A

irreversible attachment loss and bone loss

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28
Q

What are the signs and symptoms of NUP

A 
punched out papilla
fever
lymphadenopathy
pain
multiple perio abscesses
necrotizing stomatis
necrosis and ulceration of marginal, papillary and attached gingiva
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29
Q

Ecology of NUP is

A

bacteria perio bugs and G- anaerobic enterics –> clostridium, klebsiella, enterococcus
fungi candida
viral EBV
other severe malnutrition, Aids, Immunocompromised

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30
Q

What is the treatment for NUG

A

debridement, abx amoxicillin, metronidazole, chi rinse, stress control SRP

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31
Q

What is the treatment for NUP

A

abx metronidazole, fluconazole, chx debridement, SRP, 2 month recall

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32
Q

Abscesses of the periodontium include what two types

A

Gingival abscess and Acute Periodontal abscess

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33
Q

Cellular components of gingivitis are

A

PMNs
T cells lymphocytes, macrophages
B-cells or Plasma cells

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34
Q

Cellular components of acute periodontitis include

A 
osteoclasts
MMP's
Cytokines
IL-1 IL-6 IL-8 TNF-a
Leukotrines
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35
Q

How do you dtermine the extent of periodontitis

A

Slight 1-2 Cal
Moderate 3-4 Cal
Severe > 5 Cal

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36
Q

Diagnosis for Chronic periodontitis inclues

A 
BOP
exudate from pockets
tooth mobility
abscess formation
Suprabony or infraboney pocket formation
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37
Q

How to treat chronic Periodontitis

A

don’t use abx,

you are likely to loose 3.5x more teeth if you don’t treat period.

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38
Q

What are the clinical ramifications to chronic perio

A

CAL .1-.3 mm/year on F and L surface, .3 mm/year IP

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39
Q

What does chronic periodontitis look like

A

Increased redness of soft tissues and altered contours- blunted/bulbus
increased bleeding on probing tooth mobility
loss of CAL
increasing probing depths and CAL
Suprabony or infrabony pocket formation

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40
Q

What is the red complex and what disease is it associated with

A

P gingivalis
T forsythia
T denticola
Agggressive peridontitis

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41
Q

What is the only type of treatment that can cure aggressive periodontitis

A

surgery

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42
Q

There is CAL clinical attachment loss in NUG

A

False there is not

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43
Q

what is the age range for aggressive periodontitis and NUG

A

15-30

44
Q

What are the different names for NUG

A

Vincent’s stomatitis/infection, ulcerative Gingivitis, gangrenous stomatitis trench mouth

45
Q

What causes the the wet sticky appearance in NUG

A

fibrin meshwork

46
Q

NUP is reversible T or F

A

False attachment loss and bone loss

47
Q

S/S for NUP include

A 
punched out papilla
low grade fever
periodontal abscesses
necrotizing stomatis- inter proximal bone exposure
Aggressive loss of alveolar bone
48
Q

What is the etiology of NUP

A

bacteria G- anaerobic enteric such as clostridium, klebsiella, enterococcus

49
Q

What is the viral etiology of NUP

A

Candida
Viral is EBVs
other include severe malnutrition or immunocompromised AIDS

50
Q

HIV/Aids and NUP

A

ulceration and necrosis of gingival tissue
rapid destruction and or exposure of alveolar bone
CD4+

51
Q

What is the treatment for NUP

A 
metronidazole
fluconazole
chlorhexidine
soft tissue debridement
SRP
2 month periodontal maintenance interval
52
Q

What type of abscess are there in the periodontium

A

Gingival
Acute Periodontal abscess
Pericoronal abscess

53
Q

Gingibal abscess S/S

A

localized pain
rapidly expansion
adjacent teeth painful to percussion

54
Q

are gingival abscess limited to marginal gingiva or do they invade the bone

A

they are limited to gingival papilla and marginal gingiva

55
Q

What are the causes etiology of gingival abscess

A

foreign body impaction w associated bacteria

56
Q

Tx for gingival abscess are

A

drain
antibiotics
SRP
Possible surgery

57
Q

Acute periodontal abscess

A 
Swelling exudate
deep pocket
vital pulp
fistula tooth mobility
fever lymphadenopathy
58
Q

What type of abscess is associated with multiple abscesses with DM and AIDS

A

Acute periodontal abscess

59
Q

What bacteria cause acute periodontal abscess

A 
G- anaerobic P. gingivalis P intermedia
 treponema spirochetes
F. nucleatum
P. micra
T. forsythia
Candida
60
Q

What are the factors required for a acute periodontal abscess

A

blockage of perio pocket
subgingibal plaaque
plaque microbes with virulence factors (endotoxins and collagenase)

61
Q

What is the his histopathology

A

infiltrate → hyperemia and thrombosis → lysis of collagen matrix in lamina propria and gingival fibers → ulceration and apical proliferation of JE → osteoclastic mediated bone resorption

62
Q

What is the treatment for acute periodontal abscess

A

drainage
antibiotics local or systemic delivery
SRP possible surgery

63
Q

SRP is scale and root planning

A

yup

64
Q

pericoronal abscess treatmetn is what

A

control infection
extract 3rd molar
irrigation with peroxide or chx antibiotics extraction
can try to remove pericoronal tissues

65
Q

what is the definition of abscess

A

dense localized collection of neutrophils with tissue necrosis
surrounded and walled off by immature connective tissue and proliferating capillaries

66
Q

If a patient has periodontitis and needs end treatment what do you do

A

get the endo finished first.

67
Q

What are some examples of developmental or acquired deformities and conditions of the periodontium

A

localized tooth related factors that modify or predispose to plaque inched gingival disease/periodontitis
mucogingival deformities
occlusal trauma

68
Q

What are examples of localized tooth related factors that modify or predispose to plaque induced gingival disease/periodontitis

A

tooth anatomic factors
dental restoration
root fracture
cervical root resorption

69
Q

Mucogingigival deformities

A 
gingival/soft tissues recession
lack of keratinized gingiva
decreased vestibular depth
aberrant frenum/muscle attachment
gingival excess
70
Q

Occlusal trauma

A

Primary occlusal trauma-grinding clenching
no bone loss no period but will have mobile teeth and widen PDL
Secondary Occlusal Tauma
normal or excessive forces are placed on a tooth with reduced periodontium

71
Q

Chronic occlusal trauma more frequent than acute, does occlusal trauma cause periodontal pockets and attachment loss

A

NO

72
Q

how can you see occlusal trauma on a radiograph

A

widened PDL space, disruption/loss of lamina dura, root resorption

73
Q

What is a perio probe used for

A

measure attachment loss/pocket depth

74
Q

what are the variables effecting probing depth

A 
inflammation
probe diameter
Tapered vs Parallel
Hand force
Band width
75
Q

Furcation probe measures

A

horizontal bone loss

76
Q

BOP bleeding on probing

A

Positive BOP
active disease
presence of microbial biofilm/plaque
Ulcerative Sulcus/ pocket epithelium

77
Q

how many data pocket depths are taken

A

6 points d->V

78
Q

average width of the PDL in the adult is

A

.17

79
Q

checking mobility we use instruments what are the different classes

A

Class 1 > .2mm but 1mm

Class 3 > 1mm + axial displacement (depressible no apical bone)

80
Q

CAL probing depth + what

A

gingival margin level

81
Q

Apical gingival margin means to do what

A

subtract ex PD is 6 and the GM is 4 mm apical

82
Q

Biological width

A

junctional epithelium+ connective tissue attachment = around 2

83
Q

CEJ to crest of alveolar bone is

A

1.5-2 mm

84
Q

attachment epithelium + gingival fiber ligament is

A

Biological width

85
Q

violations of the biologic width induce

A

inflammation
increasing probing depth
inconsistent resorption of alveolar bone

86
Q

what do we see clinically with inflammation

A

vascular component of gingival inflammation

color edema swelling bleeding

87
Q

What are the cell types involved with inflammation

A

Neutrophils basophils/mast cells monocytes/macrophages lymphocytes plasma cells

88
Q

what is the job of the basophil

A 
histamine causes vasodilation and increased vascular permeability
platelet activating factor
Heparin anticoagulant
TNF-a
SRS-As leukotriene C4 D4 E4
89
Q

What are the jobs of monocytes and macrophages

A

secrete cytokines and lymphokines

90
Q

What are the cytokines and lymphkines

A

IL-1 Osteoclastic activation beta lymphocyte activation and activation of CD8 lymphocytes
IL-6 osteoclastic activation
TNF-alpha inflammatory
INF interferon interferes with virus
Lipid mediators of inflammation prostaglandins, leukotrienes platelet activating factor

91
Q

Lymphocytes = CD4 helper cells do what

A

key to the immune response
activates macrophages
activated CD8 cytotoxic T lymphocytes
Activates B lymphocytes to secrete immunoglobulin
Activates B lymphocytes to secrete immunoglobulin

92
Q

Lymphocytes CD8 Cytotoxic T lymphocytes

A

destroy target cells by synthesis and release of cytotoxins Synthesis and release of
INF-y
Tumor Necrosis Factor alpha
Tumor Necrosis factor beta

93
Q

Plasma cells

A

B lymphocyte is a precursor of plasma cells and both secrete IgG IgM IgE IgD IgA

94
Q

IL-1

A

stimulates osteoclasts, fibroblasts macrophages

95
Q

IL-6 stimulates

A

B and T clls

96
Q

IL-8

A

attracts and activated PMS

97
Q

TNF-a

A

activate osteoclasts

98
Q

PGE2

A

vasodilation, pyrogenic, release mediator from mast cells, cell-mediated cytotoxicity

99
Q

what is the average clinical attachment lost per year

A

.1-.3 per year for facial and lingual surfaces and .3 mm per year for inter proximal areas
In ten years a untreated patient may loose 3.5-5mm while those patients who receive treatment will loose one

100
Q

what are the patterns of bone loss requires how much bone loss to show up on a radiograph

A

30-50%

101
Q

Intrabony pockets are classified as walls remaining

A

3 walls being the best

102
Q

Intradental craters

A

35% of maxillary intrabony defects

63% of mandibular intrabony defects most common in posterior teeth

103
Q

How does a pocket form

A

apical migration of JE

loss of CT fiber attachment

104
Q

how is a pseudo pocket formed

A

aka gingival pocket by excessive PD without loss of clinical attachment bc of increased bulk of gingiva
commonly found in edemas overgrowth or inflammatory hyperplasia

105
Q

Periodontal pocket are formed by

A

excessive PD with loss of clinical attachment

associated with chronic aggressive periodontitis

Periodontics (4 decks)

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