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
2
Q
What are the systemic factors of gingivitis
A
endocrine and blood dycrasias or leukemia
3
Q
What are the endocrine factors that effect the gingiva
A
Puberty, Pregnancy, Diabetes
4
Q
What are the medications associated with gingivitis
A
Dylantin (Phenytoin sodium)
Nifedipine (Ca blocker)
cyclosporin (sand…)
5
Q
What non plaque bacteria can cause gingivitis
A
N. gonorrhea, T. pallidum and Streptococcal (Betta-hemolytic)
6
Q
What viral factors are involved in gingivitis
A
Herpes 1 and 2
Varicell-zoster infections
7
Q
What are all the non-plaque induced gingivitis?
A
Bacterial,
Viral
Fungal
8
Q
What are the 3 fungal infections associated with gingivitis
A
Hisoplasmosis
Candidia albicans
linear gingival erythema
9
Q
What type of gingival manifestations of systemic conditions are there
A
Muccocutaneous disorders
Allergic reactions
Traumatic Lesions
Foreign Body Reactions
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
11
Q
Treatment of gingivitis include use of a
A
electric tooth brush, water pick, chx rinse, flossing, toothpics
12
Q
What does gingivitis look like
A
red blunted papilla
13
Q
What are the 5 types of Acute periodontitis
A
Acute pericoronitis Acute Herpetic gingivostomatitis ANUG Acute Periodontal Abscess Acute Gingival Abscess
14
Q
What is the Diagnosis of Acute periodontitis
A
S/S: pain > swelling and edema > lymphadenopathy > fever
15
Q
What is the treatment of Acute periodontitis
A
control infection
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
17
Q
Chronic Periodontitis is characterized as what
A
Localized where the % is 30%
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
19
Q
Aggressive Periodontitis is characterized as
A
Localized Aggressive Periodontitis (Vertical bone loss)
Generalized Aggressive Periodontitis (Horizontal bone loss or jevenile.=)
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
21
Q
What are the necrotizing Periodontal Diseases
A
NUG NUP
22
Q
What is NUG
A
reversible not contagious age of onset is 15-30
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.
24
Q
how does NUG progress and what is the etology
A
anterior to posterior
stressed induced, smoking systemic diseases (AIDS,EBV)
25
What are the layers of NUG
Bacterial zone --> PMN rich zone --> necrosis--> spirochetes (lamina propia)
26
What cells are involved with NUG
PMN's, macrophages (defect in chemotaxis or phagocytosis)
27
NUP is described as
irreversible attachment loss and bone loss
28
What are the signs and symptoms of NUP
```
punched out papilla
fever
lymphadenopathy
pain
multiple perio abscesses
necrotizing stomatis
necrosis and ulceration of marginal, papillary and attached gingiva
```
29
Ecology of NUP is
bacteria perio bugs and G- anaerobic enterics --> clostridium, klebsiella, enterococcus
fungi candida
viral EBV
other severe malnutrition, Aids, Immunocompromised
30
What is the treatment for NUG
debridement, abx amoxicillin, metronidazole, chi rinse, stress control SRP
31
What is the treatment for NUP
abx metronidazole, fluconazole, chx debridement, SRP, 2 month recall
32
Abscesses of the periodontium include what two types
Gingival abscess and Acute Periodontal abscess
33
Cellular components of gingivitis are
PMNs
T cells lymphocytes, macrophages
B-cells or Plasma cells
34
Cellular components of acute periodontitis include
```
osteoclasts
MMP's
Cytokines
IL-1 IL-6 IL-8 TNF-a
Leukotrines
```
35
How do you dtermine the extent of periodontitis
Slight 1-2 Cal
Moderate 3-4 Cal
Severe > 5 Cal
36
Diagnosis for Chronic periodontitis inclues
```
BOP
exudate from pockets
tooth mobility
abscess formation
Suprabony or infraboney pocket formation
```
37
How to treat chronic Periodontitis
don't use abx,
| you are likely to loose 3.5x more teeth if you don't treat period.
38
What are the clinical ramifications to chronic perio
CAL .1-.3 mm/year on F and L surface, .3 mm/year IP
39
What does chronic periodontitis look like
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
40
What is the red complex and what disease is it associated with
P gingivalis
T forsythia
T denticola
Agggressive peridontitis
41
What is the only type of treatment that can cure aggressive periodontitis
surgery
42
There is CAL clinical attachment loss in NUG
False there is not
43
what is the age range for aggressive periodontitis and NUG
15-30
44
What are the different names for NUG
Vincent's stomatitis/infection, ulcerative Gingivitis, gangrenous stomatitis trench mouth
45
What causes the the wet sticky appearance in NUG
fibrin meshwork
46
NUP is reversible T or F
False attachment loss and bone loss
47
S/S for NUP include
```
punched out papilla
low grade fever
periodontal abscesses
necrotizing stomatis- inter proximal bone exposure
Aggressive loss of alveolar bone
```
48
What is the etiology of NUP
bacteria G- anaerobic enteric such as clostridium, klebsiella, enterococcus
49
What is the viral etiology of NUP
Candida
Viral is EBVs
other include severe malnutrition or immunocompromised AIDS
50
HIV/Aids and NUP
ulceration and necrosis of gingival tissue
rapid destruction and or exposure of alveolar bone
CD4+
51
What is the treatment for NUP
```
metronidazole
fluconazole
chlorhexidine
soft tissue debridement
SRP
2 month periodontal maintenance interval
```
52
What type of abscess are there in the periodontium
Gingival
Acute Periodontal abscess
Pericoronal abscess
53
Gingibal abscess S/S
localized pain
rapidly expansion
adjacent teeth painful to percussion
54
are gingival abscess limited to marginal gingiva or do they invade the bone
they are limited to gingival papilla and marginal gingiva
55
What are the causes etiology of gingival abscess
foreign body impaction w associated bacteria
56
Tx for gingival abscess are
drain
antibiotics
SRP
Possible surgery
57
Acute periodontal abscess
```
Swelling exudate
deep pocket
vital pulp
fistula tooth mobility
fever lymphadenopathy
```
58
What type of abscess is associated with multiple abscesses with DM and AIDS
Acute periodontal abscess
59
What bacteria cause acute periodontal abscess
```
G- anaerobic P. gingivalis P intermedia
treponema spirochetes
F. nucleatum
P. micra
T. forsythia
Candida
```
60
What are the factors required for a acute periodontal abscess
blockage of perio pocket
subgingibal plaaque
plaque microbes with virulence factors (endotoxins and collagenase)
61
What is the his histopathology
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
What is the treatment for acute periodontal abscess
drainage
antibiotics local or systemic delivery
SRP possible surgery
63
SRP is scale and root planning
yup
64
pericoronal abscess treatmetn is what
control infection
extract 3rd molar
irrigation with peroxide or chx antibiotics extraction
can try to remove pericoronal tissues
65
what is the definition of abscess
dense localized collection of neutrophils with tissue necrosis
surrounded and walled off by immature connective tissue and proliferating capillaries
66
If a patient has periodontitis and needs end treatment what do you do
get the endo finished first.
67
What are some examples of developmental or acquired deformities and conditions of the periodontium
localized tooth related factors that modify or predispose to plaque inched gingival disease/periodontitis
mucogingival deformities
occlusal trauma
68
What are examples of localized tooth related factors that modify or predispose to plaque induced gingival disease/periodontitis
tooth anatomic factors
dental restoration
root fracture
cervical root resorption
69
Mucogingigival deformities
```
gingival/soft tissues recession
lack of keratinized gingiva
decreased vestibular depth
aberrant frenum/muscle attachment
gingival excess
```
70
Occlusal trauma
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
Chronic occlusal trauma more frequent than acute, does occlusal trauma cause periodontal pockets and attachment loss
NO
72
how can you see occlusal trauma on a radiograph
widened PDL space, disruption/loss of lamina dura, root resorption
73
What is a perio probe used for
measure attachment loss/pocket depth
74
what are the variables effecting probing depth
```
inflammation
probe diameter
Tapered vs Parallel
Hand force
Band width
```
75
Furcation probe measures
horizontal bone loss
76
BOP bleeding on probing
Positive BOP
active disease
presence of microbial biofilm/plaque
Ulcerative Sulcus/ pocket epithelium
77
how many data pocket depths are taken
6 points d->V
78
average width of the PDL in the adult is
.17
79
checking mobility we use instruments what are the different classes
Class 1 > .2mm but 1mm
| Class 3 > 1mm + axial displacement (depressible no apical bone)
80
CAL probing depth + what
gingival margin level
81
Apical gingival margin means to do what
subtract ex PD is 6 and the GM is 4 mm apical
82
Biological width
junctional epithelium+ connective tissue attachment = around 2
83
CEJ to crest of alveolar bone is
1.5-2 mm
84
attachment epithelium + gingival fiber ligament is
Biological width
85
violations of the biologic width induce
inflammation
increasing probing depth
inconsistent resorption of alveolar bone
86
what do we see clinically with inflammation
vascular component of gingival inflammation
| color edema swelling bleeding
87
What are the cell types involved with inflammation
Neutrophils basophils/mast cells monocytes/macrophages lymphocytes plasma cells
88
what is the job of the basophil
```
histamine causes vasodilation and increased vascular permeability
platelet activating factor
Heparin anticoagulant
TNF-a
SRS-As leukotriene C4 D4 E4
```
89
What are the jobs of monocytes and macrophages
secrete cytokines and lymphokines
90
What are the cytokines and lymphkines
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
Lymphocytes = CD4 helper cells do what
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
Lymphocytes CD8 Cytotoxic T lymphocytes
destroy target cells by synthesis and release of cytotoxins Synthesis and release of
INF-y
Tumor Necrosis Factor alpha
Tumor Necrosis factor beta
93
Plasma cells
B lymphocyte is a precursor of plasma cells and both secrete IgG IgM IgE IgD IgA
94
IL-1
stimulates osteoclasts, fibroblasts macrophages
95
IL-6 stimulates
B and T clls
96
IL-8
attracts and activated PMS
97
TNF-a
activate osteoclasts
98
PGE2
vasodilation, pyrogenic, release mediator from mast cells, cell-mediated cytotoxicity
99
what is the average clinical attachment lost per year
.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
what are the patterns of bone loss requires how much bone loss to show up on a radiograph
30-50%
101
Intrabony pockets are classified as walls remaining
3 walls being the best
102
Intradental craters
35% of maxillary intrabony defects
| 63% of mandibular intrabony defects most common in posterior teeth
103
How does a pocket form
apical migration of JE
| loss of CT fiber attachment
104
how is a pseudo pocket formed
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
Periodontal pocket are formed by
excessive PD with loss of clinical attachment
| associated with chronic aggressive periodontitis
