Final Revision Flashcards
(143 cards)
1
Q
Appropriate management for life threatening systemic conditions:
A
§ Shorter appointments
§ Complete pain control using LA w/ or w/o
minimal vasoconstrictive substitutes
2
Q
Patients with cardiac disease involving the endocardium are susceptible to:
A
bacterial endocarditis
-as a result of blood-borne infection
3
Q
Major procedures causing bacterial endocarditis are:
A
§ Extractions
§ Scaling + root planing
§ Periodontal and implant surgeries
4
Q
Bacterial endocarditis can lead to:
A
bleeding and bacteremia
5
Q
How to treat Bacterial endocarditis?
A
FOLLOW GUIDELINES for antibiotic prophylaxis
6
Q
How is Bacteremia caused?
A
by tooth brushing or chewing and invasive oral therapeutic procedures, rather than by
single procedures causing bleeding
7
Q
Which patients have bigger tendency to bleed?
A
§ Patients with liver cirrhosis
§ Patients with high alcohol consumption
§ Patients w/ blood dyscrasia or hemophilia
8
Q
Cardiac patients often treated w/:
A
anticoagulants
9
Q
Stress for cardiac patients may cause:
A
congestive heart failure
angina pain
10
Q
Patients are more prone on having allergic rxns to..?
A
§ local anesthetics (Novocain)
§ Penicillin
§ Sulfa derivatives
§ Disinfectants, such as iodine
11
Q
Healing response of the periodontal tissues for Controlled Diabetes Mellitus patients is:
a. as good in as in healthy individuals
b. better than in healthy individuals
c. worse than in in healthy individuals
d. no response
A
a. as good in as in healthy individuals
12
Q
To accomplish infection control involved teeth with repeated abscesses and pus formation should be:
A
extracted
13
Q
Bisphosphonates as a threat to implant therapy:
A
Nitrogen-containing bisphosphonates inhibit an enzyme that controls
osteoclastic function + the cell migration responsible for osseous healing, leading to osteonecrosis
Bisphosphonate-related osteonecrosis of the jaws, represents a risk in patients taking bisphosphonates
14
Q
Bisphosphonates:
A
- real thread, avoid it
- older ppl taking it
- control w/ this medication
- treat osteoporosis
15
Q
Which way is at a higher risk of inducing Bisphosphonate-related osteonecrosis of the jaws:
a. tongue
b. intravenous
c. pills (per-os)
d. anticancer ppl
A
pills (per-os) - MINIMAL risk
tongue
intravenous
anticancer ppl - HIGHER risk
16
Q
How to handle stress patients prior to therapy?
A
w/ diazepams
§ The night before
§ In the morning
§ 1/2 h before an extensive + surgical procedure
17
Q
How to handle stress patients after therapy?
A
Non- steroidal anti-inflammatory drugs w/ analgesic and
antipyretic properties
Diclofenac K/Na inhibits prostaglandin synthesis by
interfering w/ prostaglandin synthetase action
Pain killers depending on the individual patient’s need and pain threshold
18
Q
For how long the patient should administer Diclofenac?
A
FOR 3 DAYS
19
Q
The success rates for smoking cessation counseling dependent on:
A
§ The amount of time spent counseling the individual
§ The prescribed drug
20
Q
What is a ulcerated pocket epithelium?
A
=provides a gate way for bacteria and their products
21
Q
p. gingivalis pathogen process:
A
p. gingivalis invades -> intracellular survival + replication -> endothelial activation: expression of adhesion molecules, secretion of cytokines -> endothelial cell apoptosis -> plaque rupture -> enter bloodstream
22
Q
C-reactive protein (CRP) marker plays a role in:
A
its presence indicates that there is:
- vascular inflammation
- vessel damage
- clinical CVD events
23
Q
Periodontitis patients have shown to display:
higher CRP
lower WBC
lower CRP
higher WBC
A
higher WBC
higher CRP
24
Q
Increased carotid artery intima-media thickness (IMT) is associated w/:
A
increased risk of:
- MI
- stroke
25
We can see glycemic blood levels with:
HbA1c !!!!
26
Severe periodontitis is entailed w/:
a. high glycemic control
b. low glycemic control
c. increased incidence of diabetes complications in individuals
d. decreased incidence of diabetes complications in individuals
b. low glycemic control
c. increased incidence of diabetes complications in individuals
- hypertention
- adverse effect on endothelial function
- CKD is associated w/ periodontitis
27
Rapid rate of periodontitis age observation:
- observed at 13-20y (usually young adults)
28
More common:
a. rapid rate periodontitis
b. slow rate periodontitis
b. slow rate periodontitis
29
Rapid rate of periodontitis symptoms:
- alter marginal gingiva color and volume
- bleeding on probing
- root furcation exposure
- increased tooth mobility
- increased alveolar bone loss !!!!!!!
- gingival margin recession
- increased loss of probing attachment level
- reduced R of soft marginal tissues on probing
30
Distance b/w alveolar crest and CEJ on BTW radiographs in young population:
< 2-3 mm
31
Which serotype for Aggregatibacter actinomycetemcomitans?
a. serotype b
b. serotype a
c. serotype e
a. serotype b
32
What pathogenic substance does A. actinomycetemcomitans produce?
leukotoxin
33
What is leukotoxin?
=destroys human polymorphonuclear leukocytes + Ma
34
Genetic studies for rapid rate periodontitis:
Mendelian inheritance of a gene
35
Smoking causes:
a. decreased IgG2 levels
b. increased IgG2 levels
c. more affected teeth w/ GAP than non-smokers
d. less affected teeth w/ GAP than non-smokers
a. decreased IgG2 levels
c. more affected teeth w/ GAP than non-smokers
- smoking is a risk factor for AgP patients
36
Treatment of a.a. :
```
scaling
root planing
soft tissue curettage
access flap
-limited sucess in elimination
```
therefore ANTIBIOTICS: amoxicillin and metronidazole needed (combination)
37
Treatment approach A:
supragingival plaque control
subgingival instrumentation w/ hand and ultrasonic intruments
-antibiotics amoxicillin and metronidazole combination
38
Treatment approach B:
mechanical instrumentation
meticulous OH
periodontal surgery or systemic antimicrobial therapy
-this option prefered to minimise overuse of antibiodics
39
Rapid rate Vs Moderate rate periodontitis:
Moderate rate:
- <2 mm over 5y
- seen in older people
Rapid rate:
- > or same as 2 mm over 5y
- seen in younger people (13-20y)
40
First you have:
a. plaque-induced gingivitis
b. periodontitis
a. plaque-induced gingivitis
if left untreated it leads to irreversible periodontitis
41
Should a splint always be placed when there is tooth mobility?
No, only when patient asks for it
42
ADV Vs DISADV of a splint:
ADV:
- increases stability during mastication
- increases patient comfort
- oral hygiene -> healing therapy for periodontium
- better healing of non-mobile teeth than mobile
DISADV:
- increases inflammation due to plaque accumulation
- tends to fracture frequently
- makes tooth mobility evaluation impossible
43
Periodontitis is influenced on:
a. genetics
b. env risk factors
c. both
c. both
44
Moderate rate priodontitis is a:
a. fast progressing form
b. slow progressing form
b. slow progressing form
45
Best predictor of disease progression:
previous disease experience
-if you have periodontitis then you will always have
46
Moderate rate periodontitis risk factors:
- bacteria -> not enough for the disease to occur
- age -> prevalence of perio disease increases w/ age (the older you are the more susceptible to have perio disease)
- smoking -> perio therapy is impraired in smokers + risk of developing the disease is enhanced by smoking
- genetics -> periodontitis has a high inherited component
- systemic disease
- stress -> immune system effect so inflammation, impaired wound healing etc
47
Periodontitis is initiated by microorganisms living in:
a. calcified biofilms
b. uncalcified biofilms
c. supragingival plaque
d. subgingival plaque
a. calcified biofilms
b. un calcified biofilms
c. supragingival plaque
d. subgingival plaque
48
Primary preventive measure of periodontitis:
prevention of gingivitis
THEN:
removal of sub and supra-gingival plaque
49
The clinical outcome of sub and supra-gingival plaque removal depends on:
- operator skills to remove plaque !!!!!!!!!
- patient's skill and motivation in home care !!!!!!!!!
- innate susceptibility of the patient
50
Established lesion:
- plasma cells predominance
- stable for years or become advanced lesion
- no bone and CT loss yet
51
Advanced lesion:
- same symptoms as established lesion
- periodontal pocket formation
- bone and PDL loss
- no linear line
- disruption of gingival tissue architecture
52
Key enzymes for tissue degradation?
MMPs proteinases
- they create a problem
- >MMP-9 predominence in perio patients
53
Bone loss stimulation process:
osteoblasts produce a molecule to differentiate osteoclasts -> produce acid -> destroy bone (break down organic matrix) -> resorb the bone (eat)
54
By which receptor are osteoclasts enhanced?
osteoprotegerin
55
Patients w/ poor glycemic control, long DM duration and other diabetic complications respond to perio therapy:
- in an unpredictable manner b/c tissue repair and wound healing are compromised
- don't respond well w/ uncontrolled DM
56
Clinical special considerations w/ DM patients:
- preferable early mornings (lower stress)
- brief procedures
- pain free and atraumatic as possible
57
Gingivitis initial lesion stages:
- EDEMA
- plaque
- increased WBC
- serum proteins
- acute exudative vasculitis
- loss of perivascular collagen (5% CT)
- inflammation
- no change in fibroblasts
58
Gingivitis early lesion stages:
- BLEEDING ON PROBING
- FIBROBLAST CHANGE
- initial lesion presence
- lymphoid cells accumulation
- basal cells proliferation
- 5-15% CT
- erythema
59
What is Gingivitis?
=well-controlled immunologic response due to plaque biofilm presence
60
What happens if plaque is removed?
- gingival tissues repair and remodel
| - no permanent tissue damage
61
Bacteria present in plaque and Gingivitis?
red complex (treponema denticola, p.gingivalis, t. forsythia)
62
Predisposing factors definition and examples:
=factors which retain/hinder plaque removal and maintain gingival inflammation
```
calculus
caries
fractures
recession
crowding
partial dentures
orthodontic appliances
sucrose intake
maxillofacial anatomic variants (I2)
overhangs
etc
```
63
Modifying factors definition:
=factors which alter the nature of inflammatory, vascular, cellular response or tissue repair
64
Progesterone effect on gingivitis:
- increases gingival vascularity
- increases permeability, thus higher vascular edematous inflammatory response
-hormonal variations do not affect healthy gingiva, but make worse the chronic gingivitis
65
Diabetes patients:
- more severe gingival inflammation
- glycation end products
- BM thickening
- vascular elasticity loss
- increased vascular permeability
- impairment of immune cell function
- reduced neutrophil function
- defective chemotaxis
66
Smoking:
- less gingival inflammation
- nicotine-induced peripheral vasoconstriction
- periodontal vascular system w/ smaller #s of large vessels but larger #s of small vessels
- more lymphocytes
- reduced migration
- reduced phagocytic capacity of PMNs
67
Neutropenia, Leukemia, HIV/AIDS:
Neutropenia: few neutrophils
Leukemia: high immature leukocytes count
HIV/AIDS: low T-cells count
68
Over response due to medication:
anticonvulants
immunosuppressants
Ca channel blockin agents
69
Gingival enlargement is related to:
- gingivitis
| - plaque control level
70
What can contribute to the transition from health to disease?
- total amount of dental plaque
| - the microbial composition of plaque
71
Gingivitis - Changes in the host status:
§ Inflammation
§ Tissue degradation
§ High gingival crevicular fluid flow may lead to a shift in the microbial population in plaque
72
What is a “keystone” pathogen and give an example of it:
=an organism that is central to the disease process, even when it is at a relatively low abundance
P. gingivalis
->subverts the host immune system and changes the microbial composition of dental plaque, ultimately leading to periodontal bone loss
73
Porphyromonas Gingivalis
- contributes to destructive periodontitis
- alters the total microbial load and composition
- overwhelms normal host tissue protective mechanisms and results in disease
- inhibits key features of the normal host protective mechanisms in the periodontium
74
When a dental implant is placed: (parts)
- endosseous part is surrounded by bone (not exposed to biofilm formation)
- transmucosal part (implant/ abutment) once exposed to the oral cavity, becomes rapidly colonized
75
Biofilm formation: Teeth vs Implants:
§ Enamel pellicles and Ti pellicles are not identical
-does not influence bacterial composition
§ Principles and sequence of biofilm formation at teeth and implants are similar
§ Common ecologic environment
76
Factors which may influence microbial colonization on tooth implants:
- surface characteristics of the implant/ abutment
- local environment
- resident oral microbiota
- implant prosthesis design
- accessibility for OH
77
Rough Ti surface characteristics of the implant/abutment:
§ greater bacterial adhesion
§ greater biofilm formation and accumulation
§ promote osseointegration
§ Increased difficulty in removing biofilm
§ More likely to develop peri-implantitis
78
Treatment of peri-implant mucositis:
- non-surgical mechanical therapy
- local rinses with CHX
- systemic antibiotics
§ Use of local antibiotics have shown initial improvements, followed by gradual recolonization and recurrence of disease
79
Aggresive periodontitis is associated with:
loss of Streptococcus sanguinis colonization
80
Special seals of teeth:
- junctional ep
| - CT
81
What Are Bacterial Biofilms?
=densely packed microbial cells growing on living/inert surfaces and surrounded with secreted polymers
82
How is dental biofilm formed?
1. acquired PELLICLE absorption -bacteria rarely colonize clean enamel
2. reversible adhesion
3. more permanent attachement
4. co-adhesion -once attached, colonizers start multiplying
5. attached cells multiplication
6. attached cells detachement
83
Key organism in plaque biofilm:
fusobacterium nucleatum
84
What are the benefits of bacteria in a biofil?
- better conditions to attach and grow
- inreased metabolic efficiency (better 'eating')
- enhanced tolerance of env stress, antimicrobial agents and host defences (better defence)
- enhanced ability to cause disease
85
Calculus definition:
=rough surface covered by an unmineralized layer of bacterial plaque
-saliva and bacteria on tooth surface to form
- suface roughness alone doesn't initiate gingivitis
- calculus helps more plaque
86
Supragingival Vs subgingival Calculus:
Supragingival:
- creamy-whitish to dark yellow/brownish hard mass
- initial pocket and sight inflammation
- mineralizes due to mineral salts in saliva
Subgingival:
- brownish to black calcified hard mass w/ rough surface may become visible if the gingival margin is retracted
- not visible to naked eye, so use of radiographs
- periodontal pocket and bone loss
- pellicle beneath bacterial plaque calcifies so more difficult to remove this calculus
- mineralizes due to mineral salt in inflammatory exudate passing through the pocket
- 2ry product of infection, NOT 1ry cause of periodontitis
87
What does calculus degree formation depend on?
- on amount of bacterial plaque present
| - on salivary glands secretion
88
Calculus Vs Implants
- there can be a removal of calculus w/o damaging the implant surface
- abutment interface associated w/ peri-implant disease
- rough surface of cement or excess cement at the abutment-crown interface provides a plaque + calculus retention and deposition
- overhangs may delay calculus removal
89
Why can't you completely eliminate all calculus from diseased root surfaces?
- develops in areas difficult to access for OH
| - keeps bacterial deposits in close contact w/ tissue surface
90
How to clean calculus?
- probing depth
- anatomy
- instruments type
- operators experience
91
Oral ep:
st sq keratinized ep
92
Layers of oral ep:
1. basal layer -stratum basale
- ep. renewed
2. pickle cell layer -stratum spinosum
3. granular cell layer -stratum granulosum
4. keratinized layer -stratum corneum
93
What type of cells does oral ep. contain?
- keratin producing cells
- melanocytes
- langerhans cells
- merkel's cells
- inflammatory cells
94
How is junctional epithelium connected to tooth?
- w/ hemidesmosomes
- in contact w/ enamel
desmosome=1 adjoining hemidesmosomes
95
What type of cells does CT contain?
fibroblasts
mast cells
Ma -> 1st defence inflammatory cells
infalmmatory cells
96
What are the uses of CT graft:
- enhances tissue around implants
- cover gingival recessions
- deepen mucogingival junction
97
Sharpey's fibers:
=collagen fiber portions penetrating in cementum and alveolar bone process
98
Cementum Vs Bone:
Cementum:
- no blood or lymph vessels
- no nerves
- continues degradation throughout life
- doesn't undergo physiologic resorption/remodelling
- attaches perio ligament fibers to root
- contributes to root surface damage repairment
- helps to adjust the tooth position to new requirements
99
Dehiscense Vs Fenestration:
Dehiscense =area w/o bone coverage in root's marginal portion
Fenestration =bone present marginally, but defeft is located apically
-buccal bone coverage thin/missing
100
Remodelling process of alveolar bone:
- alveolar bone is constantly renewed in response to functional demands
- teeth erupt and migrate in M direction throughout life to compensate for attrition
- osteoclasts and osteoblasts work simultaneously
- bone trabeculae are resorbed and reformed
- cortical bone is dissolved and replaced by new bone
101
Gingival supply:
- mainly supraperiosteal blood supply
- greater palatine a from greater palatine canal
- numerous anastomoses
- periodontal ligaments blood vessels
- alveolar bone blood vessels
102
Lymph node direction:
goes the opposite way than artery direction
103
Gingivitis Vs Gingival diseases induced by:
Gingivitis induced by plaque biofilm
Gingival diseases not induced by plaque biofilm
104
Health definition:
=95% of the population fitting that definition
- 10% > BoP (if MORE PROBLEM)
- PPD < 3 mm
- PPD < 4 mm
105
BoP for Localised Vs Generalised Gingivitis:
Localised Gingivitis:
BoP 10-30%
Generalised Gingivitis:
BoP > 30%
106
Modyfing factors (systemic risk factors):
```
smoking
hyperglycemia -> causes abnormal gingival bleeding
low antioxidant micronutrient intake
sex steroids
drugs
haematological disorders
```
107
What is Periodontitis?
=chronic multifactorial inflammatory disease associated w/ dysbiotic plaque biofilms + progressive tooth supporting apparatus destruction
=inflammation resulting in periodontal attachment loss
108
Stages Vs Grades:
Stages: disease severity and extent (present)
Grades: progression rate (future)
109
Periodontitis is characterized by:
- gingival bleeding
- periodontal pockets
- periodontal tissue support and attachment loss
- alveolar bone loss radiographically
110
Interdental CAL:
| Buccal/Oral CAL:
Interdental CAL: > 2 non-adjacent teeth
Buccal/Oral CAL: > 3 mm pockets at > 2 adjacent teeth
111
Periodontitis staging:
extend described as:
localized
generalized
molar/incisor pattern
112
If you have x-rays do you proceed w/ diagnosis?
yes
113
Gingival recession is based on:
- interproximal attachment loss
- gingival phenotype
- exposed root surface characteristics
114
What is gingival recession type 2?
- interproximal CAL loss
| - interproximal CAL loss < or equal to B CAL loss
115
What is gingival recession type 3?
- interproximal CAL loss
| - interproximal CAL loss > than loss of buccal CAL
116
What is gingival recession type 1?
- NO interproximal CAL loss
| - interproximal CEJ not visible
117
What is biological width?
=supracrestal tissue attachment / =junction ep + supracrestal CT
118
BoP is used to distinguish b/w:
healthy Vs inflamed peri-implant mucosa
119
Bone loss is used to distinguish b/w:
peri-implant mucositis Vs peri-implantitis
120
Signs of peri-implant mucositis:
- plaque
- lesions
- bleeding on gentle probing
- NO bone loss
- NO pockets
(like gingivitis)
121
Signs of peri-implantitis:
- increased probing depth compared to previous exams
- bleeding on gentle probing
- bone loss
-> peri-implant mucositis patients may develop peri-implantitis
122
Correct Angulation of Subgingival debridement/scaling:
80 degrees
123
Obtuse Angulation Vs Acute Angulation:
Obtuse Angulation > 80 - 90 degrees
- Ineffective calculus removal
- Surface cratering
Acute Angulation < 80 degrees
- Ineffective calculus removal
- Burnishing calculus deposits
124
The base of the periodontal pocket is identified with:
the lower edge of the blade
125
Graceys Curettes:
```
1/2, 3/4 - GREY - anterior
5/6 - YELLOW - anterior
7/8, 9/10 - GREEN - posterior B/L
11/12, 15/16 - ORANGE - posterior M
13/14, 17/18 - BLUE - posterior D
```
126
Which is not the clinical feature of the healthy gingiva?
pigmentation
127
Inflammatory changes confined to the soft tissue surrounding an implant is called:
A. Periodontitis
B. Gingivitis
C. Peri-implant mucositis
D. Peri-implantitis
C. Peri-implant mucositis
128
Calculus attaches to tooth surfaces by:
Acquired pellicle
129
Clinical signs of gingivitis appear in:
A. Initial gingivitis
B. Early gingivitis
C. Late gingivitis
D. Advanced gingivitis
B. Early gingivitis
130
The most common sequelae of gingivitis is:
A. Pericoronitis
B. Periodontitis
C. Periodontosis
D. Periapical pathology
B. Periodontitis
131
Which of the following is a feature of gingivitis?
A. Inflamed tissue
B. Bleeding on probing
C. Increased gingival fluid
D. All of the above
D. All of the above
132
Risk and secondary factors in periodontitis:
* Age
* Gender
* Race
* Heredity/gene polymorphisms
* Smoking habits
* Diabetes mellitus
* Osteoporosis
* Stress & psychosocial factors
* Obesity
* HIV infection & immunodeficiencies
133
Which statement about Gracey curettes is correct:
a. 2 sharp cutting edges
b. rounded tip
c. shank angles with working end at 90 degrees
c. shank angles with working end at 80 degrees
a. 2 sharp cutting edges
| c. shank angles with working end at 80 degrees
134
Red complex of periodontal microorganisms:
a. cause gingiva redness
b. are colored red by hematoxylin-eosin
c. group of the most important periodontal pathogens
d. main part of supragingival dental plaque
c. group of the most important periodontal pathogens
135
3. Probing depth of healthy perio pocket is:
a. 0.5 mm
b. 1.0 mm
c. 2.5 mm
d. 4.0 mm
a. 0.5 mm
b. 1.0 mm
c. 2.5 mm
136
Periodontal ligaments:
- soft
- richly vascular and cellular CT
- surrounds teeth roots
- joins cementum w/ socket wall
- separated from gingiva by alveolar crest fibers
- hourglass shape
- narrowest at mid-root level
- width: +/- 0.25 mm
137
What is the diameter of the narrowest point of periodontal probe?
0.5 mm
138
Periodontal ligaments functions:
- essential for tooth mobility
- permit forces (mastication and other tooth contacts) to be distributed and resorbed by alveolar process via alveolar bone process
139
How is tooth mobility determined?
by the width, height and quality of periodontal ligaments
140
Periodontal ligaments fibers:
```
alveolar crest fibers
horizontal fibers
oblique fibers
apical fibers
sharpey fibers
```
141
Grading w/o previous existing periodontal records:
- the bone loss:age ratio calculated from full-mouth radiographs
- if it is < 0.25 then Grade A
- if it is 0.25 - 1 then Grade B
- if it is > 1 then Grade C
- accordingly you apply grade modifiers (smocking or diabetes) if is is GRADE A or GRADE B periodontitis
- no smoking/diabetes = no change in grade
- smoking less than 10 cigarettes OR HbA1c is less than 7: upgrade to B
- smoking 10 or more cigarettes per day OR HbA1c is 7 or more: upgrade to C
142
Grading w previous existing periodontal records:
- calculate the rate of periodontitis progression over the previous 5y
- If progression is less than 2 mm, it is Grade B periodontitis
- If there's no progression in 5y, it is Grade A periodontitis
- When the progression has been 2 mm or more, it is Grade C periodontitis
- Grades A and B can be upgraded to a higher grade if the patient smokes or is diabetic
- a patient who smokes fewer than 10 cigarettes will be upgraded to B
- a patient who smokes 10 or more cigarettes per day will be changed to Grade C
- a diabetic patient w/ HbA1c below 7 will be upgraded to B
- a diabetic patient w/ HbA1c of 7 or more upgraded to C
143
Periodontitis bacteria:
```
red complex (treponema denticola, p.gingivalis, t. forsythia)
a.a.
```
