TEST 2 Flashcards
1
Q
3 things a clinician should be able to do to manage perio disease
A
Diagnose accurately
Predict effect of systemic status of disease
Confirm prediction with assessment of therapeutics
2
Q
4 systemic factors that can modify gingival diseases
A
Endocrine system
Blood dyscrasias
Medications
Nutrition
3
Q
Endocrine events that can cause gingivitis
A
Puberty
Menstruation
Pregnancy (gingivitis and pyogenic granuloma)
Diabetes
4
Q
Blood dyscrasia that can cause gingival disease
How to limit severity
A
Leukemia (acute)
Reduce dental plaque
5
Q
2 ways medications can modify gingival diseases
A
Gingival enlargement
Oral contraceptive gingivitis
6
Q
Nutrition deficiency that can cause gingival disease
A
Ascorbic acid-deficiency
7
Q
Clinical signs of chronic (adult) periodontitis
A
Pocket formation Loss of attachment Bleeding/suppuration Bone loss Tooth mobility and drifting
8
Q
_ is a frequent finding in chronic perio
A
Subgingival calculus
9
Q
Chronic perio is classified by _ and _
A
Extent and severity
10
Q
3 common features of aggressive perio
A
Systemically healthy
Rapid attachment loss and bone destruction
Familial aggregation
11
Q
Aggressive perio often has elevated levels of what two bacteria
A
A. a
P. Gingivalis
12
Q
White cell abnormalities secondary to aggressive perio
A
Phagocyte abnormalities
Hyper-responsive macrophage (high PGE2 and IL-1B)
13
Q
Localized aggressive periodontitis
Onset
Response to infecting agents
Presentation where?
A
Circumpubertal onset
Robust serum antibody response
Localized first molar/incisor presentation
14
Q
Generalized aggressive perio usually affects who
A
People under 30
15
Q
Serum antibody response in GAP vs. LAP
A
LAP - robust serum antibody response
GAP - poor response
16
Q
In GAP, destruction of attachment and bone is _
A
Episodic
17
Q
Periodontitis is associated with what two types of disorders
A
Hematologic
Genetic
18
Q
The two types of Necrotizing periodontal disease are
A
NUG - necrotizing ulcerative gingivitis
NUP - Necrotizing ulcerative periodontitis
19
Q
Clinical signs of NPD
Early
Advanced
A
Early - necrotic lesion on papilla first, then moving to gingival margin. Punched out appearance. Spontaneous bleeding.
Advanced - lack deep pockets, papillary and margin lesions merge, stinks, periodontal ligament and alveolar bone
20
Q
NUP is typically seen in who
A
Severely immunocompromised people (HIV)
21
Q
4 characteristics of periodontal health
A
Functional dentition
Painless function
Stability of periodontal apparatus
Psychological and social well being
22
Q
5 values in assessing inflammation
A
Color Texture/edema Bleeding Exudate Plaque
23
Q
Plaque index
A
Amount of plaque at gingival margin
24
Q
PSR:
Purpose
Benefits
Limitations
A
Perio screening and recording
Rapid and effective way to screen and summarizes necessary info
Early detection, speed, simple, cheap, risk management
Not the same as a comp. perio exam, adults only
25
How to tell if a diagnostic test is valid
Sensitive
Specific
26
3 categories of diagnostic methods for Perio Diseases, and examples
1. Clinical examination
- inflammation, probe depth
2. Lab tests
- biochemistry, genetic analysis
3. Non-invasive tools
- NIR, OCT, ultrasound
27
CBCT
What is it
Promising in what areas
Cone beam computed tomography
```
Intrabony defects
Dehiscence
Fenestration defects
Periodontal cysts
Furcation defects
Thickness of palatal mucosa
```
28
Sensitivity vs. specificity
Probability the test is positive when disease is present
Spec - probability test being negative when disease is not present
29
Micro testing:
Sensitivity
Low
30
Immunodiagnostic methods are used mainly to detect
Aa and Pg
31
3 types of immunodiagnostic methods
Cytofluorography
ELISA
Latex agglutination
32
Several pathogens like Pg, Tf, and Aa have a ___ that hydrolyzes ___
Trypsin like enzyme
BANA
33
3 molecular biology techniques
Nucleic acid probes
Checkerboard DNA-DNA hybridization
PCR (real time too)
34
PCR sensitivity and specificity
High
| High
35
_ components of GCF have been evaluated
3 main things
65
Host enzymes and inhibitors
Tissue breakdown byproducts
Inflammatory and host response mediators
36
Intracellular destruction enzymes
What?
Come from?
Examples of some
Markers of active perio destruction
From dead or dying PMN/neutrophils from perio
Aspartate amino-transferase
Alkaline phosphatase
B-glucuronidase
Elastase
37
Extracellular destruction enzymes are associated with activity of _
Come from _
Matrix metalloproteinases
Inflammatory, epith. And connective tissue cells
38
MMPs are secreted from
MMPs are responsible for _
Fibroblasts and macrophages
Remodeling and degradation of ECM components
39
ECM is composed mainly of what 3 things
Collagen
Proteoglycan
Non-collagen proteins
40
When collagen breaks down, _ is formed
Hydroxyproline
41
Tissue oxygen at periodontitis is _ compared to gingivitis and healthy sites
Significantly lower
42
What is SOBT, is it effective?
Salivary Occult Blood Test
Simple & for when thorough perio exam isn’t possible
Not a substitute
43
Bone loss % =
CEJ - Crest - 2 mm
__________________
CEJ - Apex - 2 mm
44
Mild vs. moderate vs. severe bone loss
Mild ≤ 20 < Moderate < 50 ≤ severe
45
Normal alveolar crest sits _
2mm below CEJ
46
T/F integrity of crestal lamina dura is related to the presence or absence of visual inflammation
FALSE
47
_ % of americans over 40 have perio disease
64
48
3 words that define Epidemiology
Origin
Spread
Pattern
49
Why use CPITN
Community perio index of treatment needs
Determine treatment patient needs
50
0-4 in CPITN
```
0 - healthy
1 - bleeding after probing
2 - calculus detected during probing
3 - pocket 4-5 mm
4 - pocket 6 mm or more
```
X - excluded
9 - not recorded
51
In 14-17 yr olds, Prevalence of:
Localized AP
Generalized AP
Incidental AL
LAP - 0.20 +/- 0.22
GAP - 0.13 +/- 0.07
Incidental AL - 1.61 +/- 0.41
52
Advanced levels of perio throughout the world
10-20%
53
Peri-mucositis
Gingivitis around implants
54
6 characteristics common to all gingival diseases
1. Signs/sympts in gingiva only
2. Dental plaque present
3. Inflammation
4. No attach. Loss or stable periodontium
5. Reversibility if etiology is removed
6. Precursor to attachment loss
55
Primary Etiologic factor of gingivitis
Bacterial plaque
56
Secondary etiologic factors for gingivitis
Calculus
Marginal def. in restorations/rough
Malocclusion
Tooth/root anomalies
57
Biologic width
2.04
0. 97 ep attachment
1. 07 connective tissue attachment
58
T/F return of inflammation to sites treated for periodontitis is still diagnosed as recurrent periodontitis
TRUE
59
3 endocrine factors that modify gingival disease
Pregnancy
Puberty
Menstrual cycle
60
Malnutrition gingivitis
Vitamin C
| Vitamins A, B2, B12 complex
61
Systemic conditions that modify gingivitis
Diabetes
Leukemia
Thrombocytopenia (bleeding)
Neutropenia (ulceration)
62
3 meds that can modify gingivitis
Anticonvulsants
Immunosuppressant
Ca channel blocking agent
63
2 things that lead to NUG
Smoking, stress
64
3 predisposing factors for NUG
Systemic disease
-ulcerative colitis, dyscrasia, nutritional deficiency states
Abnormalities of WBC function
AIDS
65
NUG vs. herpetic gingivostomatitis
Etiology
Symptoms
Duration
Contagious
```
NUG:
Bacteria
Ulceration, necrotic tissue, yellow plaque
1-2 days treated
Not contagious
```
```
PHS:
Herpes simplex virus
Multiple vesicles which burst, leaving small fibrin covered ulcers
1-2 weeks
CONTAGIOUS
```
66
Bacteria that cause gingival lesions
N. gonorrhea
T. pallidum
Strep
Mycobacterium chelonae
67
Which herpes simplex causes oral manifestations
1
68
Treatment of viral gingival lesions
Plaque removal
| Antiviral medication
69
Herpes zoster oral lesions treatment
Soft diet
Removal of plaque
Diluted chlorhexidine rinse
Antiviral drugs
70
3 fungal oral infections
Candidiasis
Linear gingival erythema
Histoplasmosis
71
Pseudomembranous vs. erythematous candidiasis
Pseudo is white
| Eryth is red
72
Linear gingival erythema
Cause
Treatment
Signs
Immunosuppression
Chlorhexidine, antimycotic therapy (don’t scale)
Linear erythematous band in free gingiva
73
Gingival lesion of Genetic origins
Hereditary gingival fibromatosis
74
Two types of allergic rxns that cause gingival lesions
Mediated by what
Type I, IgE
Type IV, T-cells
75
6 types of gingival lesions of systemic origins
1. Lichen Plano’s
2. Pemphigoid
3. Pemphigus vulgaris
4. Erythema multiforme
5. Lupus erythematosus
6. Drug induced mucocutaneous disorders
76
Lichen planus characteristic skin lesion
Wickham striae (white lacy)
77
3 characteristics of lichen planus
Subepithelial band of lymphocytes (type IV rxn)
Fibrin in basement membrane
Deposits of IgM, C3, C4, C5
78
Pemphigoid
Detachment of the epithelium from connective tissue
79
In pemphigoid, autoantibodies attack what two things
Hemidesmosomes
Lamina Lucinda components
80
Nicholsky sign indicates whtat
Pemphigoid
81
Treatment of pemphigoid
Chlorhexidine
| Topical corticosteroid
82
Pemphigus
Main sign
In who
Intraepithelial bullae (acantholysis)
Mediterranean and Jewish (middle age and up)
83
T/F pemphigus bleeds profusely
False
84
Erythema multiforme
What is it?
How often in mouth
Sign
Cytotoxic immune rxn against keratinocytes from HSV and drugs
Oral involvement in 25-60% of cases
Swollen lips
85
Lupus erythematosus
Clinically
Histologically
White striae
Telangiectasia
Butterfly skin lesion
Wide basement membrane
86
Reactive processes of periodontal soft tissues
What are they
```
Fibroma/ focal fibrous hyperplasia
- caused by irritation
Calcified fibroblastic granuloma
- reddish, ulcerated reactive lesion
Pyogenic Granuloma
- Ulcerated, bleeding common
Peripheral giant cell granuloma
- has a stalk, broad base
```
87
Reactive processes of periodontal hard tissues
Periapical cemental dysplasia
- fibrous/osseus cemental lesions
- vital tooth, no symptoms
88
Benign neoplasms of perio soft tissue (4)
Hemangioma
- soft, blue/red, asymptomatic, may bleed, blanch on pressure
Nevus
- brown/black, melanocytes
Papilloma
- filiform, white or red, HPV common
- Verruca vulgaris
- white, Hyperkeritinization, HPV 2/4
Peripheral odontogenic tumors
- non-ulcerated, similar to intraosseous forms
89
Benign neoplasms of hard perio tissues
Ameloblastoma
- From odontogenic epithelium
- well circumscribed radiolucency
Squamous odontogenic tumor
- From PDL
Benign cementoblastoma
- around apex
90
Malignant neoplasms of soft perio tissues (4)
Squamous cell carcinoma
- mandible, post. To premolars
- regional lymph node metastasis
Metastasis to the gingiva
- majority intraosseous
- soft tiss. Metastasis from lung cancer
- most carcinoma
Kaposi’s sarcoma
- skin then oral lesions
- AIDS
Malignant lymphoma
- Primary is rare
- Frequent among HIV
91
Malignant neoplasms of hard tissues (2)
Osteosarcoma
-widening of PDL
Langerhans cell disease
- swelling, tender, pain, loose teeth
92
5 cysts of periodontium
```
Gingival
Lateral perio
Inflammatory paradental
Odontogenic keratocyst
Radical are
```
93
Primary vs. secondary occlusal trauma
Primary = excessive on normal periodontium
Secondary = on weakened perio
94
Codestruction theory
Vs
Advancing plaque front theory
Occlusal trauma is co-destructive that alters perio disease
Occlusal trauma has no role
95
T/F occlusal trauma w/o periodontitis may be reversible and result in adaptation
TRUE
96
When occlusal trauma and perio is present
Do perio treatment first then occlusal therapy
97
Implant healing times
Mandible 3 months
Max 6 months
98
Before and after implant threshold and force loading that is perceptible
Before: 20 um thickness, 1-2 g load
After: 50-100 um thickness, 50-100 g loading
99
T/F 100% bone-implant surface contact is possible
FALSE
100
Occlusal trauma can be _ for peri-implant disease
Primary etiological factor
101
In reducing bone stress, _ is more important than _
Diameter
| Length
102
Clinical features of chronic perio
```
Change in gingiva (color, texture, volume)
BoP
Inc. probe depth
A loss
Gingival recession
Alveolar bone loss (vert/horiz)
Furcation involvement
Mobility
Drifting of teeth
Tooth loss
```
103
Chronic perio:
Pain?
Sensation?
Localized dull pain
Itching
Root sensitivity
104
Extent vs severity of chronic perio
Extent: localized < 30 < generalized
Severity:
Slight (1-2), moderate (3-4), severe (5+)
105
Risk factor
2 ex
Increase likelihood an individual will develop disease
Smoking
Diabetes
106
Risk determinant
2 ex
Non-modifiable factors
Age
Gender
107
Risk indicators
3 ex
Well known risk factors
HIV/AIDS
Osteoporosis
Infrequent dental visits
108
```
Risk predictors (markers)
3
```
Characteristic associated with elevated risk for disease, not necessarily part of causal chain
Furcation inv.
Calculus
History of A loss
109
T/F you cannot maintain 6 mm pockets
TRUE
110
Aggressive perio
Otherwise healthy
Severe and rapid bone and attach loss
Familial aggregation
111
LAP:
Most frequent age
Pattern/Distribution
B/t puberty and 20 yrs
At least 1 first molar, no more than 2 teeth other than incisors and first molars
112
T/F CAL is consistent with amount of plaque and calculus
FALSE - inconsistent
113
Serum antibody response in LAP vs. GAP
LAP - strong
| GAP - poor
114
Pathogenesis of LAP
Aggressive causative agents
| High level of susceptibility
115
_ (organism) is associated with LAP
Why?
A.a.
Fac. Anaerobe, non-motile
Virulence factors (kills mphage, degrades collagen, suppresses immune)
Translocate across JE
Invade CT
116
Neutrophils in AP hosts
Impaired
117
In AP, crevicular levels of _ are increased
PGE2
118
Loe and Silness plaque index
Gingival index
Amount of plaque at G margin
Plaque 0 to 3
Probe distinguishes 0 and 1
Gingival:
0 to 3, bleeding is 2+ automatically
119
O’Leary index
Plaque
Percentage of tooth surfaces positive for plaque
Disclosing solution, count red
120
PSR
Perio screening and recording
```
0 - colored, no calc, no BOP
1 - BoP
2 - calc, BoP
3 - colored partially visible, calc, BoP
4 - no colored area
```
121
NIDCR calculus and bleeding
0 - no calculus
1 - supragingival calc./ no sub calc
2 - Supra and sub, or sub only
122
Fibroma/fibrous hyperplasia
S
123
Osteosarcoma
S
124
Hereditary gingival fibromatosis
S
