E1 Flashcards
1
Q
Periodontist is composed of 4 structures
A
Gingiva
PDL
Root Cementum
Alveolar bone
2
Q
Alveolar bone is broken down into 2
A
Alveolar bone proper (bundle bone)
Alveolar process
3
Q
Echo mesenchyme condenses around ______ and forms _____
A
Dental organ
Dental papilla
4
Q
Dental papilla gives rise to
A
Dentin and pulp
5
Q
Dental follicl gives rise to
A
Periodontist
6
Q
Dental papilla determines
A
Shape and form of tooth
7
Q
Gingiva is part of the
A
Masticatory mucosa which covers the alveolar process and surrounds the cervical portion of teeth
8
Q
3 parts of Gingiva
A
Free Gingiva
Attached Gingiva
Interdental papilla
9
Q
Free Gingiva
A
Gingival sulcus
Marginal Gingiva
Sulcus Depth
Extends from FGM to FGG
Keratinized epithelium
10
Q
Free gingival margin
A
Coronal end of Gingiva
Located 1.5-2 mm coronal to CEJ
11
Q
Probe depth is a measure of
A
Free gingival space
12
Q
Free Gingival groove
A
Junction between free and attached Gingiva
Corresponds to CEJ
30-40% of adults
13
Q
Oral sulcular epithelium faces
A
Tooth surface without contacting it
14
Q
Oral epithelium faces
A
Oral cavity
15
Q
Junctional epithelium provides
A
Contact between Gingiva and the tooth
16
Q
Junctional epithelium is _______ to CEJ
A
1 mm above CEJ
17
Q
Attached gingiva should be
A
Firm, coral pink, immobile, width varies
18
Q
Attached Gingiva: Width ____ with age
A
Increases
19
Q
Attached Gingiva: widest in
A
Incisors
Narrowest in premolar
20
Q
Attached Gingiva: Mandibular lingual
A
Narrowest in incisors, widest in molars
21
Q
Stippling
A
Small depressions on attached Gingiva
40% of adults
Sign of health
Loss=inflammation
22
Q
No mucoginvial junction on
A
The palate
23
Q
MGJ is the junction between
A
Keratinized and non keratinized
24
Q
Attached Gingiva is important because
A
Supports marginal gingiva
Base for movable elements
Withstand frictional and functional stresses
Barrier for passage of inflammation
25
Attached gingiva can withstand stresses because
Thick CT layer
Firmly bound to perisoteum and bone
26
For patient with less than optimal oral hygiene width and thickness
Matter to prevent inflammation
27
Width
What you would call height
28
Thickness
Buccolingula measuremnt
29
Shape of interdental papilla depends on
Contact relationship of teeth
Width of approximately tooth surfaces
Course of CEJ
30
COL
Concavity seen in contact areas of premolar/molar region
Non keratinized epithelium
31
Golden rule of interdental papilla
Papilla is complete when the distance from the contact point to the crest of the bone was less than 5 mm
32
The base of the gingival sulcus in a healthy mouth is positioned apical to the CEJ. When is this condition most likely to occur
40-60 years of age
33
Orthokeratinzed
No nucleus
34
Parakeratinized
Nuclear remnants
35
Oral epitlium layers
Basal layer
Prickle layer
Granular layer
Keratinized layer
36
From basal layer to granular layer
Cytoplasmic tonofilaments and number of desmosomes increase
Organelles decrease
37
Merkel cells
Sensory
38
Melanocytes
Melanin
39
Langerhans cells
Defense cells
40
Basement membrane
Present between basal layer of oral epithelium and CT
1-2 um wide
Rich in glycoproteins
Contains protein polysaccharide complexes
41
Glycoproteins
Keep tissues hydrated and maintains space
42
2 layers of basement membrane
Lamina Lucinda
Lamina dense
43
Lamina Lucinda
Adjacent to basal class
44
Lamina densa
Adjacent to CT
Anchoring fibers project form LD into CT
45
He I desmosomes
Dense plaques that attach epithelium to the basement membrane
46
Does Mose
Pairs of HEMA desmosomes
47
When retention pegs fuse
It is seen as stippling
48
Where are there no retention pegs
JE site
49
When 2 rete pegs fuse
Drop down you will see stippling
50
Rete pegs are
Epithelial ridges
Thicker the gingiva the easier to see
51
After tooth eruption cells of oral epithelium possess ability to differentiate into cells of
JE
52
JE widest in _____ and thinnest towards ________
Coronal 15-20 cell layers
CEJ 3-4 cells
53
JE is continuously
Renewed
Turnover rate faster than oral epithelium
54
Difference between JE and OE: Size fo cells
JE> OE
55
Difference between JE and OE: Size of intracellular space
JE>OE
56
Difference between JE and OE:Number of desmosomes
JE
57
Difference between JE and OE: Keratinization
JE has potential to keratinized
58
JE is _______ to tooth
Physically attached
59
Periodontitis occurs when
JE migrates apically down root surface
60
Viable junctional epithelium necessary for
Pocket formation
61
Necrosis of junctional epithelium
Junctional epithelial cells die so no pocketing
Bone exposed
62
Cells of gingival CT
```
Fibroblasts
Mast cells
Macrophages
Neutrophils
Lymphocytes
Plasma cells
```
63
Collagen
Characteristic cross banding
Produced by fibroblasts, cementoblasts and osteoblasts
Most abundant
64
Reticulin
Numerous adjacent to basement membrane
| Around blood vessels
65
OXytalan
Mostly in pdl
| Run parallel to Long axis of tooth
66
Elastic
Around blood vessels
67
CT fibers of Gingiva
Collagen
Reticulin
OXytalan
Elastic
68
Gingival fibers provide
Resilience and tone
Maintain architectural form and integrity
Reinforce the gingiva
69
Circular fibers
Encircle tooth like a cuff
Only fibers not connected to cementum
70
Dentogingival fibers
Fan out from supracrestal cementum into free gingiva
Upwards
71
Dentoperiosteal fibers
Run from supracretal cementum into attached gingiva
Down
72
Transseptal Fibers
Run from tooth to tooth
Embedded in cementum
Only not connected to gingiva
73
PDL permits
Forces to be distributed
Essential for tooth mobility
74
PDL is richly
Vascular and cellular CT surrounding the roots and joining cementum and alveolar bone
75
Fibers of PDL
Alveaolar crest fibers
Horizontal fibers
Oblique fibers
Apical fibers
76
Cells of PDL
```
Fibroblasts
Osteoblasts
Cementoblasts
Osteoclasts
Nerve fibers
Epithelial cells rest of mallassez (remnants of herweigs epithelaial root sheath)
```
77
Cementum is similar to bone tissue but
No blood vessels
No lymph vessels
No innervation
No remodeling
78
Cementum can
Continue deposition throughout life
Collagen fibers embedded in organic matrix
High mineral content 65%
79
Cementum fibers
Intrinsic
| Extrinsic
80
Intrinsic cementum fibers
Produced by cementoblasts
Composed of fibers oriented parallel to root
81
Extrinsic cemental fibers
Sharpeys fibers
| Produced by PDL fibroblasts
82
Different forms of cemental fibers
Acellular extrinsic fiber cementum
-coronal or middle portion of the root
Cellular mixed strained cementum
-apical third of the root and in fraction
Cellular intrinsic fiber cementum
-in resorption lacunae
83
Cellular intrinsic fiber cementum
-in resorption lacunae
84
Cellular mixed strained cementum
-apical third of the root and in fraction
85
Acellular extrinsic fiber cementum
-coronal or middle portion of the root
86
Cementum thickness throughout life
Increases by gradual apposition
87
Cementum thickness in cervical portion of root
20-50 um
88
Cementum thickness in apical portion of root
150-250 um
89
Alveolar bone consists of bone formed by both
Cells from dental follicle
Cells independent of tooth development
90
The dental tissue that most closely resembles bone is
Cementum
91
Diagnosis of periodontitis is based on
Attachment loss NOT probe depths
-apical migration
92
When bone is being resorted junctional epithelium moves to
Root surface
93
False pocket
The probe doesn’t go past CEJ—gingivitis
94
When gingival margin is coronal to CEJ
It is a negative recession
95
When gingival margin is apical to CEJ
Positive recession
96
CAL
Pocket depth+ gingival recesssion
97
Connective tissue attachment
1.06 mm to 1.08 mm
98
Epithelial attachment
1.4 mm
99
Whole attachment
2-2.5 mm
100
Distance from CEJ to alveolar crest
Is 2 mm
101
Distance from crown margins to alveolar crest HAS to be
2 mm
102
If you don’t have enough distance from CEJ to alveolar crest then
Crown lengthening is necessary
103
Initial thinking of giniglave width and recesssion
Less than 2 mm predisposed to recession
104
Why does small width of keratinized tissue predispose to recession
Can’t protect from friction or buffer muscle pull
Facilitates subgingival plaque formation mobile tissue causes pockets to open
105
Can gingival health be maintenance independent of its dimensions?
YES
Narrow gingiva has same resistance to attachment loss as wide gingiva
106
Thin phenotype
Increased recession
More vulnerable to trauma
More inflammation
Less favorable treatment outcome
107
When would you recommend gingival grafts
When recession causes symptoms
Subgingival restoration margins on thin biotype
Preortho therapy
108
The characteristic of the gingiva are _______ determined
Genetically
Rather than being the result of functional adaptation to environmental stimuli
109
Connective tissue grafts
Connective tissue determines epithelial prototype
Slid under gum
110
Thin elastic CT will create
Non keratinized
111
Healing after extraction
```
1 clot formation
2 wound cleansing -PMNs monocytes macrophages migrate into wound
3 New vasculature mesenchymal cells from PDL form granulation tissue
4Provisional CT
5 Immature bone forms
6 Bundle bone is restored
7 Wound filled with woven bone
8 Bone maturation
```
112
Healing is important because
Socket preservation important for preserving bone morphology
113
Guided Tissue Regenration
Epithelium grows faster than bone or connective tissue
Epithelial exclusion will allow selective growth of these cells
114
Barrier membranes
When furcation involvement
Fill with bone and bow tie thing
115
Planktons bacteria adhere to
Acquired pellicle
116
_____ and ______ in pellicle
Salivary glycoproteins
Antibodies
117
Bacterial characteristics change following attachment
Synthesis of new outer membrane proteins
Active cellular growth
118
Rapid attacker’s
Specific attachment structures such as fimbriae extracellular polymers glycolclax
119
Co-aggregation
Cell to cell recognition of genetically distinct cell types
| -forms giant clumps
120
Co-aggregations is mediated ______on one cell and ______ on the other
Protein or glycoproteins
Carbohydrates
121
Co-Adhesion
Interactions between suspended and already adhering microgansims
122
Co-adhesion is influenced by
Temperature (no if temp > 37)
| Lactose (decreases co adhesion)
123
Primary colonizers are gram__
Gram + mostly
124
Secondary colonizers are gram__
Gram -
125
Tertiary colonizers are gram__
-
126
What happens as biofilm develops?
An oxygen gradient develops because it begins to become difficult to diffuse in out
127
Completely anaerobic condition are present where in biofilm
Deepest layer
The primary colonizers die and pathogen expansion
128
________ develop as a result of bacterial metabolism in thickening biofilm
Reverse gradients of fermentation
129
Bacterial hydrolytic enzymes breakdown host macro-molecules into
Peptides and amino acids
130
Cervicular fluid is protective but bacteria can use it
As food
131
Crevicular fluid comes out from plasma leading to inflammation resulting
In more vasodilation and more crevicular fluid
132
Biofilm is composed of
Microcolonies (15-20%)
+
Interbacterial matrix
133
Interbacterial matrix of biofilm comes from 3 sources
Dead bacterial cells
Saliva
Gingival exudate (crevicular)
134
The back bone of the biofilm
Exopolysaccharides
135
3 layers of biofilm
Lower layer
Loose Layer
Fluid layer
136
Lower layer of biofilm
Dense layer of microbes
Polysaccharide matrix
Tightly bound together
Steep diffusion gradients
137
Loose layer of biofilm
Irregular appearance
| Extends into surrounding medi
138
Fluid layer of biofilm
Stationary sublayer
Fluid layer in motion
Nourishes the biofilm by molecular diffusion
139
Shape of micro-colonies depends on
Shear force
140
Low shear force
Towers or mushrooms
141
High shear force
Elongated Colonies capable of oscillation
142
________ are areas of high shear
Facial
143
______ are areas of low shear force
Interdental surfaces
144
Gram positive ineterbacterial matrix is very ________ due to _____ and _______
Very fibrillar
Dextrans
Evans
145
Dextran and levans
Polysaccharide sugar molecules and very sticky
Gram positive
S. Mutans
146
Gram negative interbacterial matrix is very_______
Regular
147
Gram negative matrix contains
Trilaminar vessicesl with with endotoxins and proteolytic enzymes
Probably involved in adherence
148
Source of energy in interbacterial
Dextrans, fructans—energy sources
149
Skeleton of plaque
Mutans
150
Cuticle forms
Primary attachment
151
How are bacterial layers near sulcular epithelium different from tooth attached
No inter-bacterial matrix
More spirochetes and flagellated bacteria
152
Bacterial collaboration is necessary for
Succession
153
S. Crostatas
Fac. Species( can live with or without O2)
154
Fusobacterium
Robust anaerobes
Binding to strep improves survival when O2 is present
155
P. Gingivalis
Micraerophilic, obligate anaerobes
Coaggregation essential to survival when O2 is present
156
What 3 bacteria form robust biofilms in the presence of O2
S. Cristatus
Fusobacteirum nucleatum
P. Gingivalis
157
______ can invade epithelial cells
F. Nucleatum
S. Cristatus does not but can be carried in by F. Nucleatum
158
transfer of information and genetic material
```
Signaling (quorum sensing)
Conjugation
Transformation
Plasmid transfer
Transposon transfer
```
159
______ important for mainting healthy biofilm and converting good to bad
Quorum sensing
160
Quorum sensing
Regulation of expression of specific genes through accumulation of signaling compounds that mediate intercellular communication
161
Auto-inducer
Turns on in response to cell density
162
Pathogens produce AI
AI-2 in high levels
This may determine switch from commensal to pathogenic community
163
Antibiotics depends on
Cell turnover for efficacy
164
Biofilm bacteria are what type of growers
Slow
165
Slow growers express
Nonspecific defense mechanism
Slow growers make more eco-polymers
166
Eco-polymers
Retard diffusion
167
Extracellular enzymes that inactivate antibiotics
Betalacatamase
Formaldehyde dehydrogenase
Formaldehyde lyase
168
Classical concept of pathogens
Not normally present
Produces “virulence factors”
-damage host directly
-Induce host to damage itself
169
Ecological concept of oral microbial disease
Ecological shift leads to changes in proportions
Balance shifts in favor of pathogens
PDD is an example of ecological catastrophe
170
One stage full mouth disinfection
Full mouth scalingin and root planing
Subliminally irrigation with chlorhexedine
Tongue brushing
Oral antimicrobial rinse
171
Non-Specific Plaque Hypothesis
All plaque bacteria considered bad
Any accumulation at or below gingival margin causes inflammation
172
Specific Plaque Hypothesis
Specific organisms in dental lacquer are the etiologic always agents
Microbial compostion different at Disease vs healthy
Local debridement and systemic antibiotics could control LAP
173
First signs of perio will be seen
Interproximal molars
Premolars and canines tend to be the last
174
Gram______ increase as gingivitis progresses to peridotontitis
Gram - rods
175
Oral Dysbiosis
House of cards
Keystone pathogens each can orchestrate destruction by bringing in different bacteria.
It itself doesn’t have to necessarily cause diseases
176
P. Gingivalis with type I and V genotypes
Healthy
177
P. Gingivalis with type II and iV genotypes
In disease
178
Pathogens must express
Virulence factors
179
Colonization by beneficial species ______pathogens
Dilute levels
180
Beneficial species can _______pathogens ex. Peroxide
Inhibit
181
Host susceptibility can be affected by
HIV
Diabetes
Smoking
182
Iron can increase ________ in P. Gingivalis
Outer membrane protein
183
S. Crsistatus can _______fimA expression
Inhibit
184
Bacteria have ______ to bind host receptors
Fimbriae and Outer membrane proteins
185
Adhesions on bacteria bind to host receptors using
Type I or IV collagen
Sialic acid
Galactosyl residues
186
Veillonella uses ______ made by ________
Lactate
Streptococci
187
Campylobacter uses ______ made by _____
Formate
Selenomonas
188
Porphyromonas uses ______ from _____ in sulcus
Hemin
Blood
189
Hydrogen peroxide production by _____ inhibits _____
S. Sanguinis
A.A.
190
Competitive inhibiton can be achieved by_______ which are peptide toxic to related strains
Bateriocins
191
Desquamtion of epithelium
Invade epithelium and bind to underlying cells
192
Antibody prevent binding so bacteria
IgG and IgA protease
Mimic host antigens
193
Bacteria can secrete leukotxin which helps
Them evade phagocytic cells. They can also use non-lethal suppression of immune cells
194
World workshop designated 3 pathogens
P. Gingivalis
A. Actinomycetemcomaitans
T. Forsythia
195
Is A.A. Motile and shape?
Non motile
Round ended rod
196
A.A. Gram___
Gram -
197
If you see star shaped colonies it must be
A.A.
198
A.A. Is capnophilic meaning
It needs CO2 to grow
199
A.A. Gets nutrients by
Saccharolytic (carbs)
200
High numbers of A.A. Have been associated with
Aggressive periodontist and detected in active sites
201
Elimination of AA affected periodontist how?
Resulted in a successful therapy
Recurrent lesions harbor the species
202
A.A. Virulence factors (5)
```
Tissue invasive
Leukotoxin
Fibroblast inhibiting factor
Endotoxin
Collagenase
```
203
A.A. Inhibits growth of
Commensals
| S. sanguis
204
Does A.A. Have to be present for periodontitis?
Not seen in all cases of aggressive and seen in healthy subjects
205
AA with _____ is more likely to be disease associated than AA with full length promoter region
530bp deletion
206
AA has____serotypes base on _____
5
| Polysaccharides on surface of organism
207
Of the 5 serotypes how many can each person have
Only 1
208
AA ________ are dominant antigens
Serotype specific surface antigens
209
A.A. Serotype __ most commonly associated with localized aggressive perio in USA
B
210
A.A Serotype A
Health associated in Finland
| Disease in japan
211
P. Gingivalis gram___
Negative
212
P. Gingivalis environment
Anaerobic
213
P gingivalis shape and movements
Non motile rods
214
P gingivalis nutrients
Asachrolytic
215
P. Gingivalis cysteine proteinases
Important to in proteins egradation and in the maturation of cell surface protein such as fimA fimbrillin
216
Pg associated with period
Elevated in lesions
Lower in healthy sites
Presence indicates risk of attachment loss
217
P. Gingivalis produce
```
Collagenase
Protease
Hemolysin s
Endotoxin
Fatty acids
NH3
H2S
Indole
```
218
T. Forsythia gram__
Gram negative
219
T. Forsythia environment
Anaerobic
220
T. Forsythia shape
Spindle shaped
Highly pleomorphic rod
221
T. Forsythia requires
NAM n-acetylmuramic acid
222
T. Forsythia co-cultivates with
F. Nucleatum
223
T. Forsythia serrated S-layer on cell
Mediates adhesion
Hemagglutination
224
Treponema denticola gram
Negative
225
Treponema denticola environment
Anaerobic
226
Treponema denticola shape
Helical shaped
Highly motile
Hard to distinguish several species
227
Prevotella intermedi/nigrescens gram
Negative
228
Prevotella intermedi/nigrescens environment
Anaerobic
229
Fusobacterium nucleatum gram
Negative
230
Fusobacterium nucleatum environment
Anaerobic
231
Fusobacterium nucleatum shape
Spindle shaped
| Early colonizer and spindle shaped
232
Most common isolate cultured from subgingival microbioat in health and disease
Fusobacterium nucleatum
233
Fusobacterium nucleatum releases _______ from leukocytes
Cytokines
Elastase
Oxygen radical
234
C. Rectus
Gram negative
Anaerobic
Short
Motile vibrio
235
E. Corrodens
Gram negative
Capnophilic
Assachrolytic
Small rod
236
P. Micros
Gram positive
Anaerobic
Small
Assachrolytic coccus
237
Selenmonas species
Gram negative
| Curved saccharolutic rods
238
Eubacteria species
Gram positive
Anaerobic
Pleomorphic rods
239
How do bacteria induce damage to periodontal tissues
Attach and colonize the gingival crevice (some go into soft tissues)
Releases substances that directly damage host cells
Activate hosts own inflammatory and immune systems leading to host tissue damage
240
Bacteria that can invade periodontal epithelium
A. A
P.G.
241
Direct cytotoxic effect of bacterial metabolic waste products
Ammonia
Indole compounds
Fatty acids
Hydrogen sulfide
242
Fatty acids like propionic and butyric acids cause damage how
Diffuse into host cells and change intracellular pH
243
Damaging bacterial enzymes
Leukotoxins
| Gingipains
244
Leukotxin
Leukotoxins from A.a kills leukocytes
245
Gingipains
Gingipains Arg Specific protease from P.g. Degrade interluekin that do inflammatory response
246
Immunostimulatory molecules
```
LPS endotoxin
Lipoteichoic acids
Gingipains
Formylpeptides
Surface antigens
```
247
Prevention of bacterial entry is done by 3 mechanisms
Shedding of epithelial cells
Intact epithelaila barrier
Positive fluid flow into the gingival crevice
248
Innate immune response uses complement system to
Induce bacterial lysis
Promote phagocyte recruitment
Opsonization
Activates mast cells which increase vascular permeability
249
Innate immune system of oral mucosa can produce ______ that can kill fungi
Anti-microbial peptides (defensins)
250
3 oral epithelium pro-inflammatory cytokines of innate immune system
IL-1B and TNF-a
| IL-8
251
IL-1B and TNF-a are universal signals
Of infection that help recruite inflammatory cells
252
IL-8 attracts
Neutrophils in the early stages of infection
253
______ second line of defense
Adaptive/acquired immunity
254
Adaptive immunity has ________ response to bacterial _____
Specific response
Bacterial Ag
255
Hallmarks of adaptive immunity
Ag recognition
Immune memory
Colonial expansion
256
Innate immunity: mucin
Bund up bacteria and allow it to be washed away
257
Toll like receptors recognize
Conserved microbial associated molecular patterns
258
TLRs signals for cells to
Produce cytokines chemokines
Antimicrobial peptides
NO
Eicosanoids
259
C3b
Attaches—>opsonizatoin—> phagocytosis
260
C5b
Membrane attac complex—> Lysis
261
C3a and C5a
PMN chemotaxis mast cell degranulation—> vascular permeability—-> inflammation
262
Prostaglandins induce
Vasodilation and cytokines production
263
PGE2 induces production of
Matrix metalloproteinases by fibroblasts and osteoclasts which damage periodontal tissues
264
Matrix metalloproteinases degrade
Extracellular matrix
265
Alpha-2 macroglobulin
Broad spectrum proteinase inhibitor
266
Alpha-1 antitrypsin
Broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase
267
Calprotectin inhibits
Bacteria and fungi by chelating zinc. Produced by epithelium, PMNs, monocytes, macrophages
268
Neutrophils kill bacteria by ____ or ______
Oxidative
Nonoxidative
269
In chronic periodontist number of cells
Plasma> B lymph> T lymph
270
Th1
IL2 IFN-G TNF-a
271
Th2
IL-4,5,6,10,13
272
Cytotoxic T cells are active by
Cytokines
273
Tc cells respond to and bind
Intracellular pathogens
MHC 1 molecules
274
Are Tc cells found in periodontist?
Not many suggesting that viruses and invasive bacteria are not major players
275
Ag-Ab complex ____ and ______
Activates complement and facilitates opsonization
276
Th2 cytokines activate
B cells to plasma cells
277
B cells humoral immunity triggered in response to
Soluble antigens
278
2 types of B cells
Conventional
| Auto reactive
279
Conventional B cells
Produce antibodies against bacteria levels decrease in healthy and treated sites
280
Autoreactive B cells
Produce auto antibodies levels do not decrease after treatment
281
Antibody alone will
Block entry of toxins and viruses
Immobilizes bacteria
Agglutinate bacteria
IgM> IgG>IgA
282
Antibody plus complement will
Lyse bacteria
IgM IgG
283
Antibody plus cells
Opsonization bacteria fungi for phagocytosis
Activates extracellular killing
IgG
284
Is IgG2 or IgG1 in chronic periodontitis
IgG1 is predominate but switches in aggressive periodontitis
285
IgG2 recognizes
Carbohydrate antigens(LPS) while other mainly recognize protein Ag
286
Are there more Th2 or Th1 cells in chronic periodontal lesions
Th2
287
_____ cells are among the most predominant and active secretory cells in advanced periodontal lesions
Plasma cells
288
An individuals ability to _______in the subgingial biofilms may indicates a patients susceptibility to the disease and ability to respond to treatment
Mount a specific Ab response
289
Tissue volumes rations
10% JE
30% OE
60% CT
290
Cell layers in JE
10-20 cell layers
291
Are there dentogingival plexus venues loops in health
No but there are capillary loops
292
Stages in development of gingivitis and periodontitist
Initial
Early
Established
Advanced
293
Initial Lesion: Subclinical stage of gingivitis
Early stage of inflammation, invisible.
Increased permeability PMNs monocytes GCF in JE
Increased vascular density
294
GCF is a plasma_____ in health or _______ in disease
Transudate
Inflammatory exudate
295
Initial lesions PMNs adhere to
Post capillary venues and begin to migrate through JE into gingival sulcus
296
Chemotaxis by PMNs is induced by
IL-8 and C5a and molecules released by bacteria
297
______ of JE is essentially what inductees the whole process
Basal cells
Stimulated by endotoxin
Release inflammatory agents
Sets off cascade
298
Initial lesions drum proteins present
Extravascularly
299
Collagen is lost where durin initial lesion
Perviascular collagen
Broken down by PMNs release of granules
300
Alteration on of the most ____of JE during initial lesion
Coronal portion
301
Early lesson occurs how many days after plaque development
4-7
302
Early lesions inflammation is now
Clinically evident
303
In the early lesion what creates space for infiltration
Collagen destruction
304
Proliferation during early lesion
Basal cells of JE and SE
305
Epithelial retention pegs in early lesion
Invade coronal portion of lesion
306
Early lesions the JE invades CT
The previously inactive capillary bed opens up and proliferates into the CT papillae
307
Early lesions accumulation of _____immediately subajacent to to JE
Lymphoid cells
Still few plasma cells
15%
308
Established lesion is clinically classified as
Chronic gingivitis
309
Established lesion increased _____ around blood vessels in ______ CT
Plasma cells
Coronal CT
310
Established lesion Activated T cells produce
Cytokines
Chemotactic substances MCP MIP RANTES
311
Established lesion Plasma cells produce
Ig and cytokines IL6 and TNF
312
established lesion fibroblast produce
MMPs and TIMPs
313
IN established lesion the JE and sulcular epithelium proliferate and ________
Migrate deep into ct
314
Established lesion the sulcus deepens and the coronal portion of JE is converted into
Permeable pocket epithelium which is not attached to the tooth surface loaded with PMNs
315
Established lease on increased proportion of plasma cells
10-35%
316
Is there apical migration of JE or bone loss at established lesion?
NO
317
What cell predominates in advanced lesion
B cells over T cells which signals the conversion from gingivitis to periodontitis
318
What are the first clinical signs of periodontitis
Destruction of CT attachment to root surface
AND
Apical migration of petoihleial attachment
319
Where does bone loss begin in advanced lesions
Around communications blood vessels along crest of septum
320
___% of infiltrating cells are plasma cells in advanced lesion
50
321
Glycemic control is improved after
Periodontal therapy
322
Dental Calculus
Mineralized plaque that forms on the surfaces of natural teeth and dental prostheses
323
2 types of calculus
Supragingival
Subgingival
324
Supragingival calculus
```
Coronal to gingival margin
White/yellow
Clay like
Easily detached
Opposite salivary ducts
```
325
Subgingival calculus
Below gingival margin
Hard dense
Dark colored
Extend to base of pocket but does not reach JE
326
Detection of calculus
tactile
Radiographs
Blast of air
Coloring of Gingiva
327
Calculus represents
A secondary product of infection
NOT a cause of periodontist
328
Attachment of calculus
Calcified pellicle
Penetration of surface irrgelaties
329
4 forms of calcium phosphate
Brushite
Octa calcium phosphate
Hydroxyapatite
Whitlockite
330
Most common calcium in subgingival calculus
Whitlockite
Hexagonal
331
Predominate calcium in old calculus
HA
Rods
332
Dominate calcium in exterior layers
Octa calcium phosphate
Platelets
333
Calcium that is the basis for supragignal calculus
Bushite
334
Calculus is removed due to
It’s plaque retentive nature
