lecture 3: initiall, early, established and advanced lesions. Flashcards
1
Q
definition of gingivitis
A
- plaque induced
- INFLAMMATION (edema, BOP)
- no destruction of PDL and bone
- no apical migration of epithelial attachment
2
Q
if there is epithelial attachment what does that mean
A
the junctional epithelium is at CEJ
3
Q
definition of periodontitis
A
- plaque-induced
- host related
- INFLAMMATION (edema and BOP)
- destruction of bone
- NOT ALL cases of gingivitis progress to periodontitis.
- this is irreversible only maintain, tx and control
4
Q
what determines whether gingivitis becomes periodontitis
A
host response
5
Q
what is the continuous model
A
that it is continuous throughout life at same rate of loss
6
Q
what is the progressive model
A
- progressive loss over time of some sites
- no destruction in others
- time of onset and extent vary among sites
- periodontal ds affects mainly post teeth
7
Q
what is the random burst model
A
- activity occurs at random at any site
- some sites show no activity
- some sites have one or more bursts of activity
- cumulative extent of destruction varies among sites
- periodontitis is different among various spots and it is hard to predict attachment loss
8
Q
this type of bone loss can be due to
A
lack of access
seen in distal areas of bone loss.
9
Q
which are the least likely teeth to loose due to periodontal ds
A
mand C and PM
10
Q
what is the most common lost tooth due to periodontal ds
A
mx 2M
11
Q
what is a secondary etiological factor of periodontal ds
A
an open contact
12
Q
signs of inflammation
A
rubor
calor
dolor - not really unless they have an abscess
tumor
functio laesa (loss of function) ** misisng of tooth, increase mobility, loss of attachment
13
Q
inflammation is what type of phenomenon
A
vascular
14
Q
the process of inflammation
A
- leukocyte migration
- vasculitis the biggest change you see
- dilation
- venous stasis (congestion)
- increased permeability
- like transudate and exudate
- why does it do this? to bring immune mediators
15
Q
what is the first defense
A
innate immunity
16
Q
what is the innate immunity
A
- the first defense system
non-adaptive and genetic
includes PMNs and monocytes/macrophages (WBC)
kill through phagocytosis
17
Q
how does the innate system kill by
A
18
Q
what is the second defense system
A
adaptive immunity
19
Q
what is adaptive immunity
A
- the second defense system
its v specific
uses B and T cells
Plasma cells produce specific ab to individual antigens
done through production of immunoglobulins by antibodies
20
Q
adaptive immune system produces
A
immunoglobulins by antibodies
21
Q
B lymphocytes are:
A
- activated b-cells that become plasma cells
- plasma cells that produce immunoglobulins
22
Q
t lymphocytes are:
A
- developed in the thymus
- several functions (antigen presentation)
- help B-cells divide; can destroy virally infected cells; can down-regulate immune response
23
Q
two major forms of T cells
A
CD4 and CD8
24
Q
MHC Class II molecules is what
A
- CD4
- T helper celss
- they help B cells to divide
- Controls leukocyte development
- activates innate cell lining
25
what is MHC Class I
- CD8
- T cytotoxic cells
- destorys virally infected target cells
26
\*\*PMNS are
phagocytosis; produces lysosomal enzymes
27
\*\* macrophages are
- phagocytosis; process antigens and cytokine secretion
28
\*\* b lymphocytes are
- **plasma cells**; produces antibodies
29
\*\* t lymphocytes are
**T helper (CD4)-** helps B cells divide
**T suppressor (CD8 and CD25) -** down-regulates t and b cells
**NK cell-** kills virally-infected cells
**T-cytotoxic cell-** destorys infected cells
**Killer T cell -** kills infected cells
30
hummoral immunity has two components
- antibodies and complement
31
antibodies are released by ____ and have ____ major immunoglobulins
1. plasma cells
2. 5
32
the 5 immunoglobulins from antibodies
1. IgM
2. IgG
3. IgA
4. IgD
5. IgE
33
what is IgM
the first responder and the largest in size
34
what is IgG
second responder and most abundant, crosses the placenta
35
what is IgA
salivary IgA; a dimer
36
what is IgD
co-expressed with IgM
37
what is IgE
on **mast cells,** allergic reactions
38
what is complement immunity
**-a part of both innate and adaptive immune systems**
- a **biochemical cascade** that helps clear pathogens by lysis, opsonization, binding, and clearance of immune complexes
- acts as a coplayer to recruit more immune cells and clearance
39
t suppressor cells
now **t regulatory cells,**
they down regulate T and B cells (CD8 and CD25 expression), it prevents autoimmune disease
40
K (killer) cells
a mononuclear cell that kills cells sensitized with antibody (via a Fc receptors)
41
NK cells
natural killer cells that kill virally infected and transformed target cells that have NOT been previously sensitized
42
other immune cells- monocytes
~5%, activation in CT
## Footnote
**WILL BECOME MACROPHAGES**
43
Other immune cells- **Neutrophils**
more than 70%.
they have a 48 hour lifespan in blood with migration to sites for phagocytosis
44
Other immune cells- esoinophils
about 2 to 5% of cells
they cause damage by exocytosis (like histamine release)
45
Other immune cells- mast cells
contain mediators of inflammation (histamine, prostaglandins, leukotrienes and cytokines)
they are involved in allergic reactions
46
Other immune cells- basophils
less than 0.5% of cells
are in some way functionally similar to mast cells
47
**definition of cytokines**
molecules that send out signals and help orchestrate the process
"soluble, locally active polypeptides; regulate cell growth, differentiation, function; **produced by cells of the immune system.**
**cytokines are depenent on:** their concentration, cells that produce them, cells being attracted and acted upon and presence and extent of extracellular matrix
48
\*\* **IL-1**
pro-inflammatory, stimulates osteoclasts, fibroblasts and macrophages
49
what are the 5 important cytokines in this lecture
**1. IL-1**
**2. IL-6**
**3. IL-8**
**4. TNF**
**5. PGE2**
50
\*\*what is IL-6
proinflammatory, stimulates T and B cells
51
\*\* what is IL-8
pro-inflammatory; attract and activates PMNs
52
\*\* what is TNF
pro-inflammatory; activates osteoclasts
53
\*\* what is PGE2
vasodilation
pyrogenic
releases mediatory from mast cells
cell-mediated cytotoxicity
54
what i smore prevelaent in caucasians and which is more prevalent in asians
caucasions - IL-1
asians - TNF
55
what is the most potent inflammatory cytokines for periodontitis
IL-1
\*have tests to see if pt is susceptible by looking at values of IL-1
56
4 growth factors covered in lecture
TGF - stims epithelial cells and fibroblasts
PDGF - stimulates fibroblasts
EGF - stimulates epithelial cells
FGF - stimulates fibroblasts
57
can we then accurately predict which patients with gingivitis are going to develop periodontitis
no
## Footnote
**the answer ius in the host's immune system and genetics**
58
well known risk factors for developing periodontitis
1. smoking (habit)
2. plaque
3. diabetes (systemic)
4. anythihng that affects the immune response
patients with risk factors are more likely to have attachment loss!!!!
59
the order of phases of periodontal ds
A. normal - healthy
B. 1. initial - gingivitis
B. 2. early - gingivitis
B. 3. established - gingivitis
C. Advanced - periodontitis
60
clinically healhty ginginva has what:
- some neutrophils and macrophages in CT
- new neutrophils mirgration through JE
- no collagen destruciton
- intact epithelial barrier
- gingival crevicular fluid is present
- appears clinically healthy (color, contour, consistency)
61
inflammatory response modifiers
## Footnote
**mechanical (plaque retention factors)**
- calculus
- caries
- restoration chaosm (defective, subg, and overcontoured margins)
- prosthesis
- tooth anatomy facots
62
inflammatory response modifiers
systemic
-**uncontrolled/controlled diabetes\*\***
**-hormonal: puberty, pregnancy \*\***
**- HIV/AIDS\*\***
**- Medications\*\***
**-** PMN defects
- hematolgoical
- immune disturbances
- nutrition deficiencies
63
inflammatory response modifiers
genetic
- **leukocyte adhesion deficiency (LAD)**
**- hypophosphatasia**
**-** agranulocytosis
- neutropenias
- lazy leukocytes
- down's syndrome
- papillon-lefevre
- chediak-higashi
- ehlers-danlos syndrome
64
what is the inital lesion
- PLAQUE IS DEPOSITED ON THE TOOTH
- bacterial biproducts are released into the periodontal tissues (**virulence factos)**
- it develops 2 to 4 days after not brushing or flossing
- cells of acute inflammation are present
- there is an increase in GCF flow
- and the start of a pseudopokcet formation (due to the margin going up coronally)
65
what are the two types of virulence factors
- stimulation of the host defense system (attracts inflammatory cells, stimulates cells to release cytokines and chemoattract factors **IL-8)**
- degradation of the host tissues (enzymes: collagensae, trypsin-like enzymes, keratinase, phospholipase A)
66
with poor plaque control what do we see
stimulation of epithelial cells and fibroblasts to relese IL-\* into the CT which attracts and activates PMNS.
PMNS in CT. PMNs are attracted and near the JE and Sulcular epithelium (JE and CT are still intact)
67
what happens with plauqe accumulation \*
stimulation of inflammatory cells to release cytokines into the CT
PMNs are still attracted and near to the JE and SE.
68
clincial features of initial lesion
- increased GCF flow
- sulcus increases from 0 to 3mm by forming a pseudopocket
- alveolar bone is normal on the radiograph but the probing depth has increasd
69
the steps of PMNs
~PMNs associated~
1. diapedesis
2. chemotaxis
3. adherence
4. phagocytosis
5. killing, digestion and aggregation
70
what is the early lesion
- 4 to 7 days without brushing or flossing
- acute inflammation persists, there is increased GCF, and pseudopocket formation
- cells of chronic inflammation appear and then **dominate,** we see IL-1 and IL-6.
**there is a shift from PMNS to t lymph = chronic.**
**collagen loss continues and MMPs activation begins**
71
how is collagen lost?
72
what is matrix metalloproteinases
MMPs
- proteases with activity against most, if not all, extracellulat matrix macromolecules
and important sub class of MMP is = interstitial collagenases.
73
histopathology of the early lesion
- loose up to **70%** of collagen
- caused by a **combination** of bacterial products and host defense system that cause the destruction
**PMN**s accumulate in gingiva --\> in the sulcus --\> chronic inflam cells (**t cell lesion**) accumulate --\> chronic predominates --\> fibroblsts show cell damage --\> rete pegs proleferation of JE into CT.
74
clinical features of an early lesion
1. edema of gingiva
2. increased GCF flow
3. loss of gingival stippling
4. erythema of gingival margin
5. no migration of JE attachmen t
6. alveolar bone is normal-no bone loss
7. reversible
75
what is the establish lesion host defenses
1. inhibit dramatic plaqu growth thus it
2. prevents infection becoming dramatically worse, but a
3. stand-off exits since plaque unable to be eliminated and there is a
4. shift to b-cell/plasma cell lesion
76
what is the established lesion
1. - acute inflammation persists, after 2-3 weeks it is a **stable** lesion
- but chronic inflammation dominates (**act b lymph --\> plasma cells\*\*) b cell lesion** which means production of abs
2. PMN wall tries to contain the infection, **micro-ulcerations of pocket epithelium,** JE not intact
3. Bystander damage
4. Two-edged "sword" of immune system
NO BONE LOSS and JE is still at CEJ
77
established lesion - ds activity
1. 2 processes: damage and repair
2. a shift to actived b cells to plasma cell lesion
3. highly vascular
4. immature CT
78
effect on the ground subtance during established lesion
79
when there is a loss of collagen there is
decreased rate of synthesis and increased rate of breakdown
(esp during the establish lesion)
80
during the established lesion although there is collagen loss there is also CT repair, how ?
1. attempt to minimze tissue damage
2. fibroblasts are cytokine regulated
3. recruitment of new cells like TGF beta, PDGF (cytokine regulated) or chemotatic collagen and elastin fragments
4. Tissue inhibitors of MMPs = TIMP "the shut down mechanism"
81
histopathology of the established lesion
1. damage of fibroblasts and eptihelium
2. loss of collagen
3. **microulcerations of pockeet epithelium**
4. acute inflamamtion still there
5. PMNs in pocket
6. degreadation of extracellular matric
7. defense infliltrate so t, b, and plasma cells
8. JE proliferation and extension into the CT so
9. Elongation fo rete peg ridges
82
clinical features of established lesion
edema
erythema
BOP
gingival cahnges
NO BONE LOSS
83
initial stages of gingivitis
time, cells, collagen loss, sulcular epithelium and clincial findings
84
**early stages of gingivitis**
## Footnote
**time, cells, collagen loss, sulcular epithelium and clincial findings**
85
**establish lesion of gingivitis**
**time, cells, collagen loss, sulcular epithelium and clincial findings**
86
the established lesion is the final stage of "pure gingivitis" this lesion can maintian stable for how long
weeks, months, years
for it to progess to periodontitis is hard to predict but host factors can identify the risk groups
87
what is the advanced lesion
PERIODONTITIS
- have pocket formation results from apical migration of JE
- loss of fiber attachment (cementum and PDL)
- LOSS OF BONE and irreversible
88
advanced leison features of periodontal breakdown
1. pocket formation through the destruction of PDL, apical migration of JE, and bone resportion
2. Asynchronous multiple burst model where there are short bursts of ds activity but long burst of quiescence
3. Bystander damage
4. Host balance of damage/repair is upset
89
during the advances lesion there is alveolar bone resportion, what is associated with this
- activation of osteoclasts
- ruffled border produced = **active site**
- hydrolytic enzymes are released
- cytokinesa are released (IL-1,-11, and TNF)
- prostaglandins are produced like PGE2
- leukotrienes are produced (inflammatory mediators and involved in allergic rxn)
90
advanced lesion mechansims of bone loss\*\*
- microbial factors: LPS
- activates inflammaroty cells to release IL-1 and PGE2
- activates PMNs to release collagenase
- **COLLAGEN LOSS**
- activates osteoclasts to release collagenase for bone (MMP-13)
91
histopathology of the advanced lesion
1. PMNs
2. b, plasma cells dominating
3. inflammatory infiltrate
4. extension of lesion into PDL and bone
5. loss of collagen continues
6. cytopathologically altered plasma cells
7. progressive pocket formation - **attachment loss**
8. quiescence and exacerbation
92
clinical features of advanced lesion
1. periodontal pocket formation
2. pocket epithelium ulceration
3. radiographic bone loss (**50% of vol/density needs to be lost before detected)**
4. Bleeding on probing
5. changes in gingival color, contour and consistency
6. attachment loss
7. mobility
93
immune cells overview
initial
early
established
advanced
initial - **PMNs**, macrophages
early - ^ + **t lymphocytes**
established AND established - ^ + b lymphocytes and **plasma cells**
94
tx of gingivitis
- reversible
- suppresion of microflora for plaque induced gingivitis (scaling, polishing, pt daily hygiene)
95
tx of periodontitis
- irreversible, no cure just **control**
- through suppresion of microflora with SRP maybe ab, surgery, maintenance
- Modulation of host with low dose doxycycline
96
doxycycline is
used at a low dose and it is a collagenase inhibitor
97
is plaque necessary to initial gingivitis and/or periodontitis
yes
98
does everybody that has poor plaque control eventually develop gingivitis
yes
99
does everyone that has gingivitis because of poor long term plaque control eventually develop periodontitis
no
100
plaque is the primary etiology for
both gingivitis and periodontits
no plaque (bacteria0 no ds
101
1. plaque is ___ and ____ to initiate gingivitis
2. plaque is ___ and ____ to initiate perdiodontitis
1. necessary and sufficient
2. necessary not sufficient
102
what is plaque dysbiosis
the primary etiology of periodontal ds is **bacterial plauqe in a susceptible host**
103
