The Inflammatory Periodontal Lesion Flashcards
- plaque induced
- inflammation (edema/bleeding upon probing)
- no destruction of PDL and bone
- no apical migration of epithelial attachment
Gingivitis
Describe the destruction of PDL and bone and apical migration of epithelial attachment with gingivitis:
No destruction of PDL & bone
No apical migration of epithelial attachment
Epithelial attachment =
junctional epithelium
- plaque-induced
- inflammation (edema/bleeding upon probing)
- destruction of bone
- apical migration of epithelial attachment
Periodontitis
If you stop brushing & flossing will you develop gingivitis?
yes
Keystone pathogens of gingivitis:
p. gingivalis & Agregatibacter actinomycetecomitans
If you stop brushing and flossing and develop gingivitis, start brushing again and have optimal oral hygeine, is the gingivitis reversible?
yes
What are some factors that make someone a susceptible host for periodontitis?
diabetics, smokers, immune conditions
T/F: Not all cases of gingivitis progress to periodontitis
True
In other words, periodontitis is:
- ______ similar to gingivitis
- _____ ( susceptible host)
- Each site is ___ or ____ environment
- A % of affects population experiences _____
- The progression of the disease is probably…
- plaque-induced
- host-related
- individualized or specific
- severe destruction
- ….
Models of disease progression:
- continuous model (1900 -1950s)
- progressive model (1940-1960s)
- Random burst model (1980s-2000s)
Why does periodontal disease start in the posterior teeth?
Due to the gingival col- it creates a perfect valley where bacteria can thrive and the tissue is NON-keratinized
Red complex: (3)
P. gingivalis
T. Forsynthia
T. Denticola
The red complex species are associated with:
- bleeding upon probing
- progressive bone loss
- progressive attachment loss
What model of disease progression states “continuous through life at same rate of loss”
Continuous Model
What model disease progression coincides with the following example:
“everyone gets perio disease”
Continuous model
What model of disease progression states:
- progressive loss over time of some sites
- no destruction in others
- time of onset and extends vary among sites
Progressive model
What model disease progression coincides with the following example:
” periodontal disease affects mainly posterior teeth”
Progressive model
What model of disease progression tends to fit best when there are random areas of disease progression while some areas seem to be unaffected?
Asynchronous multiple burst model (1980s-2000s)
T/F: Maxillary teeth are less susceptible to perio disease than mandibular teeth
false- maxillary teeth more susceptible due to the trifurcated roots
What would be the reason for seeing bone loss progression more severely on the maxillary 2nd molars compared to the mandibular second molar?
The maxillary teeth have trifurcation vs. the bifurcation on the mandibular molars- this trifurcation can make it harder to keep clean
What teeth are least likely to be lost to perio disease?
mandibular canine & mandibular 1st premolar
(because the maxillary canine is right next to the first premolar which has a mesial concavity)
Signs of inflammation: (5)
- rubor (redness)
- calor (heat)
- dolor (pain)
- tumor (swelling)
- functio laesa (loss of function)
When there is an insult to the body - the first Lin e of defense is ____ and the body sends these players to the area by _____.
WBCs (neutrophils)
Dilation of blood vessels
Inflammation is a ____ phenomenon
vascular
When you see purplish change in the gingiva this is a sign of:
stagnant blood flow (chronic inflammation)
What type of cells are the “migrators” in inflammation?
leukocytes
Signs of vasculitis in an inflammatory response include:
- dilation
- venous stasis (congestion)
- increased permeability (transudate & exudate)
List some examples of innate immunity:
- skin
- saliva
- gingival crevicular fluid
Anytime the immune system goes out of control, this can result in:
autoimmunity
T cells can differentiate into 2 major forms:
CD4 & CD8
T/F: The innate and adaptive immune system work completely separate
False- the adaptive immune system goes back and helps out the innate immune system and they kinda work together
Two individuals with
- Same plaque
- Same amounts of bacteria
- Same species of bacteria
One person develops periodontitis and the other does not. Why might this be?
Due to the host immune response differing
Molecules that are secreted to send signals to other cells. A component of humoral immunity:
Complement
Bacteria cause disease when _____.
attach to the epithelium
One of the biggest mediators of destruction in periodontal disease:
Cytokines
Pro-Inflammatory cytokine: stimulates osteoclasts, fibroblasts macrophages
IL-1
What destroys bone, osteoclasts or osteoblasts?
osteoclasts
Pro-inflammatory cytokine: stimulates T and B cells:
IL-6
Pro-inflammatory cytokine: attracts and activates PMNs:
IL-8
Pro-inflammatory cytokine: activates osteoclasts
TNF
Cytokine that is responsible for vasodilation, is pyrogenic, releases mediator from mast cells and is involved in cell-mediated cytotoxicity:
PGE2
In women, what cytokine is regulated by estrogen levels, causing more issues in menopausal women?
IL-6
Whenever there is tissue breakdown, ____ is released
prostaglandin
Growth factor that stimulates epithelial cells AND fibroblasts:
TGF
Growth factors that stimulates fibroblasts: (2)
PDGF & FGF
Growth factor that stimulates/ heals epithelial cells:
EGF
FGF:
Fibroblast growth factors
EGF:
Epithelial growth factor
What causes bleeding upon probing?
ulceration of the junctional epithelium
In health when we probe, the probe stops short of the:
junctional epithelium
When probing, if the sulcular epithelium is in tact:
there will be no bleeding upon probing
When probing, if the sulcular epithelium is NOT in tact, this would result in:
bleeding upon probing
What situation might there be abscence of bleeding upon probing if someone has gingivitis/periodontitis?
smokers
Can we accurately predict which patients with gingivitis are going to progress to periodontitis?
Exactly, NO but we can identify risk factors
Risk factors for gingivitis progressing into periodontitis?
- habits (smoking)
- systemic disorders (HIV and diabetes)
Patients with risk factors are more likely to have:
attachment loss
In clinically healthy gingiva
1. Some ____ and ____ are present in connective tissue
2. A few ____ are migrating through the ___
3. No ____ destruction
4. Intact ____ barrier
5. ____ is present
6. Appears _____ healthy (color, contours, consistency)
- neutrophils & macrophages
- neutrophils; JE
- collagen
- epithelial
- gingival crevicular fluid
- clinically
A condition that may cause young kids to have susceptibility to periodontal disease:
Hypophosphotasia
List some examples of GENETIC inflammatory response modifiers: (9)
- Agranulocytosis
- Neutropenias
- Lazy leukocyte
- Leukocyte adhesion deficiency (LAD)
- Down syndrome
- Papillon-Lefevre
- Chediak-Higashi
- Hypophosphatasia
- Ehlers-Danlos syndrome
Initial lesion of gingivitis develops in:
2-4 days
- Develops in 2-4 days
- Cells of acute inflammation present
- Increased GCF flow
- Start of pseudo-pocket formation
Initial lesion
Cells of acute inflammation:
PMNs
Cells of chronic inflammation:
lymphocytes
As inflammation increases in chronicity what cells may be present?
Plasma cells
What are two types of virulence factors?
- stimulation of the host defense systems
- Degradation of host tissues
Virulence factors that stimulate the host defense systems stimulate cells to release ____ (examples: ____) & _____ (example: ___)
cytokines (ie. IL-1, TNF and PGE) & chemoattractant factors (ie. IL-8)
Virulence factors that degrade host tissues are enzymes which include: (4)
- collagenase
- trypsin-like enzymes
- keratinase
- phospholipase A
Early lesion of gingivitis occurs in:
4-7 days
- Develops in 4-7 days
- Acute inflammation persists (from initial lesion)
- Increase GCF
- Pseudopocket formation
- Cells of chronic inflammation appear and then DOMINATE
Early Lesion
Describe the shift of cells present we see form initial lesions to early lesions:
PMNs—> T Lymphocytes
Early lesion may also be known as:
T-Cell lesion
What is the dominate cell of early lesion?
T-cells
In early lesions, ______ continues and _______ begins
collagen loss; MMPs Activation
Clinical features of early lesion: (7)
- Edema of gingiva
- Increased GCF flow
- Loss of gingival stippling
- Erythema of gingival margin
- No migration of JE attachment
- Alveolar bone is normal- no bone loss
- Reversible
If you see a patient that has bleeding upon probing, what stage of lesion presents?
Established
Established lesion is characterized by breakage in the:
sulcular epithelium
The established lesion is characterized by loss of:
collagen
The loss of collagen in an established lesion results in: (2)
- decreased rate of synthesis
- increased rate of breakdown
Histopathology of the established lesion:
- Cellular damage of _____ & ____
- ____ loss increases
- ____ of pocket epithelium
- Persistence of ____
- Marked numbers of _____ in pocket
- Degradation of _____
- Dense ___, ___, & ___ infiltrate
- ____ proliferation & extension into ___
- Elongation of ___
- fibroblasts & epithelium
- collagen
- micro-ulcerations
- acute inflammation
- PMN’s
- extracellular matrix
- T-cell, B- cell, & plasma cell
- JE; CT
- rete peg ridges
Attachment loss ____ bone loss by about _____
PRECEDES; 6 months
