The Inflammatory Periodontal Lesion Flashcards
- Plaque-induced
- Inflammation (edema/bleeding upon probing)
- No destruction of PDL & bone
- No apical migration of epithelial attachment
Gingivitis
Describe the destruction of PDL and bone and apical migration of epithelial attachment associated with gingivitis:
No destruction of PDL & bone
No apical migration of epithelial attachment
Epithelial attachment =
Junctional epithelium
- Plaque-indued
- Inflammation (edema/bleeding upon probing)
- Destruction of bone
- Apical migration of epithelial attachment
- Not all cases of gingivitis progress to periodontitis
Periodontitis
If you stop brushing & flossing will you develop gingivitis?
yes
Keystone pathogen of gingivitis:
p. Gingivalis & Aggregatibacter actinomycetemcomitans
If you stop brushing and flossing and develop gingivitis, and then you resume brushing and flossing with optimal oral hygiene, is the gingivitis reversible?
Yes
What determines if a case of gingivitis will progress to peridontitis?
the susceptibility of the host
What are some factors that result in a susceptible host in terms of gingivitis progressing to periodontitis?
- smoker
- diabetes
- immune conditions
T/F: Not all cases of gingivitis progress to peridontisis
True
In other words periodontitis is:
- _____ similar to gingivitis
- _____ (susceptible host)
- Each site is ____ or ____ environment
- A % of the affected population experiences _____
- The progression of the disease is probably..
- Plaque-induced
- Host-related
- individualized or specific
- severe destruction
- ….
Why does periodontal disease start in the posterior teeth?
Due to the gingival col-
it creates a perfect valley where bacteria can thrive
What bacteria are in the red complex?
- P. Gingivalis
- Tanerella Forsyth..
- 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 (1900-1950s)
What model of 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 extent may vary among sites
progressive model (1940-1960s)
What model of 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 radome areas of disease progression while some areas tend to be unaffected?
Asynchronous multiple burst model (1980-2000s)
What would be a reason for seeing bone loss progress more severely on the maxillary 2nd molar compared to the mandibular 2nd molar?
The maxillary teeth have a trifurcation vs. the bifurcation on the mandibular molars- this trifurcation can make it harder to keep clean
T/F: Maxillary teeth are less susceptible to perio disease than the mandibular teeth
False- maxillary teeth are more susceptible due to trifurcated roots
Which teeth are the least likely to be lost to periodontal disease?
Mandibular canine & mandibular 1st premolar
This is because the bone is more dense in the mamdinular in addition to the maxillary canine being next to the maxillary first premolar which has a mesial concavity leading to collateral damage)
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 line 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 of color in inflammation this is a sign of ______ and is due to _____
chronic inflammation; blood flow is stagnant
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
Any time the immune system goes out of control this can result in:
autoimmunity
T cells can differentiate into two forms:
CD4
CD8
T/F: The innate & adaptive immune system work completely separately
False- they 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
(one may have a heightened response compared to the other)
Molecules that are selected 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; critical because it can stimulate osteoclasts (destructive), fibroblasts & macrophages:
IL-1
What destroys bone- Osteoclasts or osteoblasts?
Osteoclasts
Periodontal susceptibility test looks for:
IL-1 genotype
Pro-inflammatory cytokine, stimulates T & B cells:
IL-6
Pro-inflammatory cytokine, attracts & activates PMNs:
IL-8
In women, this cytokine is regulated by estrogen levels:
IL-6
Pro-inflammatory cytokine that activates osteoclasts:
TNF
Cytokine that is responsible for vasodilation, is pyrogenic, releases mediator from mast cells and is involved in cell-mediated immunity:
PGE2
Whenever there is tissue breakdown ____ is released
Prostaglandin
Growth factor that stimulates/heals epithelial cells and fibroblasts:
TGF
Growth factor that stimulates/heals fibroblasts:
PDGF & FGF
Growth factor that stimulates/heals epithelial cells:
EGF
FGF:
Fibroblasts growth factor
EGF:
Epithelial growth factor
What causes bleeding upon probing when pressure is too hard:
ulceration of junctional epithelium
In health when we probe, the probe stops short of the:
junctional epithelium
When probing, if the sulcular epithelium is intact:
there will be no bleeding upon probing
When probing, if the sulcular epithelium is NOT intact, this would result in:
bleeding upon probing
What situation might there be an absence of bleeding upon probing if someone has gingivitis/periodontitis?
smokers
Can we accurately predict which patients with gingivitis are going to develop periodontitis?
Exactly- no, but we can identify risk factors
so one appointment no, but if we are seeing the patient over time and are seeing the etiology and knowing the risk factors it is easier to predict
Risk factors for gingivitis progressing into periodontitis?
- habits (smoking)
- systemic disorders (HIV & DM)
Patients with risk factors are more likely to have:
attachment loss
In clinically health 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
List some examples of GENETIC inflammatory modifiers: (9)
- agranulocytosis
- neutropenias
- lazy leukocyte
- leukocyte adhesion deficiency (LAD)
- Down’s syndrome
- Papillon-Lefevre
- Hypophosphatasia
- Chediak-Higashi
- Ehlers-Danlos syndrome
A condition that may cause young kids to have susceptibility to periodontal disease:
Hypophosphatasia
Initial lesion of gingivitis develop in:
2-4 days
- developed in 2-4 days
- cells of acute inflammation present
- increased GCF flow
- start of pseudopocket formation
Initial lesion
Cells of acute inflammation:
PNMs
Cells of chronic inflammation:
Lymphocytes
As inflammation increases in chronicity what cells may be present?
Plasma cells
What are the 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 ____ (example: ____) & ____
cytokines (i.e. IL-1, TNF & PGE) & chemoattractant factors (IL-8)
Virulence factors that degrade host tissues are enzymes which include: (4)
- collagenase
- trypsin-like enxymes
- keratinase
- phospholipase A
Early lesions of gingivitis develop in:
4-7 days
- Develop in 4-7 days
- acute inflammation persists, increased GCF, pseudopocket formation
- cells of chronic inflammation appear and then dominate
Early lesion
Describe the shift of cells present we see from initial lesions to early lesions:
PNMs —-> T lymphocytes
Early lesions may also be known as:
T cell lesion
What is the dominate cells of early lesions?
T cells
In early lesions _____ loss 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
What causes the loss of collagen in an established lesion? (2)
- decreased rate of synthesis
- increased rate 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
- PNMs
- extracellular matrix
- T-cell, B-cell & plasma cell
- JE; CT
- rete peg ridges
Attachment loss precedes bone loss by about:
6 months
