Evolution of Inflamm Perio Lesion (Lecture 4) Flashcards
What are the 1st wave of cells to the inflammatory site?
Neutrophils (PMNs)
Interesting: Cytoplasmic granules of Basophils contain-Histamine (duh), Platelet Acivating factor, Heparin (anticoagulant-so why have platelet active..nvm), my favorite _____, and SRS-As (Slow-reacting substances of anaphylaxis-leukotrienes)
TNF-a
What are the 5 main cytokines/lymphokines released by monocytes/macrophages?
- IL-1 (osteoclastic activation, B-lymphocyte activation, and activation of CD8 lymphocytes)… 2. IL-6 (osteoclast activation) 3.TNF-a (activator of endothelium and inflammatory mediator) 4.INF (interferon – interferes with virus replication) 5.LIPID mediators of inflammation: prostaglandins, leukotrienes, and platelet activating factor (PAF)
What cell Activates macrophages, Activates CD8 (cytotoxic) T lymphocytes, and Activates B-lymphocytes to secrete immunoglobulin????
CD4 Helper T Lymphocyte
Which cell Destroys target cells by synthesis and release of cytotoxin, e.g., perforin and granzyme??
CD8 Cytotoxic Lymphocyte
What do CD8’s do their damage with? (4)
1.Cytotoxins (lymphokines) 2.INF-g 3.TNF-a 4. TNF-b
MOST DEFINITELY on the test: Cellular Stages of inflame—-Intial: _____……ACUTE: ______…..Chronic: _____
PMNs….PMNs, Macrophages, few Lymphocytes….FEW PMNs and Macrophages…MOSTLY Lymphocytes and Plasma Cells
________:defined as a dense localized collection of inflammatory cells, primarily neutrophils, accompanied by tissue necrosis. With time the accumulation of inflammatory cells are surrounded and walled off by immature connective tissue and proliferating capillaries.
Abscess
GINGIVITIS VS PERIODONTITIS! Plaque necessary
to initiate the disease?
G: YES P: YES
GINGIVITIS VS PERIODONTITIS! Clinical signs of inflammation?
G: YES P: MAYBE!!!
GINGIVITIS VS PERIODONTITIS! Bone loss
G: hell no P: hell YES
GINGIVITIS VS PERIODONTITIS! PDL destruction
G. nope P. yep
GINGIVITIS VS PERIODONTITIS! Apical migration of JE
G. nope P. yep
Does everybody with poor plaque control eventually develop gingivitis?
YES
Does everybody that has gingivitis because of poor long-term plaque control eventually develop periodontitis?
NO
_______ is necessary and sufficient to initiate gingivitis
Plaque
Plaque is necessary but not _______ to initiate periodontitis…IN ORDER to DEVELOP periodontitis it requires _________!!!!!
sufficient… A susceptible host!!!!!!
A patient’s _______ is extremely important in the pathogenesis of perio disease.
immunology
Immune system = provides a defensive process but also may account for most of the ________ observed in gingivitis and periodontitis
tissue injury
What did the Shri Lanka study show us?
That with uncontrolled plaque only 8% had rapid periodontal disease! 81% had mild progression and 11% had no problems!
The progression of perio disease is probably an ________ multiple burst model
asynchronous
Since perio disease is typically a ‘random burst model’ see your pt every ___ months.
3 months (bacteria take 9-12wks to recolonize)
What do we use to slow down MMP (metalo matrix proteinase)
deoxycycline
________: soluble, locally active polypeptides that regulate cell growth, differentiation and/or function
Cytokines
IMPORTANT CYTOKINES: Pro-inflammatory: stimulates osteoclasts, fibroblasts, macrophages
IL-1
IMPORTANT CYTOKINES: Pro-inflammatory: stimulates B and T cells
IL-6
IMPORTANT CYTOKINES: Pro-inflammatory: attract and activates PMNs
IL-8
IMPORTANT CYTOKINES: Pro-inflammatory: activate osteoclasts
TNF-a
IMPORTANT CYTOKINES: Vasodilation Pyrogenic Release mediator from mast cells Cell-mediated cytotoxicity
PGE2
What are the 4 Growth Factors?
TGF, PDGF, EGF, FGF
Is there Gingival Crevicular Fluid present in clinically healthy gingiva? Art there PMNs and Macrophages?
Yes there sure is!…yep a small amount of PMNs and MO’s
When does an INITIAL gingivitis inflammatory lesion develop?
2 to 4 days
REMEMBER: Acute = PMNs, Chronic = Lymphocytes
Increase in chronicity = _______
plasma cells
What are the two basic categories that virulence factors cause?
- Stimulates the host (IL-1, TNF-a,PGE2, LPS induced) 2.Degrades the host (hyaluronidase, collagenase, phospholipase a)
WHEN does the EARLY lesion develop? (NOT INITIAL lesion :)
4-7days
70% loss of collagen in gingival lamina propria.
Early Lesion
A chronic inflammatory cell infiltrate begins to appear, i.e., lymphocytes and macrophages.
Early Lesion
eginnings of pseudopocket formation.
Early Lesion
Loss of gingival stippling, Bleeding on probing
Early Lesion
The ____ gene family encodes 28 metal-dependent endopeptidases with activity against most, if not all, extracellular matrix macromolecules.
Matrix Metalloproteinases MMP
______ most active in periodontal disease: • Interstitial Collagenases • Stromelysins • Gelatinases • Metalloelastases
MMP’s
Host MMPs most active in periodontal disease are:
MMP-1 MMP-2 MMP-8 MMP-9 MMP-12 MMP-13
After ___-___ weeks the early lesion transitions to the established lesion.
2-3 weeks
No or slight histologic evidence of bone loss
established gingival inflammatory lesion
The _______ lesion is the final stage of
gingivitis
established
RETE PEGS in JE?
Early gingivitis
RETE PEGS and MicroUlcers in JE?
Established Gingivitis
The _______ Lesion: Alveolar bone resorption, Activation of osteoclasts, MMPs, Cytokines
• IL-1, IL-6, IL-8, TNF-α, Prostaglandins • PGE2, Leukotrienes
ADVANCED
What 3 things causes pocket formation in periodontitis?
1.Apical migration of JE 2.Loss of CT fiber attachment: Gingival fiber ligament, PDL 3. Loss of bone
What % of bone loss occurs BEFORE its detected on a radiograph????
30%-50% of volume/density needs to be lost before
detection on radiograph!!!!
What is the Normal CEJ-Bone Crest distance? (biological width)
1.5-2mm
