The Inflammation Periodontal Lesion (initial, early, established, advanced) Flashcards
1
Q
What is gingivitis?
A
- Plaque-induced
- Inflammation (edema/BOP)
- No destruction of PDL and bone
- No apical migration of epithelial attachment
2
Q
Where is the epithelial attachment (juntioncal epithelium) at in health?
A
the CEJ
3
Q
What is periodontitis?
A
- Plaque-induced
- Inflammation (edema/BOP)
- Destruction of bone
- Apical migration of epithelial attachment
- Not all cases of gingivitis progress to periodontitis
4
Q
What two big things lead to periodontitis?
A
- plaque-induced
- host-related (susceptible host)
5
Q
What type of teeth are more susceptible to periodontisis (posterior or anterior)?
A
posterior
- bc of the col (nonkeratinized epithelium)
6
Q
What are the models of disease progression for periodontitis?
A
*Continuous model
*Progressive model
*Random burst model
*Asynchronous multiple burst model
7
Q
What is the continous model of periodontitis?
A
- continuous throughout life at same rate of loss (everyone gets perio)
- 1900-1950s
8
Q
What is the progressive model of periodontitis?
A
- progressive loss over time of some sites
- no destruction in others
- time of onset and extent vary among sites
- 1940-1960s
9
Q
What is the random burst model of periodontitis?
A
- acitivity occurs at random at any site
- some sites show no activity
- some sites have one or more bursts of activity
- cumulative extend of destruction varies among sites
- Periodontitis is different in various sites in the same individual and it is difficult to predict attachment loss
- 1980-2000s
10
Q
Why would this area have more bone loss than other areas on the same patient?
A
slightly open contact allows for food impaction (more bone loss)
11
Q
What is the asynchronous multiple burst model of periodontitis?
A
- several sites have one or more bursts of activity during one period of life
- prolonged period of inactivity (remission
- some sites don’t develop attachment loss
- bursts due to risk factors
- cumulative extend of destruction varies among sites
- 1980-2000s
12
Q
Why are the mandibular molars not having as much bone loss as the maxillary?
A
- maxillary molar furcations are closer to the col than in mandibular
- maxilla bone is more cancellous while mandibular is more cortical
13
Q
What is the most common tooth lost to periodontitis?
A
maxillary 2nd molars
14
Q
What are the least common teeth lost to periodontitis?
A
mandibular canine/premolars
15
Q
What makes maxillary premolars more likely to develop periodontitis?
A
mesial concavity
- this is the reason the max canine is also likely to develop periodontitis
16
Q
What are the signs of inflammation?
A
- rubor (red)
- calor (heat)
- dolor (pain)
- tumor (swelling)
- functio laesa (loss of function)
17
Q
Inflammation is a __________ phenomenon
A
vascular
18
Q
What does inflammation involve?
A
- Leukocyte migration
- Vasculitis
— dilation
— venous stasis (congestion)
— increased permeability (transudate, exudate)
19
Q
What is the 1st immune defense?
A
innate (non-adaptive, genetic)
- kills by phagocytosis
- monocytes/macrophages
- PMNs
20
Q
What is the 2nd immune defense?
A
adaptive (production of immunoglobulins by antibodies)
- highly specific
- B/T cells
- plasama cells produce antibodies
21
Q
What are B lymphocytes?
A
- activated B cells are plasma cells (produce immunoglobulins)
22
Q
What are T lymphocytes?
A
- developed in the thymus
- several functions (antigen presentation)
- help B-cells divide; destory virally infected cells; down-regulate immune response
23
Q
What are the CD4 T cells?
A
MHC class II molcuels
- T helper cells
— help B cells divide
— activate innate cell lining
24
Q
What are the CD8 T cells?
A
MHC class I molecules
- T cytotoxic
— destory virally infected target cells
25
What are the different antibodies?
* IgM: first responder
* IgG: second responder; most abundant
* IgA: salivary
* IgD: co-expressed with IgM
* IgE: mast cells; allergic reaction
26
What cells use IgE?
Mast cells
| (important)
27
What is the complement system?
part of both innate and adaptive immunity systems (biological cascade tha helps clear pathogens by lysis, opsonization, binding, and clearance of immune complexes)
28
What are T suppressor cells?
T-regulatory cells
- down regulate T and B cells
- prevent autoimmune disease
29
What are killer cells?
mononuclear cells that kill cells sensitized with antibody
30
What are natural killer cells?
kill virally infected and transofrmed target cells that have not been previously sensitized
31
Monocytes become activated in connective tissue to form...
macrophages
| (important)
32
What are cytokines?
- soluble, locally active polypeptides
- regulate cell growth, differentiation, function
- produced by cells of the immune system
33
Specific cytokines may have different biologic properties dependent on...
- their concentration
- the cells that produce them
- the cells being attracted and acted upon
- presence and extent of ECM
34
What is IL-1?
pro-inflammatory: stimulates osteoclasts, fibroblasts, macrophages
35
What is IL-6?
pro-inflammatory: stimulates T and B cells
36
What is IL-8?
pro-inflammatory: attracts and activates PMNs
37
What is TNF?
pro-inflammatory: actives osetoclasts
38
What are the growth factors?
TGF - Stimulates epithelial cells and fibroblasts
PDGF - Stimulates fibroblasts
EGF - Stimulates epithelial cells
FGF - Stimulates fibroblasts
39
Can we accurately predict which patients with gingivitis are going to develop to periodontitis?
NO
- we only can identify risk factors
40
What are the risk factors for periodontitis?
- smoking
- HIV and diabetes (systemic disorders)
41
What are the histologic phases of periodontal disease?
1. Normal
2. Initial gingival lesion
3. Early gingival lesion
4. Established gingival lesion
5. Advanced gingival/periodontal lesion
42
What does clinically healthy gingiva look like?
- some neutrophils and macrophages are present in connective tissue
- few neutrophils are migrating through JE
- no collagen destruction
- intact epithelia barrier
- gingival crevicular fluid is present
- appears clinically healthy
43
What are the mechanical inflammatory response modifiers?
- calculus
- caries
- restorations (defects, margins, over contoured)
- prosthesis
- tooth anatomical factors
44
What are the systemic inflammatory response modifiers?
- uncontrolled diabetes
- hormonal (puberty/pregnancy)
- HIV/AIDS
- medications
- PMN defects
- hematological
- immune disturbances
- nutrition deficiencies
45
What are the genetic inflammatory response modifiers?
- luekocyte adhesion deficiency (LAD)
- hypophosphatasia
- agranulocytosis
- neutropenias
- lazy leukocyte
- down syndrome
- papillon-lefevre
- chediak-higashi
- ehlers-danlos syndrome
46
What is the intial lesion?
- develops in 2-4 days
- cells of acute inflammation present
- increased GCF flow
- start of pseudopocket formation
47
Acute inflammation has what cells?
PMNs
48
Chronic inflammation has what cells?
lymphocytes
49
What are the 2 types of virulence factors?
- stimulation of host defense system
- degradation of the host tissues
50
What happens when there is poor plaque control (early)?
- Bacterial byproducts are released into the periodontal tissues (virulence factors)
- Stimulation of epithelial cells and fibroblasts to release **IL-8** into the CT which attracts and activates PMNs
- PMNs are present in the connective tissue
- PMN’s are attracted to and near JE and sulcular epithelium
| (know IL-8)
51
What are the clinical features of the inital lesion?
- increased GCF flow
- sulcus increases from 0-3 mm (pseudopocket)
- alveolar bone is normal on the radiograph
52
What do selectins do?
slow the PMNs and cause them to roll during diapedesis
53
What are the features of the early lesion?
* 4-7 days
* acute inflammation persists, increased GCF, psueopocket
* cells of chronic inflammation appear and dominate (shift from T cells to PMNs)
* collagen loss continues
* MMPs activation begins
54
Collagen loss is around ___% in the early lesion
70%
| (important)
55
What are matrix metalloproteinases (MMPs)?
28 metal-dependent endopeptidases with activity against most, if not all, ECM macromolecules
56
What is the histopathology of the early lesion?
- PMNs accumulate in gingiva
- PMNs accumulate in sulcus
- cells of chronic inflammation accumulates and predominates
- fibroblasts show cell damage
- rete pegs proliferation of JE into CT
57
What are the clinical features of early lesion?
- 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
58
What do the host defenses do during established lesion?
- inhibit dramatic plaque growth
- prevents infection
- shift to a B cell lesion
59
What is an established lesion?
1. acute inflammation persists (2-3 weeks)
2. PMN wall (host tries to contain the infection
**- micro-ulcerations of pocket epithelium (BOP)**
3. Bystander Damage
4. NO bone loss
60
When is there microulcerations (bleeding on probing)?
established lesion
61
What is the disease activity during an established lesion?
*Damage
*Repair
*Shift to activated B cells (plasma cells)
*highly vascular
62
What are the clinical features of an established lesion?
- edema
- erthema
- BOP
- gingival changes
- no bone loss
63
What is the histopathology of the established lesion?
- cellular damage of fibroblasts
- collagen loss increases
- microulcerations
- persistence of acute inflammation
- marked numbers of PMNs
- degradation of ECM
- JE proliferation
- elongation of rete peg ridges
64
What is the time for an initial, early, and established lesion?
initial - 2-4 days
early - 4-7 dyas
established - 14-21 days
65
What are the cells for an initial, early, and established lesion?
initial - PMNs
early - T-cell
established - B-cell or plasma cell
66
What is the collagen loss level for an initial, early, and established lesion?
initial - perivascular
early - CT up to 70%
established - more than 70%
67
What is the sulcular epithelium makeup for an initial, early, and established lesion?
initial - infiltrated with PMNs
early - rete pegs
established - more rete pegs; microulcerations
68
What are the clinical findings for an initial, early, and established lesion?
initial - increased GCF
early - erythema and increased GCF
established - changes in color, size, and texture; BOP
69
What are the features of periodontal breakdown?
- pocket formation (PDL destruction, apical migration of JE, bone resorption)
- asynchronous multiple burst model
- bystander damage
- host balance of damage and repair is lost
- alveolar bone resorption
70
Pocket formation results from apical migration of...
JE (junctional epithelium)
71
What is the histopathology of the advanced lesion?
- B-cells, plasma cells dominate
- progressive pocket formation (attachment loss)
- PMNs
- inflammatory infiltrate
- extension of lesion into PDL na dbone
- loss of collagen continues
72
What are the clinical features of the advanced lesion?
- periodontal pocket formation
- pocket epithelium ulceration
- radiographic bone loss
- BOP
- changes in gingival color, contour, consistency
- attachment loss
- mobility
73
What is are the cells for inital lesion?
PMNs, macrophages
74
What is are the cells for early lesion?
PMNs, macrophages, T-cell
75
What is are the cells for established lesion?
PMNs, macrophages, T-cells, B-cells, plasma cells
76
What is are the cells for advanced lesion?
PMNs, macrophages, T-cells, B-cells, plasma cells
77
What is the treatment for gingivitis?
- scaling
- polishing
- patient's dialy removal of plaque
78
What is the treatment for periodontitis?
- No cure for periodontitis (only control)
- scaling and root planing
- surgery
- low dose doxycycline
79
Plaque is necessary and sufficient to initiate ___________
gingivits
| plaque is neccessary but not sufficient to initiate periodontitis
80
The primary etiology of periodontal disease is...
Bacterial plaque in a susceptible host
