Exam #1 Review Flashcards
Gingivitis
Signs and symptoms that are confined to the gingiva
Presence of plaque that causes the issue
No CAL
Reversibility of the disease by removing the etiology
Periodontitis
Attachment loss
Chronic periodontiis
Slow to moderate progression
Seen in adults
Can be modified by systemic factors
Extent of chronic periodontitis
Localized = 30%
Severity of periodontitis
Slight = 1-2mm CAL Moderate = 3-4mm CAL Severe = 5+mm CAL
Aggressive Periodontitis
Systemically healthy
Familial aggregation
Localized Aggressive Periodontitis
Young patients
1st molars and incisors plus =2 other teeth
Generalized Aggressive Periodontitis
1st molars and incisors plus >2 other teet
Mendelian trait
If you have the gene, you have the trait
If you don’t have the gene, you don’t have the trait
Polygenic traits
Requires a bunch of different genes develop one phenotype
Represented on a bell curve (most people in the middle, but some on the extremes)
Periodontitis Association with Mendelian genetics
There are only certain periodontic conditions associated with single gene mutations
Ehlers Danlos Syndrome mutation
Collagen defects
Neutropenias mutation
Neutrophil anomalies
Leukocyte Adhesion deficiency mutation
B-subunit leukocyte adhesion molecule
Hypophosphetasia mutation
B-alkaline phosphatase
Papillon Lefevre syndrome mutation
Cathepsin C defect
Haim Munk Syndrom mutation
Cathepsin C defect
Prepubertal Periodontitis mutation
Cathepsin C defect
Affresive periodontitis mutation
Cathepsin C defect
Monozygotic twins
Have identical genes
Diazygotic twins
Share half of genes
Disease cause wholly or partially by genetic factors has a higher rate in what type of twins?
Monozygotic
If monozygotic twids are not fully concordinant, what does this tell us about a disease?
Environmental factors must be etiologic
What do twin studies tell us about periodontitis?
Monozygotic twins were twice as likely to develop chronic periodontitis than diazygotics
This suggests that genetics make an important contribution
What does a segregation analysis tell us?
Tells us the pattern of diseases segregating in families - can determine if occurence in family is constant with the genetic model
Which genetic model passes periodontitis?
Almost all of them
What did a linkage analysis tell us about the chromosomal location of aggressive periodontitis?
There are multiple forms and many locations where it can be found
How do you measure CAL?
CAL = PD + recession
What is biologic width measurement
2mm
KEratinized gingiva
The marginal gingiva and the attached gingiva
Free gingival groove
Junction between the attached gingiva and the marginal gingiva
Corresponds with the CEJ
Only observable in 30-40% of adults
Free gingival margin
Coronal end of the gingiva
Located 1.5-2.0mm coronal to the CEJ
Mucogingival junction
Border between the keratinized gingiva and the alveolar mucosa
What does the ‘width’ of the gingiva mean?
Height occluso-cervically
What does the ‘thickness’ of the gingiva mean?
Thickness B-L
T/F - The mucogingival junction moves as the tooth erupts
False - so when the tooth erupts, the entire gingiva moves with it. Since marginal or free gingiva is also fixed in dimensions, the width of the attached gingiva increases
What is the purpose of gingival fibers?
Reinforce the gingiva
Provide resilience and tone
Maintain architechtural form and integrity
What are the different types of gingival fibers?
Circular
Dentogingival
Dentoperiosteal
Transseptal
Circular fibers
Encircle the tooth like a cuff
Dentogingival fibers
Fan out from the supra-crestal cementum into the free gingiva
Dentoperiosteal fibers
Run from supra-crestal cementum into attached fibers
Transseptal fibers
Run from tooth to tooth and embed into the cementum
What are the different theories about plaque as an etiological agent?
Non-specific plaque hypothesis
Specific plaque hypothesis
Ecological Plaque hypothesis
Oral dysbiosis
Non-specific plaque hypothesis
Plaque control is important in perio treatment
All plaque is considered bad
Any accumulation of micro-organisms at or below the gingival margin causes inflammation
Specific plaque hypothesis
Specific organisms in the dental plaque are etiological agents
Not all bacteria are bad
This guides our clinical thinking today
Ecological plaque hypothesis
There are no ‘good’ or ‘bad’ bacteria, but only certain things the body can tolerate
If there is a shift in ecology, bad things can happen
Oral dysbiosis
Pathogens require 1’ colonizer for attachment, and possibly other things
Pathogens are always present, but their numbers spike when the environment changes
1’ Colonizers
Gram+ and Gram-
Streptococci that bind pellicle proteins
2’ Colonizers
Bridge species - F. nucleatum
3’ Colonizers
P. gingivalis
Quorum sensing
What does Regulation of expression of specific genes through accumulation of signaling compounds that mediate intracellular communication
Provides antibiotic resistance in dense biofilms
Encourages growth of beneficial species
What does quorum sensing depend on?
Cell density
Auto-inducer 1 or 2
Turns on in response to cell density
Pathogenic bacteria produce what in high levels?
AI-2
AI-2 may determine what?
The switch from comensal to pathogenic community
What is more resistant, planktonic or biofilm bacteria?
Biofilm bacteria are 1000-1500x more resistance than planktonic
What are biofilms more resistant?
They grow more slowly
-Antibiotics depend on cell turnover for efficacy
-Slow growers express ‘non-specific defense mechanisms’
Exopolymers retard diffusion
Biofilm bacteria express different genes
Exo-polymers
Retard diffusion
- ion-exchange mechanism prevents highly charged molecules from reaching deeper zones
- Extra-cellular enzymes inactivate antibiotics (B-lactamases, formaldehyde dehyrogenase)
Neutrophil chemotaxis
Neutrophils start in circulation
Presence of plaque can be communicated to the CT by proteases, LPS, F-Met-Leu-Phe
Those things talk to macrophages, which release cytokines (TNF, IL-1)
This increases adhesion molecule expression, and these can bind to neutrophils, which then go to the site
T-cell structure
2 glycoprotein chains (a and B) with variable segments
What do variable segments of T-cells determine?
The type of immune response
TCR in periodontitis
Differ before and after surgery
Differ between chronic and aggressive periodontitis
What are the two T-cell types and what do they differ in?
Th1 and Th2
They differ in cytokine profile
What cytokines coincide with Th1?
IL-2
IFN-y
TNF-a
What cytokines coincide with Th2?
IL-4 IL-5 IL-6 IL-10 IL-13
B-cell response
Humoral immunity triggered in response to soluble antigens
Ag-Ab complex
Activates complement
Facilitates opsonization
What T cells activate B-cell response?
Th2
What are the two types of B-cells?
Conventional (B2)
Autoreactive (B1)
Conventional B cells (B2)
Produce antibodies against bacteria
Levels decrease in healthy and treated sites
Autoreacttive B cells (B1)
Produce auto-antibodies
Levels do not decrease after treatment
IL-10
Con contribute to both Th1 and Th2
Normally knocks down cell-mediated response and increases humoral response
What is lots of IL-10 an indicator of?
Stabalized perio lesion
What is little IL-10 an indicator of?
Lesion is progressing
Initial lesion
Vasculitis subadjacent to JE
Exudaiton of fluid into tissue and gingival sulcus
Increased migration of leukocytes into JE and sulcus
Serum proteins present extravascularly
Alteration of the most coronal portion of JE
Loss of perivascular collagen
Early lesion
Accentuation of features of the initial lesion
Accumulation of lymphoid cells immediately subadjacent to JE
Cytopathic alteration in resident fibroblasts
Further loss of collagen network
Early proliferation of basal cells of JE
Inflammation changes are clinically evident
Established lesion
Persistence of features of acute inflammation
Increased proportion of plasma cells
Presence of extravascular immunoglobulins in CT, JE, and sulcus
Continuing loss of collagen and matrix
Proliferation and lateral extension of JE
Early pocket formation may be evident
No apical migration of JE or bone loss yet
Advanced lesion
Persistence of established lesion deatures
Increased proportion of plasma cells (~50%)
Extension of lesion into alveolar bone and PDL with significant bone loss
Continued loss of collagen fibers and matrix subadjacent to PE
Formation of pockets
Apical migration of JE
