Week 4 Flashcards
What are the 5 methods of measuring gingivitis/periodontitis discussed in lecture?
- Plaque index- measure of plaque,
- Gingival Index- redness and inflammation,
- Pocket depth,
- Gingival Crevicular Fluid- inflammatory exudate collected with paper points or perio papers measure rates of paper taking up fluid,
- Bleeding on Probing- least biased
Which are the most subjective and best measures for gingivitis status?
BOP is least biased along with GCF flow rate.
What are the 3 major differences between Plaque Induced Gingivitis and Periodontitis as discussed in the Lecture?
- No bone loss 2. No attachment loss 3. Gingivitis is Reversible
Can someone have attachment and or bone loss and still have gingivitis? If so under what condition is highlighted in your lecture?
A site with previous bone loss but no current progression. Grey area not on exam- probably perio
What type of bacteria benefit from primary colonizers and the increasing reduced environment of the developing biofilm (decreasing oxygen)?
Facultative Gram-negative rods
What was a limitation of Loe et al. 1965 in identifying bacteria associated with gingival health and disease?
Just looked at plaque and bacteria, it was small too. Blamed plaque. Only types of bacteria not species or strains.
What was a limitation of Socransky et al. 1998 in the Checkerboard DNA-DNA hybridization approach?
They only looked at 43 species. Older methods- new high throughput could identify more potential bacterial. Did not look at host genetic and immune response.
Do these two studies are foundational in gingival health and disease research. What evidence in your lecture suggests that they may be out of date?
The number of different species, immune responses, saliva flow and content differences. Modern methods.
What are the major shifts in types of bacteria from Healthy to Gingivitis?
Gram positive Aerobes to facultative anaerobes and gram-negative rods
What is significant about microbial complexes defined by Sorcransky? What is the Orange complex associated with? What is the Red Complex associated with?
They linked them to stages of disease. Orange= Gingivitis and early periodontitis Red = periodontitis
Orange: P intermedia, P nigrescens, P micros, F. nuc nucleatum, F nuc vicentii, F nuc polymorphum, F periodonticum
Red: P. gingivalis, T forsythia, T denticola
Is the epidemiology of gingivitis well established? Why or Why not?
There is still work to be done because of how complex it is
- Describe the periodontal diseases.
- Perio- Inflammation and destruction of the tissues supporting the teeth resulting in attachment loss.
- Chronic perio- slow to moderate progression that is aggravated by systemic or environmental factors
- Aggressive perio- Rapid progression both localized and generalized
- Necrotizing perio- Trench mouth, painful, fusospirochaetal etiology
Describe the Koch’s Postulates and its limitations within the periodontal diseases.
Subject has disease, Take organism causing disease- pure culture, transfer it, watch it cause disease, isolate same organism from 2nd diseased subject. Doesn’t work as well for oral disease because there are many causes that all tie together from pathogens to host response. Pathogens are there in health and disease- in different amounts. Some can’t be grown in lab easily.
Compare and contrast between the “Specific Plaque Hypothesis”, “Non-Specific Plaque Hypothesis”, and “Ecological Plaque Hypothesis”.
- Specific ▸Pathogenicity of plaque depends on the presence of, or relative increase of, specific microorganisms.▸Not all plaque bacteria are equally pathogenic▸Can be used to explain A. actinomycetemcomitansin localized aggressive periodontitis
- Non-specific▸Periodontitis caused by dental plaque as a whole, accumulating over time on the teeth. ▸All plaque bacteria equally capable of causing disease Describe the etiology of caries and periodontitis as explained by the different plaque hypothesis. (Be prepared to provide specific examples).
- Ecological- Disease is a result of an imbalance in the total microbiome due to ecological stress, resulting in an enrichment of disease-related microorganisms. Everything including our reactions are caused by the bacteria.
Define keystone pathogen hypothesis and its significance in disease progression. (Be prepared to provide examples).
One pathogen P gingivalis can throw things off and cause dysbiosis. Low numbers of a keystone pathogen can disproportionately modulate the host response. This includes our specific different genetic immune response- host genetic factors vary and cause different outcomes.
Understand the concept of homeostasis and dysbiosis in relation to health and disease.
Bacteria can combine together to cause disease when they aren’t harmful alone. Specifically T Forsythia and F nucleatum.
P gingivalis can trigger a community to become more pathogenic.
Identify and describe the five common mechanisms of pathogenesis.
- Colonization and adhesion- fimbrea
- Invasion- ruffling and Zipping
- Enzymes- proteases
- Toxins and Cell Constituents
- Subversion of host immunity
Identify the major adhesions of periopathogens.
Auto aggregation- binding to others of same species
Co-aggregation- binding to genetically distinct microbial partners
P. gingivalis-
- FimA fimbriae- Integrin receptors on host cells; GAPDH on streptococcal surfaces; T. denticola dentilisin; host matrix proteins; lactoferrin and hemoglobin,
- Mfa1-Streptococcal surface proteins SspA/B,
- Hemagglutinins- RBS and other host cells; extracellular matrix components
A. a-
- Flp1- Intraspecies binding, salivary components
F. Nucleatum-
- FadA- Attachment and invasion of epithelial and endothelial cells,
- FomA-Interspecies binding,
- RadA –Arginine-containing receptors; interspecies binding
T forsythia-
- BspA- Epithelial cells, matrix proteins, interspecies binding, salivary agglutinins, epithelial cell invasion and alveolar bone loss in mice
Describe “Ruffling” and identify the pathogens capable of this technique.
P. gingivalis and A. a.
Engulfment of bacteria by non-phagocytic epithelial cells into vacuoles- allow spread into other tissues and evasion of immune responses
Describe the “Zipping” mechanism, the proteins involved, and the oral bacteria that does this.
F. nucleatum
FadA adhesion binding that triggers uptake like a zipper into vacuole in cell
Be able to match a bacterial toxin to their respective periopathogen.
A.a. - leukotoxins kill neutrophils and monocytes, Cytolethal distending toxin/Cdt DNase
Gram neg- LPS/Lipid A
Anaerobes- Fatty Acids-propionic, butyric, iso-butyric
Describe the mechanisms employed by Porphyromonas gingivalis in subverting host defense.
Gingipains- proteases
Cytokine paralysis- Inhibits/disrupts IL 8 gradient with SerB enzyme that binds IL 8 transcription factor so no IL 8 is made and neutrophils don’t where to go
Subvert Complement Pathway
Antagonize TLR4 recognizes LPS/Lipid A ie turning off the inflammatory response so host can’t fight it and other pathogens
Can agonize the host response too.
TLR 4 recognizes LPS triggers IL1 and TNF alpha cytokines which trigger metallomatrix proteases which cause tissue destruction
Define antagonism and agonism.
Agonizing is turning something on and antagonizing turns things off
Up regulating versus down regulating
- Understand the unique characteristics of Porphyromonas gingivalis LPS.
Changeable LipidA/LPS- 4-5 tails with different structures that antagonize TLR4
Also can agonize host response- TLR 4 recognizes LPS triggers IL1 TNF alpha cytokines which trigger metallomatrix proteases which cause tissue destruction
- Provide at least two examples of the link between oral and systemic health/disease.
Atherosclerosis,
Diabetes,
Pregnancy complications,
CRC/Colorectal Cancer, IBS (Galgnac is a receptor in colon that F nucleatum likes and may be a competitive inhibitor of lymphocytes)
▸Low grade bacteremia; spread/infection of oral bacteria to other tissues
▸Increase in inflammatory burden systemically
▸Autoimmune responses triggered by bacterial products
