Lecture 3 Flashcards
What are 6 infections in the oral cavity?
Caries
Periapical lesions
Fungal
Viral
Abscesses
Periodontal
Difference b/t gingivitis and periodontitis?
Periodontitis has attachment loss and bone loss
Those with periodontitis may experience how much attachment loss?
0.1 mm/year loss of attachment
If periodontitis is present, what else is happening?
Gingivitis
T/F - Patients can go flux back and forth from periodontal health to periodontal disease.
TRUE
What are the 3 triangles that confluence into the disease triangle?
Microbial plaque
Genetics/Host factors
Acquired/Environmental factors
What is the most elementary distinction to be made during periodontal diagnosis?
Differentiation b/t health, gingivitis, and periodontitis
T/F - SRP is done with periodontitis, but not necessarily with gingivitis.
TRUE
What is Koch’s Postulates?
Take a pathogen from diseased tissue, grow it, and re-isolated it to show the causative agent of an infectious disease
What is the route PMNs take to get to site of infection?
Blood vessels -> CT -> Junctional epithelium -> Site of infection
1965 study on dental plaque.
Students underwent a rigorous program to have periodontal health.
One half the class did not brush teeth
Other half the class did brush teeth
What were the major findings of Loe, 1965?
Time necessary for clinical gingivitis to occur varied from 10-21 days
Re-institution of oral hygiene resulted in resolution of gingival inflammation in about 1 week
Appearance of gram (-) flora preceded the onset of clinically detectable gingivitis by 3-10 days.
What 2 results were drawn from the Loe study?
Showed gingivitis could be experimentally produced in humans by allowing plaque to accumulate
Reversal of gingivitis can be accomplished by plaque removal
T/F - If you’ve had gingivitis, then you are at the greatest risk for gingivitis and periodontitis.
TRUE
Clinical health means what?
What we see clinically
Does not mean that that site is physiologically healthy
What is the nonspecific plaque hypothesis?
Increased plaque mass directly related to increased severity of disease
What is the 1970’s model of periodontal disease?
Poor oral hygiene
Bacterial plaque formation
Calculus formation
Periodontal pockets
Alveolar bone loss
Tooth loss
3 things believed in the 70s about periodontal disease?
All bacteria on tooth surface are harmful
Host response important and protective against bacteria from invading
Gingivitis progresses to periodontitis with bone and tooth loss
- Untreated periodontitis progresses slowly and steadily
- all individuals and all teeth are susceptible
- Hygiene and age are major risk factors for disease
Does gingivitis always lead to periodontitis.
No. Not always
What is the specific plaque hypothesis from the 70s and 80s?
Single or limited number of periodontopathic organisms are responsible for disease and severity of disease
T/F - Both the specific and nonspecific hypotheses are very dependent on the potential direct pathologic effects of dental plaque.
TRUE
Name some enzymes that cause tissue destruction.
Collagenase
Hyaluronidase
Chondroitin sulfatase
Proteases
What other things do bacteria release that cause cell death?
Exotoxin
Endotoxin (gram negative)
Mucopeptides (gram positive)
Ammonia
T/F - Loe also found that not all individuals get periodontitis.
TRUE
What did Goodson find?
Recurrent acute episodes followed by remission independent site activity
What is the modern plaque hypothesis?
Periodontopathic flora are necessary, and not sufficient, for disease
Periodontal diseases are specific mixed infections which cause periodontal destruction in the appropriately susceptible host
Microbial plaque comes from what 5 things?
Bacteria
Fungus
Protozoans
Viruses
Mycoplasm
Define periodontal disease.
Infectious disease process that involves inflammation
What does periodontal disease involve?
The structures of the periodontium resulting in loss of tissue attachment and destruction of the alveolar bone
Periodontal disease is any disease of the periodontium with what two basic forms?
Gingivitis
Periodontitis
Define clinical periodontal health.
The tissues are free from clinical inflammation
Define gingivitis.
Inflammatory process confined to the gingival tissues
- Caused by nonspecific accumulation of plaque
- Usually is reversible
Define periodontitis.
Inflammation not confined to the gingiva, but involves the attachment apparatus: cementum, PDL, alveolar bone, and soft tissues
THIS STARTS AS GINGIVITIS, BUT PROGRESSES TO DESTROY THE BONE AND SOFT TISSUES THAT SUPPORT THE TOOTH
Characteristics of health teeth and gingiva.
Pink gingiva
No bleeding with flossing and brushing
Fresh breath
What does gingivitis look like?
Red, swollen gingiva
Bleeding gingiva w/ flossing and brushing
Possible bad breath or taste
No bone loss
No tooth mobility
What does early periodontitis look like?
Red, swollen gingiva
Bleeding gingiva on flossing and brushing
Persistent bad breath or taste
Slight bone loss
Possible tooth mobility
Moderate periodontitis looks like what?
Red, swollen gingiva
Bleeding gums on flossing and brushing
Persistent bad breath or taste
Moderate bone loss
Tooth mobility and root exposure
What does advanced periodontitis look like?
Red, swollen gingiva
Bleeding gingiva on flossing and brushing
Persistent bad breath or taste
Severe bone loss
Severe tooth mobility and root exposure
Possible tooth loss
In the 1970s, what was the hypothesis for periodontal disease?
Increased plaque mass directly related to increased severity of disease
All bacteria on teeth are harmful
ALL INDIVIDUALS AND ALL TEETH W/IN AN INDIVIDUAL ARE SUSCEPTIBLE
WHAT CAUSES PERIODONTAL DISEASE? 2 THINGS
DENTAL/MICROBIAL PLAQUE
ENDOTOXINS
What is the modern plaque hypothesis (90s)?
Periodontopathic flora necessary, but not sufficient, for disease.
Diseases are specific mixed infections which causes periodontal destruction in the appropriately susceptible host
What are some acquired and environmental risk factors for periodontal disease?
Poor hygiene Age Meds Tobacco Stress Immune defects Nutritional deficiencies
What are some INNATE risk factors for periodontal disease?
Race Sex Genetics Congenital immunodeficiencies Phagocytosis dysfunction Down’s Syndrome Papillon-Lefevre/Ehlers-Dantos syndrome
What is the etiologic factor that causes periodontal disease?
DENTAL PLAQUE
What is calculus?
Mineralized biofilm (dead bacteria)
Inert, but the biofilm adhered to it is the issue causing disease
What does calculus do?
Provides a surface for the plaque to attach
What are two types calculus?
Supragingival calculus
Subgingival calculus
What are some properties of biofilms?
Cooperating community of microorganisms
-Arranged in microcolonies with channels b/t the microcolonies
-Microcolonies are surrounded by protective matrix
-Differing environments w/in the microcolonies in the biofilm
-Primitive communication system
-QUORUM SENSING
—Microbial gene expression differs when microorganisms are in a biofilm
-RESISTANT TO ANTIBIOTICS, ANTIMICROBIALS, AND HOST RESPONSE
What are the Koch’s Postulates for Periodontics?
Putative pathogens must be found in large numbers in diseased sites
Absence of pathogens in health
Must be able to demonstrate immune response to putative pathogens
Virulence factors can often be demonstrated
Animal models should simulate human disease
Elimination should result in clinical improvement
How long does it take to re-establish pathogenicity?
6 weeks
*After SRP, it takes 3 weeks to accumulate and then 3 more weeks to go bad
WHAT 3 ORGANISMS ARE IN THE RED COMPLEX?
Porphyromonas gingivalis
Tannerella forsythensis (Bacteroides forsythus)
Treponema denticola
Red: TF/BF PG TD!
What are the other complexes and how are they organized?
EARLY COLONIZERS
- Blue
- Purple
- Green
- Yellow
LATE COLONIZERS
- Orange
- Red
Bacteria bind to what?
NOT THE TOOTH SURFACE!
ATTACHED TO GLYCOPROTEINS ON THE SURFACE (PELLICLE)
What do the early colonizers bind to?
The pellicle (glycoproteins from the saliva)
What do the late colonizers bind to?
The early colonizers
*It takes about 42 days (6 wks) to get to a pathogenic biofilm
So it goes: tooth structure->biofilm pellicle->early colonizers->late colonizers (orange and red complexes)
What happens to the early colonizers after the late colonizers bind?
They die due to lack of nutrients and O2
This creates calculus
What are the steps of plaque formation? 6 steps
Association - Pellicle forms
Adhesion - W/in hrs, bacteria loosely bind to pellicle (planktonic bacteria)
Proliferation - Bacteria spreads throughout mouth and multiplies
Microcolonies - Steptococci secrete protective layer*
Biofilm formation - Microcolonies form complex groups with metabolic advantages
Growth/Maturation - Biofilm develops a primitive circulatory system
How does fluid flow thru a biofilm?
Thru fluid channels “under” the biofilm b/t the biofilm and pellicle
Quorum sensing in G- organisms involves 2 regulatory components: the ____________ __________ protein (R protein) and the ______ ____________ produced by the autoinducer synthase.
Transcriptional activator
AI molecule
Tell me the layers of biofilm.
Tooth surface
Pellicle
Dead bacteria in an anaerobic environment
Live, aerobic bacteria
Oxygen
Substrate
In the anaerobic layer, what is the REDOX potential?
LOW REDOX POTENTIAL
What are 4 mechanisms of antibiotic resistance w/in biofilms?
1 - Antibiotic poorly/slowly penetrates
2 - A conc gradient of a metabolic substrate leads to zones of slow or non-growing bacteria
3 - Adaptive stress response is expressed by some of the cells
4 - Small fraction of cells differentiate into a highly protected persistent state
T/F - Bioflims provide a source of antibiotic resistance.
T/F - Antibiotics don’t do anything to dead bacteria.
TRUE
TRUE
Give me a summary of biofilm.
Advanced ecosystem that is the etiology of periodontal disease
Fluid gradient helps move nutrients around and allows for bacterial communication
Keeps the inhabitants safe by making host defense mechanisms difficult to penetrate the environment and resist the effects of antimicrobials
T/F - Biofilm needs to be disrupted, even if we can’t completely remove it.
TRUE
T/F - SRP only disrupts about 13% of the biofilm.
TRUE
*If done correctly, the biofilm can grow w/o needing to be disrupted for up to 48 hours w/o problems
What is periodontitis caused by? (Interaction-wise)
Interaction of plaque and the susceptible host defense immune system
Periodontal disease:
Etiology?
Initiation?
Progression?
Etiology: Microbial plaque
Initiation: Non-specific plaque accumulation
Progression: G- bacteria and susceptible host
Sub-gingival plaque samples were analyzed from the distal, mid-buccal, and lingual aspects of canines, pre-molars, and molars after 96 hours of plaque accumulation. Tell me which site had greater plaque accumulation in the following list?
Distal - Mid-buccal
Mid-buccal - Lingual
Posterior - Anterior
Distal > Mid-buccal
Mid-buccal > Lingual
Posterior > Anterior
The majority of dental and periodontal diseases originate where on the tooth?
The interproximal area
*Any tooth brush, regardless of brushing method, does not completely remove interdental plaque - it is unkeratinized!
In general, there is a strong relation b/t poor oral _________ and __________.
Hygiene
Gingivitis
T/F - The relation b/t poor oral hygiene and the risk for developing periodontitis is not as strong as the relation b/t poor oral hygiene and gingivitis.
TRUE
Not all _________ progresses to __________, BUT all _____________ is preceded by _____________.
Gingivitis
Periodontitis
Periodontitis
Gingivitis
What are virulence factors?
Properties that enable the bacteria to cause disease
The virulence factors of fimbrea, pili, and fibrillae, what are their mechanisms of action?
Bacterial attachment, prevention of phagocytosis
What is the mechanism of action for the capsule virulence factor?
Protection, attachment, prevent phagocytosis
What is the mechanism of action for the endotoxin virulence factor?
Activation of inflammatory response, cytokine production, bone resorption
Exotoxins are released by what?
From viable organisms into environment
-Very susceptible to denaturation
Endotoxins are made by what?
LPS - Lipopolysaccharides
-Resistant to heat and chemical denaturation
By attaching to the pellicle, the bacteria avoid displacement by the ______ flow.
GCF
This is another bacterial virulence factor - the ability to adhere
Bacteria may enter the host by _________ in the epi or by direct ________ into the host tissues (less common).
Ulcerations
Penetration
Most bacteria enter the CT via what?
PASSIVE INVASION
-Swallowing creates a force and can drive bacteria into the CT
More than ___% of all Americans suffer from gingivitis.
90%
About ___% of all American adults suffer from periodontitis.
50%
How does the body respond to bacteria entering the tissue?
Inflammation, immune response, damage to soft tissue, and cell signals to start bone resorption
What is the formula for periodontal disease?
Pathogenic flora + lack of beneficial bacteria + susceptible host = Periodontal disease
Aggregatibacter actinomycetemcomitans was formerly known as?
Actinobacillus actinomycetemcomitans
*This bug is associated with aggressive periodontitis
Healthy bacteria tend to be what?
Aerobic G+ cocci,
Bad bacteria tend to be what?
Anaerobic, G- bacteria
What are some other bad bacteria present in periodontitis?
Porphyromonas gingivalis
Prevotella intermedia
Tannerella forsythia
Fusobacterium nucleatum
Peptostreptococcus micros
Campylobacter rectus - THIS ONE IS MOTILE**
What are 5 beneficial bacteria?
Actinomyces sp.
Strep mitis
Strep sanguis
Capnocytophaga sp
V parvula
Pellicle is made up of what?
Glycoproteins
-Proteins with carbohydrate moieties
**A thin, BACTERIA-FREE layer of salivary proteins that attach to the tooth surface w/in minutes of a professional cleaning
What are some factors that INCREASE a host’s susceptibility?
Impaired neutrophils
Inadequate immune response
LPS responsiveness
AIDS
Diabetes
Smoking
Drugs
Other
W/in hours of the pellicle forming, what happens?
Bacteria begin to attach to the outer surface of the pellicle (via fimbriae on bacteria)
Supragingival plaque is found where?
Coronal plaque
Marginal plaque
Subgingival plaque is found where?
Attached plaque*
- Tooth
- Epithelium
- Connective tissue
Unattached plaque (Planktonic - this can be the worst)
Attached sub-gingival plaque is what?
Zone of subgingival plaque directly attached to the surface of the tooth (coated in biofilm) of calculus in the sulcus and pocket
Unattached subgingival plaque is what?
Zone of sub-g plaque not directly attached to the tooth surface
Mostly G-, motile bacteria and resides b/t the outer position of the attached plaque and sulcular epithelium
In direct contact with both the junctional and sulcular epithelium
____________ plaque influences (increases the ability to grow) subgingival plaque, however, once ___________ plaque is established, the ___________ plaque, in essence, no longer affects it.
Supragingival
Subgingival
Supragingival
Which plaque is being disrupted through tooth brushing and/or SRP?
Supragingival plaque
Tell me the process of how subgingival plaque is created.
Biofilm -> supragingival plaque (which creates an anaerobic environment) -> Subgingival plaque (now unaffected by supragingival plaque)
The water in the ultrasonic does what?
Helps to flush away debris and endotoxins
How is calculus attached to the tooth? 2 ways
Mechanical retention on tooth, still covered by biofilm, in nooks and crannies
Direct on the pellicle
T/F - Unattached plaque is typically the most pathogenic.
TRUE
What is the critically important zone in a pocket?
The partially lysed CT fibers.
*Causes JE to move apically and can be the beginning of bone resorption
Young, supragingivial plaque is made of what?
Mostly G+ cocci and rods, with some G- cocci and rods
Aged supragingival plaque has an increase in what type of bacteria?
G- anaerobic
*This can get down into the sulcus and cause pocketing
How can young and aged supragingival plaque be distinguished?
Disclosing tablet
Differences b/t Supra and sub gingival plaque?
Matrix Flora Motile bacteria Oxygen req’s Metabolism
Supra
- Matrix - 50% matrix
- Flora - Mostly G+
- Motility - Few
- Oxygen req’s - Aerobic, unless thick
- Metabolism - Predominately carbs
Sub
- Matrix - Little or no matrix
- Flora - Mostly G-
- Motility - Common
- Oxygen req’s - High anaerobic areas
- Metabolism - Predominately proteins (usually from body tissues [breakdown of collagen in the pocket])
Planktonic bacteria is typically what? G+/G-?
G-
Subgingival plaque can be tooth-associated or epithelium-associated. Tell me the differences b/t the two.
Tooth-Associated
- Mostly G+, but turns into G-
- Does NOT extend to JE
- May penetrate cementum
- Associated with calculus formation and root caries
Epi-Associated
- G+ and G-
- DOES extend to JE
- May penetrate epi and CT
- Associated with gingivitis and periodontitis
What is the litmus test of how good SRP was?
Tissue state a few weeks (~6) later
Which bacteria have a very strong association with periodontal diseases?
RED Complex
- Porphyromonas gingivalis
- Tannerella forsythensis (Bacteroides forsythensis)
- Treponema denticola
- *Also:
- Aggregatibacter actinomycetemcomitans**
What 5 bacteria are associated with abscesses of the periodontium?
Fusobactrium nucleatum
Prevotella intermedia
Peptostreptococcus micros
Bacteroides forsythus
Porphyromonas gingivalis
Less than 5% of the population has what?
Refractory disease
- T. Forsythia
- P. Gingivalis
- P. Intermedia
- C. Recta
What bacteria are associated with chronic periodontitis?
P. Gingivalis P. Intermedia F. Nucleatum A.a C. Recta T. Forsythia
What is associated with localized, aggressive periodontitis (LAP)?
A.a
P. Intermedia
P. Gingivalis
What is ANUG?
Necrotizing, ulcerated gingivitis
-P. Intermedia - can burrow into epi cells
HIV-associated gingivitis is mostly due to what?
CANDIDA ALBICANS
Tell me about Aggregatibacter actinomycetemcomitans.
Small, non-motile
G-
Fac ana
Saccharolytic - Digest sugars
Coccobacillus
Small convex colonies with a star-shaped center
What is the most pathogenic serotype of Aggregatibacter actinomycetemcomitans?
B
Aggregatibacter actinomycetemcomitans has the ability to __________ host epi cells.
INVADE
*Like spirochetes
What is an exotoxin?
Extracellular substance produced by bacteria which are toxic to certain cells or tissues of the body
-Botulinum, tetanus
*Actively released from living cells
For some reason, know that LEUKOTOXIN is and EXOTOXIN
What is an endotoxin?
Released when cells die
LPS
What do leukotoxins do?
Produced by Aggregatibacter actinomycetemcomitans and is thought to KILL PMNs and MONOCYTES from blood and PMNs from the pocket
When LPS is released what 3 things can happen?
Cytotoxic effects
Complement activation
Bone resorption (Direct or indirect)
Tell me about Porphyromonas gingivalis.
G-, nonmotile, rod
Ana
Asaccharolytic
Invades epi cells
Able to grow at elevated pH
Thick capsule - Resist phagocytosis
Forms dark brown-black colonies
“Black pigmented bacteroides”
What other virulence factors does Porphyromonas gingivalis have, besides a capsule?
LPS - Stims cytokine secretion in monocytes and macrophages
Fimbriae - Binds bacterium to host tissues, produce and deliver of toxins and colonization antigens
Proteinases - Including collagenase
Toxic products
Tell me about Tannerella forsythia.
G-
Ana
Spindle-shape
Pleopmorphic
Invades epi cells
-Formerly know as bacteroides forsythus
Tell me about Prevotella intermedia.
G-
Ana
Short, round rod
Elevated in ANUG
“Black pigmented bacteroides”
—Uses heme as a primary foodstuff
Tell me about fusobacterium nucleatum.
G-
Ana
Spindle
MOST COMMON ISOLATE FROM SUBGINGIVAL SAMPLES
Tell me about campylobacter rectus.
G-
Ana
Short, motile vibrio
Produces a leukotoxin
Forms convex, spreading, or corroding colonies on blood agar plates
Tell me about peptostreptococcus micros.
G+ - THIS IS THE ONLY PERIO PATHOGEN THAT IS GRAM +*
Ana
Small coccus
Asaccharolytic
Tell me about spirochetes.
G-
Ana - Very anaerobic, they stink
Helical shaped
Related to NUG
Their intermediates are bad
Tell me the layers of a tooth with stuff on it.
Enamel
Pellicle
Biofilm/plaque
Calculus
