Exam 1 part 2 Flashcards
What type of category does pregnancy and gingivitis fall into for gingivitis
Pregnancy associated gingivitis –> Plaque induced gingivitis
What are the medications involved in gingival overgrowth
Anti-convulsants/Anti-seizure - Dilantin
Ca channel blockers - Nifedipine
Immunosuppresants - Cyclosporin
(as well as oral contraceptives)
What is the difference between risk and risk factor
Risk: the likelihood a person will get a disease in a specified time period
Risk factor: Before manifestation, a factor that puts them at a greater risk for developing the disease
Identify the microorganisms involved in Chronic PD
Porphyromonas gingivalis (Proteases)
Tannerella forsythia
Treponema denticola
Aggregatibacter actinomycetemcomitans (leukotoxin)
Identify the microorganisms involved in Aggressive PD
Aggregatibacter actinomycetemcomitans Porphyromonas gingivalis (some patients)
Identify the microorganisms involved in Necrotizing PD
Prevotella intermedia ( also seen in preg. ass. gingivitis)
Spirochetes (invade CT)
Fusiform bacilli
What is the portal of entry for microorganisms involved in PD
Sulcular epithelium ulcerations and direct penetration of host epithelial or CT cells
Define biofilm
Cooperating community of microorganisms arranged in microcolonies surrounded by protective matrix
- Dental plaque is a biofilm
T or F, Plaque spreads horizontally across buccal surface of tooth
False, Spreads apically along rot surface
What is calculus?
Calcified dental plaque
T or F, Calculus is a secondary contributing factor to PD
True
Calculus’s role in disease
Harbors bacteria –> induces damage
What immune cells first come to the pocket
PMN –> first repsonder
- phagocytize material in sulcus.
- Migrate into sulcus/pocket from leaky ulcerative gingival epithelium
What do mast cells do
Release amines
Increases vascular permeability
What do macrophages do
Present antigen to T cells
T-lymphocytes
lymphokines and delayed hypersensitivity
B-lymphocytes
may differentiate into plasma cells
- Active in antibody formation
Describe the 5 points of tooth associated subgingival plaque
- Densely, adherent, biofilm
- G+ rods, cocci, filaments
- Facultative aerobes/anaerobes
- Remove by SRP (mechanical removal)
- Less virulent
Describe tissue associated subgingival plaque (5)
- Loosely adherent
- G- motile anaerobes
- Spriochetes
- Remove surgically
- More virulent
Describe unattached subgingival plaque
- Free swimming in pocket
- G- motile anaerobes
- Spirochetes
- Remove by flushing
- More virulent
Describe microbial shift, healthy –> gingivitis –> periodontitis
From G+ to G-
from Cocci to rods (later spirochetes)
From non-motile to motile
From facultative to obligate anaerobes
Describe the color of supragingival and subgingival calculus
supragingival: whitish, yellow
Subgingival: dark brown, hard and dense
T or F, Roughness of calculus increases surface area
true
But it is not a mechanical irritant
T or F, Calculus increases density in which plaque can accumulate but decreases bacteria concentration
First statement true
Second statement false, it increases bacteria concentration
4 factors that can cause calculus
- Anatomical abnormalities (enamel pearl, fluted root)
- Physical irritants: amalgam overhang, rest. contours
- Habits: mouth breathing, factitious injuries
- Systemic disease: DM
4 calculus attachments
- Pellicle
- Penetrate cementum
- Lock into surface irregularities (CEJ, crown margin)
- Into depression/concavities in roots (ex: premolar roots > canine roots, multirooted teeth more prone to perio disease)
Describe the Initial stage of pathogenesis
- Onset after plaque formation
- Histopathological
- Features
- 2-4 days
- Acute inflammation: vasculitis, PMNs, Macrophages
- subclinical, no gingivitis, increased flow of gingival crevicular flow
Describe the Early stage of pathogenesis
- Onset after plaque formation
- Histopathological
- Features
- 4-7 days
- T-cell lesion
- Clinical signs of gingivitis, redness, bleeding, edema
Describe the Established stage of pathogenesis
- Onset after plaque formation
- Histopathological
- Features
- 2-3 weeks
- B-cell lesion: plasma cells
- Chronic gingivitis
Describe the Advanced stage of pathogenesis
- Onset after plaque formation
- Histopathological
- Features
- Undetermined time (not sure if periodontitis will occur)
- Alveolar bone loss, pocket formation, B-cell lesion
- Periodontitis
Which cytokines cause bone resorption
IL-1 B
TNFalpha
What is the genetic influence of Interleukin-1 on periodontal disease?
It has been shown that polymorphisms associated with the activity of IL-1 are resonsible for 2-4 times increase in macrophage IL-1 production. This profile has shown to have individuals with more severe periodontal disease.
-The polymorphism does not cause disease, it makes the individual response more severe.
T or F, MMP(1&8) is a cytokine and is involved in bone resorption
False, it is a proteinase, not a cytokine, but is found with cytokines. It breaks down connective tissue
What cells are involved in advanced lesion of paige and schroder
B cell lesion
T or F, Smoking decreases the clinical expression of inflammation and therefore less clinical inflammation than non-smokers
True,
Does smoking contribute to PD? What if one stops smoking?
Yes, Current smokers have 4 times as much periodontal disease and Former smokers have only 1.6 times as much periodontal disease
T or F, smokeless tobacco has a systemic effect on PD
False, only a localized effect on attachment loss, no effects on periodontitis
T or F, Smoking effects are irreversible.
False, they are reversible with cessation of smoking
T or F, Smoking has increases the rate of plaque accumulation
False, No effect
Does smoking allow for an increased number of pathogens?
Yes, increased in both shallow and deep pockets
How does smoking effect the immune response to challenge
It decreases the immune response, decreases PMN chemotaxis and pagocytosis and Increases TNF-alpha, PGE2, MMP-8 expression
Do smokers have an increased response or decreased response to nonsurgical therapy & surgical therapy
Decreased response to: S&RP Less pocket depth reduction Less gain in attachment Increase likelihood for failed implants
T or f, Smokers have trends toward recurrent disease after tx
true
What is the difference between recurrent and refractory
Recurrent: relapse
Refractory: non-responsive to tx modalities
T or f, smokers have less overall tooth loss
False, more
What causes a significant portion of the damage seen in periodontal disease?
Normal host response
Host response is mediated by what:
MMPs such as collagenase (collagen breakdown)
Prostaglandins (bone resorption)
Osteoclasts (bone resorption)
What is the main goal of host modulation?
Change host response to bacteria
- Regulating the tissue damaging host response, typically using drugs
- target MMPs, Prostaglandins, Osteoclasts
What is the major drug for host modulation
Periostat, which is a small does of the antibiotic doxycycline
When we collect data, what is most important in all the data we collect when diagnosing PD?
Clinical attachment loss
CAL and probing depths increasing can tell if disease is getting worse
What does healthy gingiva look like?
Scalloped gingival margin
Papillas between teeth are knife-like
Pink (salmon) indicative of health
What does diseased gingiva look like?
Blunted/bulbous/rounded interproximally
Red (inflammation)
Increased bleeding on probing
Loss of clinical attachment levels/recession
T or F, Only increasing probing depths and clinical attachment loss are associated with disease progression
True
What are the percentages of different occurrences at the cemento-enamel junction
Overlap (60-65%)
Butt (30%)
Exposed dentin (5-10%)
Dimensions of cementum
16-60 u Coronal
150+ u apical
T or F, Apical, Furcal and Distal surfaces increases with age
True
