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NBDE II > Perio > Flashcards

Perio Flashcards

1
Q

What are the three parts of the oral epithelium

A

oral epithelium; Keri
Sulcular: non keri
Junctional; non keri

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2
Q

What is the name of the GCF once inflammation has occurred

A

inflammatory exudate

I contains a higher level of serum proteins and leukocytes

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3
Q

What is the epithelial attachment

A

Special part of the junctional epithelium.

consists of lamina lucida, lamina densa and hemidesmosomes.

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4
Q

What is the alveolar bone proper

A

immediately surrounds the roots of the tooth and to which PDL fibers are attached to.
Perforated cribiform plate

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5
Q

What is the origin of the PDL and what is it primarily made up of

A 
Dental sac
collagen fibers (connective tissue fibers)
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6
Q

What are the three specialized cells found in the PDL area

A

cementoblast/cementoclast
Fibroblasts ( Most abundant) /Fibroclasts
Osteoblasts/Osteoclasts

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7
Q

What is the terminal portion of the gingival fibers called

A

Sharpey’s fibers

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8
Q

What are the components of the free gingva

A

gingival margin
Free gingival groove
gingival sulcus
interdental gingiva

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9
Q

What does pathological mobility depend on

A

quantity of remaining bony support
degree of inflammation
magnitude of occlusal forces

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10
Q

What are the most common medications that cause hyperplasia

A

Phenytoin (Dilantin)
Cyclosporine A
Nifedipine

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11
Q

What is present in dilantin-induced hyperplasia

A

Increased accumulation of inflammatory cells

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12
Q

What is pseudo pocketing

A

pocketing occurs without attachment loss

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13
Q

What are RG signs of O trauma

A 
Widening of PDL
Thickening of lamina dura
Angular bone loss and infrabony pocket defect
root resorption 
Hypercementosis
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14
Q

What’s necessary for apical shift of the attachment

A

local irritant and inflamation

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15
Q

What is secondary O trauma

A

excessive force applied to a tooth or teeth with inadequate bone support (periodontal disease)

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16
Q

What RG changes can be seen in teeth that are no longer in function

A

reduced trabeculation of bone

narrowing of the PDL space.

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17
Q

What is gingivitis

A

form of perio disease associated with PLAQUE

No loss of attachment or bone loss

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18
Q

What is the first stage of gingivitis

A

Transient (incipient) stage; within 2-4 days after cessation of OH.
Margination of PMN’s in vessels close to JE.

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19
Q

What is the second stage of gingivitis

A

Developing stage; Area of collagen destruction becomes larger and is occupied by fluid containing: Fibrin, immunoglobulin (IgG), complement, inflammatory cells (B or T lymphocytes, macrophages.
LYMPHOCYTES are the predominant cell

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20
Q

What is the third stage of gingivitis

A

Chronic stage; cytologic characteristics of the inflammatory infiltrate in the gingival lamina propria are changed.
PLASMA cells predominate
IgG is produced by most the plasma cells
Few cells containing IgA are present, mostly in saliva
IgM containing cells are rarely seen

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21
Q

What are cytokines

A

Infection-fighting factors involved in healing.

In excess they can cause inflammation and severe damage.

22
Q

T-cells are important in

A

Cell mediated immunity.
Type IV hypersinsitivity reactions (contact dermatitis)
Modulation of antibody-mediated immunity.

23
Q

What are the major classes of T-cells

A

Helper T-cells
Suppressor T-cells
Cytotoxic T-cells

24
Q

What is neutropenia

A

Abnormal decrease in the number of PMNs in the blood

Associated with: Acute leukemia, infection, RA, vit B12 def, chronic splenomegaly.

25
Q

What is leukemia

A

malignant neoplasm of immature WBC
Pt’s with acute leukemia have more oral complications than those with chronic leukemias.
Gingiva; grosly enlarged, bluish-red in color, soft spongy consistency and blunted papilla

26
Q

What is pregnancy gingivitis

A

bleeding is the most common complaint
severity increases from second to eighth month.
Similar increase seen at or around puberty and with long term use of oral contraceptives.
Tx; OHI and scaling

27
Q

What are the four local signs of acute inflammation

A

Rubor
calor; dilation of blood vessels and high metabolic rate of PMNs and macrophages.
Tumor; from increased cellular permeability
Dolor; due to lysis of cells triggers production of Bradykinin and prostaglandins

28
Q

What does a mast cell release

A

heparin and histamine due to injury or inflammation.

29
Q

What is the purpose of histamine

A

causes vasodilation and increased vascular permeability

30
Q

Where histamine stored

A

Mast cells
Platelets
basophils

31
Q

What is the extent of localized perio

A

<30% of sites involved

32
Q

What is the extent of generalized perio

A

> 3O%

33
Q

What is the severity of 1-2 mm of CAL

A

Slight

34
Q

What is the severity of 3-4 mm of CAL

A

Moderate

35
Q

What is the severity of >5 mm of CAL

A

Severe

36
Q

What are the two bacteria associated with Generalized Aggressive perio and occurs at what age

A 
prevotella intermedia
Eikenella corrodens 
12 to 25 yo 
Episodic, rapid and severe attachment loss
Weak serum response
37
Q

what are the two bacteria that dominate on Local aggressive perio and occurs at what age

A 
Gram negative anaerobes:
Actinobacillus Actinomycetemcomitans 
Capnocytophaga 
8-22 y/o
Strong serum response
Confined to incisors and first molars.
relative lack of local factors to explain it, possible genetic predespostion or dysfunction of PMNs  (chemotactic defect)
38
Q

What are the characteristics of ANUG

A

Interproximal necrosis and pseudomembrane formation on marginal tissues.
History of : Soreness, bleeding gums, fetor otis, low grade fever, malaise.
Age; 18-30

39
Q

What are the predisposing factors to ANUG

A 
18-30 y/o
Smoking
gingivitis 
poor OH
fatigue 
stress
poor nutrition
immune-compromised pts
40
Q

Wha is the tx for ANUG

A

debriment
Hydrogen peroxide rinses
Abx therapy

41
Q

What are the characteristics of HIV gingivitis

A

defined linear marginal gingival erythema

resistant to conventional therapy

42
Q

What are the characteristics of HIV periodontitis

A

rapid progression of destruction of gingiva with ulceration and cratering.
Necrosis leading to sequestration of alveolar bone.
Extremely painful

43
Q

Where does an endotoxin comes from and where is it found

A

Cell wall of gram negative bacteria.

Free endotoxin found in dental plaque and inflamed gingiva.

44
Q

What do endotoxins promote

A

bone resorption
inhibit osteogenesis
chemotaxis of PMNs

45
Q

What are the three methods for treating a periodontal abscess

A

cuettage via the sulcus
Flap surgery
I and D

46
Q

What is the bacterial count on plaque

A

10^10 bacteria per milligram

47
Q

What material contributes to the ability of plaque to adhere to teeth

A

Dextrans

48
Q

What inorganic compounds are found in plaque

A

Ca and phosphate

49
Q

What two species are early tooth colonizers

A

neisseria and streptococci

50
Q

What are the O components of calculus

A

microorganisms, desquamated epithelial cells, leukocytes and mucin

51
Q

What are the objectives of perio surgery

A 
pocket reduction
promotion of gingival reattachment
tx the etiology
remove or eliminate lesion 
restore form and function
52
Q

modified Widman flap

A

new attachment at a more coronal level

Preserves adequate zone of attached gingiva

NBDE II (5 decks)

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