OST Exam II Review Flashcards

Question 1

Q

1) What are the Periodontal Treatment Phases?

Answer

A

Phase 1: Initial (soft tissue) Therapy:

Scaling and Root Planing (SRP) - removal of accretions on the root
(OHI)

Re-evaluation:

4-6 weeks after initial therapy is completed
re-collect and analyze data
Phase 2: Surgical Therapy (hard tissue)
Bony defects
grow bone backMaintenance Phase

Question 2

Q

2) Be able to calculate AG and CAL?

Answer

A

-Attached gingiva:
○ 1. AG= KG minus Probing
Depth
○ 2. AG= (GM to MGJ) minus Probing Depth

-CAL:
CAL= PD(mm) + CEJ to GM (mm) = CEJ to BOTTOM OF PERIO POCKET

○ (+) Positive if apical to CEJ (i.e recession present)

○ (-) if coronal to CEJ (i.e excess tissue covering)

Question 3

Q

3) where does PD starts in the mouth?

Answer

A

-PD starts at most coronal part of inter proximal tissue and migrates apically

Question 4

Q

4) Know cells found in gingiva

Answer

A

Squamous Epithelium
Keratinocytes
Nonkeratinocytes
Melanocytes: pigment
Langerhan’s Cells
Merkel Cells: free nerve endings

Question 5

Q

5) Know GINGIVAL fiber groups (made of Type I & III collagen)

Answer

A

Gingival fibers:

1) Circular: Support & contour to free gingiva
2) Dentogingival: support of the gingiva
3) Dentoperiosteal: anchors tooth to bone
4) Alveologingival: attaches gingiva to alveolar bone
5) Transseptal**: Keeps teeth in alignment and protects bone

**Not on implants: dentogingival, dentoperiosteal, transseptal

Question 6

Q

5) Know PERIO fiber groups (made of Type I & III collagen)

Answer

A

Perio fibers:

1) Alveolar Crest: Resists lateral movement
2) Horizontal: Opposes lateral forces
3) Oblique: Absorbs occlusal forces (LARGEST GROUP)
4) Apical: Resists tipping of the tooth
5) Interradicular: Resists forces of lunation (pulling out) and tipping

Question 7

Q

6) What MGJ is?

Answer

A

1 ) The MGJ does not change, that line is permanent

2) Location: at base of gingival mucosa and the top of the alveolar mucosa
3) MGJ is point at which keratinized and non-keratinized epithelium meet
4) Keratinized epithelium goes to gingival epithelium → MGJ
5) Attached gingiva is measured from the gingival margin (GM) to the MGJ minus PD

Question 8

Q

7) Know about smoking and GCF

Answer

A

1) Immediate transient but marked increase
2) INCREASED crevicular fluid at the smoking event
3) Smoking has stunted inflammatory reaction

Question 9

Q

8) Know about GCF

Answer

A

Type of host defense mechanism
Sulcular fluid or Gingival Crevicular Fluid (GCF)
Test w/ filter paper (threads or micropipette) at gingival sulcus & analyzed w/ Perioton
Continuous inflammatory exudate, from peril pocket
Present in small amount in healthy people but in present in larger higher quantity people w/ gingivitis causing the tissue to look wet
Composition: proteins, Ag, Ab (IgG), Enzymes, epithelial cells, leukocytes, Electrolytes (K, Ca, Na), Organic compounds (metabolic and bacterial)
Determines permeability of sulcular epithelium
Normal = 0.43 to 1.56 uL (no gingivitis)

Question 10

Q

8) What do GCP Levels INCREASE WITH?

Answer

A

1) Circadian: from 6 AM to 10 PM
2) Inflammation: removes products
3) Time w/ female sex hormones (ex: pregnancy)
4) Mechanical: excess chewing (ex: gum)
5) Initial pathogenesis stage
6) Immediate increase w/ smoking event
7) [tetracycline] higher in GCF than in serum

Question 11

Q

9) What is Drug induced Enlargements (gingivitis) ?

Answer

A

1) Starts @ INTERDENTAL papilla and extends to facial/lingual margins, can cover root surfaces
2) Enlargements unite & cause tissue fusion
3) May or may not be plaque-associated

Examples of Med associated:

Anti-Convulsants/Anti-Seizure
Calcium Channel Blockers
Immunosuppressant
Oral Contraceptives

Question 12

Q

9) Describe Anti-Convulsants/Anti-Seizure

Answer

A

Dilantin (phenytoin)
stimulates fibroblast proliferation, inactivation of collagenase
plaque induced
dose response is questionable

Question 13

Q

9) Describe Calcium Channel Blockers

Answer

A

Nifedipine, Diltizen, Verpamil
Verapamil + Cyclosporine given to kidney transplant pts in combination
increase in cellular production and breakdown

Question 14

Q

9) Describe Immunosuppressants

Answer

A

Cyclosporine, Tacrolimus

MORE vascular than phenytoin enlargement
Dose related
LESS overgrowth w/ tacrolimus

Question 15

Q

10) Describe Paige and Schroder models of Gingivitis

Answer

A

Pathogenesis Stages (Summary)
Initial: increased GCF (gingival crevicular fluid), tissue looks wet, PMNs
Early: start to see signs of gingivitis (redness/bleeding/edema), T-cell lesion
Established: B-cell lesion, plasma cells, chronic gingivitis

-Advanced = periodontitis (B-cell lesion, bone loss, pocket formation); don’t know how long this will take or if gingivitis will ever develop into periodontitis
De

Question 16

Q

11) Know types of gingivitis plaque induced ?

Answer

A

**Systemic factors
Endocrine (puberty, pregnancy, diabetes)
Blood dyscrasias (leukemia)
**Drugs:
Anti-seizure meds (Dilantin)
Ca channel blockers (Nifedipine)
Immunosuppressants, ex: with transplant pts (Cyclosporin)
Oral contraceptives
tx via cauterizing tissue/vessels (decrease bleeding), will come back as long as pt is on medication
*Malnutrition → rare in US
Vitamin deficiency
Scorbutic gingivitis “Scurvy”

Question 17

Q

11) What is Non-plaque Induced disease?

Answer

A

1) Bacteria: E. Coli, Streptococcus, Neisseria, Treponema
2) Viruses: Herpes
3) Fungal infections: Candidiasis, Histoplasmosis
4) Systemic diseases: Benign Mucous Membrane Pemphigoid, anywhere there is a mucous membrane
5) Trauma: toothbrush abrasion
6) Foreign Body reactions: popcorn kernel, dental materials, ortho brackets
7) Genetic: Hereditary Gingival Fibromatosis

Question 18

Q

What is CHRONIC GINGIVITIS?

Answer

A

1) MOST prevalent in ADULTS but can occur in children or adults
2) Plaque & calculus present, redness, BOP
3) Inflammation spreads from papilla → GM → AG

**Extent: each tooth has 6 sites so total number teeth x 6. Sites = mesial buccal, straight buccal, distal buccal, distal palate, straight palate, mesial palate
localized < 30% of sites involved
generalized > 30% of sites involved
diffuse: GM + AG + papilla
***Severity: CAL = soft tissues loss, bone loss, probing
slight: 1 or 2 mm clinical attachment loss
moderate = 3 to 4 mm CAL
severe = 5+ mm CAL

***Acute/Aggressive:

Occurs in younger patients (< 30 yo) who are otherwise healthy
Based on location & # of teeth involved, not % of sites

1) Localized (LAP): (first) molars/incisors, large Ab response, at least 2 perm. teeth involved
2) Generalized (GAP): molars/incisors/and other teeth, smaller Ab response, at least 3 perm. teeth involved, generalized inter proximal (IP) attachment loss

Aggregatibacter a. plays significant role
More prevalent in African Americans
Highly amenable to surgery (essentially can cure the disease by surgical resection)

Question 19

Q

12) Abscesses: GINGIVAL typically acute, (treat ASAP)

Answer

A

Localized purulent infection involving marginal gingival & interdental papilla

fluctuant mass w/ exudate
not a cyst, not encapsulated
no bone loss or pocket
S/S: edematous (marginal or interdental), erythematous, smooth, shiny, soft w/ exudate out of sulcus

-CAUSES: bacteria that has been carried into gingival tissue (ex: foreign bodies, dental materials left behind)

Tx: Drainage if fluctuant, debridement, rinse (saline or CHX), antibiotic + follow-up
if you don’t drain pressure will accumulate → pain

Question 20

Q

12) Describe PERIODONTAL Abscesses: typically acute, (treat ASAP)

Answer

A

Marginal gingival & interdental papilla + periodontium (bone)

-Classified as LEVEL 3 (management of pts with PD)

Perio abscess has pocket associated with it, can be an extension of an infected pocket
Deep pocket depth w/ possibility of mobile teeth
Microscopically: PMN accumulation
Microbio: G- (P.g, P.i, F.n, T.f, P.m, A.a ), fusiform bacteria, spirochetes

CAUSES:
1) Infected pocket

2) Incomplete calculus removal: best we can do
is 5 mm subgingivally

3) Root fracture: can’t see vertical on x-ray, only see if fracture is oblique or if x-ray is tilted so you can see the roots

*Clinical application: if pt has severe vertical bone loss must extract b/c bone loss can affect adjacent teeth → extract, do bone graft then implant
longer it sits there the more damage to the bone

Question 21

Q

12) Describe Pericoronal & Multiple Abscesses: typically acute, (treat ASAP)

Answer

A

*Pericoronal: over a partially erupted tooth (over the crown)
pt is in pain
trouble w/ occlusion and poor OH
tx: extract partially erupted tooth, laser cut it off

***Multiple abscesses = uncontrolled/diagnosed DM, immunosuppressive diseases, something is going on systemically

Question 22

Q

13) Know about pregnancy and gingivitis/PD

Pregnancy associated gingivitis: plaque induced gingivitis

Answer

A

Including [prevotella intermedia] → uses steroids as growth factor
Marginal & generalized gingival enlargement
Causes increase in GCF
Single or multiple tumor like lesions
Pyogenic granuloma = pregnancy tumor (non-cancerous)
Tx: cutoff tumor lesions, send for biopsy just as COA, can re-occur, filled w/ blood
PREVENTION: plaque control

-TX: cleaning and debridement, OH (trophy, cavitron), antibacterial mouthwash (chlorhexidine)
(goes away after pregnancy)

– Complications can include: preterm labor and low-birth-weight (<2500g)

Question 23

Q

14) What is a risk factor for PD?

Answer

A

1) Microbial:
specific organism, total microbial burden, biofilm pathogenicity

2) Systemic:
diabetes (DM), genetics, sex, race, HIV

3) Behavioral:
tobacco use, patient (pt) compliance

4) Local:
restorations, tooth anatomy, malocclusion

Gingivitis: OH, hormonal, smoking
Aggressive perio: A.a, defective PMN function, African American
Chronic perio: microorganisms, diabetes, osteoporosis, genetics, smoking, nutrition, HIV/AIDS, stress

Question 24

Q

15) What is NUG? In HIV patients?

Answer

A

*Still NUG = necrotizing ulcerative gingivitis

● Acute necrotizing inflammation of the gingival margin
● involves both stratified squamous epithelium & underlying CT
● Forms Pseudomembrane
- Replaces destroyed epithelium
- Meshwork of fibrin, necrotic epithelial cells, PMN’s and various microorganisms
● Infiltration of PMN’s in intercellular spaces
● CT is hyperemic
- Engorged capillarie
- Dense infiltration of PMN’s
● Age groups= Occurs in all ages but mainly 20-30
● Not contagious
● “Trench mouth”
● Rare in US before 1914 (WWI, WWII)
● S/S: lymphadenopathy, possible fever
○ If severe: high fever, inc. HR, leukocytosis, loss of appetite, lassitude

Question 25

Q

15) Clinical features of NUG?

Answer

A

● Rapid onset
● Severe pain
● Gingival bleeding; may or may not be spontaneous
● Interdental Crater, punched out papilla, pseudomembrane, fetid (sulfur) breath

Question 26

Q

15) What is the Host Response for NUG?

Answer

A

Host Response:
●	Systemic Predisposing Factors
●	Immunosuppression-AIDS 
●	Stress
●	Smoking 
●	Diet

Question 27

Q

15) What are other factors of NUG?

Answer

A

● Host resistance and smoking
● Oral hygiene (Pre-existing gingivitis and Opportunistic microorganisms)
● Local irritants

Question 28

Q

15) What are the Listgarden’s 4 Zones for NUG?

Answer

A

● Zone 1: Bacterial Zone
- Superficial, contains bacteria
● Zone 2: Neutrophil-rich Zone
- Numerous Leukocytes, mostly PMNs, bacteria, spirochetes
● Zone 3: Necrotic Zone
- Dead cells, fibers, spirochetes, and other bacteria
● Zone 4: Zone of spirochetal infiltration
- Well-preserved tissue infiltrated with spirochetes

Question 29

Q

15) NUG-Treatment?

Answer

A

● First treatment- debridement, OHI, evaluate systemic factors
● Recall visit- 1-2 wks, eval. OH, further tx
● Final re-eval- 4-6 wks, consider surgery (gingivectomy)
● If fever present give antibiotics first: Amoxicillin and Metronidazole (G-, bad aftertaste/metallic), take 3x a day for 1 week, no alcohol use while taking (including alcoholic mouthwash)
○ If allergic then prescribed clindamycin

Question 30

Q

15) What is NUP?

Answer

A

● Essentially the same, except NUP involves bone loss
Extraoral and Systemic Signs and Symptoms:
● Patients usually ambulatory w/ no systemic complications
● Locally lymphadenopathy
● Slight elevation in temperature
● Severe cases may have systemic complications:
-High fever
-Increase pulse rate
-Leukocytosis
-Loss of appetite
-General Lassitude

Question 31

Q

15) Systemic Signs & Symptoms:

Answer

A

Severe, deep pain, & rapid onset
Soft tissue & attachment loss
Exposed bone
Low CD4 & high viral counts

● Consider Antibiotics
● Amoxicillin and/or Metronidazole(Given in severe perio cases, tastes bad, and not to be taken with alcohol)

Question 32

Q

16) Know about Primary Herpes

Answer

A

■ Contagious
■ Herpes Simplex Virus- 1 (HSV-1)
■ can happen in kids and immunocompromised adults
■ occured in bound and unbound tissue: attached gingiva and alveolar mucosa (ex: soft tissue lip, cheeks, palate, mucosa), non-keratinized
■ if young adults contract it, it’s more severe
■ most cases are subclinical (exposure but no S/S)

■ Most adults have developed immunity to HSV with most cases being subclinical

■ Both sexes affected

■ All races affected equally

■ Primary infection- early in life
- Children ages 1-10

More severe in young adults 15-25

Question 33

Q

16) What is the Tx for Primary Herpes?

Answer

A

■ TX: bed rest, bland mouthwash (no alcohol in them b/c it will burn), fluids, antipyretics (not ASA), lidocaine gel, CHX (chlorhexidine)

Ab: Valacyclovir, Vibraadine, Acyclovir
Topicals: Acyclovir (Zovirax), Penciclovir (Denavir), Docosanol (Abreva - prevents virus getting into the cell, not an antiviral)

Question 34

Q

16) What is the Prodromal phase for primary herpes vs recurrent herpes?

Answer

A

■ Prodromal phase: abreva and valacyclovir works at this phase

Fever
Irritability
Headache
Gingival inflammation

Question 35

Q

16) What is, active phase, latency and reactivation herpes?

Answer

A

■ Active phase

Vesicles rupture, yellow ulcers, red halo
viral shedding (average 12 days)
Mobile and Attached tissue
Heal in 7-14 days with no scarring

■ Latency

Virus resides in ganglia
non-replicating state
latency associated transcripts (LAT)

■ Reactivation

Caused by stress, sun, palatal injections etc.
Put on Ab to prevent outbreak or dec. severity of outbreak

Question 36

Q

16) What is Recurrent Herpes?

Answer

A

■ Spontaneous or stimuli related
■ Virus migrates
■ Herpes labialis (extra-oral)
■ Virus overwhelms local immune response
■ Intraoral only on Bound down Tissue/ attached gingiva (palate, lip, extra-orally)
■ Herpes will present as more than one dot (grape cluster), looks like outburst of necrotic spots

Question 37

Q

16) Herpetic Whitlow?

Answer

A

■ RECURRENT infection
■ fingers and hands
■ latent site- dorsal root ganglion
■ debilitating

Question 38

Q

16) Recurrent Herpes Virus activation and Tx?

Answer

A

■ Sunlight
■ Trauma
■ Fever
■ Stress

○ Treatment
■ Acyclovir

Note: aphthous ulcer (immune mediated) is not a virus (non-contagious), it happens on moveable mucosal tissues only, will not be on keratinized attached tissue → looks same as herpes but different etiology, one spot = canker sore

Question 39

Q

17) In Pediatric dentistry what is normal periodontium :

Answer

A

○ Normal Periodontium:
■ Pale pink firm gingiva
■ Either smooth or stippled
- stippling found in 35% of children between ages of 5-13 years
■ Interdental gingiva is broad facio-lingually and narrow mesiodistally
- No sharp papilla points b/c of tooth spacing
■ Mean gingival sulcus depth average 1mm
■ PDL is wider than the PDL of permanent teeth
■ Radiographically, the trabeculae in the alveolar bone are fewer but thicker than in the adult
*The crests of interdental bony septa are flat

Trabeculae in alveolar bone are fewer but thicker than in adult
Calculus can be present, less plaque etiology than adults
BOP(bleeding on probing) and pocketing is less common
Root planing = roots are exposed, most children don’t have exposed roots so would just do scaling on kids
No need to probe deciduous/mixed dentition unless concerns
Malpositioned teeth:
Accumulate more plaque

*Localized marginal recession:
-tooth position in arch is most important
can correct itself as tooth alignment improves
-Increased gingivitis with:
-excessive overbite/ excessive overjet
-Nasal obstruction
-Mouth breathing

Disease altering oral mucosa including gingiva
Varicella
Rubeola (measles)
Scarlatina (scarlet fever)
Diphtheria

Question 40

Q

In Pediatric teeth what are Malpositioned teeth?

Answer

A

○	Malpositioned teeth
■	Accumulate more plaque 
■	Increased gingivitis with:
-	excessive overbite
-	excessive overjet
-	Nasal obstruction
-	Mouth breathing
○	Disease altering oral mucosa including the gingiva
■	Varicella
■	Rubeola (measles)
■	Scarlatina (scarlet fever)
■	Diphtheria

Question 41

Q

18) What are Suprabony vs Infrabony/Intrabony pockets?

Answer

A

○ Suprabony - Base of pocket is coronal to level of underlying bone
■ Horizontal bone loss
■ transseptal CT fibers are horizontal

○ Intra(infra)bony - Base of pocket is apical to the level of the adjacent bone
■ Vertical bone loss
■ always have underlying angular defects
■ transseptal CT fibers run length of defect vertically (obliquely)

Question 42

Q

Why do we do pocket reduction therapy? What is the basis of it?

Answer

A

○ Rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation
○ Pockets create area where daily plaque removal becomes impossible

Question 43

Q

20) What is a periodontal abscess vs a gingival abscess. What are the clinical manifestations.

Answer

A

○ PERIODONTAL ABSCESSES: Acute localized accumulation of viable & nonviable PMNs w/in pocket wall.
■ Extension from infected pocket: G- microorganisms i.e. fusiforms and spirochetes
■ Incomplete removal of calculus
■ Root fracture
- Does it hurt?
- dull, constant pain, recent origin
- Bone Loss?
- Bone destruction is responsible for tooth loss
■ Multiple abscesses = uncontrolled/diagnosed DM, immunosuppressive diseases, something is going on systemically

○ GINGIVAL ABSCESSES: Acute localized purulent infection that involves the marginal gingiva and interdental papilla due to bacteria carried into gingival tissue (i.e. popcorn hull, toothbrush bristle, fingernail, dental material)

■ S/S
Localized swelling - marginal or interdental
Red, smooth, shiny surface
May present purulent exudate

■	Treatment
If fluctuant, establish drainage
Debridement
Rinse (saline or CHX)
Follow up

Fenestrations - “window” in bone on facial or lingual - places exposed root surface in direct contact with gingiva or alveolar mucosa
Dehiscence - Loss of alveolar bone on the facial (rarely lingual) aspect of a tooth that leaves a characteristic oval, root-exposed defect from cementoenamel junction apically. The defect may be 1-2 millimeters long or extend full length of root.
3 Features of Dehiscence: 1)gingival recession, 2) alveolar bone loss & 3) root exposure.

Question 44

Q

21) What is Normal bone morphology?

Answer

A

1) Crest follows the CEJ and is 1-2mm apical
2) Interproximal higher (more coronal) than facial and lingual
3) Scalloped

4) Related to fenestrations & dehiscences
- Fenestrations - “window” of bone loss/absence on facial or lingual - places exposed root surface in direct contact with gingiva or alveolar mucosa

- Important to note that this is developmental flaw. Not active PD
 - Dehiscence - An absence of normal bone growth. Most common on facial (rarely lingual) aspect of a tooth.

5) Related to: interdental septa
- Thickness, width, & crestal angulation

   - “ When attempting to determine if bone morphology is correct, first compare CEJs then compare the bone (and bone loss) to the relationship of the position of the teeth”
     - Essentially she is saying that bone morphology is unique to the patient.

Question 45

Q

22) Patterns of bone loss:

○What is the difference between primary vs secondary?
○ how do you see it on the radiograph?
○ what happens when there is no occlusal surface?

Answer

A

○ 4 types:

1) Horizontal
2) Vertical
3) Osseous crater
4) Reverse architecture (aka inconsistent margins)

■ PRIMARY Occlusal Trauma:

Occurs when EXCESSIVE (GREATER than normal) occlusal forces occlusal forces exerted on a tooth w/ “NORMAL” periodontium
NO bone loss, NO perio disease, will have generalized mobile teeth

■ SECONDARY Occlusal Trauma:

Occurs when NORMAL or excessive forces are placed on tooth w/ REDUCED periodontium
Occurs when there is a compromised periodontal attachment and, thus, a pre-existing periodontal condition.

Does occlusal trauma cause periodontal pockets and attachment loss??? NO

○How do you see it on the Radiograph???
*Widened PDL space, *Disruption/ LOSS of lamina DURA, and *ROOT RESORPTION.

○What happens when there is NO occlusal surface
■	HYPO-FUNCTION:
1.	a lack of occlusion
2.	atrophy of the periodontium
3.	narrowing of the PDL space
4.	tendency towards extrusion
5.	increase in cementum thickness
6.	thinning of alveolar bone

○MOST COMMON = HORIZONTAL bone loss

○What regenerates BEST =3 wall defect (vertical bone loss)

○Regenerates LEAST = 1 wall defect (hemiseptum)

○ 4 wall defects= circumferential
■ Does not exist in natural dentition

Question 46

Q

23) Scenarios of diagnosis for type of PD - know the numbers associated with each type?

Answer

A

Scenarios of diagnosis for type of PD - know the numbers associated with each type:

***CHRONIC Periodontitis:
Classification based on EXTENT:
- Localized is ≤ 30% sites involved
- Generalized is > 30% sites involved

Classification based on SEVERITY:

Slight (mild) - 1-2 mm CAL
Moderate - 3-4 mm CAL
Severe - > 5 mm CAL
***AGGRESSIVE Periodontitis:
1) LOCALIZED Aggressive Periodontitis (LAP):
Circumpubertal onset!
Involves NO MORE than 2 teeth other than 1st Molar
Involves no more than 2 teeth other than 1st molars and incisors.

2) GENERALIZED Aggressive Periodontitis (GAP):
* Usually < age 30 by may be older
* Generalized IP attachment loss
* **At least 3 Permanent teeth other than 1st molars and incisors

Familial aggregation
(Based on LOCATION & # of teeth involved. NOT on percentage of sites)

Question 47

Q

24) What are common PD pathogens?

Answer

A

●	Porphyromonas gingivalis
●	Tannerella forsythia
●	Treponema denticola
●	Aggregatibacter actinomycetemcomitans
●	Prevotella intermedia

Question 48

Q

What is the Difference between aggressive localized and generalized HIV?

Oral manifestations what do we typically see in our patients in the mouth?

Answer

A

1) Oral Hairy leukoplakia
- Lateral border of tongue
- Keratotic area, corrugated, may appear shaggy

2) Oral candidiasis:
-Diminished host resistance
-Candida albicans
Often refractory (meaning it is non-responsive to treatment)

3) Bacilliary (epitheliod) angiomatosis
- Infectious vascular disease similar to Kaposi sarcoma
- Rickettsia-like organism etiology
- Red, purple, blue soft lesion

4) Kaposi sarcoma: can be extra-orally
Vascular neoplasm
HHV 8
LOCALIZED, slow growing

5) Hyper pigmentation ( from HIV meds)
- Seen on PALATE, buccal mucosa, gingiva, tongue

AIDS: Periodontal disease

1) NUG
2) NUP
3) NUS (necrotizing ulcerative stomatititis

4) Linear Gingival Erythema: around GM, generalized, diffuse gingivitis
-Fiery red, non-painful gingival band
-Common in AIDS patients with unpredictable response to Tx
-Tx: SRP, polish & re-treat if necessary
-May be refractory
-May spontaneously remiss
does NOT indicate low CD4 count

Question 49

Q

What are the secondary features of AGGRESSIVE PERIODONTITIS?

Answer

A

1) Deposits inconsistent w/ destruction
2) Elevated proportions of A.a
3) In some populations, elevated P.g
4) Phagocyte abnormalities
5) Hyper-responsive macrophage phenotype
6) Elevated levels of PGE2 and IL-1B
7) Progression of attachment loss may be self-limiting

Note: generally not universally present

Question 50

Q

What is one of the MOST prevalent disease in childhood?

Answer

A

Chronic marginal gingivitis (looks like chronic gingivitis)

Pre-eruption bulge: before crown breaks gingiva, gingiva is blanched, firm and conforms to shape of underlying crown
Gingivitis is associated with tooth eruption → prominent rolled gingival margin, inflamed, edematous
Normal prominence of gingival margin: prominent and rolled esp. in maxillary anterior region
Poor OH with ortho tx → remove brackets/wires until OH improves

Question 51

Q

Know about saliva

Answer

A

● Defense Mechanisms of Gingiva Saliva
- Lubrication/Physical protection
● Salivary components: Glycoproteins, mucoids
● Probable mechanism: Coating similar to gastric mucin
- Cleansing
● Salivary components: Bicarbonate and phosphate
● Probable mechanism: Antacids
- Buffering
● Salivary components: Physical flow
● Probable mechanism: Clearance of debris and bacteria
- Antibacterial action
● IgA: Control of bacterial colonization
● Lysozyme: Breaks bacterial cell walls
● Lactoperoxidase: Oxidation of susceptible bacteria

Question 52

Q

What is the MOST frequently occurring osseous defect?

Answer

A

OSSEOUS CRATER
■ concavities in the crest of the alveolar bone
■ confined within facial & lingual walls

Brainscape's Knowledge GenomeTM

OST Exam II Review Flashcards

Brainscape's Knowledge Genome^TM