oral hygiene

Question 1

main component of dentrifices
cpf
hw
bp
fsc

Answer 1

cleansing +polishing agent 10-40%
foaming agents 1-3%

humectant 20-70%
water 5-30%

binder/gelling agent 1-2%
preservative 2-%

flavoring2%, sweeteners 2-3%
coloring 2-3%

Question 2

CAT vs S. +p04

cleaning vs polishing agents made of what ?

Answer 2

CAT- Ca2+, Al3, Sn[Tin] cleaning agent

polishing - silica; phosphate

Question 3

foaming agents

Answer 3

SLS sodium lauryl sulfate - antibacterial

Question 4

Binders/gelling agent

Answer 4

natural gums - thickening agent
or
seaweed extracts- stabilizers

Question 5

Humectant

Answer 5

sorbitol and mannitol -maintain moisture and prevent evaporation

Question 6

type of dentifrices

Answer 6

anti caries F 100-1450/ 5000 prescription based
desensitizing agents
=eg ACP, Knitrate-reduce nerve excitability, SnF2 [stannous fluoride] ; arginine

antigingivitis ; antiplaque - stannous fluoride; triclosan - historical value

Question 7

Type of F

Answer 7

NaF 0.22% at 1000 ppm
Na MFP monofluorophosphate 0.76% at 1000ppm
NaF 5000ppm - prescription based

Question 8

active ingredient of oral antiseptic m/w

Answer 8

CHX
EO
CPC- cetylpyridinium chloride

Question 9

CHX adv

Answer 9

1gold standard of therapeutic m/w
2most effective antiplaque and antiging
3antibacterial via disruption of cell membrane, increase premeability, cell lysis and death
superior 4substantivity - 8-12hr bind to oral tissue

Question 10

chx disadv

Answer 10

tooth and tongue staining
unpleasant taste
increased calculus formation

Question 11

chx instructions- eg

Answer 11

15ml - 30-60 sec bid 14days ; rinse and spit
30 mins btw rinsing and brushing avoid interaction with SLS which deactivates CHX// eat/drink /rinse - periogard, peridex

Question 12

EO moaction

Answer 12

contain phenolic compounds that destroy microorg by compromising cell membrane and inhibit ENZYME activity

Question 13

benefit of EO

Answer 13

slow bacterial multiplication
2 prevent bact. agg
3reduce bact. load
4 prevent biof. maturation
5 reduce pathogenicity of biofilm

Question 14

Adalimumab (Humira®) Facts
General class:
(MOA):
Excretion:
side effect

Answer 14

General class: Monoclonal antibody
Mechanism of Action (MOA): Blocks action of TNF ; Tumor Necrosis Factor [chrons dx]
Excretion: Half-life changes between 10 to 20 days and may be longer depending on dose.
s/effect: Can lower the ability of the immune system to fight infections.

Question 15

Zolpidem tartrate Facts
General class:
(MOA):
Brand names:

Answer 15

General class: Hypnotic
Brand names: Ambien®, Edluar®, Intermezzo®, Zolpimist®
Mechanism of Action (MOA): Inhibits GABA action through benzodiazepine 1 receptor, but medication is not benzodiazepine; this leads to sedation and hypnosis
Excretion: 1:1 Urine/feces; fast onset (1/2 hour)

Question 16

Etanercept Facts
General class:
(MOA)

Answer 16

General class: Tumor Necrosis Factor (TNF) Blocking Agent; Antirheumatic
Brand name: Enbrel®
Mechanism of Action (MOA): Anti-inflammatory effect in affected joints through blockage of TNF action
Trivia: Injectable recombinant protein combining TNF receptor portion and Fc portion of IgG antibodies

Question 17

Gabapentin Facts
General class:
(MOA)
Excretion:
side effects:
Gabapentin Clinical Significance
Treats:
Interacts with:

Answer 17

General class: GABA analog
Brand names for Gabapentin: Neurontin®, Gralise®
Mechanism of Action (MOA): Even though related to GABA, does not bind GABA receptors. Generally reduces excitatory neurotransmitters associated with voltage-gated calcium channels in presynaptic neurons.
Excretion: urine
Trivia: May cause dry throat sensation; Caries risk+ Xerostomia

Treats: Postherpetic neuralgia, seizures
Interacts with:
Opioids: increased sedative effect
Buprenorphine (tobacco cessation): increased sedative effect

Question 18

Lisinopril Facts
General class:
MOA):

Answer 18

General class: Angiotensin-converting enzyme (ACE) inhibitors (~pril ending)
Common examples: Benazepril (Lotensin®), Captopril, Enalapril (Vasotec®), Lisinopril (Zestril®, Prinivil®)
Mechanism of Action (MOA): Inhibits conversion of Angiotensin I to Angiotensin II
Angiotensin II is vasoconstrictor

ACE inhibitors can cause dry, hacking, non-productive cough that is highly irritating to individuals taking ACE inhibitors
ACE inhibitors are associated with angioedema, Stevens-Johnson syndrome

Question 19

Lisinopril Clinical Significance

Treats:
Indicates risk for:
Interacts

Answer 19

Treats: Hypertension
Indicates risk for: MI, stroke (as related to hypertension risk)
Orthostatic hypotension risk during dental appointments
Interacts with: causes increase in NSAID renal toxicity

Question 20

Losartan Facts
General class:
(MOA):
Excretion:
tx
risk
interacts

Answer 20

Angiotensin II Receptor Blocker (~sartan)
examples: Losartan (Cozaar®), Valsartan (Diovan®), Olmesartan (Benicar®), Telmisartan (Micardis®)
Mechanism of Action (MOA): Blocks vasoconstrictor and aldosterone-secreting effects of Angiotensin II, resulting in lower blood pressure
Excretion: 1/3 urine, 2/3 feces
Clinical Significance

Treats: Hypertension
Indicates risk for:
Orthostatic hypotension
MI, stroke risk related to hypertension
Interacts with: NSAIDs diminish effect of Angiotensin II receptor blockers

Question 21

Glipizide Facts

General class:
(MOA):

Answer 21

Sulfonylureas
Common examples: Glipizide (Glucotrol®), Glimepiride (Amaryl®), Glyburide
Mechanism of Action (MOA): Stimulates insulin release from beta cells; reduces hepatic glucose release; increases insulin sensitivity in tissues
Excretion: Mostly Urine

Question 22

Allopurinol Facts

General class:
moa:

Answer 22

Xanthine Oxidase Inhibitor
Mechanism of Action (MOA): Inhibits conversion of hypoxanthine to xanthine to uric acid in joints in GOUT pt

Question 23

Diclofenac Facts

General class:
(MOA):
Excretion:
used for-dose?

Post Op risk:

Answer 23

Non-steroidal anti-inflammatory drug (NSAID), non-selective COX-1 & COX-2 inhibitor
examples: Ibuprofen ;Naproxen, Diclofenac (Voltaren®.)
Mechanism of Action (MOA): Inhibition of COX enzymes results in diminished prostaglandins formation; antipyretic, analgesic, anti-inflammatory effects
Excretion: 2/3 urine, 1/3 feces
used for mild-moderate oral pain
50 mg Diclofenac Sodium 3 times/day; Maximum dose 150 mg/day

Post Op risk: Possible bleeding risk through inhibition of platelet aggregation

Question 24

no in-office dental treatment that has the potential for severe bleeding (i.e., extractions, scaling/root planing) should be rendered, IF:
Bleeding time >
Platelet count <
PTT >
PT >
INR >

Answer 24

Bleeding time > 10 minutes
Platelet count < 50,000
PTT > 45 seconds
PT > 22 seconds
INR > 3

Question 25

LPS (Endotoxin)
Source:
Effects:

Answer 25

Gram-negatives (e.g., TF,AA, PG, )
Effects: Increases cytokine release from PMNs, macrophages, and fibroblasts
Induces NO secretion in macrophages
Increases differentiation of osteoclast precursors->Activates osteoclasts
Stimulates T helper cell proliferation

Question 26

HSP (Heat Shock Proteins)

Source:
Effects:

Answer 26

TF, AA, PG, CR, PI, FN, Capnocytophaga
Promotes PDL epithelial cell proliferation and osteolytic activity
Molecular mimicry between bacterial and host HSP leading to autoimmune response

Question 27

Extracellular Proteolytic Enzymes
Source:
\effects:

Answer 27

TF, PG
Degrade “LAFF” proteins: Laminin, Albumin, Fibrinogen, Fibronectin
Hydrolyze collagen IV, IgG, and IgA

Question 28

Leukotoxin
Source:
Effects:

Answer 28

AA
Low levels: Promote apoptosis of WBCs (T cells, NK cells, PMNs), aiding in immune evasion
High levels: Cause cell death by necrosis

Question 29

Differences Between Leukotoxin and Endotoxin
Leukotoxin:

Answer 29

Produced by AA only -leukotoxin
Specifically targets white blood cells (WBCs)
Low levels: Promote apoptosis of WBCs (immune evasion)
High levels: Cause necrosis of cells

VS Endotoxin (LPS):
Found in the outer membrane of Gram-negative bacteria (e.g., TF, AA, PG)
Acts broadly on multiple cell types (PMNs, macrophages, fibroblasts)
Increases cytokine release, NO secretion, and promotes differentiation and activation of osteoclasts

Question 30

Scaler Type+ Recommendation for Pacemaker Patients ?
Magnetostrictive Ultrasonic Scalers,eg

Answer 30

Contraindicated, eg Cavitron

Question 31

Advantages of the ovate pontic include

Answer 31

1aesthetic quality, which mimics the natural emergence of a tooth from the gums,
2 easy to clean; avoiding food impaction due to its recessed form.
3 its structural strength, compared to a modified ridge lap pontic, often eliminating the issue of unsupported, weak porcelain that can be present at the gum-facing edge of the pontic.

Question 32

Piezoelectric Ultrasonic Scalers
Manual Scalers (e.g., Curettes)
used for pacemaker pt?

Answer 32

yes, Indicated

Question 33

Intensity-Modulated Radiation Therapy (IMRT) 6x

Answer 33

1Advanced form of 3D-CRT: Utilizes non-uniform radiation intensities optimized by computer techniques.
2 Greater conformity to target/tumor; higher doses to be focused on the tumor.
3 Sparing of normal tissues/parotid gland+ 4 Reduces adjacent tissue toxicities.
5 Lower risk of osteoradionecrosis
6 Suitable for treating recurrent tumors. can-re-irradiation.

Question 34

Disc Displacement with Reduction
Description:
Symptoms:

Answer 34

Condition: The disc is anterior to the condylar head in the closed mouth position and reduces upon opening.
Symptoms: Clicking, popping, or snapping noises in last 30 days with jaw m/m. Medial and lateral displacement of the disc possible.

Question 35

Disc Displacement with Reduction with Intermittent Locking
Description:

Answer 35

Condition: The disc is anterior in the closed mouth position and intermittently reduces with opening. Limited mandibular opening occurs when the disc does not reduce.
Symptoms: Clicking, popping, or snapping noises[last 30 days with jaw m/m]. Medial and lateral displacement of the disc possible. Requires a maneuver to unlock the TMJ.
Imaging: MRI- disc displacement with reduction.

Question 36

Disc displacement without reduction with limited opening

Answer 36

In the closed mouth position, the disc is in
an anterior position relative to the condylar head, and the disc does not reduce with opening of the mouth.
Persistent LMO that does not reduce with the clinician or patient performing a manipulative maneuver AND INTERFERing with ability to eat; <40mm.
This is also referred to as “closed lock.” This disorder is associated with limited mandibular opening.

Question 37

Disc displacement without reduction without limited opening

Answer 37

In the closed mouth position, the disc is
in an anterior position relative the condylar head and the disc does not reduce with opening of the mouth. This disorder is NOT associated with current limited opening.

1. Maximum assisted opening (passive stretch) movement including vertical incisal overlap ≥ 40 mm.

Question 38

Brännström’s Hydrodynamic Theory of Dentine Hypersensitivity -define/symptom

Theory Basis:

Answer 38

A short, sharp pain arising from exposed dentine [enamel loss or gingival recession] in response to stimuli such as thermal, tactile, osmotic, or chemical.

Theory Basis: Dentine hypersensitivity is caused by the movement of fluid within the dentinal tubules dt external stimuli (hot, cold, touch). This movement of fluid stimulates mechanoreceptors [nerve endings] located at the pulp-dentine interface, leading to pain.

Cold Stimuli: Cause fluid to contract and move inward.
Hot Stimuli: Cause fluid to expand and move outward.

Question 39

Arginine Mechanism:

Answer 39

Arginine +Calcium Carbonate: work together to occlude (block) the open dentinal tubules and prevents fluid movement, which is the main cause of dentine hypersensitivity according to Brännström’s Hydrodynamic Theory.
=Colgate Sensitive Pro-Relief// 8%