33 - Medications Impacting Periodontium

Question 1

Proper term for the overgrowth of gingiva that occurs with some medications

Answer 1

Drug-influenced gingival enlargement

Question 2

What drug class most commonly causes GE?

Why?

Answer 2

Calcium channel blockers

Most widely prescribed drug

Question 3

What drug has the highest prevalence of GE

Answer 3

Nifedipine

Question 4

Other CCBs w/ GE

Answer 4

Verapamil
Diltiazem
Felodipine

Question 5

Incidence/prevalence of the 3 drug classes in order

Answer 5

Phenytoin > cyclosporine > CCB

Question 6

50% prevalence GE w/ what drug

Answer 6

Phenytoin

Question 7

25-40% prevalence GE w/ what drug (~1/3)

Answer 7

Cyclosporine

Question 8

30-40% prevalence GE w/ what drug (~25%)

Answer 8

CCBs

Question 9

Regions of mouth/gingiva affected by GE

Answer 9

Max/man anterior
Starts in papillary gingiva
Localized or generalized

Question 10

Description of GE

Answer 10

Fibrotic pebbly papillae THEN diffuse fibrotic enlargement at GM

Redness and bleeding w/ poor plaque control

Question 11

Histology of GE

Answer 11

Increased fibroblasts and inflammatory cells

Increased collagen bundles

Question 12

GE and MP mechanism

Answer 12

1) Phenytoin and cyclosporine may regulate MP phenotype, upregulate PDGF and IL-1 from MP that stimulates OB proliferation/differentiation

Question 13

3 other GE mechanisms

Answer 13

1) Increased collagen production by FB
2) Decreases apoptosis of fibroblasts
3) Decreased MMP (cyclosporine) or increased TIMP

Question 14

Effect of oral hygiene on GE

Answer 14

Good OH may decrease inflammation and inhibit GE

Improved OH can cause regression of GE

Question 15

Dose dependent relationship of drug to GE?

Answer 15

Some say yes, some say no

Question 16

What drugs are host modulating agents

Answer 16

NSAIDs

MMP inhibitors

Question 17

Where is arachidonic acid found?

Answer 17

Cell membranes in membrane phospholipid bilayer

Question 18

Arachidonic acid metabolism

Answer 18

Cyclooxygenase (COX) 1/2 metabolize into prostaglandin and thromboxane

Question 19

Characteristics of COX-1

Answer 19

Constitutive

Protects cells in GI tract

Question 20

Characteristics of COX-2

Answer 20

Inducible

Upregulated by pro-inflammatory cytokines

Question 21

Pathway from Arachidonic acid

Answer 21

PGG2 > PGH2 > PGI2 OR TXA2 OR PGD2/PGE2/PGF2

Question 22

PGI2 is what? Does what?

Answer 22

Prostacyclin

Vasodilation
Inhibit platelet aggregation

Question 23

TXA2 is what? Does what?

Answer 23

Thromboxane A2

Vasoconstriction, promotes platelet aggregation

Question 24

PGD2/PGE2/PGF2 do what?

Answer 24

Vasodilation

Potentiate edema

Question 25

How do NSAIDs work?

Answer 25

Block COX-1 and/or COX-2 leading to decreased prostaglandin production.

Thus, decreased inflammation

Question 26

Can NSAIDs block periodontal inflammation?

Answer 26

Yes, with chronic drug administration to maintain effect

Prevents alveolar bone loss

Question 27

What is the primary agent available for MMP inhibition?

Answer 27

Periostat (20mg doxycycline)

These are tetracycline derivatives

Question 28

What does Periostat do?

Answer 28

Decreases collagenase production

Question 29

Why are chemically-modified tetracyclines a thing?

Answer 29

Produced to have effects on different MMPs or other molecules

Example: Decrease formation of AGEs in diabetes

Question 30

What name is associated with CMTs?

Answer 30

Lorne Golub

SUNY Stony Brook

Discovered that tetracyclines have non-antimicrobial effects in reducing collagenase production