1. Analgesics and pain control in
Dentistry
Iyad Abou Rabii
DDS. OMFS. MRes. PhD

2. Analgesics
Central Analgesics
Peripheral Analgesics (NSAID)

3. Central Analgesics

4. Central Analgesics
Centrally acting analgesics are thought to
affect the opiate receptors in the brain and
perhaps also those in the spinal cord.
(Receptors are specialized sites with which a
drug interacts to produce its effects.)
The most widely used and effective of these
narcotic analgesics are derived from opium
alkaloids. Morphine is one typical example

5. Central Analgesics
Opiums
(Morphine, Heroine, Codeine, Fentanyl,
Meperidine, Tramadol, Alfetanil)
Increase pain threshold and decrease reaction
movements
Decreasing Respiratory Center`s sensibility for
CO2
Some of them cause addiction

6. Central Analgesics
Non-opiums
Nevopame
Not anti-inflamatory
Don`t causes sleep
Pain is reduced on the CNS level

7. Central Analgesics - opiums
Morphine

8. Morphine receptors
Morphine is attached to special cellular
receptors in order to perform its effects
Three kind of receprors are been
identified
Mu µ
Kappa κ
Delta δ

9. Morphine receptors

10. Morphine receptors
Mechanism of action
Morphine is linked to theses receptors
Activating receptor activated Potassium channels
causing rapid burst of K outside the neuron cell
(hyperpolarization)
Decrease the voltage-gated calcium chanels
activity preventing calcium ions entrance (More
hyperpolarization)
Hyperplorisation prevent propagation of the
action potential (electrical signals) along the
axon.

11. Morphines
For sever and mild pain, two types
Opium derived from opium plant
Opium agonists
Natural (Endomorphine)
Synthetic (Methadon, meperidine, Alfantenyl))

12. Morphine Agonists
Classified to
1. Strong Agonists
1. Morphine 4 h
2. Meperidine 2 h
3. Methadone 24h
4. Heroine 2 h
5. Alfentanyl‫ 5 ا‬to 45 min
2. Mild Agonists (Hydropoxyphene, Codeine)

13. Morphine
3. mixed agonists and antagonists
1. Pentazocaine: Agonist on κ and weak antagonist on µ and
δ
2. Nalbuphine : same as Pentozocaine but stronger afonist to
µ
3. Buprenorphine : 0.4 mg from it is equal to 10 mg of
Morphene it is partial agonist to µ and antagonist to κ

14. Morphines
4. Antagonists
1. Naloxon : Rapidly emove opiums linked to the receptors µ ،
κ and δ (30 sec after inhection)
2. Naltrixone its effects are longer than naloxon (one oral
administration can block heroine effects for more than 48 h)

15. Morphines

16. Pharmaceutical effects
Opium can affect CNS, Digestive tube,
pupil, and cardio vascular system.
CNS
1. Prevent pain reception with a dose related effect
2. Sedation but with high doses convulsion may
occur
3. Euphoria (False feeling of happiness)
4. 10 mg (IV) for mild pain
15-20 mg (IV) for severe pain (respiratory
depression is possible at this dose)

17. Pharmaceutical effects
CNS (suite)
6. Decrease the RC (Respiratory Center) sensibility
to CO2 blood level. In that case no benefit of
giving pure Oxygen (apnea may develop)
7. Nausea and vomiting (Phenothiazine is
administrated to overcome these effects)
8. cough suppressant (specially Codeine)

18. Pharmaceutical effects
Digestive system
1. Spasm of sphincters
2. Constipation
3. These effects can be reversed by the
administration of atropine (Acetylcholine
receptors antagonists)

19. Pharmaceutical effects
Other
1. Morphine pin point pupils
2. Hypotension
3. Bronchospasme
4. ischuria (urinary retention)

20. Pharmacodynamic
Can be used orally, mostly used by injection
Analgesic for the treatment of pain (except
spasmodic origin , why?)
Its effect starts
IV : 7 min
IM : 20 min
SC (subcutaneous) : 40 min

21. Pharmacodynamic
Metabolized in the liver (not to be used with
hepatic pathology)
Eliminated by kidneys as inactive metabolites
Also eliminated by sweat, bile, and maternal
milk (not to be administrated to breast
feeding woman)

22. Opium in Dentistry
1. Low to mild pain (codeine ,hydrocodone
oxycodone Propoxyphene, and tramadol)
2. For severe pain :Morphine, Pentazocaine
Butorfanol, Meperidine, and Fentanyl

23. Opium in Dentistry
In most cases dental pain is accompanied or
caused by an inflammation process, so
NSAIDs is the first choice.
Anyhow it is not uncommon to use a
combination of opium with Aspirin or other
NSAID, thus two pain control mechanisms are
combined.

24. Opium in Dentistry
Oral way is the preferred way of opium
administrations
Most opiums have their effects appears
after 2 hours, dose cant be repeated
safely after 2 hours of the first
administration if needed
Injection forms of opium can not be
administrated in dental clinics

25. Codeine
30 to 60 mg orally every 4-6 h
With this dose side effects of Codeine is
negligable
In higher dose constipation and nausee
may be noticed
Used normally in combination with
NAISD

26. Hydrocodone and oxycodone
Used orally
Hydrocodone 30 mg every 4-6 h
oxycodone 5 mg every 4 to 6 h
Pharmaceutical effects of 5 mg of
Oxycodone equal to 30-60 mg of
Codeine

27. ‫ا‬Propoxyphene
Some false rumors about the addiction
capacity of Codeine led to the development of
Propoxyphene
Used for mild pain
Its sedative action is lower than Codeine
Normally used in combination with
Paracetamol (60 to 100mg)

28. Morphine
For severe pain
The dose for 70 kg weight patient is 10 mg
The best sedative effect between opium
but also side effects (constipation, nausea,
respiratory depression, addiction) are most
obvious comparing to other opiums

29. Non Steroidal Anti-Inflammatory
Drugs (NSAIDs)

30. NSAIDs
Have analgesic, antipyretic V, and anti-
inflammatory effects
NSAIDs are Prostaglandin Antagonist
Prostaglandin is important mediator of
inflammation, pain and fever

31. Prostaglandin and Cyclooxygenases
Prostaglandins are produced
following the sequential
oxidation of AA, DGLA or EPA
by cyclooxygenases (COX-1 and
COX-2) and terminal
prostaglandin synthases:
COX-1 is responsible for the
baseline levels of
prostaglandins.
COX-2 produces prostaglandins
through stimulation.
(GLA) Gamma-linolenic acid
(AA) Arachidonic acid
(EPA) Eicosapentaenoic acid

32. NSAIDs
COX-1 and COX-2 are both located in the blood
vessels, stomach and the kidneys,
Prostaglandin levels are increased by COX-2 in
scenarios of inflammation.
Inhibiting COX-1 is responsible of NSAIDs side
effects
A third form of COX, termed COX-3 is thought to
exist in the brain and may be associated with
relief of Headaches when on NSAID therapy.

33. NSAIDs
COX-2 selective inhibitor is an anti-inflammatory
drug (NSAID) that directly targets COX-2, with such NSAID
pharmaceutical effect are maximal while side effects are
minimal

34. NSAIDs-Pharmacodynamics
Well absorbed in the digestive tube
Metabolized in the liver
Essentially eliminated by the Kidney

35. Paracetamol
Most used NSAID especially when Aspirin is
contraindicated
Inhibit prostaglandin formation in the CNS level only
(cox-3)
Thais explains its maximal antipyretic and analgesic
effects, and minimal anti-inflammatory effects
(preferred with infection)
500 to 650 mg x4 daily
Can be increased to 1000 mg X4 daily if needed

36. Paracetamol
Side effects
No side effects with therapeutic dose
Allergy is rar
Extensive use mais
Excessive use of paracetamol can damage multiple
organs, especially the liver and kidney.
Non Tetragenic, can be administrated to pregnant
and breast feeding woman.

37. Aspirin
Aspirin also known as acetylsalicylic
acid abbreviated ASA
First choice in non-infection origin dental pain
treatment (when there is no contraindication)
Very effective in acute dental pain (650 mg of
Aspirin is more effective than 60 mg of Codeine)
The maximum effect of aspirin is not dose related
(all or none), increasing the dose more than 650
mg is useless
This dose is repeated four time daily.

38. Aspirin
Aspirin use has been shown to increase the risk
of gastrointestinal bleeding.
Although some enteric coated formulations of
aspirin are advertised as being "gentle to the
stomach", in one study enteric coating did not
seem to reduce this risk.

39. Aspirin
Combining aspirin with other NSAIDs has also
been shown to further increase this risk.
Using aspirin in combination
with clopidogrel or warfarin also increases the risk
of upper gastrointestinal bleeding.

40. Aspirin
Large doses of salicylate, a metabolite of aspirin,
have been proposed to cause tinnitus
Reye's syndrome, a severe illness characterized by
acute encephalopathy and fatty liver, can occur
when children or adolescents are given aspirin for
a fever or other illnesses or infections
Aspirin (or aspirin-containing products) should
not be given to anyone under the age of 12 who
has a fever

41. Propionic Acid derivatives
Ibuprofen, fenoprofen, ketoprofen, and
flurbuprofen.
Effective for mild pain
Used safely with children

42. Propionic Acid derivatives
Ibuprofen
400 mg X4 daily
May be administrated preoperatively to reduce
postoperative pain
Naproxen
For mild pain
500 mg then 250 mg X3 daily

43. Propionic Acid derivatives
Flurbuprofen
More effctive than Ibuprofen
50-100 mg of it equal 400 mg of Ibuprofen in
efficacity
Daily dose is 300 mg divided on 2 to 3
administration. (150 X2 or 100 X 3)

44. Etodolac
Etodolac
Efective dose for dental pain is 200 – 400
X3 daily
Analgesic effect with this dose starts after
30 min and last for 4-6 h
Daily dose shouldn`t exceed 1200 mg

45. Diclofenac
Diclofenac
Its pharmaceutics and side effects are
similar to Naproxen
Dose is 25-50 mg X3 daily

46. Nimesulide
Its side effects are minor, excellent
analgesic and anti-inflammatory effects
Analegesic effect are stronger than
Ketoprofen (most effective propionic
acid)
Given orally 100 mg X2 daily

47. Possible analgesics
combinations
Opiums + non-opiums
Non-opiums + non-opiums
NSAIDs + Caffeine
NSAIDs + Sedative

48. Opiums + non-opiums
Good strategy (two pain control
mechanisms are involved)
Most used non-opium used is Codeine
(60 mg)
Dextropropoxyphene (65 mg) might
also be used but it is less effective than
Codeine

49. NSAIDs + Sedative
NSAIDs can be combined with sedatives
(Diphenhydramine hydrochloride)
This help to release dental origin pain
normally accompanied with insomnia
But increased possibility of Drug-drug
interaction should be considered when
administrated with other drugs

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