antibiotics and analgesics in dentistry

1. Antibiotics and Analgesics in Endodontics
Under the guidance of :
Dr. Azhar Malik( Prof.&HOD )
Presented by : Dr Ankit kumar
PG(1st Year)

2. INTRODUCTION
HISTORY
CLASSIFICATION
SYSTEMIC ANTIBIOTICS IN ENDODONTICS
LOCAL ANTIBIOTICS IN ENDODONTICS
DENTAL PROCEDURE AT HIGH RISK AND LOW RISK OF BACTEREMIA
ANTIBIOTIC PROPHYLAXIS
ANALGESICS
CLASSSIFICATION OF NSAIDS
OPIODS
CONCLUSION

3. INTRODUCTION
Antibiotics : These are the substances produced by microorganisms, which
selectively suppress the growth of or kill other microorganisms at very low
concentrations.
 Antimicrobial agent (AMA)-synthetic as well as naturally obtained drugs that
attenuate microorganisms .
 Chemotherapy-Treatment of systemic infections with specific drugs that
selectively suppress the infecting microorganism without significantly affecting
the host.

4. HISTORY
3 Phases
Empirical phase Ehrlich’s phase
The Modern Era
of
Chemotherapy

5. Empirical phase
Mouldy curd by Chinese on boils.
Chauloogra oil for leprosy.
Chenopodium by Aztees for intestinal worms.
Mercury by Paracelsus(16th
century) for syphilis.
Cinchona bark(17th
century) for fevers.

6. Ehrlich’s phase(1890-1935).
Ehrlich’s given the idea that if certain dyes could selectively stain microbes, they could
also be selectively toxic to these organisms. He tried methylene blue, trypan red, etc.
• Developed arsphenamine in 1906 and neo arsphenamine in 1909 for syphilis.
• Coined the term 'chemotherapy’.

7. Modern Era
Domagk(1935)-The therapeutic effect of Prontosil.
Pasteur(1877)- Demonstrated the phenomenon of
antibiosis : growth of anthrax bacilli in urine was
inhibited by air born bacteria.

8. Fleming(1929)- Discovered pencillin.
Chain and Florey(1941)- Clinical use of pencillin.
Waksman and his colleagues (1944)- Discovered
Streptomycin.

9. Classification of Antibiotics
Based on :
a) Mechanism of Action
b) Type of organisms against which primarily effective
c) Spectrum of activity
d) Mode of Action

10. Classification
Based on mechanism of action :
1.Inhibitors of cell wall synthesis :-Eg: Penicillin, cephalosporins, vancomycin,
bacitracin.
2.Inhibitors of protein synthesis:-Eg: Chloramphenicol, erythromycin, tetracycline,
clindamycin.
3. Inhibit DNA gyrase :-
Eg: Ciprofloxacin (Other quinolones).
TRIPATHI 6th
edition

11. 4.Cause misreading of m-RNA code and affect permeability:
Aminoglycosides—Streptomycin, Gentamicin
5.Interfere with intermediatory metabolism: Sulfonamides, Sulfones,
Trimethoprim, Pyrimethamine, Metronidazole

12. Lippincott's pharmacology 5th
edition

13. Type of organisms against which primarily active :
A. Antibacterial: Penicillin, Aminoglycosides, Erythromycin, Fluoroquinolones, etc.
B. Antifungal: Griseofulvin, Amphotericin B, Ketoconazole, etc.
C. Antiviral: Acyclovir, Amantadine, Zidovudine, etc.
D. Antiprotozoal: Chloroquine, Pyrimethamine, Metronidazole, Diloxanide, etc
E. Anthelmintic: Mebendazole, Pyrantel, Diethyl carbamazine, etc.
TRIPATHI 6th
edition

14. Spectrum of Activity :
Narrow-spectrum:
Pencillin G
Streptomycin
Erythromycin
Extended Spectrum :
Ampicillin
Amoxycillin
Broad Spectrum :
Tetracyclines
Chloramphenicol
Lippincotts pharmacology 5th
edition

15. Mode of action :
1.Bacteriostatic antibiotics :
Tetracycline
Chloramphenicol
Erythromycin
Lincomycin
2.Bactericidal antibiotics :
Cephalosporin
Penicillin
Erythromycin
Aminoglycosides
Metronidazole TRIPATHI 6th
edition

16. SELECTION OF ANTIMICROBIAL AGENTS :
a. The organism’s identity
b. Patient factors
c. The site of the infection
d. The safety of the agent
e. The cost of therapy
Lippincott's pharmacology 5th
edition

17. BACTERIOLOGY
ENDODONTIC
INFECTIONS
INTRARADICULAR
PRIMARY SECONDARY
EXTRARADICULAR
PERSISITANT
Cohen 10th
edition

18. Primary infection, caused by microorganisms that initially invade and colonize the
necrotic pulp tissue (initial or “virgin” infection)
Secondary infection, caused by microorganisms not present in the primary
infection but introduced in the root canal at some time after professional
intervention (i.e., secondary to intervention)
Persistent infection, caused by microorganisms that were members of a primary or
secondary infection and in some way resisted intracanal antimicrobial procedures
and were able to endure periods of nutrient deprivation in treated canals.
Cohen 10th
edition

19. Sequeira jr et al : update endodontic microbiology 2008

20. When you need the drugs to kill the bugs
?
• Fever > 100° F
• Malaise
• Lymphadenopathy
• Trismus
• Cellulitis
• Osteomyelitis
• Persistent Infection
American Association of Endodontists, 2006

21. . Just say NO! Kill the bugs without
the drugs
•Irreversible pulpitis.
•Acute apical periodontitis.
•Draining sinus tracts.
•After endodontic surgery.
•To prevent flare-ups.
•After incision for drainage of a localized swelling (without cellulitis, fever, or
lymphadenopathy)
COHEN 10th edition

22. Complications of Antibiotic Therapy
 Hypersensitivity
Direct toxicity
Superinfections
Lippincott's pharmacology 5th
edition

23. SYSTEMIC USE OF ANTIBIOTICS IN
ENDODONTIC INFECTIONS
 Adjunctive antibiotic strategies may be needed in cases where there
is abscess formation.
In cases of discrete and localized swelling, drinage itself is
considered sufficient.
Segura-Egea etal. Antibiotics in Endodontics: a review

24. Segura-Egea JJ, Gould K, Şen BH, Jonasson P, Cotti E, Mazzoni A, Sunay H, Tjäderhane L, Dummer PMH. Antibiotics in Endodontics: a
review. Int Endod J. 2017 Dec;

25. Antibiotics in Endodontics: a review Segura-Egea et al

26. Systemic antibiotics not indicated in Endodontics :
1. Symptomatic irreversible pulpitis (pain, with no other symptoms and
signs of infection).
2. Pulp necrosis.
3. Symptomatic apical periodontitis (pain, pain to percussion and biting
and widening of periodontal ligament space).
4. Chronic apical abscess (teeth with sinus tract and periapical
radiolucency);
5. Acute apical abscess without systemic involvement (localized
fluctuant swellings)

27. Balasubramaniam R, Jayakumar S. Antibiotics in endodontics-A concise review. Int J Appl Dent Sci.
2017;3(4):323-9.

28. TYPES OF ANTIBIOTICS, RECOMMENDED
DOSAGES AND DURATION
Beta-lactam antibiotics (penicillin V and amoxicillin) are
recommended for the treatment of endodontic infections.
 Antibiotics should be prescribed at the correct frequency, dose and
duration so that the minimal inhibitory concentration is surpassed
and so that side effects and the selection of resistant bacteria are
prevented.

30. If penicillin V is used and therapy is ineffective.
Combination of penicillin V with metronidazole (loading dose 1000
mg followed by 500 mg every 6 h) or amoxicillin with clavulanic acid
is recommended.

31. Local use in Endodontics Antibiotics
It can be used in various modalities in endodontics.
 First local use of Antibiotics in endodontics was by Grossman -
Father of Endodontics.
In 1951 he proposed (PBSC) Poly antibiotic paste – combination of
penicillin, bacitracin, streptomycin and caprylate sodium suspended
in silicon vehicle.
Later in 1975 banned PBSC for endodontic use, because of the risk
of allergic reactions.

32. Locally used antibiotic agents in endodontics
1. TAP - Triple Antibiotic Paste
2. MTAD
3. Tetraclean
4. Ledermix Paste
5. Odontopaste
6.Medicated Gutta Percha
International Journal of Applied Dental Sciences 2017

33. Advantages of locally used antibiotic agents
Efficient and predictable disinfection.
 A high drug concentration at the local site.
 Reducing systemic complications of antibiotic medication.
 Disadvantage
 Possible development of bacterial resistant strains (antimicrobial
resistance).
 Allergic reactions.
Tooth staining or discoloration.

34. TAP –Triple antibiotic paste
First used by Sato et al., now commercially available as 3-MIX.MP
Cohen 10th
edition

35. Hoshino et al. recommended metronidazole (500 mg) minocycline
(100mg) and ciprofloxacin (200mg) at 1:1:1 ratio for 3mix formulation.
The carrier is propylene glycol and macrogol ointment at 1:1 ratio .
This formulation was later modified by Takushige et al. as
metronidazole, minocycline and ciprofloxacin mixed in a ratio of 3:3:1

36. Disadvantage
Bacterial resistance.
Use of Minocycline can cause tooth discolouration.

37. MTAD
 3% Doxycycline + 4.25% citric acid +0.5% Polysorbate 80 detergent.
 MTAD is capable of :
Removing the smear layer.
Disinfecting the root canal system.
Commercially available as BioPure MTAD.
Cohen 10th
edition

38. TETRACLEAN
Mixture of an antibiotic, acid and detergent, but it differs from MTAD by
the concentration of doxycycline (50mg/ml) and the type of detergent
polypropylene glycol.
 Teraclean is more effective than MTAD against the endodontic
pathogen E. Faecalis in the planktonic culture and mixed species in
invitro biofilm .
Giardino et al. also proved that tetraclean resulted in a high degree of
biofilm disintegration on nitrate membrane filters when compared with
MTAD and 5.25% Naocl.

39. Odontopaste
Zinc oxide based endodontic dressing.
Composition :
•Clindamycin hydrochloride-5%
•Triamcinolone acetonide-1%
•Calcium hydroxide -0.5%
Antibiotics in Endodontics – A Concise review

40. LEDERMIX PASTE
 3.2% demeclocycline Hcl and a steroid 1% triamcinolone acetomide.
Steroids mainly reduce the inflammation and pain, while the
antibiotics limit the infection by the microbes.
Modification of the paste-
0.7% triamcinolone, 3% demeclocycline and calcium salts.

41. Medicated Gutta percha
 Howard Martin introduced medicated gutta percha containing 10%
Iodoform and 10% tetracycline impregnated gutta percha (TGP)
 Intended to reduce the growth of bacteria inside the obturated root
canal.
TGP prevent the colonization of bacteria on the gutta percha points
and within the root canals.

42. Septomixine forte
Contains two antibiotics :
Neomycin.
polymixine B sulphate.
•Neomycin : bactericidal against gram-negative bacilli(Tang et al )
• Polymixine B sulphate is effective against gram positive bacteria.
Australian Dental Journal Endodontic Supplement 2007;52

43. Chlorhexidine
Chlorhexidine (CHX) is a broad spectrum antimicrobial agent. The
property is due to its cationic bisbiguanide molecular structure.
It is bacteriostatic at lower concentrations and bactericidal at higher
concentrations.
Effective against Gram positive than Gram negative bacteria.

44. Chlorhexidine can be applied in varies forms.
1. Mouthwash (0.12% and 0.2%),
2. Gels (2%)- medicament
Ercan et al showed 2% CHX gel was the most effective against E.facalis inside the
dentinal tubules, followed by a Ca(OH)2/ CHX mix , whilst Ca(OH)2, alone was totally
ineffective, even after 30 days.

45. Calcium hydroxide
Hermann introduced Ca(OH)2 paste as an ICM in 1920.
Calcium hydroxide paste for intracanal use is a thick
suspension of Ca(OH)2 powder in sterile water or saline or
glycerine.

46. Used to obtain;
1. Microbial control.
2. Dissolve organic remnants.
3. Heal periapical inflammation.
4. Inhibit inflammatory root resorption.
5. Stimulate hard tissue formation and
6. Serve as a temporary obturating material between appointments.

47. Its antimicrobial action is related to its high pH, which results in the
inactivation of bacterial membrane enzymes. Mahmoud Reza Hamidi et al.
2012

48. Studies done to test the antibacterial efficacy of calcium hydroxide
show that calcium hydroxide is ineffective against E. Faecalis. It
resists calcium hydroxide for about 10 days. Calcium hydroxide
shows limited action against facultative anaerobes and Candida
species but is effective against obligate anaerobes.
Hemanshi kumar. An in vitro evaluation of the antimicrobial efficacy of Curcuma longa, Tachyspermum ammi, chlorhexidine
gluconate, and calcium hydroxide on Enterococcus faecalis. Journal of conservative dentistry. Year : 2013 Volume : 16
Issue : 2 Page : 144-147

49. ANTIBIOTIC PROPHYLAXIS IN ENDODONTICS
The use of prophylactic antibiotics in medically compromised
patients undergoing endodontic therapy is controversial and should
only be considered when the benefit has been demonstrated or
when there is consensus for such use.

50. Segura-Egea JJ, Gould K, Şen BH, Jonasson P, Cotti E, Mazzoni A, Sunay H, Tjäderhane L, Dummer PMH. European Society of
Endodontology position statement: the use of antibiotics in endodontics. Int Endod J. 2018 Jan;5

51. American Heart Association,2021

52. The FDA has divided antibiotics into five categories
based on their side effects during pregnancy:
Category A: This category includes antibiotics that have been adequately controlled in studies
and have not reported any specific side effects during pregnancy.
Category B: Antibiotics have not been observed any specific complications in humans during
pregnancy, but side effects have been observed in animals.
Category C: Antibiotics do not have sufficient information about their side effects in pregnant
women or animals.
Category D: Antibiotics that have side effects, but they have been proven in pregnancy, but
when necessary, their benefits are more than their disadvantages.
Category X: Antibiotics those side effects have been proven in humans and animals and their
disadvantages are more than their advantages.
Antibiotics in endodontic treatment during pregnancy Eur J Transl Myol 32, 2022

53. Antibiotics in endodontic treatment during pregnancy Eur J Transl Myol 32, 2022

54. Dental procedures at high risk and
low risk of Bacteremia

55. High risks
•Dental extractions.
• Periodontal procedures – surgeries, SRP.
• Dental implants placement, Reimplantation of avulsed tooth.
• Endodontic instrumentation beyond apex.
• Endodontic surgery.
• Placement of orthodontic bands.
• Intraligamentary and intraosseous injections.
•Prophylactic cleaning of teeth or implants where bleeding is anticipated.
ANTIBIOTIC PROPHYLAXIS IN DENTISTRY: A REVIEW AND PRACTICE RECOMMENDATIONS
TONG, DARRYL C. et al.The Journal of the American Dental Association, Volume 131, Issue 3

56. Low risks
•Restorative procedures.
• Intracanal endodontic treatment and post placement and core.
•Placement of rubber dam.
• Removable partial dentures.
•Orthodontic appliance adjustments.
• Taking oral impressions, oral radiographs, fluoride gels application.

57. Analgesics
Algesia : An unpleasant emotional experience associate with actual
or potential tissue damage or describe in terms of such damage.
Analgesic : A drug that selectively relieves pain by acting in the
CNS or peripheral pain mechanism, without significantly altering the
consciousness.
International association for the study of pain (IASP)

58. PAIN PATHWAY

59. Classification
ANALGESICS
Non-opioid analgesics(NSAIDS) Opioid analgesics
Non-
selective
COX
Inhibitors
Preferential
COX-2
Inhibitors
Selective
COX-2
Inhibitors
Analgesic –
antipyretics with
poor
antiinflammatory
action
Natural opioids Semi-synthetic
opioids
Synthetic opioids
Essentials of medical pharmacology, K.D TRIPATHY 6th
edition.

60. NSAIDS
- Analgesic, Antipyretic & Anti-inflammatory actions.
-Act primarily on Peripheral Pain Receptors.
& CNS to raise the pain threshold
-Compared to Morphine
- Weaker analgesics
- Do not depress CNS
- Do not produce physical dependence
& have no abuse liability

61. NSAIDS
Classification :
Nonselective COX inhibitors :
Salicylates : Aspirin.
Propionic acid derivatives : Ibuprofen,Naproxen,Ketoprofen
Enolic Acid Derivative :Piroxicam, Tenoxicam
Acetic Acid Derivative : Ketorolac, Indomethacin, Nabumetone.
Pyrazolone derivative :propyphenazone.

62. Preferential COX-2 inhibitors :
Nimesulide , Diclofenac, Acelofenac, meloxicam.
Selective COX-2 inhibitors:
Celecoxib , Etoriocoxib, Paracoxib.
Analgesic – antipyretics with poor anti-inflammatory action :
Para aminophenol derivative : paracetamol(Acetaminophen).
Pyrazolone derivatives : metamizole , propyphenazone.
Benzoazocine derivative: nefopam

63. CLINICAL FEATURES OF NSAIDs
Analgesia.
Antipyresis.
Anti-inflammatory.
Antithrombotic.
J Can Dent Assoc 2002; 68(8):Journal of the Canadian Dental Association

64. Adverse effects
Dyspepsia
 Gastric mucosal damage
 Increased bleeding
 Possible renal impairment
 Anaphylactoid reaction
J Can Dent Assoc 2002; 68(8):Journal of the Canadian Dental Association

65. SALICYLATES
Aspirin
•Acetylsalicylic acid.
•Rapidly converted in the body to salicylic acid which is responsible for
most of the actions.
Pharmacological actions:
1. Analgesic, antipyretic, anti-inflammatory actions-
Weaker analgesic than morphine type drugs.
Anti-inflammatory action exerted at high doses (3-5g/day)

66. PHARMACOKINETICS
Aspirin is absorbed from stomach and small intestine.
Slowly enters brain but freely crosses placenta.
Plasma t ½ of aspirin 15-20 min; salicylic acid 3-5 hrs.
Both are metabolized in liver and excreted in urine.

67. ADVERSE EFFECTS
At analgesic dose (0.3-0.6g/day) – nausea , vomiting , epigastric
distress ,increased occult blood loss in stools.
Hypersensitivity – rashes, urticaria, angioedema.
Anti-inflammatory doses (3-6g/day) – dizziness, vertigo , excitement and mental
confusion, hyperventilation and electrolyte imbalance.
Acute salicylate poisoning- fatal dose in adults 15-30g.
- vomiting ,dehydration, electrolyte imbalance ,
hallucinations, petechial haemorrhages, hyperpyrexia,
convulsions, coma.

68. Dental Considerations:
Patients taking aspirin as secondary drug for thrombogenic cardiovascular
problems such as Myocardial infarction:-
The need for continuous anticoagulation must be weighed against the
need for blood clotting.
Consult physician to determine the safety of stoppage of the drug.
Extra measures during and after surgery to help promote clot formation
and retention.
Local hemostatic measures such as oxidized cellulose (surgical), collagen
sponge(haemocollagen), or resorbable gelatin sponge.

69. Dental Considerations :
Individual not taking anticoagulant or antiplatelet drugs, normal coagulation profile is an INR of
1.0.
The INR must be measured prior to dental procedures, ideally this should be done within 24
hours before the procedure.
Patients with stable INR, measured within 72 hours before the procedure is acceptable.
Minor dental surgical procedures can be done with INR within therapeutic range of (2.0-4.0)
when local haemostatic measures are used to control bleeding.
Optimal INR value for dental procedures is 2.5 because it minimizes the risk of hemorrhage.
Journal of Oral science, Vol 49,No.4<253-258,2007 Dental Management of patients receiving anticoagulantion or antiplatelet treatment

70. Ibuprofen
Propionic acid derivative.
Introduced as a better tolerated alternative to aspirin.
PHARMACOKINETICS
Well absorbed orally; highly bound to plasma proteins(90-99%)
Inhibit platelet function, use with anticoagulants should be avoided.
Largely metabolized in liver and excreted in urine and bile.
Plasma t ½ is 2-4 hrs.
 DOSAGE – 400-600mg TDS.

71. •CLINICAL USES
•Used as simple analgesic and antipyretic;
•Rheumatoid arthritis
•Osteoarthritis
•Soft tissue injuries
•Suppress postoperative swelling and inflammation.

72. ADVERSE EFFECTS
Gastric discomfort, nausea and vomiting.
Headache , dizziness, blurring of vision etc.
Rashes , itching – rare
Not to be prescribed to pregnant women and should be avoided in
peptic ulcer patients.

73. Diclofenac sodium
Potent analgesic-antipyretic-anti-inflammatory agent.

PHARMACOKINETICS
Well absorbed orally.
Plasma t ½ is 2 hrs.
Metabolized and excreted both in urine and bile.
Concentration in synovial fluid is maintained for 3 times longer period than in plasma –
extended therapeutic action in joints.
DOSAGE – 50 mg TDS ,75 mg deep i.m.

74. CLINICAL USES
Rheumatoid and osteoarthritis.
Toothache.
Ankylosing spondylitis.
Post traumatic and postoperative inflammatory conditions.
ADVERSE EFFECTS
Epigastric pain
Nausea
Fever
Headache
Rashes

75. Ketorolac
It is acetic acid derivative.
Potent analgesic; modest anti-inflammatory.

PHARMACOKINETICS
Rapidly absorbed after oral and im administration.
Plasma t ½ is 5-7 hrs.

DOSAGE –

Oral 20 mg starting dose than 10 mg 4-6 h

15-30 mg im or iv 24 h

76. CLINICAL USES
Post operative and acute musculoskeletal pain.
Renal colic
Pain due to bony metastasis
ADVERSE EFFECTS
Nausea
Abdominal pain
Ulceration
Headache , dizziness, nervousness
Pain at injection site

77. Paracetamol
Para amino phenol derivative.
Good antipyretic; negligible anti-inflammatory action.
PHARMACOKINETICS
Well absorbed orally.
Plasma t ½ - 2-3 hrs
Effects after an oral dose lasts 3-5 hrs.

78. DOSAGE –
Adults :- 325-650mg TDS
Childrens :10-15mg/kg

79. ACTIONS:
 Central analgesic action -Raises the pain threshold.
Poor inhibitor of prostaglandin synthesis in peripheral tissues but more
active on COX in brain.
Negligible anti-inflammatory action – poor ability to inhibit COX in the
presence of peroxides generated at sites of inflammation.

80. CLINICAL USES
Headache
Musculoskeletal pain
Much safer than aspirin in terms of gastric irritation; ulceration and
bleeding.
Does not prolong bleeding time
Can be used in all age groups.

81. ADVERSE EFFECTS
Can cause liver damage.
Analgesic nephropathy occurs after years of heavy ingestion.
Acute paracetamol poisoning-
If a large dose is taken (150mg/kg or >10g in an adult) , serious toxicity
can occur.
Early manifestations- nausea , vomiting, abdominal pain & liver
tenderness.
After 12-18 hrs - hepatic necrosis ; may be accompanied by renal
tubular necrosis and hypoglycemia.

82. Mefenamic acid
Commercial names : Mefegesic (Uniorange), meftal Forte (Blue Cross) ,
mefac (P&B), Gefplus (Madhav Biotech), Lenagesic (Wockhardt),
Ponstan (Pfizer)
Dosages :
PO 500mg , then 250 mg q6h, not to exceed 1 week.
Adverse side effects :
◦ Diarrhoea.
◦ Epigastric distress is complained.
◦ Drowsiness, dizziness, confusion, headache, nausea, vomiting, GI bleeding
◦ Tachycardia, palpitation

83.  Oligouria, hematuria.
 Hearing loss, blurred vision.
 Rashes, sweating.
Uses:
Indicated primarily as analgesics in muscle, joint and soft tissue pain where strong
anti –inflammatory action is not needed.

84. J Can Dent Assoc 2002
An Update on Analgesics for the Management of Acute Postoperative Dental Pain

85. J Can Dent Assoc 2002; 68(8):Journal of the Canadian Dental Association
An Update on Analgesics for the Management of Acute Postoperative Dental Pain

87. Opioid Analgesics
Classified as :-
Natural opium alkaloids
- morphine & codeine
Semisynthetic opiates
- Diacetylmorphine (Heroin), Pholcodeine.
Synthetic opioids
- Pethidine (Meperidine)
- Fentanyl
- Methadone
- Tramadol.

89. Morphine
Natural opium alkaloid
Pharmacological actions:-
1. CNS
Analgesia
Sedation
Mood and subjective effects.
Nausea & vomiting

90. . CVS
Causes vasodilatation
3.GIT
Constipation is a prominent feature.
4.Other smooth muscles
Biliary tract – biliary colic
Uterus – slightly prolong labour
Bronchi – bronchoconstriction
5.ANS
Mild hyperglycaemia.

91. Preparation and dosage:-
-10-30 mg oral
-10-15 mg i.m or s.c
-Children 0.1-0.2mg/kg.
Adverse effects:-
Side effects – sedation, mental clouding, vomiting, constipation, blurring of vision , fall in
BP.
Urticaria , itching , swelling of lips.
Apnea .
Acute morphine poisoning – lethal dose 250 mg.
- specific antidote - naloxone 0.4-0.8 mg i.v. repeated every
2-3 minutes.

92. Therapeutic uses of morphine
For relief of pain.
Sedation and sleep
Preanesthetic medication.
In acute left ventricular failure.
Precautions and contraindications
Infants and elderly
Respiratory insufficiency
Bronchial asthma
Head injury
Hypothyroidism ,liver & kidney disease
Unstable personalities.

93. Tramadol
Centrally acting analgesic.
Treatment of mild to moderate pain – as effective as
morphine.
Severe or chronic pain – less effective
Indicated- medium intensity short lasting pain due to
diagnostic procedures, injury, surgery etc.

94. Oral bioavailability – 68 %
I.M administration – 100 % Bioavailability.
T ½ is 3-5 hrs and effects last 4-6 hrs.
Causes less respiratory depression , sedation, constipation than
morphine.
Abuse potential is low.
Dose – 50-100mg /6 h orally and parenteral.
Maximum recommended daily dose is 400 mg.
300 mg in patients > 75 years old and for extended-release formulations

95. Mechanism of action
Opioid receptor binding.
Inhibition of Serotonin and norepinephrine reuptake.

96. Opioid receptor binding :
Act as weak mu-opioid receptor agonist.
Binds to mu-opioid receptors in the central nervous system,
Pain relief by reducing the perception of pain signals and altering the brain response to pain.
Inhibition of Serotonin and norepinephrine reuptake :
 The (+)-enantiomer binds to the receptor and inhibits 5HT uptake
. The (–)-enantiomer inhibits NE uptake and stimulates α2 adrenergic receptors.

97.  SIDE EFFECTS
Nausea
Vomiting
Dizziness
Sedation
Headache
Can cause seizures and possibly exacerbate seizures in patients with
predisposing factors.

98. Haas DA.J Can Dent Assoc 2002 An Update on Analgesics for the Management of Acute
Postoperative Dental Pain

99. OTHER DRUGS WITH ANALGESIC EFFECT
GLUCOCORTICOIDS :
The potent anti-inflammatory properties of glucocorticoids
were first appreciated & utilized as an adjunct to
endodontic therapy more than 50years ago.
Used as an intracanal medicament & systemically as a
means to decrease pain & inflammation in endodontic
patients
Ingle’s endodontics 6th
Ed

100. Intracanal administration
In the form of a paste mixed with antibiotics
Dexamethasone solution.
Kenacomb: Each gram contains 100 000 units nystatin, 2.5 mg
neomycin base (as sulphate), 0.25 mg gramicidin, and 1.0 mg
triamcinolone acetonide.

101. LEDERMIX PASTE
 3.2% demeclocycline Hcl and a steroid 1% triamcinolone acetomide.
Steroids mainly reduce the inflammation and pain, while the
antibiotics limit the infection by the microbes.
Modification of the paste-
0.7% triamcinolone, 3% demeclocycline and calcium salts.
Australian Dental Journal Endodontic Supplement 2007;52 ,The use of calcium hydroxide, antibiotics and biocides as
antimicrobial medicaments in endodontics.

102. Systemic administration
Dexamethasone :
Very potent & highly selective glucocorticoid.
Long acting.
Pituitary depression.
Used in inflammatory & allergic condition.
•Dose: 8mg loading dose, followed by 4 mg every eight hours (upto
max. 5 days).

103. CONCLUSION
Analgesics are definitely useful in reducing pain & improving the quality of life
but have their own spectrum of adverse effects.
No single drug is superior to all others for every patient. Choice of drug is
inescapably empirical.

104. REFERENCE
The pharmacological basis of therapeutics, GOODMAN & GILMAN 10th
edition.
Lippincott pharmacology 5th
edition.
Essentials of medical pharmacology, K.D TRIPATHY 6th
edition.
Pathways of Pulp 10th
Edition Stephen Cohen.
Ingles Endodontics 6th
edition.
Segura-Egea JJ, Gould K, Şen BH, Jonasson P, Cotti E, Mazzoni A, Sunay H, Tjäderhane L,
Dummer PMH. European Society of Endodontology position statement: the use of
antibiotics in endodontics. Int Endod J. 2018 Jan;5
Segura-Egea JJ, International Endodontic Journal, 50, 1169–1184, 2017
Antibiotics in endodontic treatment during pregnancy Eur J Transl Myol 32, 2022

105. Sequeira jr et al : update endodontic microbiology 2008
International Journal of Applied Dental Sciences 2017; 3(4): 323-329
Use of non steroidal anti-inflammatory drugs in dental practice : A Review. Med
Oral Patol Oral Cir Bucal 2007;12:E10-8.
Haas DA. An update on analgesics for the management of acute post-operative
dental pain. J Can Dent Assoc 2002;68(8):476-82.
2021 American Heart Association, Inc., a 501(c)(3)
JADA, Vol. 131, March 2000
Australian Dental Journal Endodontic Supplement 2007;52:1