Therapeutics in endodontics:
by:
Dr: Doaa Gamal
Lecturer of Endodontics,Sinai University
Root canal treatment can be made comfortable, pain-free and successful for the
patient by appropriate management of patient’s fear and anxiety,pain and elimination
of infection, when present.
It gives an overview of various drugs used in Endodontics.
HOW TO MANAGE FEAR and ANXIETY IN an ENDODONTIC PATIENT?
Clinician must recognize patient’s dental fear for following reasons:
• Unrecognized fear and stress can result in a medical emergency situation such as
syncope, hyperventilation, bronchospasm, etc on the dental chair
• It prevents the cooperation from the patient.
• It acts as a barrier for the clinician to the delivery of quality dental care.
• Ignoring fear will complicate Endodontic treatment unnecessarily.
• Fear lowers the pain reaction threshold.
Once the clinician recognizes patient’s fears, appropriate measures can be taken to
manage it prior to and during the root canal treatment procedure
Management of fear and anxiety:
A-Iatrosedation(behavioral intervention)
Dr Friedman formulated a term called ‘Iatrosedation’, meaning relaxation of a patient by doctor’s
behavior (hypnosis, audioanalgesia, biofeedback)
Effective management of patient’s anxiety and fear by:
• Explaining each step of root canal treatment procedure before beginning it.
•Making local anesthetic injections comfortable and atraumatic by application of topical anesthetic at
the site of injection to avoid even the pain from the needle prick.
-Slow administration of local anesthetic solution Inform the patient about the possible discomfort and
how it can be managed.
Pharmacosedation:
In few cases, behavioral intervention may not be effective and pharmacologic management of anxiety
needs to be carried out. This includes use of sedatives and tranquillizers that can calm the patient
without producing sleep, but may cause drowsiness to some extent. They act by depressing the
central nervous system (CNS) and decreasing cortical excitability decreasing the patient’s awareness
and distracting their minds from the dental procedure.
Minimal, moderate or deep sedation can be achieved with the help of drugs that used for conscious
sedation. Inhalation, oral and parenteral routes such as intramuscular, intravenous and intranasal are
the routes of administration of CNS-depressant drugs. Inhalation and oral routes are commonly used
Sedation:
-Nitrous oxide
A-Benzodiazepines:
(anti-anxiety) are the main drugs orally administrated used for minimal sedation because they
produce sedation, anxiolysis, and amnesia, which are desirable attributes for moderate sedation.
There is no respiratory depression like with the opioids.
Alprazolam (Xanax)
Clorazepate (Tranxene)
Diazepam (Valium)
Lorazepam (Ativan)
Midazolam (Versed)
common adverse effects of benzodiazepines :
A. Sedation (do not drive a car), drowsiness, xerostomia, blurred vision, diarrhea, nausea,
decrease respiratory rate.
b. Other agents :
Barbiturates are not routinely used:
A-Barbiturates have more of an effect on the heart, CNS, and lungs than the benzodiazepines. Their
popularity over the years has been reduced by the benzodiazepines, which have fewer adverse
effects.
Longer-acting barbiturates such as phenobarbital are usually used as anticonvulsants and shorter-
acting barbiturates such as pentobarbital and secobarbital are used as sedative/hypnotics.
Propofol is a very potent sedative/hypnotic nonbarbiturate that is administered intravenously with
minimal amnesic and analgesic properties. Rapid oncet and raped recovery.
Fentanyl:
A. Fentanyl, an analgesic, has a quick onset of action (highly lipophilic) and short duration so it is
frequently used for intravenous moderate sedation. It is 100 times more potent than morphine. In
addition its duration is relatively short compared to other opioids, usually lasting only 30 to 60
minutes. Fentanyl is safe for patients with renal failure.
Analgesics
Analgesics:
A-Non-opioid or non narcotic analgesics(NSAIDS):
1-Nonselective COX (cyclooxygenase) inhibitors:
-Salicylates (Acetyle salicelic): Aspirin
-(Propionic acid derivatives )Ibuprofen(Brufen), ketoprofen ( ketofan )
-Naproxen
-Acetic acid derivatives Ketorolac ( ketolac )
-Diclofenac sodium R ( Voltaren ) R ( Declophen )
-Diclofenac potassium ( cataflam ) R ( flector ) R ( dolphin k )
2-Highly selective COX-2 inhibitors:celecoxib(celebrix)
3-Analgesics and antipyretics with poor anti-inflammatory effect: Paracetamol (Acetaminophen)
B-Opioid or narcotic analgesic Drugs:
Natural,Semisynthetic,Synthetic
Mechanism of action of NSAIDS:
Mechanism of NSAIDs
Most NSAIDs(non selective cox inhibitor) inhibit COX-1 and COX-2
nonselectively .
❖But some newer NSAIDs; like: celecoxib and rofecoxib are selective inhibitors of COX-2.
Theoretically, COX-2 inhibitors have less adverse effects but have caused death in cardiac patients and have
been banned in any countries.
Mechanism of action of NSAIDs:
Non-narcotic Analgesics Nonsteroidal anti-inflammatory drugs: Produce analgesic and anti-
inflammatory effect. • Mechanism: Inhibition of cyclooxygenase (COX)
• Classification:
NSAIDs:
-Cox 1 inhibitor
-Cox 2 inhibitor
Ibuprofen is considered the prototype of contemporary NSAIDS derived from propanoic acid.
It can inhibit both COX 1 and COX 2 enzymes, so it can be termed as “mixed COX” inhibitor,
more so, that of COX 1 enzyme. • Blockade of COX 1 can have gastrointestinal adverse
effects such as ulcers. Blockade of COX 2 can have cardiovascular adverse effects such as
thrombotic events. • NSAIDs are very effective in managing pain of inflammatory origin. •
Adverse effects: – GIT side effects – CNS side effects (Dizziness, headache) •
Contraindications: NSAIDs are contraindicated in patients with ulcers and aspirin
hypersensitivity.
Drug interaction:
NSAIDs interact with number of drugs such as: – Anticoagulants – b-blockers – Cyclosporine –
Dosage: Ibuprofen 200 mg, 400 mg, 600 mg.800, 400 mg and 600 mg doses of ibuprofen produce greater
levels of analgesia. NSAIDs can be considered as a primary class of analgesics for treating acute inflammatory
pain •
Research has found that: Since NSAIDs reduce the levels of prostaglandins in inflamed tissue, they can
increase the effectiveness of local anesthetics if given 1 hour prior to anesthetic administration.
Drug interactions of profen:
Antihypertensive medications
Aspirin
• Lithium
Warfarin
Aspirin
• Aspirin is the most useful salicylate for treating pain.
• Aspirin works by inhibiting prostaglandin synthesis.
• It primarily inhibits the enzyme cyclooxygenase (COX).
Aspirin is rapidly and almost completely absorbed from the stomach and small intestine.
Aspirin:
Uses
Mild to moderate pain
Fever
Inflammation
Prevention of stroke or heart attack
Antiplatelet effects
Adverse effects:
Gastric irritation
Prolonged bleeding time
Nausea and vomiting
Epigastric pain
Constipation
Asprin toxicity(salicilism):
Confusion and drowziness
• Sweating and hyperventilation
• Nausea, vomiting
• Marked acid-base disturbances
• Hyperpyrexia
• Dehydration
• Cardiovascular and respiratory collapse, coma convulsions and death
-Diclofenac is a nonsteroidal anti-inflammatory drug
taken to reduce inflammation and pain
USES:
Pain associated with dental surgery.
post traumatic and postoperative inflammatory conditions
Oseto-arthritis
ADVERSE DRUG REACTIONS:
Liver damage
• Nausea
Dizziness
Headache
Abdominal Pain
• Peptic Ulceration Hypertension
• GI Bleeding
Skin Rashes
Cardiac Failure
Selective COX-2 inhibitors Ex(Celebrex)
General advantages :
Potent anti-inflammatory
Potent Antipyretic & analgesic
Lower incidence of gastric upset
No effect on platelet aggregation (cox1)
General adverse effects:
Renal toxicity
• Dyspepsia & heartburn
• Allergy
Cardiovascular ( do not offer the cardioprotective effects of non-selective group).
Celecoxib(celebrex)
Selective COX-2 inhibitors
Food decrease its absorption
Highly bound to plasma proteins
Celecoxib (Celebrex) 200 mg
once/day
Acetaminophen: it is thought to involve inhibition of prostaglandin synthesis within the central nervous system
Acetaminophen is not related to salicylates or NSAIDs.
It is rapidly and completely absorbed from the gastrointestinal tract.
It achieves peak levels in 1-3 hours.
Acetaminophen is metabolized by the liver.
If large doses are ingested, an intermediate toxic metabolite ,N-acetyl-p-benzoquinone-amine is formed.
Mechanism:
Inhibits prostaglandin synthesis via CNS inhibition of COX (not peripheral)
doesn’t promote ulcers, bleeding or renal failure;(SAFE)
*peripherally blocks generation of pain impulses,
*inhibits hypothalamic heat-regulation center
Acetaminophen:
Acetaminophen has both analgesic and antipyretic effects.
Therapeutic doses have no effect on the cardiovascular and respiratory system.
It does not have any real gastrointestinal effects.
Acetaminophen
Adverse Effects:
Hepatotoxicity
Can occur after the ingestion of a single toxic dose
(20-25 gm) or after long term use of therapeutic
doses.
Children are at high risk for hepatotoxicity because
they are often given doses that are not age- and
weight-appropriate.
Signs and symptoms include nausea, vomiting, abdominal pain, anorexia
Nephrotoxicity: It has been associated with long-term use
Goals of Combination Therapy:
To use lower doses of the component drugs
Increasing range of action by combining a fast-onset, short acting analgesic for milder pain and aslower-onset,
longer-duration analgesic.
Targeting different pain pathways simultaneously
Acetaminophen Combinations
Acetaminophen combined with NSAID (For mild pain)
Acetaminophen combined with opioid (For severe pain)
Indications of NSAIDS in Endodontics:
Irreversible pulpitis
• Apical periodontitis
• Acute alveolar abscess
• Infected cyst
Adverse effects shared by NSAIDs
GIT upsets ( nausea,vomiting)
GIT bleeding & ulceration
• Bleeding
Hypersensitivity reaction
• Inhibition of uterine contraction.
Salt & water retention
B-Opioid Analgesic Drugs:
Opioids analgesics are used to relieve acute, moderate to- severe pain. The
opioid receptors are located at several important sites in brain, and their
activation inhibits the transmission of nociceptive signals from trigeminal nucleus
to higher brain regions
Classification:
-Natural :
Morphine • Codeine
-Semisynthetic:
• Diacetylmorphine (heroin) • Pholcodine
-Synthetic:
• Pethidine (Meperidine) • Tramadol • Fentanyl • Methadone •
Dextropropoxyphene
Codeine It is a methylmorphine. Occurs naturally in opium, partly converted into
morphine in body It is less potent than morphine. Codeine is 1/6–1/10 as analgesic to
morphine. When compared to aspirin, it is more potent 60 mg codeine–600 mg aspirin.
Morphine It has site-specific depressant and stimulant actions in CNS. Degree of
analgesia increases with dose Depresses respiratory center, death in morphine poisoning is
due to respiratory failure Oral bioavailability averages one fourth of parenterally
administered drug About 30% bound to plasma protein, and high first pass metabolism
Plasma t1/2 = 2 to 3 h Morphine is noncumulative Doses: 10–15 mg intramuscular or
subcutaneous (SC). Side effects Sedation, constipation, respiratory depression, nausea and
vomiting
Antidote Naloxone 0.4 to 0.8 mg IV repeated every 2 to 3 min till respiration picks up; used
in acute morphine poisoning.
Dextropropoxyphene Half as potent as codeine Plasma t1/2 is 4–12 h Doses: 60–
120 mg three times a day.
Tramadol Centrally acting analgesic; relieves pain by opioid as well as additional
mechanism Injected IV 100 mg tramadol is equianalgesic to 10 mg morphine
Adverse effect of opioids:
-Respiratory depression
-Dependance
-Nausia
-Constipation
-Dizness
Differences between Opioids and Non Opioids
Opioid Analgesics Non Opioid Analgesics
Act centrally Act peripherally
Cause addiction Do not cause addiction
Produce CNS depression No CNS depression
Do not produce gastritis Produce gastric irritation
Do not provide antiinflammatory effect Provide anti inflammatory
Corticosteroids
CORTICOSTEROIDS:
• Mechanism: Glucocorticoids reduce the acute inflammatory response
by inhibiting the formation of arachidonic acid, and – by suppressing
vasodilatation, migration of polymorphonuclear (PMN) leukocytes and
phagocytosis ↓ Thus, they block the cyclooxygenase (COX) and lipooxygenase
(LOX) pathways ↓ Blocking synthesis of prostaglandins and leukotrienes ↓ Pain
control
• Steroids have been used in the past as: – Pulp capping agent – Intracanal
medicamentalone or in combination with antibiotics/antihistaminics – Systemic
administration to decrease pain and inflammation in Endodontic patients
• Steroids have been found to be more effective in pain from pulpal necrosis
with associated radiolucency compared to pain from irreversible pulpitis
because of the chronic inflammation Dosage: 6–8 mg of dexamethasone or 40
mg of methylprednisolone can be given by an intraoral ,IM or an intraosseous
injection
but theyfor
killing significant
medicines
are anti- post-treatment pain relief.
killing medicines
but they are anti-
But due to their
inflammatory
processes, they
can reduce pain.
Antibiotics
For Prevention or Elimination of Infection:
Not all Endodontic cases require antibiotics.
• Conditions that require adjunctive antibiotics:
1. Cases with show signs of systemic involvement such as fever, malaise, lymphadenopathy, trismus, etc.
2. Acute alveolar abscess is the condition which may show such systemic involvement and will need antibiotic
treatment in addition to debridement of root canal and drainage of any accumulated purulence.
3. Progressive infections—increased swelling, cellulitis, osteomyelitis.
4. Persistent infections
5. Prophylactic antibiotics are prescribed in medically compromised patients to prevent infection.
6. Surgical Endodontics
Conditions that donot require adjunctive Antibiotics:
1- Most of the infections of Endodontic origin, such as symptomatic irreversible pulpitis or apical periodontitis.
2-Necrotic teeth with radiolucency or a draining sinus tract or localized fluctuant swellings can be effectively
managed without the use of antibiotics
Other methods for management:
Analgesics , combination of Appropriate Endodontic procedure , use of intracanal medicament in few cases and
Occlusal reduction (Bite relief )
Systemically administered antibiotics cannot substitute timely Endodontic
treatment.
Chemomechanical debridement of the infected root canal system and incision and drainage if there is swelling,
usually begins the healing process in case of a normal healthy patient.
Incision and drainage provides pathway for removal of inflammatory mediators and helps prevent further
spread of cellulitis.
– Overprescribing of antibiotics, in cases where not indicated can result in bacterial resistance
NB– Sometimes, severe pain may be from a vital tooth where bacteria are not a causative factor, where
antibiotics are not needed.
Antibiotics commonly used in dentistry:
• Penicillins:
– Effective against both facultative and anaerobic microorganisms associated with polymicrobial Endodontic
infections.
– Mechanism of action: Inhibition of cell wall synthesis during multiplication of microorganisms. Exerts
bactericidal action,l east toxic antibiotic and accumulate in the kidney – 1g of penicillin VK can be orally
administered followed by 500 mg every 4–6 hours. –
Amoxicillin 1 g—as a loading dose can be very effective to treat infections followed by 500 mg every 8 hours
Clavulanate: – It causes competitive inhibition of beta-lactamase.
– Clavulanate + amoxicillin (Augmentin) combination is very useful in Endodontic infections. This
combination is effective in immunocompromised patients also.
Erythromycin and other macrolides:
– Mainly used in patients allergic to penicillin – Not effective against anaerobes associated with Endodontic
infections –
-Bacteriostatic.
-It has serious drug interactions with certain antihistaminics and bronchodilators.
Clarithromycin and azithromycin are other macrolides with some advantages over erythromycin.
– Dosage: Clarithomycin 250–500 mg every 12 hours for 6–10 days
Azithromycin loading dose: 500 mg followed by 250 mg daily. – These antimicrobials can block the metabolism
of anticoagulant drugs like warfarin causing serious bleeding in patients undergoing anticoagulation therapy.
• Clindamycin:
-Bacteriostatic , wide spectrum antibiotic and penetrate well into abscesses.
Effective against both facultative and strict anaerobic bacteria associated with Endodontic infections –
-Overgrowth of clostridium difficile causing pseudomembranous colitis
• Metronidazole:
-Bacterecidal.
Effective against anaerobic bacteria.
– Combined with penicillin to treat severe or persistent Endodontic infections.
– Patients taking metronidazole should not consume alcohol during therapy and at least 3 days afterward.
• Cephalosporins :Usually not indicated for treating Endodontic infections.
• Doxycycline: May be occasionally prescribed when the above antibiotics are
contraindicated.
Usually excellent in endo-perio lesions.
Not to be given to children ,pregnant or lactating women.
May cause photo sensitivity.
Fluoroquinolones:
Ciprofloxacin: May be indicated in persistent infections
Fluoroquinolones interfere with DNA replication classifying them as bactericidal.
They are not effective against microbes commonly
seen in endodontic infections.
Their use in dentistry should probably be limited to
cases in which culture results prove their indication.
DAP Intracanal mediction:=(Ciprofloxacin)+Metronidazole
Prophylactic antibiotics
Are recommended for both nonsurgical and surgical Endodontic procedures in
patients with cardiac conditions who are at risk of developing bacterial endocarditis
or in medically compromised patients in general before and after treatment
Intracanal Irrigants and Disinfectants Such as sodium hypochloride, EDTA,
chlorhexidine, etc, are the agents used during root canal treatment for debridement
and cleansing of infected root canal of all necrotic debris and for removal of smear
layer.
Thank you