Botulinum toxin for OFP Flashcards
How does botulinum toxin work?
Neurotoxin produced by clostridium botulinum bacteria A to G strains. A is the most potent strain. Allergan (botox) and Dysport (Ipsen) are type A. Type B is rarely used.
Inhibits acetylcholine release by cleaving SNARE proteins and preventing release of acetylcholine into the synaptic cleft. This causes skeletal muscle paralysis. Takes between 24 hours and 72 hours to take effect and reaches peak effect at 10 days. 2 - 6 months after injection everything returns to normal because neurons form new collateral axonal sprouts (buds from the neuron) which create new neuromuscular junctions.
In pain it normalizes muscular hyperactivity, it normalizes excessive muscle spindle activity, retrograde neuronal flow to the CNS, suppresses neuropeptide secretion in nociceptors in cental and peripheral NS.
Suppression of substance P and decreases calcitonin GRP, decreased inflammation, decreased glutamate secretion, and reduces spinal dorsal horn neurone activity leading to pain relief and anti-inflammatory effects.
What are the approved orofacial indications for botulinum toxin use?
Strabismus
Cervical dystonia
Chronic migraine (more than 15 days per month of headaches)
Belpharospasm (uncoordinted muscle spasms)
Cosmetic use (forehead lines, glabellar, lines, Crow’s feet)
What are the contraindications to botulinum toxin use?
Known hypersensitivity/allergy
Pre-existing neuromuscular/neurological disease (Myaesthenia gravis, Eaton Lambert syndrome, Amyotrophic lateral sclerosis, motor neurone disease)
Infection at injection site.
Inflammation/inflammatory skin disorders at intended injection site.
Previous lower eyelid surgery
Pregnancy
Lactation
Psychological issues?
Theoretically medications that decrease neuromuscular transmission such as aminoglycosides, Ca channel blockers, penicillamine, and quinine
What are the adverse effects of using botulinum toxin?
Short term: Local = ecchymosis, pain, oedema, purpura, and transient hypoaesthesia. Post injection headaches, prolonged migraines, nausea, and malaise/flu-like symptoms. Botulism symptoms. Anaphylaxis
Medium to long term: Unwanted muscle weakness, ptosis (eyelid/lip), altered or reduced facial expression, dysphagia, neck weakness, muscle atrophy, osteopaenia of mandibular condyle.
Treatment failure often occurs due to antibody development and this occurs in 5 - 10% of patients. It is avoidable with the use of booster injections.
What are the therapeutic uses of botulinum toxin in dentistry?
Lack of clear evidence but is effective for:
Motor/neurological problems (Bruxism/pathological clenching, oromandibular dystonia)
Pain (TMD, myogenous TMD, arthrogenous TMD and neuropathic orofacial pain)
What does the dental board of Australia advise regarding use of botulinum toxin for OFP?
Dentists must perform only those dental procedures for which they have been educated, trained and are competent.
Current scope of practice includes use of botulinum toxin.
BT should only be used if treatment can be justified. It is off-label.
Administering botox would require additional training.
How does botox reduce pain?
It normalizes muscular hyperactivity
It normalizes excessive muscle spindle activity
Produces effects by retrograde neuronal flow to the CNS reducing exocytosis of pain molecules.
Suppresses neuropeptide secretion in nociceptors in central and peripheral NS.
Suppression of substance P and decreases calcitonin GRP, decreased inflammation, decreased glutamate secretion, and reduces spinal dorsal horn neurone activity leading to pain relief and anti-inflammatory effects.
How does botox reduce pain?
It normalizes muscular hyperactivity
It normalizes excessive muscle spindle activity
Produces effects by retrograde neuronal flow to the CNS reducing exocytosis of pain molecules.
Suppresses neuropeptide secretion in nociceptors in central and peripheral NS.
Suppression of substance P and decreases calcitonin Gene Related Peptide, decreased inflammation, decreased glutamate secretion, and reduces spinal dorsal horn neurone activity leading to pain relief and anti-inflammatory effects.
How does botox reduce pain?
It normalizes muscular hyperactivity
It normalizes excessive muscle spindle activity
Produces effects by retrograde neuronal flow to the CNS reducing exocytosis of pain molecules.
Suppresses neuropeptide secretion in nociceptors in central and peripheral NS.
Suppression of substance P and decreases calcitonin Gene Related Peptide,
Decreased inflammation,
Decreased glutamate secretion
Reduces spinal dorsal horn neurone activity leading to pain relief and anti-inflammatory effects.
How does botox reduce pain?
It normalizes muscular hyperactivity
It normalizes excessive muscle spindle activity
Produces effects by retrograde neuronal flow to the CNS reducing exocytosis of pain molecules.
Suppresses neuropeptide secretion in nociceptors in central and peripheral NS.
Suppression of substance P and decreases calcitonin Gene Related Peptide,
Decreased inflammation,
Decreased glutamate secretion
Reduces spinal dorsal horn neurone activity
These effects lead to pain relief and anti-inflammatory effects.
What is oromandibular dystonia?
Movement disorder characterised by involuntary spasms and muscle contractions affecting the mandible. Manifests as distorted mandibular position. It is focal in 50% of cases, segmental in 33%, and generalised in 17%.
It causes dysfunction of speech, swallowing, and eating. Can cause jaw pain.
What is the evidence of efficacy of botox for oromandibular dystonia?
No RCTs mostly case reports.
Tan et al 1999 and 2000 found that 69.7% of patients demonstrated improvement functionally.
Sinclair et al 2013 also showed improvement in >60% of patients
What are the outcomes of botox for treatment of oromandibular dystonia?
Requires botox every few months
Long term management with botox has minimal morbidity (no facial nerve paresis)
Loss of treatment effect noted in case reports.
How common is bruxism?
14 - 20% in children.
How is bruxism managed?
Self-care including improved sleep hygiene, reduction of stress, meditation, cognitive behavioral therapy.
Physical therapies
Systemic medications (eg benzos)
Oral appliances
