Bruxism, a widespread condition excacerbated by stress, refers to grinding or clenching the teeth. The chronic condition may lead to tooth wear, periodontal disease, headaches and temporomandibular joint disorders. This article discusses how the use of Botox, professionally administerd by a dentist trained in its use, can alleviate this condition.

By Afreen Hoque and Maureen McAndrew

Currently an increasing number of dentists are providing botulinum toxin to their patients for a multitude of non-cosmetic reasons. Botulinum toxin type A is being used to address facial and oral pains and syndromes, including bruxism, masseteric hypertrophy, sialorrhea, hemifacial spasm, temporomandibular disorders, temporomandibular joint dislocation, salivary fistula and oromandibular dystonia. This article will particularly focus on the mechanism and use of botulinum toxin in bruxism as determined by recently published research.

The effects of Botulinum toxin type A
Botulinum toxin (BTX) type A (USA trade named “Botox”) is produced by the bacterium Clostridium botulinum. Botulinum toxin functions by inhibiting the release of acetylcholine at the neuromuscular junction. Normally, acetylcholine diffuses across the synaptic cleft at the neuromuscular junction to bind acetylcholine receptors on the motor end plate of the muscle cell. The binding of acetylcholine to its receptors triggers an increase in the opening of sodium and potassium ion channels. This initiates depolarisation of the motor end plate and ultimately causes a muscle contraction. Botulinum toxin serotype A, however, inhibits the release of acetylcholine at the neuromuscular junction. This toxin binds to cholinergic nerve terminals where it is internalised and released into the cytoplasm of the neuron. It then forms a complex with neuronal proteins and causes the proteolysis of SNAP-25—a synaptosomal-associated protein utilised in synaptic vesicle fusion with the nerve terminal membrane. Subsequently there is a decrease in the frequency of acetylcholine released at the synaptic cleft, which eventually leads to the inhibition of its exocytosis. Consequentially, there is a loss of acetylcholine receptors at the motor end plate resulting in a loss of neuronal activity in the target organ, and muscular denervation [1 - 3]. More recent data on the subject suggest that the neurotoxin also plays a role in reducing the release of inflammatory mediators (calcitonin gene-related peptide (CGRP), substance P, glutamate, etc) that cause pain [4].

This neurotoxin therefore interrupts a vital step in the contraction process of a skeletal muscle and causes temporary muscle paralysis. Eventually, however, the muscle initiates the formation of new acetylcholine receptors. As the axon terminal begins to sprout with the growth of branches to form new synaptic contacts, there is a gradual return to full muscle function, usually with minimal side effects.

Bruxism
Bruxism refers to the grinding or clenching of the teeth. Bruxism is a widespread condition that affects children, adults, the elderly, and may in fact be more frequent in patients with developmental disabilities [5]. It is most often a result of psychological stress and manifests both nocturnally and diurnally. Subsequent signs of bruxism may include myofacial pain and limited range of motion of the mandible. Bruxism also may or may not be audible. Chronic bruxism may lead to tooth wear, periodontal disease, headaches, and TMJ disorders [5]. Botox has been shown to provide treatment in a range of bruxism-related conditions, such as in patients with developmental disabilities, nocturnal bruxism and myofascial pain [5 - 7]. It is therefore essential that dentists be well versed in the condition and possible management techniques [8]. Traditional treatment for bruxism include mouthguards and other intraoral appliances. Additional treatment modalities include relaxation therapy, behavioural modification techniques and medications such as benzodiazepine or L-dopa [7, 9, 10].
 
The use of Botox is a longer-term solution to the problem of bruxism. Current treatment with Botox involves a bilateral injection into the masseter and temporalis muscles. However the injection of Botox into the temporalis muscle has not conclusively been found to eliminate bruxism. Rather, the bilateral action of Botox on the masseter muscles, just superior to the angle of the mandible, has been found to be effective in numerous clinical trials. The neurotoxin functions by inhibiting the excessive masseter muscle contractions, thereby reducing bruxism. This method of treatment typically provides relief for four to six months [6, 7, 9, 11]. At the conclusion of the cycle of relief, Botox may be re-administered for continued management of the condition. Similarly, because the neurotoxin provides a treatment that is reversible, it gives patients the option to stop the therapy at any time. Additionally, the neurotoxin may also work to inhibit periodontal mechanoreceptors, which may provide a solution to problems with jaw closure related to bruxism [8]. Bruxism may also result in masseteric hypertrophy. Botox may provide a much less invasive option for this condition compared to surgery. Surgical removal of the medial bulk of the masseter muscles can lead to complications associated with the use of general anesthesia, postoperative hemorrhage, edema, hematoma, infection, scarring and facial nerve damage [3, 12].

Potential complications
It is important to note that there are a number of complications associated with the use of Botox. Possible complications may include the following:

• Mild pain or soreness at the  injection site.
• Local edema.
• Erythema.
• Transient numbness.
• Mild drooling.
• Mild nausea.
• Transient headache.
• Production of neutralising (IgG) antibodies against Btx-A (in injections over 200U given at once, or repeated injections within one month of treatment session)
• Muscle weakness at site of injection.
• Post-injection bruising.
• Local spread, causing unwanted paralysis of nearby muscles.
• Flu-like symptoms.
• Development of tolerance

If there is an accidental overdose, an antitoxin is available that will neutralise the toxin if given within a few hours of the overdose. Also, Botox is contraindicated for people with diseases that affect neuromuscular transmission, such as myasthenia gravis, as well as for women who are pregnant or nursing [1].

As evidenced by this research, Botox may serve as a valuable addition to the beneficial non-cosmetic treatments, particularly for bruxism, which a dentist can provide to his or her patient. Because dentists’ training and knowledge encompasses all of the head and neck, dentists can conservatively and safely treat certain problems of the face and oral cavity when given the appropriate training specifically related to Botox use.

References
1. Bhogal PS et al. Dental Update April 2006;33(3):165-168.
2. Fuster Torres MA et al. Med Oral Patol Oral Cir Bucal 2007 Nov 1;12(7):E511-7.
3. Hoque A, McAndrew M. Use of botulinum toxin in dentistry. New York State Dental Journal November 2009;75(6):52-55.
4. Song PC et al. Oral Diseases May 2007;13(3): 253-260.
5. Lang R et al. Research in Developmental Disabilites 2009; 30: 809-818.
6. Guarda-Nardini L et al. The Journal of Craniomandibular Practice. April 2008;26(2):126.
7. Lee SJ et al. American Journal of Physical Medicine & Rehabilitation 2010; 89(1):16-23.
8. See SJ et al. Acta Neurologica Scandinavica 16 May 2002;107(2):161-163.
9. El Maaytah M et al. Head and Face Medicine 2006; 2:41.
10. Monroy Philip G. Special Care in Dentistry 2006;26(1):37-39.
11. Tan Eng-King et al. The Journal of the American Dental Association 2000; 131: 211-216.
12. Kim HJ et al. Dematologic Surgery 2003;29(5):484-489.

The authors
Afreen Hoque, B.A.
and
Maureen McAndrew, D.D.S., MS.Ed.
New York University College of Dentistry
New York, NY, USA.
afreen.hoque@nyu.edu