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"If parafunctional symptomatic condition is suspected, liaising with a dental professional will allow for a holistic approach and more effective management."
DDS (Brazil), Stat Exam (UK), MSc Aesth Medicine (UK)
Having qualified in Brazil at the prestigious São Paulo State University (UNESP), Dr Hiratsuka Dalmedo has been working in the UK for the past 25 years.
She obtained the ‘Certificate of Facial Aesthetics Masterclass’ from the Royal College of Surgeons of England followed by the Master’s degree in Aesthetic Medicine with Distinction from the renowned Queen Mary University of London, with the topic “Management of Bruxism and Masseteric Hypertrophy with Botulinum Toxin A”.
Currently holding the post of Clinical Senior Lecturer & Lead for Training Activities in the Postgraduate Programme in Aesthetic Medicine at Queen Mary University of London.
Dr Hiratsuka Dalmedo is engaged in teaching at all levels, with a particular emphasis for non-surgical treatments and special interest in cadaveric courses with anatomy applied to injectables and workshops with live models, having contributed as a speaker in numerous conferences throughout the UK, Europe and Middle East.
National and international tutor for the S.A.F.E. (Stylage & Anatomy for Facial Experience) Training in association with Thinkin by Dr. Benjamin Ascher (France) and International Key Opinion Leader for Vivacy UK.
Balancing her time between clinical practice in dentistry and aesthetics, as well as her teaching responsibilities in London, she remains passionate about elevating standards and fostering excellence in Aesthetic Medicine.
In 2013, an international panel of experts defined bruxism as “repetitive jaw-muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible” [1]. Definitions are currently reviewed to update it from a ‘movement disorder in otherwise health individuals to a risk factor’, as the abnormal high levels of muscle activity increase the risk of detrimental effects on oral health, and also to establish differences between Sleep Bruxism (SB) and Awake Bruxism (AB) [2].
These two circadian manifestations are considered overlapping conditions with AB characterized by repetitive or sustained tooth contact and/or bracing or thrusting of the mandible, and SB as abnormal rhythmic or arrhythmic muscle activity during sleep arousals [3].
Rhythmic Masticatory Muscle Activity (RMMA) is considered a physiologic activity of the jaw muscles during sleep and present in 60% of the adult population, with a recurrent and repetitive pattern of bruxism, with up to three times higher frequency than in control patients [4]. Sleep arousal is defined as a momentary awakening from sleep, marked by an increase in respiratory and autonomic cardiac activity that occurs 6 to 14 times per hour during sleep without complete return to consciousness [5,6].
The precise etiology remains unknown, while in the past bruxism was linked to dental occlusal discrepancies and abnormalities of the orofacial structures, the emphasis now is towards central factors regulation particularly the basal ganglia network and arousal during the sleep [7,8].
Other important factors that may play a role are of psychosocial nature such as stress, anxiety and personality type, and pathophysiological such as genetics, smoking, heavy intake of alcohol and caffeine, illicit drugs (i.e., cocaine and ecstasy) and certain medications (e.g. selective serotonin reuptake inhibitor) [9].
The great variation in methodology applied for diagnosis, characteristics of subjects studied and types of bruxism (SB or AB) result in a broad difference of prevalence in the literature, affecting 6 to 91% of the adult population with no significant diferences regarding gender [10].
First described by Legg in 1880, masseteric hypertrophy (MH) is a rare entity and it can be presented as either unilateral or bilateral benign enlargement of the masseter muscles. There is no gender prevalence and patients are generally in their 20s to 40s [11].
The etiology of the condition is unknown and not always linked to parafunctional conditions such as bruxism, but it can be related to masseteric hyperfunction by abnormal habits such as chewing gum and type of diet, especially hard food.
MH or enlargement of the masseter muscles is one of the causative factors leading to significant changes in the definition of the jawline and mandibular angle.
The heaviness of the lower face with a prominent mandibular angle is generally not considered as aesthetically pleasing by female patients, who perceive these characteristics as a masculine trait.
Self-esteem can be affected, furthermore if the condition is accompanied or caused by bruxism, it can lead to long – term impairment in functions and symptoms such as orofacial and temporomandibular joint pain, headaches and dental issues.
MH and bruxism are two linked entities but require individual evaluation.
Treatment demand is determined by presence of signs and symptoms. Clinical examination including palpation and inspection of the MM while relaxed and clenching should be performed to assess strength and stiffness of the muscle. The clinician should be able to differentiate benign masseteric enlargement from other conditions such as tumours, salivary gland diseases, parotid gland hypertrophy and isolated mandibular bony protuberance [12]. The current thinking reinforces the concept of conservative interventions; therefore irreversible and invasive occlusal therapies are not in line with the current management of bruxism [13].
Some behavioural interventions such as relaxation, hypnotherapy, biofeedback, and cognitive behavioural therapy may provide some relief of symptoms but with no remarkable evidence or advantage over occlusal splint therapy [14].
There is a lack of sufficient evidence for the prolonged use of pharmacotherapy such as anxiolytics or antidepressants.
Early work from Tan et al. in 2000 suggested Botulinum Toxin A (BoTN-A) as a safe and effective treatment for bruxism, reducing muscular activity [15]. In recent years the use of BoTN-A in bruxism therapies has gained more relevance. Due to its affinity for cholinergic synapses and its mechanism of action at the neuromuscular junction, it will block the release of acetylcholine from motor nerves causing muscular relaxation in therapeutic dosages.
This will result in a decrease of the intense levels of motor activity of the masseter muscle (MM) and has been shown to be beneficial to bruxist patients and for those aiming for cosmetic improvement of lower face contouring [16].
Despite the increasing use of BoTN-A to control muscle activity in bruxism, there is a lack of standardization regarding the optimum dosage.
Literature shows evidence of effectiveness from using 20 – 30 IU of Onabotulinum toxin on each side in Caucasian patients to 40 – 60 IU in Asian patients on each side, and the use of Abobotulinum toxin from 60 – 120 SU for both sides [17,18]. Recent studies using Prabotulinum toxin demonstrated that even the lower dose of 15 IU promoted decrease of symptoms and reduction of masseter thickness leading to a noticeable improvement in facial contouring [19].
To identify the ‘safest zone’ for injections, I would recommend palpation of the MM and knowledge of the important anatomical neighbouring structures (Fig 1):
Anatomical variations exist and they only acts as guidelines to theoretically locate the safest site for injections [20].
In my own practice, I outline the following boundaries (Fig.2):
A. Ear lobe to cheilion.
B. Posterior: 1 cm from tragus.
C. Anterior: 1 cm behind the anterior border of the MM, this can be felt by asking the patient to clench and palpating the border.
D. Lower: 1 cm above the inferior margin of the mandible.
Three to four injection points are marked, 1 cm apart; the marking is best performed while the patient is clenching.
Injection points may differ depending on the bulk and width of the MM, together with variable dosage.
The injection plane is deep and perpendicular to bone, therefore a 13 mm needle is recommended instead of the 8 mm needles more commonly used for BoTN-A for anti-wrinkle injections.
To ascertain that the toxin is equally distributed in all muscle layers, a retrograde delivery of the toxin can be also be adopted.
Results are gradual, with muscle weakness shown as early as two weeks after injections, and statistically significant differences in facial changes and relief of symptoms peaked at three months post-treatment and decreased at six months follow up [21].
The effect of muscle atrophy is secondary to relaxation, therefore awareness of longevity is relevant as it will determine the need for booster injections.
Despite the safety profile, localised mild complications such as pain, soreness, hematoma and bruising may occur but these are self-limiting and of intermitent nature.
Peng in 2018, grouped complications that occurred in 680 patients who received 2036 sessions of BoTN-A during the period of 6 years. The highest incidence was concerning decrease in mastication force and pain (30%), which improved within a week, bruising (2.5%), headaches (0.58%), sunken cheeks (0.44%), sagging (0.20%) and smile limitation (0.15) [22].
Undesirable and more long lasting complications include sunken cheek and asymmetric smile by likely injections into the zygomatic muscles causing subzygomatic volume loss, change in smiling expression by toxin diffusion into the risorius muscle and worsening of jowling and sagging of the skin due a substantial volume reduction, mainly in more mature patients [23,24].
One notable complication is known as paradoxical bulging (Fig.3) which is characterized by a muscular bulging during chewing or clenching, the suggested etiology is the overactivity of masseter fibers not affected by toxin, the author has adopted the retrograde delivery of the product, in order to reach all muscle layers and reduce the likelihood of this adverse effect [22]. Management of this adverse effect is by reinjecting the bulging area of the MM.
Botulinum Toxin A has been shown to be a safe and effective treatment for bruxism and masseter hypertrophy.
If parafunctional symptomatic condition is suspected, liaising with a dental professional will allow for a holistic approach and more effective management.
Treatment of masseter hypertrophy should be bespoke and in conjunction with thorough assessment of the other facial areas with a view to achieve balance and harmony.
Knowledge of anatomical structures will enable safer injection techniques with less complications.
Fig.1
Fig.2
Fig.3
Label:
A- Before treatment
B- Results after 12 months
Treated with Abobotulinum toxin 80 SU each side, reduced to 60 SU each side after 6 months.
Interval between injections: 3 months
Label:
A- Before Treatment
B- Results after 2 months
Treated with Onabotulinum toxin 20U each side, followed by 10U each side to address paradoxical bulging 2 weeks after initial treatment.
