Bruxism, Masseter Hypertrophy, and Botulinum Toxin: A Comprehensive Review

Introduction

Bruxism is a common parafunctional activity characterised by involuntary, excessive clenching or grinding of the teeth, often accompanied by rhythmic contractions of the jaw muscles. It can occur during sleep (sleep bruxism) or wakefulness (awake bruxism), and both forms are widespread globally. Recent meta-analytic data indicate that roughly one in five adults experiences bruxism: the combined global prevalence is about 22% (sleep bruxism ~21%, awake bruxism ~23%).

Bruxism is often overlooked in general practice, yet it can have significant consequences for oral and facial health. Patients may present with tooth wear (flattening or chipping of teeth), jaw pain, morning temporal headaches, or temporomandibular joint (TMJ) stiffness. In severe or chronic bruxism, the excessive loading of the masticatory muscles (primarily the masseter and temporalis) can lead to muscle hypertrophy and orofacial pain.

Importantly, bruxism has a multifactorial aetiology and is now understood to be at least partly a centrally mediated phenomenon. Sleep bruxism in particular is considered a sleep-related movement disorder tied to micro-arousals of the central nervous system. This central origin explains why traditional peripheral treatments (e.g. mouthguards) may alleviate symptoms and protect the teeth but do not necessarily cure the underlying driver of bruxism.

Pathophysiology of Bruxism

Bruxism is broadly classified into sleep bruxism (SB) and awake bruxism (AB), which differ in their triggers and awareness. Sleep bruxism often occurs during micro-arousals in sleep; the brainstem arousal leads to a rise in autonomic activity and activation of jaw muscles in an unconscious rhythmic pattern. In contrast, awake bruxism is usually semi-voluntary clenching or grinding during daytime, often driven by stress, concentration, or habit.

Over time, this neuromuscular overactivity can cause hypertrophy of the masseter (and sometimes temporalis) muscles, similar to how repetitive exercise enlarges skeletal muscles. Patients with long-standing bruxism often develop visibly enlarged jaw muscles and a stronger bite force. Ultrasonographic and electromyographic studies have confirmed that bruxism is associated with increased masseter muscle thickness and activity.

Orofacial pain in bruxism arises from sustained muscle contraction and joint overload. The constant clenching can lead to myalgia in the jaw muscles – patients often report sore, stiff masseters or tenderness in the temples upon waking. This can manifest as tension-type headaches, especially in the temporal region.

Masseter Muscle Hypertrophy

The masseter muscle is the primary jaw-closing muscle, originating from the zygomatic arch (cheekbone) and inserting at the mandibular angle. With chronic hyperactivity as in bruxism, this muscle can undergo hypertrophy, meaning an increase in bulk and cross-sectional size. Masseter hypertrophy may be unilateral or bilateral, and patients present with a noticeably wider lower face or a more square jawline.

From an aesthetic perspective, masseter hypertrophy can dramatically alter facial shape. An attractive or youthful female face is often described as having a "V-shape" or triangle of youth, where the widest part of the face is at the cheeks and it tapers to a slimmer jaw and chin. Excessive growth of the masseters makes the lower third of the face wider relative to the upper and middle thirds, creating what has been termed "pseudo-ageing".