--- title: Bruxism Explained: Causes, Types, and the Hidden Dangers of Teeth Grinding canonical_url: https://directory.smilesolutions.com.au/dental-sleep-health/tmd-bruxism-sleep-disordered-breathing-treatment/bruxism-explained-causes-types-and-the-hidden-dangers-of-teeth-grinding/ category: description: geography: city: state: country: metadata: phone: email: website: publishedAt: --- # Bruxism Explained: Causes, Types, and the Hidden Dangers of Teeth Grinding ## Bruxism Explained: Causes, Types, and the Hidden Dangers of Teeth Grinding Most people who grind their teeth at night have no idea they're doing it. There's no alarm, no conscious sensation, and often no obvious sign - until a dentist discovers flattened canines, shattered enamel, or a jaw that clicks ominously on opening. This is the defining challenge of bruxism: it is, by its very nature, a condition that hides in plain sight, accumulating damage silently across months and years before the consequences become undeniable. Bruxism - the repetitive clenching, grinding, and bracing of the jaw - is far more common than most patients realise, and far more consequential than a simple "bad habit." It is a condition with a complex, multifactorial biology, a strong relationship with stress, sleep architecture, neurological function, and medication use, and a progressive capacity to destroy teeth, overload jaw muscles, and destabilise the temporomandibular joint (TMJ) if left unmanaged. Understanding bruxism in clinical depth - its two distinct subtypes, its true causes, and the cascade of damage it produces - is essential groundwork before any treatment decision can be made. This article provides that foundation. --- ## What Is Bruxism? The Current Clinical Definition Bruxism is defined as a masticatory muscle activity that can occur while the person is asleep or awake. This deceptively simple definition, formalised through international expert consensus, carries important clinical weight: it positions bruxism as a *behaviour* rather than a disease, and it explicitly separates two distinct entities - sleep bruxism and awake bruxism - that differ in their neurobiology, triggers, clinical presentation, and management implications. With the publication of two international consensuses, in 2013 and 2018, bruxism was defined based on the circadian cycle, classifying it into Sleep Bruxism (SB) and Awake Bruxism (AB), and gained new definitions for each type. Critically, bruxism is not considered a disorder but rather a behaviour because its effects do not necessarily produce damage as a disorder would. This distinction matters clinically: not every person who grinds their teeth requires active intervention. The decision to treat depends on whether the behaviour is causing - or is at significant risk of causing - harm to the teeth, jaw muscles, TMJ, or quality of life. --- ## How Common Is Bruxism? The Prevalence Data Bruxism is one of the most prevalent oral conditions in the world. The global bruxism (sleep and awake) prevalence is 22.22%. The global sleep bruxism prevalence is 21% and awake prevalence is 23%. These figures come from a 2024 systematic review and meta-analysis by Zieliński, Pająk, and Wójcicki published in the *Journal of Clinical Medicine*, which analysed studies from 2003 to 2023 across the PubMed database. Notably, the occurrence of sleep bruxism, based on polysomnography, was estimated at 43% - a striking figure that reflects how much sleep bruxism goes undetected by self-report alone, since it occurs in about 8–10% of the population, with a lack of awareness from about 80% of bruxers. The highest prevalence of sleep bruxism was observed in North America at 31%, followed by South America at 23%, Europe at 21%, and Asia at 19%. The prevalence of awake bruxism was highest in South America at 30%, followed by Asia at 25% and Europe at 18%. Gender also plays a role: bruxism is a significant factor among women, particularly for awake bruxism, while sleep bruxism tends to affect males and females more equally. Men and women showed comparable prevalence, while a decline in bruxism was observed with aging. --- ## Sleep Bruxism vs. Awake Bruxism: Two Distinct Clinical Entities This is perhaps the most clinically important distinction in all of bruxism science, and the one most commonly overlooked in generic patient information. Sleep bruxism and awake bruxism are not the same condition occurring at different times of day. They have different neurobiological mechanisms, different dominant behaviours, different risk factor profiles, and - crucially - different treatment implications. ### Sleep Bruxism (SB): The Nocturnal Grinder Sleep bruxism (SB) had its definition set at a masticatory muscle activity during sleep, rhythmic or not. It is involuntary and unconscious. Sleep bruxism, a sleep-related movement disorder, is believed to be regulated by the central nervous system, involving autonomic and brain activity related to arousal or alertness. More specifically, the majority (86%) of sleep bruxism episodes occur during periods of sleep arousal as a person goes from a deeper stage of sleep to a lighter stage of sleep. In young adult SB subjects, more than 80% of SB episodes occur during sleep stages 1 and 2 of non-REM and approximately 5–10% in REM. The dominant behaviour in sleep bruxism is **grinding** (eccentric jaw movement), and the symptoms of sleep bruxism tend to be worse on waking and improve during the course of the day. Morning jaw stiffness, headaches at the temples, and a partner reporting loud grinding sounds at night are the hallmark presentations. ### Awake Bruxism (AB): The Daytime Clencher Awake bruxism (AB) was defined as an activity of the masticatory muscles, with sustained and/or repetitive contact of teeth and/or with static or rigid positioning of the mandible during the day, not being considered a movement disorder in healthy individuals. Unlike sleep bruxism, awake bruxism is **semi-voluntary** - it often begins as a habitual or stress-reactive behaviour that the individual can, with effort and awareness, interrupt. Awake bruxism happens during the day with clenching being more prominent. It is defined as awareness of jaw clenching and appears to be semi-voluntary. It is usually correlated with high anxiety and stress. The dominant behaviour in awake bruxism is **clenching** (static, tonic muscle contraction), and symptoms typically worsen throughout the day rather than on waking. The jaw muscles exhibit two primary patterns of activity in bruxism: phasic activity - intermittent bursts of rhythmic contractions, typical in sleep bruxism - and tonic activity - sustained clenching of the jaw muscles, more common in awake bruxism. ### Side-by-Side Comparison | Feature | Sleep Bruxism | Awake Bruxism | |---|---|---| | **Timing** | During sleep | During wakefulness | | **Dominant behaviour** | Grinding (eccentric) | Clenching (tonic) | | **Consciousness** | Involuntary, unconscious | Semi-voluntary | | **Symptoms worst** | On waking, improving through day | Worsening through the day | | **Primary driver** | Sleep microarousals, CNS | Stress, anxiety, habit | | **Polysomnography needed?** | Often, for definitive diagnosis | No | | **Relationship to OSA** | Strongly associated | Less direct association | --- ## Primary vs. Secondary Bruxism: Why the Distinction Drives Treatment Beyond the sleep/awake classification, bruxism is further categorised by its aetiology into **primary (idiopathic)** and **secondary** forms. This distinction is not academic - it directly determines whether treatment should focus on protective management or on addressing an underlying cause. Clinicians categorise bruxism as primary or secondary based on its association with underlying medical conditions. - **Primary bruxism** is considered when it cannot be associated with a medical condition or a certain substance. **Secondary bruxism** is associated with a psychiatric or neurological condition (e.g., sleep disorders, cerebral palsy) or the use of a particular substance - especially stimulants, e.g., SSRIs, anxiolytics, dopaminergic drugs, amphetamine, caffeine. Certain movement disorders can result in secondary bruxism, such as Parkinson's disease, oral tardive dyskinesia, oromandibular dystonia (Meige's syndrome), tic disorders, Huntington's disease, and hemifacial spasm. Certain neurologic or psychiatric disorders are known to precipitate or worsen bruxism, including intracranial haemorrhages or infarcts, neurodegenerative diseases, coma, dementia, depression, mental retardation, autism, and attention deficit hyperactivity disorder (ADHD). In secondary bruxism, treating the underlying cause - adjusting medication, managing a sleep disorder, addressing a neurological condition - is a primary therapeutic step. In primary bruxism, management is directed at protecting structures and reducing contributing factors such as stress. --- ## The Multifactorial Causes of Bruxism One of the most important conceptual shifts in modern bruxism science is the abandonment of single-cause explanations. Accumulated scientific evidence spanning the last three decades has considered sleep bruxism to have a multifactorial aetiology. While psychological factors are often emphasised as key contributors, sleep bruxism is now understood to originate from complex multisystem physiological processes involving both the central and autonomic nervous systems. ### 1. Psychological and Psychosocial Factors Stress and anxiety are among the most consistently identified risk factors for bruxism - particularly awake bruxism. Sleep-related microarousals correlate with sleep bruxism, whereas stress and heightened alertness often cause awake bruxism. Heavy alcohol use, excessive caffeine consumption, tobacco use, and highly stressful life circumstances also contribute to bruxism. ### 2. Neurological and Central Nervous System Factors Studies demonstrate that neurotransmitters in the central nervous system (CNS) and their associated genes may be factors in the pathophysiology of sleep bruxism. The serotonin receptor encoding gene HTR2A, catechol-O-methyltransferase (COMT), and the dopamine receptor gene (DRD1) have been shown to be associated with sleep bruxism. Hyperactivity of the masticatory muscles is influenced by brainstem centres that regulate motor activity, particularly during sleep arousals. Dysregulation of neurotransmitters such as dopamine and serotonin may contribute to increased jaw-muscle activity. ### 3. Medications and Substances Drug-induced bruxism is a clinically significant and under-recognised phenomenon. The use of amphetamines, antipsychotics, selective serotonin reuptake inhibitors (SSRIs), serotonin-noradrenaline reuptake inhibitors (SNRIs), noradrenaline-dopamine reuptake inhibitors, and drugs of abuse with catecholaminergic effects such as cocaine and MDMA can be associated with sleep bruxism. Disturbances in the neurotransmitters and their receptors in the central nervous system may play a significant role, particularly in sleep bruxism. Drugs that interfere with the normal secretion and function of neurotransmitters are documented to be capable of inducing bruxism. Such psychotropic drugs are being used in clinical practice chiefly for the management of mood disorders, anxiety, and depression. This is clinically critical: a patient presenting with new-onset or worsening bruxism who is also taking an antidepressant or stimulant medication should be assessed for drug-induced secondary bruxism, and their prescribing physician consulted. ### 4. Sleep Disorders - Including Obstructive Sleep Apnoea Risk factors for bruxism include sleep apnoea, anxiety, genetic predisposition, sleep disorders, medication use, and neurologic and psychiatric disorders. The relationship between sleep bruxism and obstructive sleep apnoea (OSA) is one of the most clinically important - and actively researched - intersections in dental sleep medicine. The prevalence of sleep bruxism was consistently higher in individuals with OSA compared to the general population. Sleep-disordered breathing induces compensatory neuromuscular responses, manifesting as increased masticatory muscle activity and nocturnal bruxism, which subsequently precipitates or exacerbates temporomandibular dysfunction (TMD) and associated orofacial pain syndromes. This connection is explored in depth in our companion article *(see our guide on The TMD–Bruxism–Sleep Apnoea Connection)*, but the key clinical implication here is this: a patient presenting with sleep bruxism should always be screened for OSA, and vice versa. ### 5. Genetic Predisposition There is moderate evidence for the role of genetics as a risk factor in the causation of sleep bruxism. A review identified 30 genes and 56 polymorphism variations potentially associated with either sleep bruxism or awake bruxism. While the field is still evolving, familial clustering of bruxism is well-recognised clinically and should prompt earlier screening in at-risk patients. ### 6. What Does NOT Cause Bruxism One of the most important corrections in modern bruxism science concerns dental occlusion. Previously held notions that attributed mechanical factors, such as occlusal discrepancies, as singular aetiologic determinants have been refuted by contemporary insights. While occlusal discrepancies and certain craniofacial morphologies were once considered primary causes of sleep bruxism, current evidence suggests they play only a minor or secondary role. Instead, these factors may act as modulators that influence the manifestation or severity of sleep bruxism in predisposed individuals, rather than serving as its underlying cause. This is why "adjusting the bite" to treat bruxism - a historically common dental approach - is not supported by current evidence as a primary intervention. --- ## The Hidden Dangers: Progressive Damage From Untreated Bruxism The word "hidden" in the context of bruxism damage is apt on two levels: the behaviour itself is often unconscious, and the structural damage it causes accumulates slowly, becoming apparent only when it reaches a clinically significant threshold. By that point, the harm is often irreversible. ### Tooth Destruction: Forces Far Beyond Normal When bruxism is involved, there is an abnormal increase in magnitude, frequency and duration, elevating the pounds of pressure to the maximum biting force of 200 to 300 pounds. The grinding force compared to regular mastication is three to ten times more powerful - enough to crack a walnut. To put this in context: normal tooth wear in non-bruxers is considered to be approximately 29 micrometres in molars and 15 micrometres in premolars per year. Dental enamel loss of 10–40 micrometres occurs from friction of normal biting or chewing, while the forces generated for mastication are between 20–120 Newtons. When bruxing, the load can be as high as 1000 Newtons, changing normal physiologic wear to severe wear, leading to fatigue failure and fractures. The clinical consequences of this force accumulate in a predictable pattern: 1. **Attrition and wear facets** - Flattened occlusal surfaces, shortened canines, and polished wear facets appear first. Canines tend to show the first visual signs of bruxism because the anatomy of a canine is longer and more pointed than other tooth types. Wear facets or flat canines are obvious visual signs of grinding. 2. **Enamel loss and dentinal exposure** - Bruxism may lead to cracks or fractures of the teeth. Tooth enamel may wear away, exposing the dentin layer underneath. Teeth then become sensitive to temperature changes and pressure. Critically, once enamel is lost, it cannot regenerate. 3. **Tooth fractures and restoration failure** - Damage from bruxism can be minor or substantial, affecting hard tissues, with attrition of occlusal surfaces of the teeth and fractures of teeth or restorations, including implant-retained restorations. 4. **Cracked tooth syndrome** - As fractures deepen under constant pressure, they will eventually chip, break a corner, or damage the pulp requiring endodontic (root canal) therapy. In extreme cases the tooth may need to be extracted. 5. **Periodontal effects** - Inflammation of the periodontal ligament of teeth may make them sore to bite on, and possibly also cause a degree of loosening of the teeth. ### Jaw Muscle Overload: Hypertrophy and Chronic Pain The masseter and temporalis muscles bear the full force of every bruxism episode. Over time, chronic overactivation leads to muscle hypertrophy, fatigue, and pain. Patients with bruxism showed masseter muscle hypertrophy, higher attrition-type tooth wear index, and more teeth with fatigue fractures and abfractions than those without bruxism. Masseter hypertrophy - a visible squaring of the lower jaw - is a common physical sign of chronic bruxism, particularly in heavy clenchers. It is also the anatomical basis for the morning headaches, jaw fatigue, and facial pain that bruxism patients frequently report. ### TMJ Damage: The Joint That Pays the Price The large forces that can be generated during bruxism can have detrimental effects on the components of the masticatory system, namely the teeth, the periodontium, and the articulation of the mandible with the skull - the temporomandibular joints. Chronic bruxism loads the TMJ with forces it was not designed to sustain over extended periods. The result can include articular disc displacement, joint inflammation, degenerative changes to the condylar cartilage, and the onset or worsening of temporomandibular disorder (TMD). A meta-analysis demonstrated a positive association between bruxism and TMDs, highlighting that the presence of bruxism increases the likelihood of developing TMDs in the future. For a detailed explanation of how these conditions interact, see our guide on *(What Is TMD? Understanding Temporomandibular Joint Disorders, Causes, and Symptoms)*. ### Dental Restoration Failure Bruxism is a significant risk factor for the failure of crowns, bridges, veneers, and dental implants. The forces generated far exceed what these restorations are engineered to withstand over normal functional use. Patients who are bruxing and have received significant restorative work - without having their bruxism managed - face a high risk of premature restoration failure, often requiring repeated and costly retreatment. --- ## Why So Many Bruxism Patients Go Undiagnosed Several factors conspire to keep bruxism under the clinical radar: - **Sleep bruxism is unconscious** - patients cannot self-report what they are not aware of - **Partners may not notice** or may not mention grinding sounds - **Early tooth wear is subtle** and may not trigger concern at routine dental check-ups - **Symptoms are diffuse** - headaches, jaw soreness, and tooth sensitivity are attributed to other causes - **The condition is episodic** - stress-related flares may be followed by quiet periods that reduce urgency Bruxism is usually detected because of the effects of the process - most commonly tooth wear and pain - rather than the process itself. By the time wear becomes clinically obvious, significant structural damage has already occurred. This is why proactive screening - particularly for patients with headaches, jaw pain, morning fatigue, or a history of stress - is a core part of a comprehensive dental assessment. *(See our guide on Recognising the Signs: When Jaw Pain, Headaches, Snoring, and Grinding Mean You Need Assessment.)* --- ## Key Takeaways - **Bruxism affects approximately 1 in 5 people globally**, with sleep bruxism and awake bruxism representing distinct clinical entities with different neurobiology, symptom patterns, and management pathways. - **Sleep bruxism is primarily driven by CNS arousal mechanisms and sleep architecture**, not dental occlusion - a critical shift from historical understanding that changes treatment logic. - **Awake bruxism is semi-voluntary and closely linked to stress and anxiety**, making behavioural and psychological interventions particularly relevant for this subtype. - **Secondary bruxism - caused by medications (especially SSRIs and stimulants), neurological disorders, or OSA - requires identification and treatment of the underlying cause**, not just protective dental management. - **The damage from untreated bruxism is progressive and cumulative**: enamel loss is irreversible, TMJ degeneration can become permanent, and the forces generated (up to 1000 Newtons) are sufficient to fracture teeth and fail dental restorations. --- ## Conclusion Bruxism is not simply "teeth grinding." It is a neurologically complex, multifactorial behaviour with two distinct clinical forms, a range of underlying causes from stress to sleep apnoea to medication side effects, and a capacity for serious, irreversible harm when left unmanaged. The distinction between sleep and awake bruxism matters for treatment. The distinction between primary and secondary bruxism matters even more. For patients in Melbourne experiencing jaw pain, morning headaches, worn teeth, or unexplained tooth sensitivity, bruxism - and its relationship to TMD and obstructive sleep apnoea - deserves proper clinical assessment, not a wait-and-see approach. Understanding what bruxism is and what it does is the essential first step. The next steps - accurate diagnosis, appropriate splint selection, and integrated management of the bruxism-TMD-OSA triad - are explored throughout this content series. We recommend continuing with *(How TMD, Bruxism, and Sleep Apnoea Are Diagnosed: From Clinical Exam to Sleep Study)* and *(Occlusal Splints vs. Mandibular Advancement Splints for Bruxism: Choosing the Right Device)* for a complete picture of the diagnostic and treatment pathway available at Smile Solutions Melbourne. --- Smile Solutions has been providing dental care from Melbourne's CBD since 1993. Located at the Manchester Unity Building, Level 1 and 10, 220 Collins Street, Smile Solutions brings together 60+ clinicians - including 25+ board-registered specialists - who have cared for over 250,000 patients. No referral is required to book a specialist appointment. Call **13 13 96** or visit smilesolutions.com.au to arrange your TMD and sleep treatment consultation. ## References - Zieliński, G., Pająk, A., & Wójcicki, M. "Global Prevalence of Sleep Bruxism and Awake Bruxism in Pediatric and Adult Populations: A Systematic Review and Meta-Analysis." *Journal of Clinical Medicine*, 2024; 13(14):4259. https://doi.org/10.3390/jcm13144259 - Lal, S.J., Sankari, A., & Weber, D.D.S. "Bruxism Management." *StatPearls*. StatPearls Publishing, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482466/ - Lobbezoo, F., Verhoeff, M.C., Ahlberg, J., Manfredini, D., et al. "A century of bruxism research in top-ranking medical journals." *Cephalalgia*, 2024. https://doi.org/10.1177/25158163241235574 - Oliveira, J.M.D., Pauletto, P., Massignan, C., et al. "Prevalence of Awake Bruxism: A systematic review." *Journal of Dentistry*, 2023; 138:104715. https://doi.org/10.1016/j.jdent.2023.104715 - Thomas, D.C. et al. 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"Diagnosis and prevalence of probable awake and sleep bruxism in adolescents: an exploratory analysis." *Brazilian Dental Journal*, 2023; 34(3):9–24. https://doi.org/10.1590/0103-6440202305202 - Lobbezoo, F. et al. "International consensus on the assessment of bruxism: Report of a work in progress." *Journal of Oral Rehabilitation*, 2018; 45(11):837–844. https://doi.org/10.1111/joor.12344 - Manfredini, D. et al. "Relationship Between Bruxism and Obstructive Sleep Apnea: A Systematic Review of the Literature." *Journal of Clinical Medicine*, 2025; 14(14):5013. https://doi.org/10.3390/jcm14145013 - Farrar, M. & Sharpling, B. "The dental demolition derby: bruxism and its impact - part 1: background." *British Dental Journal*, 2022. https://doi.org/10.1038/s41415-022-4143-8 - Ekman, E. et al. "Sleep Bruxism: A Narrative Review of Current Concepts, Mechanisms, and Clinical Implications." *PMC*, 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC13094812/