Sleep Bruxism in Geriatric Population: When Aging Changes the Grinding Game

Story-at-a-Glance

• Sleep bruxism prevalence decreases significantly with age, dropping from 13% in young adults to approximately 3% in those over 60, yet remains clinically important in elderly populations
• Neurodegenerative disorders like Parkinson’s disease, Alzheimer’s disease, and frontotemporal dementia show a 52% higher prevalence of bruxism compared to healthy elderly controls
• The relationship between sleep bruxism and aging involves dopaminergic and serotonergic pathway disruptions, which become more pronounced with neurodegeneration
• Polysomnographic studies reveal that rhythmic masticatory muscle activity patterns change dramatically in geriatric populations, with diagnostic thresholds needing recalibration
• Elderly bruxism presents unique challenges: increased medication interactions, higher risk of dental complications, and complex associations with hypertension and sleep-disordered breathing
• Clinical recognition remains problematic, as neither neurologists routinely screen for bruxism as a motor disorder nor dentists consistently recognize its neurological origins in older adults

The Unexpected Pattern That Changed Our Understanding

When Dr. Gilles Lavigne, Canada Research Chair in Pain, Sleep and Trauma at the University of Montreal, first examined polysomnographic recordings from elderly bruxers in the 1990s, he noticed something that would reshape decades of assumptions about teeth grinding. The rhythmic masticatory muscle activity that defined sleep bruxism in younger adults didn’t quite behave the same way in people over 65.

His groundbreaking 1996 study established critical diagnostic thresholds for sleep bruxism. While asymptomatic individuals showed only 1.7 episodes per hour on average, the patterns shifted dramatically with aging. This wasn’t simply a matter of decreased frequency—the nature of the grinding itself transformed. In many elderly patients, particularly those with neurological conditions, the supposedly “nocturnal” disorder began appearing during waking hours with surprising regularity.

Fast forward to 2025, and we’re witnessing a demographic shift that makes this research more urgent than ever. By 2030, roughly one in five Americans will be over 65, according to recent epidemiological data. Sleep complaints are already prevalent in up to 50% of the elderly population, and as this segment grows, so too will the complexity of managing conditions like sleep bruxism in geriatric populations—a disorder that’s been largely overlooked in aging research until recently.

When the Grinding Doesn’t Fade: Understanding the Geriatric Paradox

Here’s where things get interesting (and perhaps counterintuitive): while the overall prevalence of sleep bruxism decreases with age, its clinical significance often increases. Think of it this way—you might have fewer episodes of teeth grinding at 75 than you did at 25. But each episode carries far greater consequences for already-compromised oral health, medication-sensitive systems, and fragile sleep architecture.

Research published in systematic reviews confirms that sleep bruxism prevalence drops from 13% in adults aged 18-29 to just 3% in those over 60. Yet paradoxically, when elderly individuals do experience bruxism, they face more severe outcomes: increased tooth wear in already aging dentition, heightened temporomandibular joint pain, and complex medication interactions that younger people simply don’t encounter.

What’s driving this peculiar pattern? The answer lies in the intricate dance between aging physiology and sleep mechanisms. As we age, sleep becomes more fragmented and lighter, with reduced slow-wave sleep and increased arousals. These are the very conditions that can both suppress and, under certain circumstances, exacerbate bruxism activity.

Additionally, the geriatric population experiences changes in neurotransmitter systems that directly influence jaw muscle activity. Dopamine levels naturally decline with age, and serotonergic pathways that help modulate rhythmic motor activities during sleep become less efficient. This creates what some researchers call a “vulnerability window” where certain individuals maintain or even develop new-onset bruxism in their later years. (Understanding how anxiety and stress trigger bruxism episodes in younger populations helps contextualize these age-related changes.)

The Neurodegenerative Connection: A Grinding Reality

Perhaps the most significant breakthrough in understanding sleep bruxism in geriatric populations came from research examining its relationship with neurodegenerative disorders. A 2024 meta-analysis demonstrated that elderly patients with neurodegenerative disorders show a relative risk of 1.52 for bruxism compared to age-matched controls—in other words, they’re 52% more likely to grind their teeth.

The connection runs deep. Consider Parkinson’s disease, where dopamine-producing cells progressively die. Dr. Frank Lobbezoo, professor at the Academic Centre for Dentistry Amsterdam and a leading bruxism researcher, has spent years investigating this association. His work with Dutch Parkinson’s patients revealed something startling: these individuals reported significantly more bruxism during both sleep and wakefulness compared to healthy controls, and they experienced notably higher pain intensity in the orofacial region.

But here’s where the neurobiology becomes fascinating (if you’re into that sort of thing, which I certainly am). In Parkinson’s disease, the basal ganglia—brain structures critical for controlling movement—function abnormally. This dysfunction extends to the basal ganglia-thalamocortical circuitry that helps regulate jaw movements. When dopamine depletion occurs, it leads to imbalanced basal ganglia output. This results in motor circuit hyperactivity and increased muscle tone. Translation? The jaw-closing muscles become overactive, manifesting as both daytime clenching and nighttime grinding.

The mechanism isn’t limited to Parkinson’s. Research on Alzheimer’s disease patients has documented awake bruxism as well, particularly in those with frontal lobe dysfunction. A Japanese study used surface electromyography to demonstrate rhythmic masseter muscle activity at rates of 1-2 contractions per second in Alzheimer’s patients—a clear neurological sign rather than a mere dental problem.

Frontotemporal dementia patients show even higher rates, with some studies reporting bruxism in up to 27.3% of cases. This makes sense when you consider that frontotemporal dementia specifically affects the frontal and temporal lobes, regions involved in motor control and behavioral regulation.

The Medication Maze: When Pills Meet Grinding

Managing sleep bruxism in the geriatric population becomes exponentially more complex when you factor in polypharmacy—the use of multiple medications simultaneously. According to recent data, 46% of Medicare beneficiaries take five or more medications daily, and this cocktail can interact with bruxism in unpredictable ways.

Some medications exacerbate bruxism. Certain antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), are well-documented bruxism triggers. This creates a cruel catch-22: elderly patients taking SSRIs for depression may develop or worsen teeth grinding, leading to jaw pain and sleep disruption—which then worsens their depression. I’ve seen this cycle play out more times than I’d like to count.

Interestingly, the same medications used to treat Parkinson’s disease can have contradictory effects on bruxism. A cross-sectional study examining levodopa equivalent daily dosages in Parkinson’s patients found no clear dose-response relationship with bruxism frequency—suggesting the mechanism is more nuanced than simply “more dopamine equals less grinding.”

Then there’s the issue of medications that affect sleep architecture directly. Beta blockers, commonly prescribed for hypertension in the elderly, suppress melatonin secretion and increase sleep fragmentation. Benzodiazepines and opiates, while potentially reducing bruxism episodes, worsen sleep-disordered breathing—which itself is associated with bruxism. It’s a pharmaceutical house of cards.

Sleep Architecture Under Siege: The Hypertension Factor

Recent research has unveiled an intriguing connection between hypertension and sleep bruxism in elderly populations that challenges our previous understanding. A 2022 polysomnographic study comparing nonapneic hypertensive patients with normotensive controls found significant differences. Hypertensive individuals showed higher arousal indices and increased sympathetic system activation during sleep—conditions that intensify bruxism activity.

The relationship appears bidirectional. On one hand, chronic hypertension creates systemic inflammation and increased sympathetic tone. This may trigger more frequent bruxism episodes through heightened arousal mechanisms. On the other, repeated bruxism episodes themselves involve bursts of cardiac and sympathetic activity, potentially contributing to blood pressure elevation over time.

This is particularly relevant for geriatric populations, where cardiovascular disease prevalence is high. Approximately 50% of elderly individuals have hypertension, meaning half of our aging population faces this compounding risk factor for sleep bruxism. The implications for clinical management are significant: treating sleep bruxism might require cardiovascular considerations, and vice versa.

The Diagnostic Challenge: Why We Keep Missing It

One of the most frustrating aspects of sleep bruxism in geriatric populations is how often it goes unrecognized. A 2020 commentary by a Parkinson’s patient-researcher noted that “while bruxism can happen at any time of day, daytime versions are seldom a complaint in someone with PD. Complaints of morning jaw pain, or the discovery of loosened or even broken teeth, may signal a case of nocturnal bruxism.”

The problem? Most neurologists don’t screen for bruxism as a motor symptom, and most dentists aren’t trained to recognize the neurological origins of tooth grinding in elderly patients. This creates a dangerous gap in care where significant symptoms fall through the cracks.

Part of the challenge lies in how bruxism manifests differently in older adults. Younger bruxers typically report loud grinding sounds that disturb bed partners, making the condition obvious. Elderly bruxers, however, may exhibit more clenching behavior than grinding, producing less noise and therefore fewer complaints. The tooth wear is often attributed to “a lifetime of chewing” rather than active pathology.

Moreover, many elderly patients live alone or sleep separately from partners due to various health concerns, removing the most common detection method—the bed partner’s report. Without that audible grinding sound, and with elderly individuals less likely to have dental insurance or regular dental checkups, bruxism can progress silently for years.

The 2018 international consensus on bruxism assessment, led by Lobbezoo and colleagues, established a grading system: “possible” bruxism based on self-report, “probable” bruxism with clinical examination findings, and “definite” bruxism confirmed by polysomnographic or electromyographic recordings. However, polysomnography—the gold standard—remains impractical for widespread screening in elderly populations due to cost, access barriers, and the challenges of having frail older adults sleep in unfamiliar laboratory settings.

The Biological Clock Gone Awry: Circadian Disruption

There’s another layer to this puzzle that deserves attention: circadian rhythm changes in aging. The suprachiasmatic nucleus—our brain’s master clock—becomes less sensitive to environmental cues as we age. Melatonin production, which peaks at night in younger adults, diminishes dramatically in elderly populations, sometimes reaching levels similar to daytime concentrations.

This circadian disruption has profound implications for sleep bruxism. Research suggests that bruxism episodes are tied to sleep micro-arousals and shifts in sleep stages, events that are themselves regulated by circadian rhythms. When that circadian system becomes dysregulated—as it does in normal aging and especially in neurodegenerative diseases—the temporal patterning of bruxism can shift unpredictably.

Additionally, aging brings a phase advance in sleep timing. Elderly individuals tend to go to bed earlier and wake up earlier, a phenomenon called “advanced sleep phase syndrome.” This shift affects when bruxism episodes occur, potentially moving them to earlier in the night when muscle tone and arousal patterns differ from later sleep cycles.

What This Means for Clinical Practice

So where does this leave us? (A question I find myself asking frequently when diving into complex medical territory.) The evidence suggests we need a fundamental rethinking of how we approach sleep bruxism in geriatric populations.

First, screening should be routine. Every elderly patient with Parkinson’s disease, Alzheimer’s disease, or other neurodegenerative conditions should be specifically asked about teeth grinding, jaw clenching, morning jaw pain, and unexplained tooth damage. The same goes for elderly patients with hypertension or those taking multiple medications.

Second, we need better diagnostic tools. While polysomnography remains the gold standard, portable single-channel electromyographic devices show promise for in-home assessment. These devices can record multiple nights—important because bruxism shows significant night-to-night variability, particularly in older adults. Lavigne’s research demonstrated coefficient variations of 25-30% across nights in the same individual, meaning one-night recordings may miss the diagnosis entirely.

Third, management must be individualized. The one-size-fits-all approach doesn’t work for elderly bruxers. Oral appliances may be appropriate for some, but others with cognitive impairment might remove them repeatedly or have difficulty with insertion. Medications that reduce bruxism in younger adults may be contraindicated due to fall risk or drug interactions. Cognitive behavioral approaches, while promising, require cognitive capacity that may be diminished in dementia patients.

The Path Forward: Emerging Approaches

Some exciting developments are on the horizon. Research into the role of dopaminergic medications in Parkinson’s-related bruxism continues, though findings remain mixed. Short-term administration of levodopa has shown some ability to suppress bruxism activity in controlled studies, but the clinical applicability for chronic use remains unclear.

Biofeedback approaches adapted for elderly populations are being explored. The idea is simple in concept but complex in execution: train individuals to recognize muscle tension in their jaw and consciously relax it. For cognitively intact elderly patients, this might offer a medication-free approach to management.

There’s also growing interest in addressing the underlying sleep architecture disruptions rather than targeting bruxism directly. Improving sleep quality through sleep hygiene modifications, treating comorbid sleep disorders like sleep apnea, and optimizing medication timing may reduce bruxism episodes indirectly.

Interestingly, some researchers are investigating whether bruxism in certain elderly populations might serve a protective function. There’s evidence that rhythmic masticatory muscle activity during sleep may help lubricate the upper alimentary tract and increase airway patency—potentially beneficial for those at risk of aspiration or sleep-disordered breathing. This is speculative, but it reminds us that not all bruxism necessarily requires aggressive treatment.

A Call for Greater Awareness

I keep coming back to one simple truth: we need to talk more about this. The intersection of aging, neurodegeneration, and sleep disorders creates a perfect storm of complexity, and sleep bruxism sits right at that intersection. As our population ages and the prevalence of neurodegenerative diseases increases, this “minor dental problem” is poised to become a significant public health concern.

What can you do if you’re an older adult concerned about bruxism—or caring for someone who is? First, don’t dismiss symptoms. Morning jaw soreness, headaches upon waking, unexplained tooth chips or fractures, or cheek/tongue indentations all warrant investigation. Second, ensure your healthcare providers are communicating. Your dentist should know about your Parkinson’s diagnosis; your neurologist should know about your dental problems. Third, consider keeping a sleep diary tracking symptoms, as the night-to-night variability can make patterns hard to spot otherwise.

For healthcare providers, the message is clear: screen intentionally, think systemically, and recognize that bruxism in elderly populations is rarely a standalone condition. It’s a window into neurological function, sleep quality, medication effects, and cardiovascular health—all intertwined in ways we’re only beginning to understand.

The research conducted by leaders like Gilles Lavigne and Frank Lobbezoo has given us the tools to recognize and manage sleep bruxism in geriatric populations more effectively. The challenge now is translating that research into widespread clinical practice and raising awareness among the professionals who work with elderly patients daily.

As someone who has spent years researching sleep disorders and their cascading effects on health, I find the story of geriatric bruxism particularly compelling. It reminds us that aging isn’t a simple linear decline but a complex reorganization of multiple systems—each affecting the others in ways both predictable and surprising. And sometimes, the grinding sound in the night is telling us far more than we might initially think.

Have you or a loved one experienced changes in teeth grinding patterns with aging? What helped—or didn’t help—in managing it? The more we share experiences and observations, the better we can fill the gaps in our understanding of this underrecognized condition. Your insights might just help someone else navigate their own sleep challenges more effectively.

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FAQ Section

Q: What is sleep bruxism, and how does it differ from awake bruxism?

A: Sleep bruxism is repetitive jaw muscle activity during sleep characterized by teeth grinding or clenching. It’s now classified as a behavior rather than a disorder in otherwise healthy individuals. Awake bruxism involves jaw clenching or teeth contact during waking hours, often in response to stress or concentration. While they can occur in the same person, they likely have different underlying mechanisms and triggers.

Q: What does “geriatric population” mean in medical research?

A: The geriatric population typically refers to adults aged 65 and older, though some studies use cutoffs of 60 or 70 years. This age group is chosen because it marks the beginning of what’s considered “older adulthood” in most healthcare systems and coincides with significant physiological changes and increased disease prevalence.

Q: What are neurodegenerative disorders, and which ones are associated with bruxism?

A: Neurodegenerative disorders (NDDs) are conditions characterized by progressive loss of neurons in the brain. The main ones associated with increased bruxism risk are Parkinson’s disease (PD), Alzheimer’s disease (AD), and frontotemporal dementia (FTD). These conditions affect brain regions and neurotransmitter systems that help control jaw movements.

Q: What is polysomnography?

A: Polysomnography (PSG) is the gold-standard sleep study that simultaneously records multiple body functions during sleep, including brain waves (EEG), eye movements, muscle activity (EMG), heart rhythm, and breathing patterns. For bruxism, it specifically captures rhythmic masticatory muscle activity (RMMA) in the jaw muscles.

Q: What are dopaminergic and serotonergic pathways?

A: These are communication systems in the brain using the neurotransmitters dopamine and serotonin. Dopaminergic pathways help control movement and motor functions; disruptions contribute to Parkinson’s disease and can trigger bruxism. Serotonergic pathways help regulate mood, sleep, and rhythmic motor activities; imbalances can affect when and how bruxism occurs during sleep.

Q: What is polypharmacy, and why does it matter for elderly bruxism?

A: Polypharmacy means taking multiple medications simultaneously, typically defined as five or more. It’s common in elderly populations (affecting about 46% of Medicare beneficiaries) and matters for bruxism because certain medications can trigger or worsen teeth grinding, while others interact with treatments. Managing bruxism often requires carefully reviewing the entire medication list.

Q: What does “circadian rhythm” mean, and how does it relate to sleep and bruxism?

A: Circadian rhythms are the body’s internal 24-hour cycles that regulate sleep-wake patterns, hormone release, and other physiological processes. They’re controlled by the suprachiasmatic nucleus in the brain and influenced by light exposure. In aging, these rhythms become less precise, affecting sleep quality and potentially the timing and frequency of bruxism episodes.

Q: What is the basal ganglia, and why is it important for understanding bruxism in Parkinson’s disease?

A: The basal ganglia are interconnected brain structures deep in the cerebral hemispheres that help control voluntary movements, including jaw movements. In Parkinson’s disease, dopamine loss causes basal ganglia dysfunction, leading to movement problems like tremor and rigidity—and also contributing to jaw muscle overactivity seen in bruxism.

Q: What does “sleep architecture” mean?

A: Sleep architecture refers to the structure and pattern of sleep cycles throughout the night, including the different sleep stages (light sleep, deep slow-wave sleep, and REM sleep) and how they’re organized. In elderly individuals, sleep architecture changes: less deep sleep, more light sleep, more frequent awakenings, and altered REM sleep patterns—all of which can affect bruxism occurrence.

Q: What is an arousal index, and why is it relevant to bruxism?

A: The arousal index is the number of brief awakenings or partial awakenings per hour of sleep, measured during polysomnography. It’s relevant because most bruxism episodes occur during or just after these micro-arousals—brief activations of the heart, brain, and muscles. Higher arousal indices, common in elderly populations and hypertension patients, can increase bruxism frequency.

Q: What is temporomandibular disorder (TMD)?

A: Temporomandibular disorder (TMD) refers to problems with the jaw joint (temporomandibular joint) and surrounding muscles. Symptoms include jaw pain, clicking sounds, difficulty opening the mouth, and headaches. While the relationship with bruxism is debated, some evidence suggests they occur together more frequently than by chance, particularly in elderly populations with neurodegenerative diseases.

Q: What does “rhythmic masticatory muscle activity” (RMMA) mean?

A: RMMA refers to repetitive contractions of the jaw-closing muscles during sleep, typically occurring at a frequency of about one contraction per second. It’s the core biomarker for diagnosing sleep bruxism through polysomnography. The pattern can be phasic (brief, rhythmic contractions), tonic (sustained contractions), or mixed. In healthy individuals, low levels of RMMA occur naturally during sleep without causing problems.