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CE: Management of Chronic Drug-Induced Bruxism and Orofacial Pain by Dr. Elfatih Eisa

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Categories: Restorative Dentistry;
CE: Management of Chronic Drug-Induced Bruxism and Orofacial Pain 

Gain the skills to treat chronic bruxism in patients with compounding dental and pharmacologic factors

by Dr. Elfatih Eisa

Short description
This course offers a comprehensive overview of managing chronic drug-induced bruxism and orofacial pain, particularly in cases complicated by dental procedures. Participants will gain insights into diagnostic and treatment planning strategies, as well as the integration of multidisciplinary approaches to enhance patient outcomes.


Abstract
The course explores the complexities of diagnosing and managing chronic drug-induced bruxism and orofacial pain. It highlights a case study involving a 40-year-old female patient presenting with symptoms exacerbated by dental treatment and psychotropic medication use. Key elements include differentiating bruxism types, understanding medication-induced triggers and crafting personalized treatment plans incorporating behavioral therapy, medication adjustments and occlusal stabilization appliances. Evidence-based approaches to mitigating associated symptoms like tinnitus, headaches and myalgia are emphasized. By the course’s conclusion, attendees will be equipped to apply multidisciplinary strategies for managing similar cases effectively.


Learning objectives
After completing this course, readers should be able to:
  1. Differentiate between sleep and awake bruxism and identify their respective triggers and manifestations.
  2. Identify the mechanisms by which specific medications contribute to sleep-induced bruxism.
  3. Recognize the role of psychotropic medications in inducing or exacerbating bruxism and develop strategies for management.
  4. Create personalized, multidisciplinary treatment plans for patients with complex orofacial pain and drug-induced bruxism.
  5. Enhance patient outcomes through effective communication, patient education and behavioral interventions.
Patient history and present illness
A 40-year-old female patient arrived at the Orofacial Pain Clinic at the University of Kentucky with a range of persistent symptoms that began following dental treatment three years before her visit. Her chief complaint was neck pain, right ear hearing loss and ear fullness after she had had dental work done. She described an aching, burning pain centered around the right post-auricular, occipital, neck and shoulder areas. The pain intensity varied from 5 on a scale of 1–10 to 9 out of 10, and it occurred almost daily, typically exacerbated by certain postures, stress, teeth clenching and lifting heavy objects.

Additional symptoms included:
  • Aural fullness and tinnitus: Right aural fullness and intermittent tinnitus.
  • Headaches: Occipital headaches on the right side with a pain intensity of 7 out of 10, occurring thrice monthly and often lasting for an entire day. These headaches were exacerbated by neck pain and relieved with Advil, heat compresses, stretching, chiropractic therapy and Botox.
  • Occlusal discrepancy: A sensation of “multiple different bites” contributed to her discomfort.

History of previous treatments
The patient had undergone several treatments with limited success:
  • Stabilization appliances: Multiple trials of stabilization appliances and orthotics did not improve her symptoms.
  • Selective teeth adjustments: Grinding adjustments postveneer placement yielded minimal improvement.
  • Botox therapy: Botox injections in the masseter muscles significantly reduced teeth clenching and pain. However, injections in the neck and shoulder areas resulted in muscle weakness, with a subsequent pain flare-up for six weeks afterward.
  • Physical therapy and dry needling: Both were reported to provide limited pain relief.

Review of systems
  • Neurological: Headaches, dizziness, tingling in fingers
  • ENT: Aural fullness, tinnitus
  • Pulmonary: Seasonal allergies
  • Musculoskeletal: Shoulder pain, neck aches
  • Other systems: Negative for additional findings

Medical, family and surgical history
  • Medical history: GERD, anxiety disorder, panic attacks, Eagle syndrome
  • Family history: Positive for myocardial infarction, bone cancer, emphysema and pneumonia
  • Surgical history: Tonsillectomy, bilateral inguinal hernia repair
  • Current medications: Wellbutrin 150 mg twice daily
  • Allergies: Adverse reaction to Demerol

Psychosocial history
The patient reported eight hours of sleep with a sleep latency of up to 30 minutes, consuming three units of caffeine daily but denying alcohol, smoking or recreational drug use. She noted a history of anxiety and panic attacks but denied depression or suicidal ideations. Wellbutrin had been part of her treatment regimen for several years, although its effectiveness in managing her anxiety was uncertain.


Clinical examination
  • Vitals: BP: 113/81 mmHg; Pulse: 85 bpm; SpO2: 96%; BMI 20.6
  • Cranial nerves: II-XII intact
  • Cervical examination: Mild restriction with movements, slight tenderness in the right occipital, splenius capitis and trapezius muscles
  • Mandibular function: Maximal comfort opening of 40 mm with slight mandibular deflection to the right. No TMJ sounds or tenderness were noted.
  • Occlusal findings: Occlusion was evaluated with shim stock. Occlusal contacts noted on teeth #2, 4, 5, 12, 13, 14, 15 with their opposing teeth, while the rest of the teeth were slightly out of occlusion.
  • Intraoral examination: Bilateral linea alba, veneers on teeth #5-12, craze lines, root exposure on tooth #25 with slight attrition noted.
  • Intraoral appliances: The patient had two intraoral appliance that were evaluated. The first appliance was a full-coverage maxillary, flexible appliance. The second appliance was a hard full-coverage mandibular appliance showing uneven occlusal contacts.

Differential diagnosis
  • Possible chronic drug-induced bruxism
  • Cervical myofascial pain
  • Cervicogenic headache
  • Masticatory myalgia
  • Minor occlusal instability
  • Contributing factors: Oral parafunctional habits (awake bruxism), loss of stable intercuspal position

Initial treatment plan
  1. Patient education: Provided reassurance about her condition and detailed explanations.
  2. Behavioral therapy: Referred for clenching awareness, self-care strategies and physical self-regulation (PSR) skills training.
  3. Medication adjustment: Recommended discontinuing Wellbutrin, with a trial of duloxetine as an alternative serotonin-norepinephrine reuptake inhibitor (SNRI). A letter was sent to her primary care physician to coordinate this change.
  4. Occlusal appliance: Fabricated a hard, full-coverage stabilization appliance to manage nocturnal clenching.
  5. Therapeutic exercises: The patient was evaluated by a physical therapist trained in managing TMD and cervicalgia. Prescribed jaw-opening exercises to improve range of motion.

Follow-up appointments
Follow-up appointment 1: Three months after initial visit
  • Improvement reported: The patient noted significant relief after discontinuing Wellbutrin, although she had not yet started duloxetine. She experienced reduced pain (2 out of 10) in the right occipital and masseter muscles.
  • Procedure: Delivered a vacuum-formed splint with hard acrylic for even bilateral contacts.
Follow-up appointment 2: Four months after initial visit
  • Further progress: Reduced TMJ sounds and diminished sense of occlusal instability. Some discomfort in the maxillary left premolar noted occasionally but a significant improvement in pain levels compared with the initial appointment.
  • Procedure: Splint adjusted for comfort.
Follow-up appointment 3: Five months after initial visit
  • Continued improvement: Mild residual aching pain (2 out of 10) in the right masseter, trapezius and occipital areas. Attributed improvement to discontinuing Wellbutrin, appliance use, PSR exercises and Botox therapy.
  • Assessment: Continue management of cervical myofascial pain and masticatory myalgia.

Overview on bruxism
Bruxism, a condition involving excessive masticatory muscle activity, is now recognized as comprising two distinct behaviors based on when it occurs: sleep bruxism and awake bruxism.1 Bruxism can lead to significant occlusal trauma, affecting dental hard tissues, restorations, prostheses and even the musculoskeletal structures involved in chewing and speech. While awake bruxism is often triggered by psychosocial factors, sleep bruxism is believed to involve more complex mechanisms within the central nervous system.

These behaviors are no longer seen as variations of a single phenomenon but rather as separate entities with specific definitions.
  1. Sleep bruxism: This is defined as involuntary masticatory muscle activity during sleep, which can manifest in several forms: rhythmic (phasic) or non-rhythmic (tonic) or mixed. Importantly, sleep bruxism is not classified as a movement disorder or sleep disorder in individuals who are otherwise healthy. It involves jaw clenching or teeth grinding during sleep without associated underlying sleep pathologies.
  2. Awake bruxism: In contrast, awake bruxism refers to masticatory muscle activity during wakefulness. It is characterized by repetitive or sustained tooth contact, as well as actions like bracing or thrusting the jaw. Similar to sleep bruxism, awake bruxism is not considered a movement disorder in healthy individuals and often occurs unconsciously, particularly in response to stress or concentration.
These updated definitions emphasize that while both forms involve the same muscle groups, their triggers, characteristics and implications may differ, thereby warranting separate classifications for more accurate diagnosis and management.1

Studies on the prevalence of bruxism indicate that it affects a significant portion of the population, ranging from 8% to 31.4% among adults and 3.5% to 40.6% among children.2,3 The condition is generally understood to have a multifactorial origin, though the precise causes and mechanisms remain unclear. Factors contributing to bruxism include dental occlusal interferences, psychological stressors, environmental influences and dysfunctions in the basal ganglia and neurotransmitter systems in the brain.

One theory suggests that bruxism is mediated by central mechanisms involving neurotransmitters such as dopamine and serotonin. Certain medications, particularly psychotropic drugs, can alter the balance of these neurotransmitters, potentially inducing or exacerbating bruxism.4,5 Despite its recognition in psychiatry, the awareness of drug-induced bruxism remains relatively low among dental professionals, which underscores the need for increased education and vigilance in dental practice to identify and manage this condition effectively.

The prevalence of lifestyle changes such as increased stress levels, poor sleep quality and inadequate nutrition has contributed to a rising incidence of mood disorders and other mental health issues worldwide.6–8 Growing awareness about mental health has led more individuals to seek professional treatment for conditions like anxiety, depression and other psychological concerns. Consequently, there has been an uptick in the prescription of psychotropic medications, including antipsychotics and antidepressants, to manage these conditions.9,10 Similarly, the number of patients requiring treatment for neurological disorders has also grown over the years. These medications, which often target the central nervous system, are used either as monotherapy or in combination therapies, reflecting an increased reliance on pharmacological interventions for managing mental and neurological health.


Review of drug-induced bruxism
Psychotropic drugs are chemical agents capable of crossing the blood-brain barrier to influence the central nervous system. These substances can stimulate or suppress neurological activity, thereby affecting mood, perception, cognition and behavior. Some psychotropic medications, particularly those affecting dopamine, serotonin, norepinephrine and histamine receptors, have been linked to the induction of bruxism by altering neurotransmitter functions and receptor responses in the brain.

Several classes of medications have been associated with the onset of bruxism. SSRIs (selective serotonin reuptake inhibitors) are one of the medications frequently reported.11–13 Research suggests that SSRI-induced bruxism may be linked to increased serotonergic activity, which can suppress dopaminergic pathways, subsequently leading to muscle hyperactivity and teeth grinding. Commonly implicated SSRIs in these cases include fluoxetine, sertraline and paroxetine, which are known to heighten serotonin levels, potentially disrupting the balance of neurotransmitter activity involved in motor control.

 The literature indicates that switching from SSRIs to SNRIs, such as duloxetine, can alleviate SSRI-induced bruxism in some patients. SNRIs are often considered effective because they balance serotonin and norepinephrine levels, with a reduced impact on dopaminergic pathways that are frequently linked to bruxism. On the other hand, Wellbutrin (bupropion) belongs to the class of norepinephrine and dopamine reuptake inhibitors (NDRIs). Unlike SNRIs and SSRIs, NDRIs primarily increase norepinephrine and dopamine levels by inhibiting their reuptake in the brain.

This increase in dopaminergic activity can sometimes lead to side effects like bruxism, as dopamine is known to play a role in muscle control and movement regulation, which may influence jaw muscle activity.

Additionally, various classes of medications, including SSRIs, SNRIs, NDRIs and others, have been reported to cause bruxism, each potentially leading to different manifestations of the condition. Table 1 (page 46) summarizes the list of medications associated with bruxism and specifies the type of bruxism they may induce, as documented in the literature.14

However, it is crucial to recognize that patient responses to medications are highly individualized. While some may find relief with SNRIs, others might experience an exacerbation of bruxism symptoms. Similarly, NDRIs can alleviate symptoms of depression and anxiety for some patients but may induce bruxism in others.


Relevance to the case
The patient’s improvement after discontinuing Wellbutrin, along with the consideration of switching to duloxetine, aligns with evidence supporting the use of SNRIs for managing medication-induced bruxism. However, it is crucial to recognize that individual patient responses can vary significantly. While certain medications may provide relief for some, the same class has also been documented to induce bruxism in others.

Notably, despite the recommendation to switch to duloxetine, the patient showed significant pain relief simply by discontinuing Wellbutrin. However, this decision should be approached with caution, as the patient’s underlying anxiety disorder was left untreated by alternative medication.

This case underscores the importance of a personalized treatment plan, combining medication adjustments with non-pharmacologic strategies such as stabilization splints, physical therapy and behavioral therapy to effectively manage complex orofacial pain conditions.


Conclusion
The comprehensive management plan, which included discontinuing Wellbutrin, incorporating behavioral therapy, physical therapy and the use of a stabilization appliance, led to substantial pain relief and functional improvement. This case highlights the importance of a multidisciplinary approach in effectively managing drug-induced bruxism and chronic orofacial pain. DT
References
1. Lobbezoo, F., et al. “International consensus on the assessment of bruxism: Report of a work in progress.” Journal of Oral Rehabilitation, vol. 45, no. 11, Nov. 2018, pp. 837–844. https://doi. org/10.1111/joor.12663.
2. Manfredini, Daniele, et al. “Epidemiology of Bruxism in Adults: A Systematic Review of the Literature.” Journal of Orofacial Pain, vol. 27, no. 2, 2013, pp. 99–110.
3. Manfredini, Daniele, et al. “Prevalence of Sleep Bruxism in Children: A Systematic Review of the Literature.” Journal of Oral Rehabilitation, vol. 40, no. 8, 2013, pp. 631–64.
4. Bader, Gudrun, and Gilles Lavigne. “Sleep Bruxism: An Overview of an Oromandibular Sleep Movement Disorder.” Sleep Medicine Reviews, vol. 4, no. 1, 2000, pp. 27–43.
5. Falisi, Giancarlo, et al. “Psychotropic Drugs and Bruxism.” Expert Opinion on Drug Safety, vol. 13, 2014, pp. 1319–1326.
6. Hidaka, Brandon H. “Depression as a Disease of Modernity: Explanations for Increasing Prevalence.” Journal of Affective Disorders, vol. 140, no. 3, 2012, pp. 205–214.
7. Rao, T. S. Sathyanarayana, et al. “Understanding Nutrition, Depression and Mental Illnesses.” Indian Journal of Psychiatry, vol. 50, no. 2, 2008, pp. 77.
8. Colten, Harvey R., and Bruce M. Altevogt. Extent and Health Consequences of Chronic Sleep Loss and Sleep Disorders. Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem, National Academies Press, 2006, pp. 55–135.
9. Feigin, Valery L., et al. “Global, Regional, and National Burden of Neurological Disorders, 1990–2016: A Systematic Analysis for the Global Burden of Disease Study 2016.” The Lancet Neurology, vol. 18, no. 5, 2019, pp. 459–480.
10. Mental Health Statistics: People Seeking Help. Mental Health Foundation, 2016, mentalhealth.org.uk/explore-mental-health/ statistics.
11. Garrett, Ashley R., and Je rey S. Hawley. “SSRI-Associated Bruxism: A Systematic Review of Published Case Reports.” Neurology: Clinical Practice, vol. 8, no. 2, Apr. 2018, pp. 135–141.
12. Uchima Koecklin, Katia H., et al. “The Neural Substrates of Bruxism: Current Knowledge and Clinical Implications.” Frontiers in Neurology, vol. 15, 2024, article 1451183.
13. de Baat, Cees, et al. “Medications and Addictive Substances Potentially Inducing or Attenuating Sleep Bruxism and/or Awake Bruxism.” Journal of Oral Rehabilitation, vol. 48, no. 3, Mar. 2021, pp. 343–354.
14. George, S., et al. “Drug-Induced Bruxism: A Comprehensive Literature Review.” Journal of Advanced Oral Research, vol. 12, no. 2, 2021, pp. 187–192.

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Author Bio
Dr. Elfatih Eisa Dr. Elfatih Eisa earned his Bachelor of Dental Surgery from Riyadh Elm University in Saudi Arabia in 2012. His passion for helping patients led him to pursue a certificate in prosthodontics at the Eastman Institute for Oral Health at the University of Rochester in New York in 2024. In addition to his prosthodontics training, Eisa earned a Master of Science degree and a certificate in orofacial pain from the University of Kentucky. He is the lead prosthodontist at ClearChoice in Edwardsville, Ill. As one of fewer than 300 board-certified orofacial pain specialists in the United States, Eisa is highly skilled in diagnosing and managing a wide range of complex orofacial pain conditions, including temporomandibular joint disorders, teeth grinding, headaches, neck pain and neuropathic pain.
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