Medications That May Contribute to TMD and Orofacial Pain

Anatomical skull model of the temporomandibular joint beside prescription medication bottles representing the potential role of commonly prescribed medications in temporomandibular disorders (TMD) and orofacial pain.

Medications That May Contribute to TMD and Orofacial Pain

Author: Donald Tanenbaum DDS MPH - Board-Certified Orofacial Pain Specialist at New York TMJ & Orofacial Pain

Date: July 10, 2026

Clinical Takeaway

When jaw pain appears disproportionate to the clinical findings or fails to respond to conventional treatment, the medication history deserves careful attention.

Commonly prescribed medications may influence muscle physiology, electrolyte balance, sleep quality, bruxism, and pain processing in ways that complicate the diagnosis and management of temporomandibular disorders.

Recognizing these potential relationships does not necessarily mean the medication is the primary cause of pain. Instead, it broadens the differential diagnosis and encourages thoughtful collaboration with the patient’s prescribing physician when appropriate.

Not every patient assessment is straightforward. In fact, figuring out why a patient has persistent jaw symptoms is not always clear-cut. Over the last few years, while searching for answers, I’ve begun to look a bit more carefully at the medications my patients are taking. What I have found is that there is a repetitive list of medications that continue to be part of the medical histories in a surprising number of patients.

As many of these medications have been identified as potential contributors to musculoskeletal pain in the orofacial region due to an impact on muscle physiology, pain modulation, electrolyte balance, sleep, or parafunctional activities, a careful review of a patient’s medication history deserves consideration whenever the clinical picture seems more complicated than expected.

Levothyroxine and synthroid

Levothyroxine and Synthroid are prescribed to replace thyroid hormone that the gland can no longer produce adequately, most commonly in patients with Hashimoto’s thyroiditis. When dosed appropriately, these medications restore euthyroid function and should improve rather than worsen musculoskeletal symptoms.

At times, however, underdosing may present a different picture. Patients may report persistent jaw muscle pain, poor sleep, fatigue, and generalized muscle discomfort that does not fit the mechanical pattern of a simple TMD problem. Their levothyroxine dose may be considered adequate by laboratory standards, yet still be insufficient for that individual’s tissue needs.

Overdosing can create the opposite problem. Excess thyroid hormone may produce sympathetic nervous system activation, elevated resting muscle tension, anxiety, and disrupted sleep, all of which may contribute to persistent masticatory muscle pain.

When a patient has remained on thyroid replacement therapy for an extended period without periodic reassessment, collaboration with the prescribing physician has often proven worthwhile.

Statins

Cholesterol-lowering statin medications produce muscle aching and fatigue in a meaningful number of patients. It is estimated that this occurs in approximately five to ten percent of patients worldwide. The underlying mechanism is believed to involve impaired energy production within skeletal muscle.

Jaw and facial muscle pain developing after initiation of statin therapy, following a dosage adjustment, or after switching from one statin to another may reflect statin-associated myopathy rather than primary TMD.

Although the masticatory muscles are not commonly discussed in the statin literature, the possibility should be considered when muscle pain appears without another satisfactory explanation. Communication with the prescribing physician is certainly justified in these scenarios.

ACE inhibitors and ARBs: Lisinopril and Losartan

ACE inhibitors such as lisinopril and ARBs such as losartan are among the most commonly prescribed antihypertensive medications because, beyond lowering blood pressure, they provide well-documented protective effects on the kidneys and cardiovascular system.

Musculoskeletal complaints including myalgia and arthralgia have been described with losartan, while lisinopril has been associated with arthritis, arthralgia, neck pain, and generalized joint pain. However, there is no published literature specifically examining ACE inhibitor- or ARB-related musculoskeletal pain involving the TMJ or masticatory system.

So, what would the connection potentially be?

ACE inhibitors increase circulating bradykinin, a peptide that has been shown to influence pain hypersensitivity following tissue injury. ARBs do not increase bradykinin to the same degree and therefore may not contribute to chronic pain through this same mechanism.

Theoretically, if circulating bradykinin levels rise in a patient who already has inflamed or sensitized masticatory tissues, those elevated levels may amplify the pain signals those tissues are generating.

In practical terms, this means that a patient taking lisinopril or another ACE inhibitor who has even modest TMJ inflammation or masticatory muscle involvement may experience pain that appears disproportionate to the degree of tissue injury present.

Therefore, in the patient whose pain seems inconsistent with the clinical findings, investigation into this possibility may be justified. I have pursued this line of thinking in a number of patients, collaborating with cardiologists who have been receptive to considering medication changes when clinically appropriate.

Omeprazole and proton pump inhibitors

Long-term proton pump inhibitor (PPI) therapy has been associated with impaired intestinal magnesium absorption. Magnesium deficiency is a well-established cause of muscle cramping, myalgia, and neuromuscular irritability.

PPIs may also impair the long-term absorption of vitamin D and vitamin B12. In patients receiving chronic PPI therapy who present with unexplained jaw muscle cramping, diffuse myalgia, or persistent muscle tenderness, evaluation of magnesium, vitamin D, and vitamin B12 levels is often a simple and productive step.

Spironolactone

Spironolactone has become one of the most commonly prescribed medications seen in women presenting for consultation. Its most widespread modern application has been in the management of hormonal acne.

The musculoskeletal consequences of spironolactone may operate through two intersecting pathways. By blocking androgen receptors, spironolactone may reduce endogenous pain-inhibitory mechanisms, shifting the nervous system toward greater pain sensitivity at precisely the time when the jaw may be under increased functional stress.

The second pathway is electrolyte-mediated. Long-term spironolactone therapy may contribute to magnesium depletion. When magnesium levels fall, the threshold for pain amplification may decrease, leaving the masticatory system less protected against the development or persistence of chronic pain.

Though this relationship may be more theoretical than predictable, there are so many women in my practice taking this medication that I believe it deserves consideration and should at least prompt discussion and collaboration with the prescribing physician when appropriate.

Amphetamines for ADHD

Stimulant medications prescribed for attention-deficit/hyperactivity disorder activate the sympathetic nervous system, increasing resting muscle tone and potentially promoting both awake and sleep bruxism.

When jaw symptoms begin or worsen following initiation of stimulant therapy, this relationship deserves careful consideration. The combination of stimulant-induced sympathetic activation and pre-existing jaw loading habits may place these patients at increased risk for the development or exacerbation of TMD symptoms.

SSRIs and SNRIs

Serotonergic antidepressants, including sertraline, fluoxetine, escitalopram, and venlafaxine, have the potential to produce sleep bruxism by altering dopamine pathways that normally suppress masticatory muscle activity during sleep.

The onset or worsening of jaw symptoms within weeks to months of initiating therapy, or following an increase in dosage, is a pattern that, when encountered in this practice, consistently prompts further discussion.

Although medication-induced bruxism is not universally recognized, increasing attention has been given to this phenomenon in both the psychiatric and dental literature and should remain part of the differential diagnosis when evaluating persistent jaw pain.

To our colleagues in the New York City metropolitan area

If your practice is located in the New York City metropolitan area, New York TMJ & Orofacial Pain has four locations staffed by board-certified orofacial pain specialists. We provide evidence-based, multidisciplinary care and collaborate closely with referring providers to assist in the diagnosis and management of patients with complex TMD and orofacial pain conditions.

Contact one of our offices →

About the author

Dr. Donald R. Tanenbaum is a co-founder of New York TMJ & Orofacial Pain. He provides care at our Manhattan and Hauppauge locations.

Frequently asked questions about medications that may contribute to TMD and orofacial pain

Can commonly prescribed medications contribute to persistent TMD?

Yes. Certain medications may influence muscle physiology, pain processing, electrolyte balance, sleep quality, or bruxism. While they are rarely the primary cause of TMD, they may amplify symptoms or interfere with recovery.

When should a medication-related contributor be suspected?

Consider the medication history when symptoms begin after medication initiation or dosage adjustment, appear disproportionate to the clinical findings, or fail to improve with appropriate treatment.

Should medications be changed if they are suspected of contributing to TMD?

Medication changes should always be coordinated with the prescribing physician. The goal is to identify potentially contributing factors while maintaining appropriate management of the patient’s underlying medical condition.