Intrinsic Injuries to the Jaw’s Temporomandibular Joint
By Dr. Bradley Eli
Sustained mouth opening and hyperextension injuries are the most common intrinsic injuries of the temporomandibular joint (TMJ).
Dental procedures are typical clinical scenarios that can result in intrinsic injury from sustained mouth opening. Hyperextension injuries can occur during oral surgery, endotracheal intubation, playing a wind instrument, cheering, snorkeling or simply yawning.
Intrinsic TMJ injuries are known risk factors for the development of temporomandibular disorders (TMDs). Data from the Orofacial Pain Prospective Evaluation and Risk Assessment (OPPERA) study shows that intrinsic injuries (sustained mouth opening and yawning) are more common than extrinsic injuries and are more likely to contribute to the incidence of painful TMDs than extrinsic injuries .
Narrow Therapeutic Window for Prompt Intrinsic TMJ Injury Treatment
According to the National Academies of Sciences, Engineering, and Medicine (NASEM), Temporomandibular Disorders: Priorities for Research and Care March 12, 2020 article, “Temporomandibular disorders (TMDs), are a set of more than 30 health disorders associated with both the temporomandibular joints and the muscles and tissues of the jaw”.
Author Enriqueta Bond also states that the current understanding of TMD pathogenesis suggests that there may be a narrow therapeutic window where prompt treatment of intrinsic TMJ injuries can halt the progression to a chronic pain disorder. Patients with TMDs require high-intensity medical care, with expenditures that are 60% greater than baseline primary care patients.
Furthermore, some people with TMDs suffer a lifetime of pain and disability. For these reasons, preventing the transition from an acute intrinsic jaw-related injury to a chronic TMD should be a clinical priority.
This paper outlines the pathophysiology of intrinsic TMJ injuries and how this leads to chronic TMD development. Clinical manifestations of intrinsic jaw-related injuries are considered and guidelines regarding patient screening and education are discussed. Finally, a multimodal treatment plan that can be used to help prevent TMD development is outlined.
Pathophysiology of Jaw Hyperextension Injuries
Intrinsic injuries occur when temporomandibular joint excursion is sustained for an unnatural period or when the opening exceeds the individual’s maximal excursion length (“hyperextension” or “hyperdepression”). Several animal models have been developed to explore the effect of prolonged excursion/hyperextension on the temporomandibular complex.
Articular cartilage: In a model developed by Fujisawa and colleagues (2013) , rabbits were administered general anesthesia and then subjected to repetitive, steady mouth opening. The results showed reactive changes to the cartilage chondrocytes, consistent with arthritis-like changes. Eiji Tanaka used a similar model and found that vascular endothelial growth factor (VEGF) was expressed in the articular cartilage, a finding usually seen only in osteoarthritic joints .
Muscles of mastication: To show that prolonged mouth opening affects the muscles of mastication, Wang GYF  used a bite block in a rat model and found evidence of mechanical allodynia and TMJ dysfunction. On histologic examination, atrophy and macrophage infiltration were found in the masseter muscle. Hawkins and Durham (2016)  developed an animal model that closely resembles the mechanical stress induced during routine dental procedures. In this rat model, near maximal opening was sustained by retractors for only 20 minutes under anesthesia. After the procedure, there was sensitivity around the masseter muscle as recorded by defensive responses to cutaneous stimulus (i.e. nocifensive responses).
Trigeminal Nerve: In the study  referenced above, inflammation of the trigeminal nerve and microglia activation in the trigeminal subnucleus caudalis was documented after prolonged mouth opening. Similar findings were found in the Hawkins and Durham (2016) study, where the upper spinal cord and trigeminal nucleus showed increased expression of proinflammatory cytokines, a sign of peripheral sensitization in trigeminal afferents.
There is limited information as to why the simple act of yawning might be responsible for TMD development. One explanation is that mechanoreceptor density in the TMJ is greatest in locations that correspond to extreme movement, such as maximal opening. Wide yawning likely triggers a large mechanoreceptor discharge, leading to a cascade of afferent nerve impulses in the surrounding tissues. This response may cause peripheral sensitization (explained below) and trigger a guarding reflex in the TMJ complex. This pathophysiology is typical of Jaw and Muscle Sprain/Strain (JAMSS) injuries, where the tissue injury is followed by sensitization and guarding.
From Intrinsic Jaw Injury to Chronic TMD Development
How does sustained jaw hyperextension trigger a chronic pain disorder?
The most widely accepted model of chronic TMD development, and of chronic pain disorders in general, is that pain is perpetuated by neural sensitization. Sensitization is where the stimulus intensity required to trigger a neural signal is decreased. In this case, a peripheral insult from sustained mouth opening or jaw hyperextension leads to a hyperexcitable state in the brain, the neuropathological hallmark of a chronic pain disorder.
Peripheral sensitization occurs in the peripheral afferent nociceptors. After an initial noxious stimulus triggers a jaw pain response, the response threshold of these neurons will be lowered. This creates an increased reactivity to noxious stimulus, a state called “hyperalgesic priming” that can last several weeks. Hyperalgesic priming appears to be mediated by pro-inflammatory cytokines such as prostaglandins .
Another step in chronic TMD pathogenesis is the generation of reflex guarding in the muscles of mastication. While this begins as a protective response, it soon becomes a contributing factor in the pathologic process of chronic pain development. Tonic activation of masticatory muscles leads to pro-inflammatory cytokine release, tissue deoxygenation, and fatigue, all of which serve to amplify peripheral sensitization.
Peripheral sensitization ultimately leads to central sensitization, the central nervous system response to persistent peripheral afferent signaling. It involves increased expression of pro-inflammatory cytokines, morphological changes in microglial and other supporting cells, and synaptic changes in the brain and spinal cord. The result of these changes is a hyperexcitable state in the central nervous system that results in the hallmark chronic pain symptoms allodynia, hyperalgesia, and secondary hyperalgesia.
Preclinical and clinical data indicate that these changes occur in the first 4 weeks after acute injury , suggesting that there is a narrow therapeutic window to prevent central sensitization and chronic pain development.
Finally, psychological factors contribute to the transition from intrinsic TMJ injury to chronic disorders. The mechanism appears to be through neuroplastic changes in the amygdala, the site of affective states such as depression and anxiety (both of which are known risk factors for TMD development). Preclinical data has confirmed that central sensitization occurs in the so-called “nociceptive amygdala,” illustrating that negative emotional states and the distortion of nociceptive sensory information in allodynia/hyperalgesia are intercorrelated .
Clinical Aspects of Intrinsic TMJ injuries
Sustained mouth opening occurs frequently during oral surgeries and dental procedures. This represents a risk for intrinsic TMJ injury and subsequent TMD development. Importantly, a significant number of patients who suffer from TMDs identify the specific cause of their symptoms to be dental work. Such patients exhibit greater disability than control TMD cases .
Further evidence that dental procedures predispose to intrinsic injuries is documented in a study that found a statistically significant number of patients who had prolonged root canals developed persistent TMD pain in the month after the procedure . Another example concerns third molar extractions, which are well-documented risk factors for TMD development. A recent metanalysis showed that the odds ratio of jaw-related disorders after third molar extraction is 1.8 to 2.2, with a relative risk of 2.1 .
Hyperextension injuries of the temporomandibular joints can occur during intubation for general anesthesia, likely because the jaw muscles are paralyzed during induction, making the TMJ more susceptible to hyperextension. Hyperextension injuries constitute 10% of all cases of airway trauma due to intubation .
Somewhat surprisingly, trauma from yawning is a common cause of TMD development. In one study of 232 subjects with TMD secondary jaw injury, 16% were due to injuries sustained from yawning .
Guidelines for TMD Prevention from Intrinsic TMJ Injuries
The difficulty with clinically assessing patients with intrinsic jaw joint injuries is that there is rarely an opportunity for assessment until chronic TMD symptoms are already well-established. However, because prolonged mouth opening or jaw hyperextension typically occurs during clinical maneuvers (dental work, oral surgery, intubation), guidelines for TMD prevention for practitioners who perform these maneuvers can be formulated.
What are Risk Factors for TMD development Caused by Jaw Hyperextension?
Factors that may increase the risk of developing a TMD disorder include:
- Pre-existing TMD symptoms.
- Limited range of motion (voluntary jaw opening less than 30mm).
- Psychological history (specifically anxiety, depression, PTSD, or somatic symptom disorder).
- Any other chronic pain disorder.
- Headache disorders.
- Sleep apnea or insomnia.
- Poor general medical status.
The most important measure for practitioners is to take a focused jaw pain patient history; note any of the known risk factors for TMD development.
After taking a clinical history, patients should be educated to contact the office if there is any sign of lingering jaw pain (more than 3-5 days). Special care and more detailed education should be given to patients with any of the above risk factors in their history. If there is lingering jaw pain or muscle spasm, patients can be directed to use a multimodal treatment strategy aimed at preventing TMD development (outlined below).
What is the Treatment for Intrinsic Jaw Injuries?
The goal of intrinsic jaw injury treatment is to mitigate the factors that contribute to central sensitization. These include peripheral sensitization, masticatory muscle guarding, and pain amplification due to negative psychological states (anxiety, depression, catastrophizing).
Since there are multiple targets that may help prevent chronic disorders, each case is individually assessed.
A multimodal approach to jaw therapy can include:
- Analgesics: Reduce inflammation and peripheral sensitization.
- Cryotherapy: Reduces inflammation, has analgesic effect, and decreases muscle tension.
- Thermotherapy: Increases circulation, tissue oxygenation, and waste elimination. Heat is soothing, promotes muscle relaxation, and facilitates mobility.
- Physical Therapy: Circulates synovial fluid, removes metabolic waste, and interrupts peripheral sensitization.
- Behavioral Pain Management: Reduces anxiety and stress that can amplify pain. Fosters resilience and decreases catastrophizing.
- Oral appliance therapy: Decreases muscle tension and guarding through joint unloading.
Prompt treatment of intrinsic TMJ injuries with this multimodal approach constitutes the best chance of preventing TMD development.
Intrinsic TMJ injuries can occur with sustained mouth opening or jaw hyperextension.
The most common clinical scenario for these injuries are oral surgeries, dental procedures, and intubation for general anesthesia, although the simple act of yawning wide can also cause an intrinsic TMJ injury.
Injury from sustained opening/hyperextension involves the cartilage, muscles, and nerves of the TMJ complex. The initial insult primes a hyperexcitable state in peripheral afferents called peripheral sensitization and triggers a guarding reflex in the masticatory muscles. Sustained peripheral nerve impulses lead to neuroplastic changes in the central nervous system called central sensitization. Negative emotional states reinforce central sensitization via the limbic system.
Once this occurs, the hallmark signs of chronic joint or soft tissue pain develop; or additionally, hyperalgesia, allodynia, and secondary hyperalgesia.
Clinical practice Intervention aimed at reducing peripheral sensitization, masticatory muscle guarding, and negative emotive states surrounding pain have the potential to prevent central sensitization from developing.
A multimodal conservative approach has the best chance of accomplishing this goal. Because it’s impossible to tell who might develop an intrinsic injury, universal education regarding the potential for sustained jaw pain should be adopted, with special attention given to patients who are at high risk of developing TMDs.
Dr. Brad Eli, DMD, MS is a graduate of UCLA’s post-doctoral Orofacial Pain program. The field of orofacial pain, temporomandibular disorders, and treatment of sleep disorders became the 12th specialty of dentistry in 2020. Over the past 29 years of clinical practice specializing in orofacial pain and sleep, Dr. Eli has also been on the educational staff at university hospitals, pain centers, and the clinical staff of Southern California hospitals.
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