Splint selection is a critical factor in treating temporomandibular joint dysfunction (TMD), ensuring that therapeutic interventions support optimal jaw physiology, neuromuscular function, and long-term health.
About the Guest Author
Dr David Stephenson, BDSc (Hons) from the University of Queensland (1983), is a highly experienced General Practitioner Dentist with over 40 years of clinical practice. He has pursued extensive further education in TMJ dysfunction, upper airway resistance syndrome (snoring and sleep apnoea), and upper cervical spine/whiplash trauma (cervicogenic headaches). His approach integrates advanced diagnostics, musculoskeletal therapy, and airway management to provide comprehensive care for patients suffering from chronic pain and sleep-related disorders, because sleep bruxism and clenching, and nasal patency airway issues, disrupt normal sleep architecture.
The Temporomandibular joint (TMJ) is one of the most misunderstood structures in dentistry. Unlike a traditional ball-and-socket joint, it is a gliding hinge joint that allows both rotational and translational movements. It consists of a single bone, the mandible, which articulates with the temporal bones at two independent but interconnected joints. It is also considered to be the highest joint in the cranio-sacral system of the spinal vertebrae.
The TMJs receive input from the Trigeminal nerve and associated muscles, including the masseter, temporalis, and pterygoid muscles, which coordinate jaw movement. The TMJ is cushioned and stabilised by a fibrocartilaginous disc, fibrous connective tissue, and synovial fluid, which together help absorb shock and prevent excessive wear.
Any dysfunction in these structures can lead to temporomandibular disorders (TMD), causing pain, clicking, or restricted movement, or chronic nociception due to parafunctional activity, swallowing, or chewing. In most cases, parafunctional activity occurs during sleep. Additionally, the mandibular branch of the Trigeminal nerve has a direct connection to the Trigeminal ganglion, and nociception produces a lot of Substance P, which leads to central sensitisation. Peripheral injuries must transmit pain signals through a junction at the spinal synapses. However, the TMJ and mandible are directly connected to the central nervous system. This direct connection lowers the nociceptive threshold of the Trigeminal system.
Unlike most joints in the body, the TMJ has a unique ability to repair cartilage damage. Stem cell activity in the distal articular cartilage allows for regeneration, making it one of the few joints capable of self-repair. This further reinforces the need for proper diagnosis and treatment, as excessive strain on the TMJ can compromise its ability to heal naturally.
Assessing TMJ dysfunction: The PDQ model
Dysfunction means anything that is not normal function.
In 2007, at the AACP Symposium in Fort Worth, Dr Clifton Simmons, DDS, introduced the PDQ model – Pain, Dysfunction, and Quality of Life. This framework helps assess and manage TMD and related orofacial pain conditions.
The PDQ model differs from traditional assessments, which often focus only on structural issues within the TMJ. Instead of treating TMD as purely a mechanical problem, the PDQ model takes a broader view, recognising that pain, joint function, and overall well-being are interconnected. This model helps practitioners evaluate not only if dysfunction occurs but also how it affects a patient’s daily life.
Pain is a primary indicator of TMD, often presenting as muscle pain, joint discomfort, headaches, or nerve-related pain. Sometimes, pain is referred from a muscle into a tooth. Chronic clenching can radiate pain into the upper lateral incisor, and sometimes into the upper first molar. Pain can be in the joint, muscles, ear, or present as a band of tension headache.
However, pain is NOT the only indicator of dysfunction. Many people use their neuromuscular (and emotional) systems to compensate or compromise to AVOID pain. This is a very important concept to understand.
Dysfunction refers to abnormal jaw movement, which may include restricted motion, difficulty chewing or speaking, and muscle fatigue. When the joint does not function properly, it can lead to joint instability and long-term wear. However, not all dysfunction is about pain. Dysfunction can include clicking, crunching, cramping, locking, an inability to open or chew properly, neck stiffness, postural compensations, ear stuffiness/itchiness, or tinnitus.
Quality of life issues can include bruxism causing disrupted sleep quality. The noise of someone bruxing can keep bed partners awake, and the sound of a popping jaw joint can be embarrassing when one is out for lunch or dinner. A locked jaw without reduction can also have a huge impact on a person’s ability to function normally, and the chronic crushing pain can compromise their normal life activities, work, parenting, or leisure. And because their disability can’t be seen, friends and family can easily STOP being empathetic.
By addressing pain relief, functional restoration, and the broader impact on quality of life, the PDQ model provides a comprehensive approach to diagnosing and treating TMD. Rather than relying on a single treatment method, the PDQ framework encourages a tailored, patient-specific approach.
Pain management may involve anti-inflammatory medications, muscle relaxants, or trigger point therapy to reduce discomfort. Restoring function may include jaw exercises, orthopaedic oral devices, orthodontic interventions, or in severe cases, surgical procedures.
Improving quality of life often requires a multidisciplinary approach, such as sleep studies for suspected apnoea, behavioural therapy for stress-related clenching, dietary modifications to reduce strain on the jaw, osteopathy or other manipulative therapy for the jaw and neck, or float tank therapy.
It’s also important to note that, in many cases, cervical spine misalignment plays a role in TMD.
Research by Dr Paul Durham and Professor Nikolai Bogduk highlights that upper cervical spine injuries also produce Substance P and Central Sensitisation. Central Sensitisation can trigger a reflexive response in the jaw, leading to increased clenching and exacerbation of TMJ parafunction.
The Trigeminal nerve, which innervates the TMJs directly, is closely linked to Upper Cervical Spine proprioception via direct neural connection between the Trigeminal Ganglion and the Trigeminal Motor Nucleus.
Misalignment at C0/C1 or C1/C2 or C2/C3 can create neuromuscular compensations that perpetuate jaw tension and headaches. Addressing cervical posture and mobility may play a crucial role in managing TMJ-related pain, and vice versa.
Rethinking splints: Terminology and purpose
For decades, the term ‘splint’ has been used in dentistry to describe a broad category of oral devices prescribed for patients experiencing jaw pain, muscle tension, and parafunctional habits.
However, this terminology fails to distinguish between devices that protect teeth and devices that support joint and muscle function.
That’s why it’s my belief that the dental profession needs to reconsider its use of the term ‘splint’ when referring to oral devices. By definition, a splint is a retainer – a device that holds something in place but does not actively correct or rehabilitate function.
We already have an ADA code for a retainer.
Unless, the dentist has completed an in-depth exam (ADA code 963: Clinical occlusal analysis including muscle and joint palpation), and come up with a diagnosis and proposed a thorough treatment plan that addresses the associated neurological and compensation symptoms of TMD, just addressing the patient’s symptoms by providing a 965 occlusal splint (which is just a retainer to protect the teeth and the expensive dentistryis not enough.
To illustrate my point, let’s compare an occlusal splint to a moon boot for a sprained ankle. A moon boot serves to immobilise and protect the injured area while it heals. However, just as a moon boot is NOT an orthopaedic orthotic restoring a functional alignment, an occlusal splint does not necessarily provide orthopaedic functional alignment of the TMJs.
Just as a podiatrist prescribes an orthotic to orthopaedically correct ankle and foot posture, reduce strain, and improve movement, a TMJ orthotic supports the jaw by optimising joint positioning, reducing muscle tension, and facilitating more balanced function. It is also important to recognise that splints and guards are not inherently therapeutic. While they may prevent further dental damage, they do not by design rehabilitate jaw muscles, restore proper occlusion, or stop bruxism at its source. In fact, long-term reliance on an occlusal splint without additional treatment can even lead to muscle adaptation, bite changes, and worsening dysfunction in some cases.
This is why the occlusal splint (ADA item code 965) should be more accurately referred to as a ‘TMJ orthotic’ – a functional orthopaedic device designed to support the temporomandibular joint both at rest and during function.
TMJ dysfunction is a multifactorial condition, often involving parafunction, muscle overuse, joint instability, airway issues, and neurological triggers. Proper treatment should extend beyond the use of a splint or guard and include physical therapy, behavioural modifications, and occlusal adjustments when necessary.
The Importance of the Shimbashi Index
The Shimbashi Index is a crucial measurement for a dentist assessing a physiological vertical dimension for TMJ health. Named after pioneering dentist and researcher, Dr Henry ‘Hank’ Shimbashi, this index identifies the optimal relationship between the upper and lower jaws. When the lower jaw is correctly positioned relative to the upper jaw, the condyle, articular disc and eminence are in centric relation.
Centric relation is not a position. It is a relationship.
Cartilage on the condyle meets the centre of the cartilage disc, and the centre of the cartilage disc meets the cartilage on the eminence. There is no cartilage on the top of the Glenoid fossae, so a retruded back position is NOT NORMAL. In centric relation, at a normal physiological vertical height, the associated muscles function at their ideal length and neuromuscular input is normalised, which reduces strain and nociception and prevents dysfunction.
Dr Shimbashi’s research, which involved more than 500 patients, demonstrated that there is a physiological range of vertical dimension where jaw muscles achieve their maximum potential without causing pain. Shimbashi Index is determined by measuring the distance from the CEJ of the upper front tooth to the CEJ of the lower front tooth. The ideal measurement is approximately 18-21mm when the patient bites in centric occlusion.
Shimbashi measured normal average upper centrals = 10-12mm, normal average lower centrals = 8-10mm, normal average over bite = 1-2mm, Therefore normal Shimbashi Index = 18-21mm.
It’s an empirical measurement, based on normal average, but is an important measurement to take BEFORE any therapy. Many patients with TMD present with significantly lower Shimbashi Index, sometimes as little as 10mm. This leads to increased overbite, excessive coverage of the lower teeth by the upper teeth, reduced lower face height, foreshortened resting muscle tension, retruded condyles in the glenoid fossae, and higher susceptibility to nociception to the CNS. Dentists should routinely measure the Shimbashi Index in patients experiencing TMD.
Conversely, a bite opened beyond the patient’s physiological norm by an oral device that places the patient at an increased face height/ dental vertical dimension will lead to discomfort and lack of device tolerance. This explains why improperly designed oral devices can fail or worsen symptoms, or be abandoned by the patient as useless. Or worse, if the patient complies, the physiological neuromuscular response may lead to occlusal and jaw relationship changes.
A proper understanding of the Shimbashi Index allows dentists to fabricate effective, well-tolerated therapeutic devices that respect the natural physiological and neuromuscular balance of the jaw.
The TMJ-migraine connection
Clenching and bruxism should be carefully evaluated in individuals who suffer from chronic migraines, as these habits may contribute to the persistence and severity of their symptoms.
A classic migraine is characterised by one-sided headaches occurring on at least 15 days per month, with at least eight of those meeting the diagnostic criteria for migraines.
A central migraine is one that debilitates the sufferer. They may need to rest in bed with no bright lights or noise, and may be accompanied with nausea and/or dizziness, vertigo, and vomiting.
One factor that may worsen this condition is excessive stimulation of pain-sensitive nerves (nociceptors) in the jaw and face. Reducing peripheral nociceptive input, which means decreasing nociceptive, adverse mechanoreceptive, and adverse proprioceptive signals that originate from the muscles, joints, and nerves in the mouth and jaw, can help lessen the overall CNS pain response in the nervous system.
When nociception is continuously triggered in these areas, it can lead to central sensitisation, a process in which the brain and spinal cord become overly responsive to pain signals. Central sensitisation is a key characteristic of chronic migraine, as it can cause heightened sensitivity to normal stimuli and contribute to the persistence of central headache pain even when the original trigger is no longer present.
The use of targeted intraoral orthotics designed to minimise strain on the TMJs during nocturnal clenching may help reduce excessive neuromuscular activity, relieve compression of the TMJs, and reduce nociception.
Remember that the TMJ articular discs have stem cells that can heal, but only if the joints are positioned in centric relation at rest and during function. By decreasing the stimulation of pain receptors in the TMJs and upper cervical spine region, and reducing the parafunctional input of the bruxing and clenching, these devices have the potential to lower the overall nociceptive burden to the CNS, and, in turn, help reduce the frequency and intensity of tension headaches and migraines. However, because chronic migraines involve complex neurological processes, collaboration between dentists and neurologists is essential. Dentists can address underlying jaw dysfunction, while neurologists can assess and treat the broader neurological components of the condition.
Hormonal fluctuations also play a significant role in TMJ dysfunction, particularly in women. During the menstrual cycle, changes in estrogen and progesterone levels affect ligament laxity and muscle tone. Research has shown that the change in androgen levels during the menstrual cycle can contribute to increased tension in the masticatory muscles, which contain hormone receptors. For patients who already exhibit bruxism or TMJ-related pain, these hormonal changes can exacerbate symptoms. Evidence from neuroscientists indicates that a decrease in androgen levels is directly linked to an increase in CNS input and reduced upregulation of nociception.
In addition, lifestyle habits such as caffeine intake and other dehydrating foods and drinks, too much salt, inflammatory substances like sucrose, and simply not enough good quality mineral rich water, lack of trace minerals for enzyme function, all affect muscle tone, lymph flow, and healing capacity.
TMJ Orthotic considerations
Now that we’ve covered TMJ dysfunction, let’s look at oral device therapy.
Any device a dentist provides should address a diagnosed issue. Otherwise, it is simply a retainer. Whether it is a mouthguard, a soft-hard splint, or a Michigan splint with cuspid guidance, if it does not address dysfunction, it is just a retainer that protects the teeth. A mouthguard is typically used for sports protection rather than therapeutic purposes, while soft-hard splints provide some cushioning but may inadvertently encourage clenching in certain patients.
Michigan splints with cuspid guidance aim to reduce muscle strain and improve occlusal guidance for patients who brux, though their effectiveness depends on the specific needs of the patient and whether the provider’s design effectively considers physiological vertical dimension.
Flat-plane occlusal splints, which are among the most commonly prescribed, serve primarily to distribute forces to help protect teeth and restorations from excessive wear, but do not actively treat TMJ dysfunction. They certainly don’t treat bruxism.
Bruxism is a neurological condition, and while splints can mitigate its effects, they do not address the root cause. Some patients even clench harder on a splint, exacerbating muscle tension rather than relieving it. Although splints do not cure bruxism or TMD, they can play an important role in managing symptoms and preventing further dental complications.
To be effective, TMJ orthotic therapy must be tailored to each patient’s condition and integrated into a broader treatment plan. True TMD management may also involve physical therapy to improve joint mobility and reduce muscle strain, behavioural therapy to address stress-related clenching, bite adjustments to correct occlusal discrepancies, medication to reduce inflammation and pain, and hopefully, achieve orthopaedic alignment of the TMJs.
Unlike some other medical devices for joint dysfunction that are used only for short-term intervention, traditional occlusal splints are worn indefinitely.
This raises an important question: “Should patients be encouraged to rely on a splint long-term as a guard against tooth wear/fracture, or should TMD treatment be focused on addressing the dysfunction itself?” Long-term reliance on a splint may provide ongoing protection, but without a comprehensive treatment approach, the underlying problem remains unresolved.
Differences between NTI and traditional occlusal splints
An NTI-tss device (Nociceptive Trigeminal Inhibition tension suppression system) is a small, custom-fitted anterior anti-clenching device designed to relieve symptoms of nocturnal clenching. Unlike full-arch occlusal splints, which cover all or most of the teeth, an NTI-tss device covers only the upper and lower front teeth (incisors and canines) and prevents the back teeth from making contact, no matter where the mandible moves.
It was invented by Dr Jim Boyd DDS, a headache sufferer, in 1996, and tested in a migraine trial for the FDA , by Dr Wesley Shankland. The trial compared the use of “the NTI-tss against bleaching guards against no input” and was found to be more effective than Imgran (a Triptan) for chronic migraine sufferers. The FDA recommended that persons suffering from chronic migraines see a dentist at the first instance, rather than be placed on medication therapy.
The NTI-tss device limits the contraction of the temporalis muscles, which are responsible for compressive clenching. By preventing full occlusion of the molars, the reflex built into the lower incisor periodontal ligaments via the huge mandibular branch of the Trigeminal nerve, reduces the temporalis muscle activity, which decreases stress on the TMJ and lowers the risk of tension headaches and migraines caused by nocturnal clenching.
Traditional occlusal splints, on the other hand, allow for posterior molar contact, which have no inhibition and allow increased clenching intensity (asleep clenching can exert 10-20 times the force that one would use to chew a nut).
As the NTI-tss device limits occlusal contact to the incisors only, it reduces temporalis contraction intensity and subsequently lowers nociceptive input from the TMJs. However, incorrect NTI fabrication can result in canine or molar contact, which negates the intended inhibition of trigeminal motor activity. Worse, incorrect design can over-open the vertical dimension beyond normal physiological limits.
Failure to respect the patient’s natural physiological vertical dimension can lead to significant discomfort and poor device tolerance. Many NTI devices, for example, have been criticised due to improper application of this concept. The issue is not with the neuro-muscular appliance itself but rather a misunderstanding of the Shimbashi Index, the concept of centric relation, and most importantly, poorly diagnosed condition, which results in poorly tolerated oral devices.
The final word
Universities in Australia still do not adequately explain these fundamental concepts. Even today, dental students misunderstand the basics of TMJ function and disorders.
This gap in knowledge results in underdiagnosed and undertreated patients who fall between the gaps of the healthcare system ) and do not receive meaningful therapeutic care.
The goal should be to provide the right device to address the patient’s PDQ, ensuring that oral device selection aligns with both function and patient comfort, rather than defaulting to generic splints that do not treat the underlying dysfunction.
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