INTRODUCTION:

Temporomandibular disorders (TMD) result from musculoskeletal dysfunction of the orofacial region affecting masticatory muscles, temporomandibular joints (TMJ), and other associated structures. The main characteristics of these problems are facial and TMJ pain, headache, earache, dizziness, masticatory muscle hypertrophy, limited mouth opening, locked jaw, abnormal teeth wear, joint sounds, and others (1). Dentist must be aware on the proper diagnosis and treatment of temporomandibular disorders, because they represent the second most frequent patients complaints (only less frequent than dental pain) (2). Skeletal muscle relaxants are frequently used to treat these conditions. The muscle relaxants are believed to exert their action either by treating spasticity secondary to upper motor neuron syndromes, or muscular pain and spasms secondary to peripheral musculoskeletal conditions (3).

Drugs classified as skeletal muscle relaxants include baclofen, carisprodol, chlorzoxazone, cyclobenzaprine, dantrolene, metaxalone, methocarbamol, orphenadrine, and tizanidine. Some centrally acting muscle relaxants such as phenprobamate and mephenoxalone have antianxiety action that may be related in part to their action (4), these muscle relaxants are useful in treating tempromandibular disorders. TMJ disorders are common and often self-limited in the adult population. In epidemiologic studies, up to 75 percent of adults show at least one sign of joint dysfunction on examination and as many as one third have at least one symptom(5,6). However, only 5 percent of adults with TMJ symptoms require treatment and even fewer develop chronic or debilitating symptoms(7).

Symptoms of TMD:

Pain and tenderness on palpation in the muscles of mastication, or of the joint itself (preauricular pain – painfelt just in front of the ear). Pain is the defining feature of TMD and is usually aggravated by manipulation or function(8),such as when chewing, clenching(9), or yawning, and is often worse upon waking. The character of the pain is usually dull or aching, poorly localized(10),and intermittent, although it can sometimes be constant. The pain is more usually unilateral (located on one side) rather than bilateral(11). It is rarely severe(12).

Limited range of mandibular movement, which may cause difficulty eating or even talking. There may be locking of the jaw, or stiffness in the jaw muscles and the joints, especially present upon waking(13).There may also be incoordination, asymmetry or deviation of mandibular movement.

Pathogensis of tempromandibular joint disorder:

Inflammation mainly affects the posterior disc attachment (14, 15). Several inflammatory mediators play an important role in the pathogenesis of TMJ disorders like tumor necrosis factor alpha (TNFalpha), interleukin-1beta (IL- 1beta) , prostaglandin E2 (PGE2), leukotriene B4 (LkB4 ), matrix metalloproteinases (MMPs), serotonin- 5- hydroxytryptamine (5-HT).(16, 17). MMPs are the early marker or detector to determine temporomandibular joint arthritis(18). Serotonin is the mediator of pain and inflammation is produced in enterocromaffin cells of the gastrointestinal mucosa and absorbed by platelets. It is also produced in the synovial membrane and in the synovial fluid which causes TMJ pain in cases of systemic inflammatory joint diseases (19,20). Inflammation results in tissue response as: vasodilatation, extravasation, release of mediators, activation of nociceptors, release of neuropeptides as substance P (SP), neuropeptide Y (NPY), which stimulate release of inflammatory mediators like histamine and serotonin and hyperalgesia.

Management of TMD:

Most of the time, patients will visit the clinician when pain and dysfunction, such as limitation of opening, episodes of joint locking (open lock/TMJ subluxation), pain with mandibular function (chewing), facial pain, or headache are present.

The treatment goals for TMD are decreasing pain, restoring normal mandibular range of motion (ROM) and restoring normal masticatory and jaw function. Many TMDs can be cyclical and self-limiting, with periods of complete remission of symptoms.

In the case of disc-condyle incoordinations, studies suggest that for some patients even though they may be progressive (for example, a disc displacement with reduction may progress to a disc displacement without reduction), they are self limiting, suggesting an adaptation of the condition and with no significant disability(21, 22, 23, 24). It is very important to emphasize that patients have no recurrence of symptoms with the use of conservative, reversible treatments (23, 25), thus conservative treatment is the modality that needs to be used at all times. Initial treatment should therefore stress a conservative and reversible approach. Primary treatment options include home care (self-care program), medical care (non-surgical care), and surgical care.

Patient education: home care program:

Home care should generally be the initial approach, at least as part of a more extensive treatment plan. The use of a home care program has proved to be effective in the management of TMD. It has been shown that patients have reported feeling less pain immediately after their initial patient education/counseling visit, perhaps as a consequence of an immediate reduction in stress/ tension-related parafunctional activity(21, 26). Patient education is a crucial aspect of home care and is one of the most subtle and underappreciated, yet effective, treatments for TMD. Therefore, informing and reassuring the patient regarding their condition and presenting symptoms may alleviate a great deal of anxiety and improve treatment outcomes.

A successful home care program consists of rest- ing the masticatory muscles by limiting jaw movements, parafunctional habit modification, emphasizing a soft diet, and moist heat and/or ice therapy(27).Muscle rest may involve limited jaw activity (eg, reduced talking, chewing, yawning)for the treatment duration, and perhaps as a preventive measure, even after symptoms have resolved. Patients with disc displacement without reduction should be instructed to avoid any forceful attempt to open the mouth wider when the condition is acute and have explained to them that, with the care provided, the ROM will improve and return to normal(21).Restricting the mandibular movements as much as possible would facilitate healing and prevent further injury(27). This could be attained with a soft food diet, avoiding chewing gum and hard foods, and limitation of opening during yawning, as well as habit awareness, such as avoiding biting objects, clenching, or bruxing(21, 28). Patients may have a diurnal (day- time) parafunctional habit (clenching, grinding, posturing) that is often not conscious, and this should be addressed to decrease sustained masticatory muscle contractions(29). Patient education and understanding of the physiological rest position (lips together, teeth apart) is imperative in reducing and eventually halting the daytime activity that contributes to the progression of TMD. If asked to pay attention to their jaw position over time, many patients will return for follow-up with the recognition that they are in fact engaging in some jaw activity that contributes to their symptoms. Additionally, suggesting habit-controlling cues may be helpful in remind- ing the patient throughout the day to check the position of their bite. As an example, saying the letter “N” throughout the day can remind the patient to unclench or discontinue grinding their teeth. A soft diet is also crucial for muscle and TMJ pain management so that the condition is not exacerbated while treatment is provided. Finally, a trial of moist heat and/or ice therapy overlying the painful areas of the face, head, and neck can be recommended. Moist heat tends to work better for muscle pain or tension by increasing circulation and relaxing involved muscles, and ice for TMJ capsulitis by reducing inflammatory symptoms.

Medical care (non-surgical):

Physical therapy:

Instructing the patient to apply moist heat or cold compresses, or alternating both modalities, has been proven to be beneficial, since it stimulates analgesia and relaxation and may improve movement (30, 31).Physical therapy is beneficial in restoring the normal function of the TMJ, muscles of mastication, and cervical muscles, as well as in reducing inflammation, promoting repair, and strength (31, 32), Physical therapy can be performed by an experienced physical therapist3 or can be provided by a qualified clinician who is treating the TMJ disorder. Primary goals of the physical therapy component of treatmentare to stretch chronically contracted and fatigued muscles, increase ROM, and reduce muscular trigger point activity(33).A number of exercises are commonly used to treat TMJ- associated muscle disorders, including N-stretch (placing the tip of the tongue on the roof of the mouth and stretching the jaw), chin to chest (gently pulling the head forward, bringing the chin toward the chest); and head tilt (turning the head to one side and then tilting it posteriorly). These exercises must be done four to six times per day to be effective. In addition, the patient should use moist heat for 10–15 minutes followed by ethyl chloride spray prior to stretching the muscles. Vapocoolant spray provides a temporary anesthesia effect to the muscles so that a more intense stretch can be achieved without pain. The heat and cooling spray should be used for at least three of the six exercising sessions throughout the day. Patients can expect an even higher likelihood of treatment success if transcutaneous electrical nerve stimulation is added to a strict stretching regimen(34),and if biofeedback training is used as a cognitive behavioral procedure to teach the patient to maintain reduced muscular tension and pain(29, 35).

Pharmacotherapy:

Medications are an effective addition in managing the symptomatology of intracapsular disorders(21). Commonly used pharmacological agents for the treatment of TMJ disorders include analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), local anesthetics, oral and injectable corticosteroids, sodium hyaluronate injections, muscle relaxants, botulinum toxininjections, and antidepressants (30, 36-38). The analgesics and corticosteroids are indicated for acute TMD pain; the NSAIDs, local anesthetics, and muscle relaxants are used for both acute and chronic conditions; and tricyclic antidepressants are usually used more for chronic TMD pain in association with tension-type headaches (36, 39). Research demonstrating the efficacy of botulinum toxin for muscular disorders related to TMD is limited (40, 41), although there is some data to support the benefit of using low concentrations and large injection volumes of botulinum toxin at multiple muscular sites (38).

Muscle relaxants:

Muscle relaxants are commonly indicated for the treatment of two different types of conditions: spasticity from upper motor neuron syndromes and muscular pain or spasms from peripheral musculoskeletal diseases or injury such as low back pain. The muscle relaxants in current use have variable mechanisms of action, efficacy and adverse effects. This class of medications is well tolerated, with the most common side effects being drowsiness and nausea. The latency of the liver injury is variable(42).Muscle relaxants make up a heterogeneous group of drugs that mainly exert their pharmacologic effect centrally at the level of the spinal cord, the brainstem, or the cerebrum, and that have an insignificant, if any effect, at the muscle fiber level. Their centrally mediated mechanism of action can exert a clinically significant peripheral therapeutic effect.

Carisprodol:

Carisoprodol is still a commonly prescribed muscle relaxant that should be dispensed with caution owing to the potentially addictive properties of its main metabolite, meprobamate. Carisoprodol produces its muscle relaxant effect by depressing the interneuronal activity at the spinal cord level as well as in the descending tracts of the reticular formation. It is not recom- mended for use in the pediatric age population. This drug is metabolized in the liver with meprobamate as its main metabolite. It is mainly excreted through the kidneys. The usual adult dosage is 350 mg four times per day. The most common side effect is drowsiness. Other central nervous system adverse effects that have been reported include ataxia, agitation, insomnia, and others. Adverse effects such as tachycardia, postural hypotension, nausea, erythema multiforme, and eosinophilia have also been seen(43).

Baclofen:

Structurally, baclofen is related to the centrally occurring inhibitory neurotransmitter GABA. Clinically, it has commonly been used for its muscle relaxant effects in the treatment of spasticity, as well as for its neuropathic analgesic properties in the treatment of trigeminal neuralgia pain. Baclofen is a GABA-B receptor agonist with presynaptic and postsynaptic effects leading to a decrease in the excitatory neurotransmitter release as well as in substance P, which is involved in transmission of nociceptive impulses (15). It is metabolized in the liver and excreted in the urine. Baclofen can be administered orally as well as intrathecally via an implanted pump mechanism when significant adverse effects preclude further dose escalation to achieve therapeutic effect. Initial dosing of baclofen should be gradual, starting with 5 to 10 mg three times per day. The maximum recommended dose is 80 mg per day in divided doses; however, higher therapeutic doses in cases of refractory spasticity have been used without any significant untoward side effects. Common side effects are weakness, sedation, and dizziness. At higher doses, baclofen can cause seizures, ataxia, and hallucinations. Abrupt withdrawal should be avoided because it can precipitate seizures and hallucinations.

Cyclobenzaprine:

Cyclobenzaprine is probably the most commonly used muscle relaxant for nonspasticity-related muscle pain. Structurally, it resembles tricyclic antidepressants and differs from amitriptyline by only one double bond. Its therapeutic effect is centrally mediated and carries no direct peripheral action on the affected muscles. Its main pharmacologic action occurs at the brainstem and spinal cord levels and is partially explained by a depressant effect on the descending serotonergic neurons (44). It is extensively metabolized in the liver and excreted as a glucuronated metabolite through the kidneys. It possesses a fairly long half-life of approximately 18 hours and can continue to accumulate for up to 4 days when administered at a frequency of three times per day. Given its structural similarity to tricyclic anti- depressants as well as potent anticholinergic properties, caution should be exercised when considering its use in the elderly or in patients with heart dis- ease. Likewise, concomitant use with monoamine oxidase inhibitors is absolutely contraindicated because this combination can cause a hyperpyretic crisis or even death. The initial starting dose should be 5 mg three times per day on as needed basis and can be titrated up to 10 mg three times per day per therapeutic effect or side effect. In patients with hepatic or renal insufficiency, it should initially be administered once per day given its relatively long half-life. Of note, one recent study showed equal efficacy of 5 and 10 mg doses, with the smaller dose showing a lower level of sedation (45).The most common side effects are drowsiness, dry mouth, fatigue, and headache, followed by less often occurring adverse effects of diarrhoea, dizziness, abdominal pain, nausea, nervousness, blurred vision, and confusion (46).

Tizanidine:

Tizanidine is a centrally acting muscle relaxant that, through its alpha-2 adrenergic agonist properties, is thought to prevent the release of excitatory amino acids by suppressing polysynaptic excitation of spinal cord interneurons. Metabolism is through the liver, and excretion is 60% through the kidneys and 20% through the feces. Tizanidine should be administered through a gradual upward titration from an initial dose of 2 to 4 mg at bedtime up to the maximum of 8 mg three times per day. The bedtime dose can provide an analgesic effect as well as improve quality of sleep owing to the commonly occurring sedating side effect. Other common side effects are daytime drowsiness, hypotension, weakness, and dry mouth. Even though tizanidine’s pharmacologic effect is similar to another alpha-2 agonist, clonidine, it possesses only a fraction of its blood pressure–lowering effect. Less commonly reported side effects of tizanidine are palpitations, bradycardia, dizziness, headache, nausea, elevated liver enzymes, and several rare cases of fulminant liver failure that led to death. Serial monitoring of liver enzymes is strongly recommended(47).

Occlusal appliance therapy:

Oral appliances (OAs) are processed acrylic devices that have been used for the management of TMD for years, with different designs. Studies have reported a reduction in TMD symptoms or at least sufficient evidence to justify their use for myalgia and arthralgia of the masticatory system(48-52). In an extensive review about the use of OAs and the management of TMD, it was concluded that OAs are still regarded as a useful adjunct therapy for some TMD cases(53).

Stabilization appliances (flat plane splints) (Figure 3) are used for the purpose of equally distributing jaw parafunctional forces, reducing the forces placed on the masticatory muscles, and protecting the occlusal surfaces of the teeth from chronic nocturnal bruxing(54). For the case of nocturnal bruxism, OAs will protect the teeth from excessive tooth wear but may not stop parafunctional habits; they may, however, decrease the frequency, duration, and intensity of these habits(53,55,56). Usually, the patient is instructed to wear the splint only at night as long as parafunctional activity is controlled during the day with education and bite relation awareness, teaching the patient to be aware of when they are clenching their teeth during the day. The splint should cover all of the maxillary or mandibular teeth and have bilateral posterior contacts with little to no anterior contacts. The stabilizationappliance should feel comfortable to the patient when fitted for the first time and be re-evaluated after 1 week. Adjustments should continue every 3–6 months due to changes that may result in the form and function of the splint due to chronic bruxing.

Anterior repositioning splint prescription varies among clinicians, but it is usually used for the chronic intermittent closed-locking patient(54), With the possibility of permanent occlusal and bite changes with long-term use of reposition- ing appliances, short-term (6 weeks) use of this appliance is strongly recommended in addition to close monitoring. If bite changes start to develop, then the patient should be instructed to discontinue the use of the splint and the splint may need to be converted to a stabilization non-repositioning appliance. A few patients may experience increased pain with the use of a splint. In this case, the splint and the initial diagnosis should be re-evaluated and, if the pain persists, discontinuation of the splint is recommended.

In a systematic review and meta-analysis of randomized controlled trials, it was found that well-adjusted hard stabilization appliances are more effective in treating joint and muscle pain when compared with the use of no appliance, soft stabilization appliances, anterior bite appliances, and non-occluding appliances(53).Even though these OAs presented some evidence of reducing joint and muscle pains, the potential adverse events (eg, occlusal changes) were higher(52).

Occlusal adjustment:

There is not enough evidence to show that occlusal adjustments are useful in treating or preventing TMD(57). As a general rule, TMD should be treated in a conservative manner and occlusal adjustments are an irreversible modality.

CONCLUSION:

Temporomandibular disorders are frequent and wide spread in general population.TMJ internal derangement is most frequent type of TMD, and in characterised by several stages of dysfunction involving the condyle- disk relationship. The chief complaint is usually pain, which can manifest itself in different ways: head ache, jaw ache, ear ache, facial pain. In early stages of conditions, treatment may involve eating a soft diet and reducing strain on the jaw with the use of a splint or bite guard. Non steroidal anti-inflammatory drugs or muscle relaxants may be prescribed.

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Received on 20.12.2016 Modified on 09.01.2017

Research J. Pharm. and Tech. 2017; 10(3): 917-922.

DOI: 10.5958/0974-360X.2017.00170.6