Patients affected by orofacial pain disorders suffer from significant disability. Even mild pain or dysfunction has a profound effect on their social life. A withdrawal from social events such as meals and social gatherings that necessitate chewing, talking, and smiling is common. Absenteeism is high, and intimacy activities such as oral sex and kissing can become uncomfortable.

Orofacial pain relates to the structures innervated by the trigeminal nerve. Branches of C2 and C3, such as the greater and lesser occipital nerve, which innervate the scalp area, also contribute to facial pain (particularly the forehead and orbits) (Fig. 44–1). Orofacial pain disorders originate from or affect the mouth, teeth, face, head, and neck. As such, orofacial pain conditions fall within the scope of several medical specialties, hence diagnosis and management are complex. For this reason, it is important to evaluate the patient in an integrative multidisciplinary setting where physiatrists, pain physicians, dentists, neurologists, physical therapists, life coaches, sleep physicians, ear/nose/throat (ENT) and pain psychologists can work together.¹

Mood disorders, depression, anxiety, catastrophizing, and lack of coping skills negatively affect the emotional burden caused by all chronic pain conditions, including temporomandibular disorders (TMD).^2–4

Evidence has also suggested that psychological problems can manifest as somatic symptoms, sometimes referred to as “masked depression” or in extreme cases, somatization.^2,5–7 An increased propensity to report orofacial pain is seen in individuals with higher levels of psychological distress and with a perception of unhappiness in childhood.

It is widely accepted that the best results for all pain conditions are obtained with conservative modalities that include both pharmacologic and nonpharmacologic aspects, with an emphasis on patient education and involvement. Procedural and surgical interventions are mostly reserved for select patients or patients refractory to conservative treatments. This equally applies to the treatment of orofacial pain.⁸

Overview

In a Canadian epidemiologic study, 48.8% of orofacial pain patients responded positively to one or more of the nine questions concerning TMD symptoms. Joint sounds (clicking, crepitus, popping), tiredness or stiffness of jaw muscles, and an uncomfortable bite were the symptoms most frequently reported. Functional pain or pain while at rest was reported by 12.9%. Sex and age differences were small although statistically significant. Females and the younger age groups were more likely than males or the older age groups to report one or more symptoms.⁹

Treatment for TMDs should be limited to conditions that are accompanied by pain and/or dysfunction. Joint sounds, even though unsettling to some, do not warrant treatment other than education, reassurance, improvement in coping mechanisms, and therapies to decrease somatization.

Temporomandibular disorders are divided into two subtypes:

1. 
   

   Arthrogenous TMD: Pain and dysfunction that is due to the joint itself (condyle or disc). The pain is usually located around the temporomandibular joint (TMJ) and ear.¹⁰ Dysfunction includes closed or open locking, anterior open bite, and difficulty chewing. Arthrogenous TMJ may be associated with imaging changes and can be either acute or chronic.

   
   
2. 
   

   Myogenous TMD: Pain and dysfunction are within the masticatory muscles. The pain is generally described as deep, diffuse, achy, and often referring to the TMJ, ear, temples, and even the teeth. Dysfunction typically consists of an inability to open the mouth wide due to pain and a deflection of the jaw. Myogenous TMD is usually associated with normal imaging and can either be acute or chronic.

Arthrogenous TMD

Anatomy of the TMJ

The TMJ is a complex joint composed of an articular disc made up of dense fibrous tissue, dividing the joint into a lower compartment and an upper compartment. In the lower compartment, the condyle rotates in relationship to the disc. The upper compartment allows for anteroposterior and mesio-lateral translation of the disc and condyle in the fossa and over the articular eminence of the temporal bone. Together, the rotation in the lower compartment and the translation allow for wide opening of the mouth. Unique to the TMJ is that all articular surfaces are covered by fibrocartilage¹¹ (Fig. 44–2).

TMD: Trauma to the Joint

The TMJ, like all other joints in the body, is subject to potential harmful influences. Macrotrauma (falls, punches) often involves tearing or rupture of the disc or ligaments, condylar fractures, or subluxation. Trauma is first characterized by joint effusion, pain, and acute change in tooth contact or locking of the joint open or closed. In the short term, this type of trauma may lead to severe joint pain lasting weeks to months. In the long term, these patients face a higher risk of traumatic arthritis, but function generally returns to normal or close to it. Intra-articular bleeding can also lead to adhesion, fibrosis, or proliferation of vascularized and innervated hyperplasia tissue.

Microtrauma (night bruxism, condylar hypermobility, recurrent dislocations, retrusive jaw position, loss of molar support), causing changes in loading pattern, has been identified as a cause of TMJ. However, a causal relationship between these and temporomandibular disorders has not been firmly established.

Stress-induced excessive parafunction, such as daytime clenching or bruxism, are certainly factors that could lead to decompensation, but recent evidence suggests that stress may also directly invoke biologic responses that may be associated with TMJ osteoarthritis. Nerve growth factor (NGF) has been shown to evoke joint and muscle pain following local or systemic administration. NGF is not only produced in response to injury (when it may stimulate sympathetic neurons to sprout into adjacent sensory ganglia), but animals and human studies have shown that psychological stress also increases plasma NGF.

Arthrogenous TMD: Osseous Pathology

Osteoarthritis

The major etiologic factor in TMJ, osteoarthritis (OA) is understood to be excessive mechanical stimuli caused by a wide variety of normal and excessive jaw function. However, the underlying mechanisms leading to activation of the chondrocytes in OA cartilage are not fully understood. There is evidence that synovitis is associated with the symptoms of pain and dysfunction and that it may promote more rapid cartilage degeneration.^12,13

Osteoarthritis is the most common disease affecting the TMJ. Radiographic studies of OA of the TMJ reveal an incidence of 40% in patients older than 40 and 100% in patients older than 80. So although about 50% of the population has radiographic changes, only 30% of these patients are symptomatic.

OA has a strong predilection for women and can affect people of any age.

Symptoms range from pain and tenderness in the joint and masticatory muscles and muscle fatigue to difficulty with and pain upon chewing and mouth opening, with occasional restriction of range of motion and crepitation. OA due to normal wear and tear usually affects older people, is slow in onset, and runs a course of mild episodic symptoms. OA secondary to microtrauma or macrotrauma will typically affect people ages 20 to 40 years old and will be more likely to be more severe and associated with dysfunction such as disc derangement.

Treatment for osteoarthritis is palliative with nonsteroidal anti-inflammatory drugs (NSAIDs), night guards, behavior modification, pain psychology, and eventually joint injections with corticosteroids. There are experimental treatments such as platelet-rich plasma and stem cell injections that may be of consideration in the future.

Rheumatoid arthritis (RA) can also affect the TMJ. It is unlikely for the TMJ to be the first joint affected. The symptoms experienced are similar to OA, with longer-lasting stiffness. Because RA is primarily a soft tissue disease, there will be few radiographic changes in the early stages, while a magnetic resonance imaging (MRI) may show disc abnormalities.

In the late stages, there is a high incidence of fibrous ankylosis and of progressive class II malocclusion and open bite, with impairment of masticatory function and speech due to condylar bone destruction.^14–17

Laboratory findings are used to confirm diagnosis. Rheumatoid factor (RF) is positive in 70% to 80% of patients. However, it is also positive in 5% of healthy subjects.¹⁸

Western blot is elevated in 90% of the patients during active stages only.

Other tests include blood count, antinuclear antibody (ANA), human leukocyte antigen (HLA)-Dw5 and HLA-DRw.^3,19,20

Treatment for rheumatoid arthritis, lupus, and Sjögren’s syndrome should be deferred to the patient’s rheumatologist, as the treatment will be more systemic than local.

Idiopathic condylar resorption (ICR), also called “cheerleader syndrome,” affects young women in ages ranging from 15 to 35.^10,21

Generally, the patient will come to the attention of the dentist or orthodontist with pain in the joint(s), a rapidly progressing anterior open bite, and difficulty in chewing and talking, which may in turn lead to myofascial pain.

Although the etiology of ICR has not been fully characterized, some have suggested that it is secondary to an extreme form of osteoarthritis linked to hormonal changes (estrogen receptors have been identified in the TMJ).^22,23

Diagnosis should also aim at ruling out other types of arthritides such as rheumatoid arthritis, scleroderma, and other autoimmune disorders. A history of joint injection with steroid and orthognatic surgery should be elicited (7% develop the disease following orthognatic surgery), as well as certain types of orthodontic appliances that put pressure on the condyles. Chin cups/straps during continuous positive airway pressure (CPAP) treatment should also be considered.¹⁹ Management is difficult, as there is much we do not know about the disease and its progression.

The classic management is very conservative. Reconstructive treatment is not started until the disease process has stopped and the condition stabilized, as confirmed by isotope bone scans, occlusal casts, bite records, and computerized tomography (CT) scans.

Following remission, depending on the degree of resorption, the modalities range from orthodontics and orthognatic surgery to autologous or alloplastic joint replacement.²⁴

At the other end of the spectrum, Wolford and his team advocate synovectomy, disc repositioning, ligament repair, and orthognatic surgery with possible TMJ replacement simultaneously at an early stage to aim at arresting the resorptive process and correcting the deformity.²⁵

Benign neoplasms of the mandibular condyle (osteochondromas, osteomas, chondromas, giant cell lesions, synovial chondromatosis) are rare, and the overlap of symptoms with the more commonly occurring temporomandibular disorders makes them difficult to diagnose.

Malignancies

Primary malignancies of the TMJ are also very rare. The most common are sarcomas. Every cartilage-producing head and neck tumor in an adult should be considered to be potentially malignant.

The typical presentation of a malignant tumor includes a painful mass associated with variable degrees of reduced jaw movement. These tumors are generally slow growing. Rarely do they cause hearing loss and Eustachian tube obstruction. Patients without a mass often get diagnosed initially as TMD. Underdiagnosis has been reported as high as 20%, and 6% to 9% of osteosarcomas occur in the jaw. In other sites, the first symptoms generally appear in the teenage years. The mean age for jaw osteosarcoma is 27 to 33 years old.²³ Head and neck radiation therapy, Paget’s disease, fibrous dysplasia, and retinoblastomas are risk factors. Metastasis from head and neck sarcomas has been reported in 50% of cases. Lungs, cervical nodes, and bones are the usual sites of spread.

Metastatic Tumors of the TMJ

Metastatic tumors account for about 3% of jaw tumors. The most common is adenocarcinoma originating from the female breast, lung, and prostate. The diagnostic dilemma is the same as with primary malignancies. The symptoms bear great commonality to those of certain TMDs.

Myofascial pain (MFP) is pain that is referred to distant sites from trigger points (TrPs) in muscle. The TrPs are focally tender spots found in taut bands of skeletal muscle. MFP is probably the most prevalent cause of pain in all parts of the body and has been reported as a common source of pain in numerous medical specialties.^26–29

It is also the most prevalent cause of painful symptoms in TMDs.³⁰

Symptoms

Any deep, dull, aching pain, whether in or over muscles or in any other structure such as a joint, tooth, sinus, or deep in the head, may be myofascial in origin. MFP is largely a referred symptom where examination and/or imaging of the painful area is typically entirely normal. The intensity of MFP should not be underestimated: the pain intensity has been documented to be equal to or slightly greater than pain from other causes.²⁶

Associated Symptoms

The referred pain from MF TrPs is often accompanied by referred physiological sensory, motor, and autonomic effects typically seen with prolonged pain and may confuse the clinical picture.

Sensory complaints may include tenderness of the referred pain site, such as scalp pain on brushing the hair, or simply tenderness to palpation at the site of pain, for example, tenderness to palpation of the lateral poles of the TMJ without concomitant pain with joint movement. Motor effects include increased motor activity in any muscles found in the pain reference zone. Autonomic changes may include localized vasoconstriction (paleness), ptosis, perspiration, tearing, runny nose, and even nausea and vomiting.

MFP worsens with increased psychological stress, cold weather, immobility, and overuse of involved muscles. Patients often report relief with hot baths, rest, warm weather, and massage.³¹ TrPs may wax and wane between latent and active states. Latent trigger points do not cause clinical pain but may be activated to cause their referred pain by additional acute muscle overload or psychological stress. Palpation of latent TrPs will cause the associated referred pain pattern, and proper palpation is a diagnostic test.

Patients are typically only aware of the referred pain site and associated symptoms. They will not recognize or report the existence of the causative TrPs. The location of TrPs and their associated referred pain patterns are predictable and reproducible from patient to patient. Thus, the pain pattern can be used in reverse to identify the probable guilty muscle TrPs. A meticulous discussion of MFP, as well as a complete compendium of the pain referral patterns for almost all muscles of the body, has been brilliantly detailed by Simons et al.³² (Fig. 44–3)

Etiology

Myofascial TrPs tend to develop either after:

• 
  

  Acute trauma, such as falls, blows, sports injuries, motor vehicle accidents, or excessive or unusual exercise

  
  
• 
  

  Insidiously over time with chronic muscle overload due to poor posture and body mechanics, abnormal strain, and repetitive motion-type injuries

  
  
• 
  

  Secondary to protective muscle splinting caused by other chronically painful conditions, such as migraine or postherpetic neuropathy

  
  
• 
  

  Secondary to referred pain from other TrPs

TrPs that develop in muscles in the referred pain site of TrPs in another muscle are called “satellite” TrPs. They are very common and may develop their own referred pain pattern. Treatment of these satellite TrPs requires recognition and treatment of the primary, or “key,” TrPs perpetuating them.

Pathogenesis

Despite the comparative ease of their clinical identification, the structure and exact pathophysiology of TrPs are still under debate. Clinically, pressure algometry studies have demonstrated that TrPs are circumscribed tender areas in muscle; pain with palpation is not due to generalized muscle soreness. In fact, non-TrP sites in people with MFP are no more tender than muscle sites in people with no myofascial pain.^33–35

Careful monopolar needle electromyographic (EMG) evaluation of TrP sites demonstrated that TrP sites exhibit spontaneous electrical activity (SEA), while similar EMG evaluation of the muscle surrounding the TrP was normal. Moreover, the amplitude of the spontaneous EMG activity was significantly higher in people who had clinical pain due to active TrPs than in people without clinical pain who had latent or no TrPs.^36,37

Increased sympathetic output due to psychological stress was shown to increase the amplitude of the SEA recorded from TrPs, whereas the EMG activity of neighboring non-TrP muscle sites remained unchanged. This finding was similar to the clinical observation that emotional stress increases clinical pain, correlating with activation or aggravation of TrPs.³¹

Other researchers using a unique in vivo microanalytical technique found that active myofascial trigger point sites have significantly higher concentrations of bradykinin, calcitonin gene-related peptide, substance P, serotonin, and norepinephrine and have significantly lower pH than latent or non-TrP sites.^38,39

Interestingly, concentrations of these neurogenic inflammatory biochemicals declined after needling the TrP and eliciting a twitch response. (A twitch response is a characteristic feature of trigger points that has been well studied in rabbits. It represents a spinal cord reflex resulting in brief contraction of the taut band containing the trigger point when it is stimulated with snapping palpation or needle penetration.)^40–42

An explanation of how pain gets referred to distant sites from muscle was proposed by Mense and Vecchiet et al and refined by Simons to relate to myofascial TrPs. Mense and Vecchiet et al suggested that convergent connections from other spinal cord segments are “unmasked” or opened by nociceptive input from skeletal muscle. Subsequent referral to other myotomes is due to the release and spread of substance P to adjacent spinal segments. Simons expanded on this theory to suggest how this may relate to the referred pain from TrPs.^43–45

Examination requires systematic fingertip or pincer-type examination of the potentially causative muscles, looking for taut bands and focal tenderness. Effective TrP palpation is a skill that must be learned and practiced. Once a suspected TrP is found, algometry studies support the application of 2 to 3 kg/cm² of pressure to elicit pain. Because referred muscle pain is delayed, the pressure should be applied for at least 5 to 10 seconds to elicit the referred pain pattern, if any. The examination may replicate the patient’s pain so precisely that there is no doubt about the diagnosis. If uncertainty exists, specific TrP therapies, such as “spray and stretch” or TrP injections, described next, may be used diagnostically.

Treatment

The most important factor in treating MFP is identification and control of causal and perpetuating factors, followed by muscle stretching. Patients must be educated to correct relevant perpetuating factors and will also need to comply with specific home stretching exercises. Once most perpetuating factors are controlled, therapeutic techniques such as “spray and stretch,” TrP pressure release, and TrP injections may help facilitate the patient’s recovery. Myogenous TMD is generally treated with a blend of home care (including sleep optimization), diet and behavior modification (more relaxed jaw position), physical therapy, and the adjunct of pain psychology if necessary, and possibly muscle injections. The use of muscle relaxants can be useful short term. The use of a night guard has shown benefits in some people, particularly those who wake up with increased symptoms. More aggressive methods would be trigger point injections with local anesthetics. The use of Botox for myofascial pain is not yet supported by a body of evidence.

Some long-term myofascial pain patients show signs of more centrally mediated pain and will respond to medications used for fibromyalgia such as gabapentin, pregabalin, duloxetine, baclofen, or nortriptyline.

Perpetuating factors most commonly include mechanical factors that place an increased load on the muscles. Teaching patients good posture and body mechanics will go a long way in reducing referred pain from myofascial TrPs, especially in the head and neck region. An intraoral stabilization splint may be indicated to decrease the frequency of clenching or bruxing as a perpetuating factor.^46–48

Psychological factors, such as stress or depression, must be addressed, as they both contribute either directly (stress activates TrPs) or indirectly (depression lowers pain thresholds) to MFP. Sleep disturbance and inactivity are also common perpetuating factors. Simple stress management and relaxation skills will reduce TrP activation. Mild depression and sleep disturbance can be treated with low doses of tricyclic antidepressant drugs and a structured exercise/activation program.

Other perpetuating factors include metabolic, endocrine, or nutritional insufficiencies that affect healthy muscle metabolism. Evaluation of patients for general good health with referral to their physician for management of any systemic abnormalities is indicated. In secondary MFP, the primary concomitant painful disorder, such as migraine, pulpitis, or chronic neuropathy, must also be treated or managed.

Spray and stretch is a useful technique that uses ethyl chloride vapocoolant spray (Gebauer, Co., Cleveland, OH) to facilitate muscle stretching in MFP. Muscle stretching has been shown to reduce the intensity of referred pain and TrP sensitivity in patients with MFP. This technique and alternatives are described in detail in the Travell and Simons text.⁴⁹

Needling of TrPs, with or without injection of solution, has been shown to be helpful in reducing the TrP activity to allow stretching.^50,51 The best clinical result occurs when the TrP itself is pierced by the needle and a twitch response is elicited.⁵²

Treating “key” myofascial TrPs with dry needling or injection has been shown to reduce the activity and tenderness of related satellite TrPs.^53,54 Although dry needling is effective, the use of a local anesthetic reduces postinjection soreness.⁵² Small amounts of low concentrations of local anesthetic, such as 0.5% procaine or 0.5% lidocaine, are recommended for TrP injection. Longer-acting amide local anesthetics or local anesthetics containing epinephrine cause permanent muscle damage.⁵⁵