This article clarifies the current state of knowledge of chronic oral, head, and facial pain (COHFP) conditions with the inclusion of temporomandibular joint disorders as just one component of the variety of conditions that can cause head and facial pain. Obtaining an accurate diagnosis in a timely manner is extremely important because COHFP symptoms can be caused by a variety of pathologic conditions that can be inflammatory, degenerative, neurologic, neoplastic, or systemic in origin. The essential role of the specialty of otolaryngology in the diagnosis and management of patients with these complex COHFP conditions is emphasized.
Key points
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Chronic oral, head, and facial pain (COHFP) disorders are frequently misdiagnosed, therefore a constant reevaluation of the diagnosis and response to treatment is required.
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Otologic symptoms are often caused by temporomandibular disorders (TMDs), and a careful history and clinical examination are the most important factors in making an accurate diagnosis and appropriate referral.
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Joint overload and lack of motion lead to pathologic changes resulting in inflammatory and degenerative temporomandibular joint disease.
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Principles for treating inflammatory and degenerative temporomandibular joint disorders are to reduce load, increase mobility with passive motion, reduce inflammation and muscle spasm, and manage pain.
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For patients with severe temporomandibular joint disorders that fail to improve with appropriate treatment, the least invasive procedure to treat the pathologic condition and improve function is indicated.
Introduction
In 1934, Costen published a paper in the Annals of Otology, Rhinology and Laryngology on “A Syndrome of Ear and Sinus Symptoms Dependent on Disturbed Function of the Temporomandibular Joint.” Costen observed patients with ear, jaw, and sinus pain and theorized that an altered occlusion resulted in temporomandibular joint disease as the major etiologic factor. Furthermore, he recommended correction of the occlusion to relieve pressure on the temporomandibular joint and surrounding structures, ultimately leading to resolution of the symptoms. Thus, the importance of the specialty of otolaryngology in the diagnosis and treatment of oral, head, and face pain was reinforced 80 years ago and continues to this day. Although Costen’s proposal that an altered occlusion was the main cause of head and facial pain has been refuted by evidence-based research, to his credit, he did understand that the site and source of complex head and facial pain are often not the same. Today, 8 decades after the introduction of Costen syndrome, there are many clinicians who still treat patients according to the observations of Dr Costen in 1934.
The diagnosis and management of COHFP has been a subject of great controversy over the years and continues to this day. This situation is unfortunate, because there have been great advances in our understanding of these conditions based on solid research over the past 25 years.
Common clinical scenarios that the otolaryngologist is presented with include the following:
- 1.
Patients with severe persistent ear pain with negative otologic findings who have inflammatory temporomandibular joint disease.
- 2.
Patients with COHFP and masticatory dysfunction who are ultimately diagnosed with neoplasia or other serious disorders (eg, trigeminal neuralgia, temporal arteritis).
- 3.
Patients with oropharyngeal cancers treated with surgery and radiation leading to trismus because of radiation fibrosis, making early detection of recurrent or second primary cancers extremely difficult if not impossible for the clinician.
- 4.
Patients with persistent maxillary dental pain, undergoing multiple dental procedures that fail to reduce symptoms (eg. extractions, root canal therapy) who eventually are diagnosed with acute or chronic maxillary sinusitis.
- 5.
Patients with tinnitus symptoms, resistant to treatment, and coexisting TMDs.
This article clarifies the current state of knowledge of COHFP conditions with the inclusion of temporomandibular joint disorders as just one component of the variety of conditions that can cause head and facial pain. Obtaining an accurate diagnosis in a timely manner is extremely important because COHFP symptoms can be caused by a variety of pathologic conditions that can be inflammatory, degenerative, neurologic, neoplastic, or systemic in origin. The essential role of the specialty of otolaryngology in the diagnosis and management of patients with these complex COHFP conditions is emphasized.
Introduction
In 1934, Costen published a paper in the Annals of Otology, Rhinology and Laryngology on “A Syndrome of Ear and Sinus Symptoms Dependent on Disturbed Function of the Temporomandibular Joint.” Costen observed patients with ear, jaw, and sinus pain and theorized that an altered occlusion resulted in temporomandibular joint disease as the major etiologic factor. Furthermore, he recommended correction of the occlusion to relieve pressure on the temporomandibular joint and surrounding structures, ultimately leading to resolution of the symptoms. Thus, the importance of the specialty of otolaryngology in the diagnosis and treatment of oral, head, and face pain was reinforced 80 years ago and continues to this day. Although Costen’s proposal that an altered occlusion was the main cause of head and facial pain has been refuted by evidence-based research, to his credit, he did understand that the site and source of complex head and facial pain are often not the same. Today, 8 decades after the introduction of Costen syndrome, there are many clinicians who still treat patients according to the observations of Dr Costen in 1934.
The diagnosis and management of COHFP has been a subject of great controversy over the years and continues to this day. This situation is unfortunate, because there have been great advances in our understanding of these conditions based on solid research over the past 25 years.
Common clinical scenarios that the otolaryngologist is presented with include the following:
- 1.
Patients with severe persistent ear pain with negative otologic findings who have inflammatory temporomandibular joint disease.
- 2.
Patients with COHFP and masticatory dysfunction who are ultimately diagnosed with neoplasia or other serious disorders (eg, trigeminal neuralgia, temporal arteritis).
- 3.
Patients with oropharyngeal cancers treated with surgery and radiation leading to trismus because of radiation fibrosis, making early detection of recurrent or second primary cancers extremely difficult if not impossible for the clinician.
- 4.
Patients with persistent maxillary dental pain, undergoing multiple dental procedures that fail to reduce symptoms (eg. extractions, root canal therapy) who eventually are diagnosed with acute or chronic maxillary sinusitis.
- 5.
Patients with tinnitus symptoms, resistant to treatment, and coexisting TMDs.
This article clarifies the current state of knowledge of COHFP conditions with the inclusion of temporomandibular joint disorders as just one component of the variety of conditions that can cause head and facial pain. Obtaining an accurate diagnosis in a timely manner is extremely important because COHFP symptoms can be caused by a variety of pathologic conditions that can be inflammatory, degenerative, neurologic, neoplastic, or systemic in origin. The essential role of the specialty of otolaryngology in the diagnosis and management of patients with these complex COHFP conditions is emphasized.
Pitfalls leading to misdiagnosis of COHFP
The reasons for the difficulty in properly diagnosing COHFP and TMDs are multifactorial. The following factors that can lead to misdiagnosis are important for the clinician to be aware:
- 1.
Complex regional anatomy of the head and neck, often resulting in disparity between the site and the source of pain.
- 2.
Symptoms of pain, limitation of mandibular movement, joint noise, tinnitus, and altered occlusion are not specific for the pathologic condition. Thus, these symptoms can be caused by local otologic and temporomandibular joint disorders or infectious, neoplastic, neurologic, and systemic conditions.
- 3.
Chronic tissue damage from trauma and/or multiple surgical procedures can lead to central sensitization of sensory nerve pathways, leading to neuropathic pain, allodynia (pain response to nonpainful stimuli), and hyperalgesia (excessive pain response to mildly painful stimuli). The presence of neuropathic pain can make accurate diagnosis extremely difficult because the clinician can easily be misled into believing that the source of the pain is localized, when in fact, there is a central-nervous-system-mediated component.
The following case scenarios are provided to demonstrate common clinical situations that can potentially lead to misdiagnosis of COHFP and TMDs.
Inflammatory/Degenerative Temporomandibular Joint Disorders Initially Presenting with Symptoms of Otalgia
A major factor contributing to confusion between otologic pathology and temporomandibular joint pathology is close anatomic proximity and common sensory innervation via the auriculotemporal nerve. Patients often cannot differentiate ear pain from temporomandibular joint pain, and thus, otologic pathology may cause temporomandibular joint pain and temporomandibular joint pathology may cause otologic pain.
A 26-year-old woman presented to the otolaryngologist with severe right-sided ear pain for the past 9 months. The patient reported having an upper respiratory tract infection 9 months ago and after the resolution of the respiratory infection, developed persistent right-sided ear pain. She also noticed that chewing made her symptoms worse and that there was limitation in her jaw opening. The otologic examination and audiometric findings were normal. Palpation of the anterior aspect of the right external auditory canal revealed significant tenderness, compared to the right. The maximum interincisal mandibular opening distance was measured at 20 mm with deviation to the right and produced severe pain in the right ear ( Fig. 1 A). The patient was unable to shift her jaw to the left because of severe pain in the right ear. The patient was given a tongue blade to bite on, and this produced severe pain in the right ear. The otolaryngologist concluded that the diagnosis was a temporomandibular joint disorder. The recommended course of action was ibuprofen, 600 mg, thrice daily and for the patient to be evaluated by an oral and maxillofacial surgeon with expertise in the diagnosis and management of temporomandibular joint disorders.
The patient was evaluated by an oral and maxillofacial surgeon who diagnosed her with right temporomandibular joint synovitis, masticatory muscle spasm with a clenching habit, as a major etiologic factor. A night guard oral appliance was fabricated to attempt to reduce the forces of nocturnal clenching. The patient was instructed to perform passive jaw motion exercises thrice daily. She was continued on ibuprofen, 600 mg, thrice daily and prescribed diazepam, 5 mg, to be taken at bedtime to help to reduce stress and act as a muscle relaxant. After using the oral appliance for 1 week, the patient’s symptoms increased, with further exacerbation of the right-sided ear pain. The patient returned to the otolaryngologist who noted severe pain on palpation over the right temporomandibular joint as well as in the external auditory canal. Although examination of the middle ear with an otoscope did cause pain, the tympanic membrane and middle ear examination was unremarkable. The maximum interincisal opening distance was now 15 mm, and the patient was unable to occlude her teeth properly on the right side because the upper and lower posterior teeth were not meeting. The otolaryngologist and the oral and maxillofacial surgeon conferred, and the patient was diagnosed with an acute temporomandibular joint synovitis. The patient was placed on a 1-week oral steroid medication with a tapering dose and was referred back to the oral and maxillofacial surgeon for further management.
The clinical findings were essentially unchanged when the patient was seen by the oral and maxillofacial surgeon. The pain level was rated as 9 on the visual analog scale (0, no pain; 10, the most severe pain); the maximum interincisal opening distance was measured at 18 mm with deviation to the right and causing severe pain localized to the right ear and temporomandibular joint region. The left lateral excursion of the mandible was severely limited to 3 mm and caused pain in the right temporomandibular joint. The right lateral excursion was 10 mm and did not exacerbate pain. The occlusion was class I with a 1-mm right-sided posterior open bite. Mild manipulation of the mandible to attempt to position the right posterior teeth to occlude caused severe right-sided temporomandibular joint and ear pain. The left temporomandibular joint was nonpainful and had normal rotational and translational movement. A panoramic radiograph was obtained, which was unremarkable. Temporomandibular joint magnetic resonance imaging (MRI) was performed, which revealed anterior disk displacement without reduction of both the right and left temporomandibular joints. A significant finding was a large effusion in the right temporomandibular joint superior joint space as demonstrated by enhanced white signal intensity on the T2 images (see Fig. 1 B). The clinical examination and MRI findings were consistent with a right temporomandibular joint synovitis. The patient was frustrated having had this problem for 9 months without any significant resolution in spite of a full course of nonsurgical management.
The oral and maxillofacial surgeon recommended right temporomandibular joint arthroscopic surgery, which was performed under sedation and local anesthesia. This surgery revealed a severe grade 4 synovitis of the posterior synovial tissues as well as adhesions in the superior joint space (see Fig. 1 C). Operative arthroscopy was performed, which involved lysis of adhesions and removal with a motorized minishaver and a 2.0 mm full radius blade. Areas of significant synovitis were localized, and under direct vision, betamethasone (6 mg/mL) was injected with a #25 gauge spinal needle. The disk was mobilized with a graded probe instrument. After the arthroscopic surgery, the patient was placed on nonsteroidal antiinflammatory drugs, muscle relaxants, and a nonchew diet for 3 weeks. Most importantly, passive motion exercises to gradually stretch the mandible open to restore normal range of motion were started immediately. The passive motion exercise sessions were performed for 15 minutes thrice daily. Three weeks after the arthroscopic surgery, the maximum interincisal opening distance was 38 mm and the pain level was reduced to 3 with maximum opening. At rest, without jaw movement, there was no ear or temporomandibular joint pain. The diet was gradually advanced, and at 3 months postoperatively, the maximum interincisal opening distance was 41 mm, the pain level on the visual analog scale was 1, and the patient was able to chew on soft foods. She continued performing her passive motion exercises twice daily. At 1 year postoperatively, the patient has no pain at rest and occasional pain levels of up to 2 with maximum opening. The patient is able to chew on almost all foods, although she avoids very chewy foods such as bagels and hero sandwiches.
Discussion Case #1
A common scenario is a patient who seeks consultation with an otolaryngologist regarding the onset of acute ear pain or the persistence of chronic ear pain. When the clinical findings do not support an otologic cause, the patient is often referred for evaluation of a temporomandibular joint disorder. The patient may seek multiple opinions from otolaryngologists, neurologists, dentists, and oral and maxillofacial surgeons in a quest for appropriate diagnosis and treatment. The importance of establishing an accurate diagnosis cannot be over emphasized because it is essential for proper treatment. Thus, failure to establish the diagnosis will often result in persistent symptoms or inappropriate treatments. In spite of this, the astute clinician can use the following guidelines to help differentiate pathologic conditions of the ear versus those of the temporomandibular joint:
- 1.
Temporomandibular joint pathology is generally increased by mandibular movement and function.
- 2.
If the pain is increased significantly because of chewing (or biting firmly on a tongue blade during the initial examination), it often indicates a temporomandibular joint or masticatory muscle disorder.
- 3.
Temporomandibular joint pathology will often cause a restriction in the range of motion of the affected joint. Thus, a right temporomandibular joint disorder often causes the mandible to deviate to the right with attempts at maximum opening. Furthermore, when a patient attempts an opposite lateral excursion (for example, sliding the lower jaw to the left in the aforementioned scenario) there will be restricted movement and increased pain.
- 4.
Temporomandibular joint noise (clicking or crepitus) does not necessarily indicate temporomandibular joint disease as the cause of the pain.
- 5.
If the patient points directly to the temporomandibular joint as the location of the source of pain during attempts at maximum jaw opening, it usually indicates a temporomandibular joint disorder.
- 6.
Patients who have excessive clenching habits will often have tender temporalis and masseter muscles on palpation.
Although none of the above guidelines are absolute, because there are always exceptions to the rule, these simple observations can give the clinician an important clue as to which direction the diagnostic workup should follow.
Neoplasia Misdiagnosed as COHFP and Temporomandibular Joint Disorders
The specialty of otolaryngology plays a vital role in educating other health professionals about the consequences of misdiagnosing serious neoplastic conditions with symptoms that mimic COFHP and temporomandibular joint disorders. Unfortunately, there are numerous examples of patients with COFHP symptoms who were initially misdiagnosed and treated unsuccessfully for a routine COFHP, Temporomandibular Joint (TMJ), or dental disorder. However, failed treatment with persistent symptoms must alert the clinician that the diagnosis may be faulty. There are serious consequences of continued failed treatment and misdiagnosis because this may lead to delayed diagnosis and treatment of a neoplastic process. An important rule for all clinicians to follow is as follows:
If the patient does not respond as expected to treatment based on the most likely diagnosis in one’s differential diagnosis, then the clinician must reevaluate the diagnosis and rule out other conditions that may be causing the patient’s symptoms.
The constant reevaluation of the diagnosis based on the patient’s response to treatment is referred to as the Flexible Diagnoses-Management Concept. It is common, even for the experienced clinician, to be uncertain of the diagnosis and treatment of a patient with chronic orofacial pain, which is unlike the more common situation in which a patient with acute pain and swelling presents with an abscess that is generally easy to diagnose, treat, and cure. As this is not the case with patients with chronic pain, it is important for the clinician to have a different mind-set with the development of differential diagnoses that remain flexible. The concept here is that the clinician develops an initial differential diagnoses and treats the patient according to the most likely condition or conditions causing the chronic pain. Based on the response to treatment, there is a continual reevaluation of the diagnoses and treatment. Failure to constantly reevaluate the response to treatment and diagnosis can lead to serious consequences with misdiagnosis of lethal pathologic conditions that mimic COFHP and temporomandibular joint disorders.
Most importantly, the clinical presentation needs to be looked at carefully. Patients with jaw pain, limitation of mobility, and deviation of the mandible to one side on opening often have an intra-articular temporomandibular joint pathology. However, there are other pathologic conditions that can lead to deviation of the mandible. The motor branches of the fifth cranial nerve provide innervation to the muscles of mastication, including the masseter, temporalis, lateral, and medial pterygoid muscles. As the lateral pterygoid muscle attaches to the mandibular condyle and anterior capsule of the temporomandibular joint, it is responsible for translation of the temporomandibular joint. Lack of motor function of the lateral pterygoid muscle will cause failure of translation of the mandibular condyle during jaw opening movements, resulting in deviation of the mandible to the affected side because of the unopposed action of the lateral pterygoid muscle on the unaffected side. The clinician must be thorough and check for normal motor function of the muscles of mastication. Lack of muscle tone of the masseter, temporalis and lateral pterygoid muscles must alert the clinician to a fifth cranial nerve deficit as the cause of the mandibular deviation with opening. Furthermore, once there is clear evidence of a cranial nerve deficit, the clinician must assume a diagnosis of neoplasia until proven otherwise.
Central lesions affecting the trigeminal ganglion often cause symptoms that are located in the peripheral distribution of the fifth cranial nerve ( Fig. 2 ). Therefore, dental pain in the absence of objective evidence of local pathologic condition must be viewed with suspicion. Complicating the clinical picture is the fact that there are many painful dental conditions that do not manifest with clear objective clinical findings.
For example, a painful inflammation of the dental pulp caused by decay may not demonstrate any pathologic condition seen on radiographs, particularly if the patient has a metal crown on the tooth. Masticatory muscle pain from clenching also has negative radiographic findings. Therefore, once treatment of these conditions is initiated, it is extremely important to evaluate the patient’s response to treatment. If the symptoms persist, it is necessary to reevaluate the diagnosis, and the clinician must consider the possibility of the local pain being caused by a central pathology.
Dental pain does not necessarily originate from the oral cavity. Central nervous system pathology can cause pain in the oral and maxillofacial region. There are numerous examples of dental pain treated by numerous clinicians without any relief because the pain was caused by a central nervous system lesion. A common condition that often presents with a history of numerous failed dental treatments is trigeminal neuralgia. A careful history reveals that the character of the pain is shocklike, usually unilateral and so severe that it stops the patient in the middle of a sentence. Although the pain is of high intensity, it is often short in duration (usually seconds) and there is often a trigger point that will suddenly bring on the severe pain with an innocuous stimulus. A light touch to the face, wind on the face, or brushing teeth is often the triggering stimulus for the severe pain from trigeminal neuralgia. Once the diagnosis is established, initial treatment is usually a course of anticonvulsant medication (eg. gabapentin, carbamazepine). It is extremely important for trigeminal neuralgia to be viewed as a symptom, and thus, a brain scan is necessary to determine if there is a central nervous system lesion compressing the trigeminal nerve. If medications fail to control the severe symptoms, the patient should be referred to a neurologic surgeon.
Another common scenario for the otolaryngologist is the patient with persist dental pain and failed dental treatment in the presence of maxillary sinusitis. Infection of the maxillary sinus will cause pain because of nociceptive stimulation of the posterior, middle, and anterior superior divisions of the maxillary nerve (V2). These sensory nerves are also stimulated when there is dental pathology of the maxillary posterior teeth, and therefore, patients with maxillary sinusitis often complain of severe tooth pain with dental interventions failing to resolve symptoms ( Fig. 3 ).
The clinician must be aware of systemic pathologic conditions that can cause temporomandibular and oral, facial, and head pain. Conditions such as fibromyalgia, rheumatoid arthritis, psoriasis, and osteoarthritis can affect the temporomandibular joint and the surrounding muscles of mastication causing severe symptoms. Patients with multiple sclerosis are more prone to trigeminal neuralgia. If there is a history of herpes zoster, facial pain can occur because of postherpetic neuralgia. Cardiac ischemia is also a common cause of facial pain. The pain may occur in the throat, mandible, temporomandibular joint, and teeth. Approximately 32% of patients with cardiac ischemia had craniofacial pain along with other cardiac symptoms. One study revealed that craniofacial pain was the only complaint in 6% of individuals with cardiac ischemia. As cardiac ischemia and acute myocardial infarction require immediate referral and management, the implications for the treating clinician are significant.
Temporomandibular joint and masticatory muscle disorders: current concepts of diagnosis and management
Perhaps one of the most common of the COHFP disorders that causes otologic symptoms without otologic pathology is the group of disorders encompassing inflammatory/degenerative temporomandibular joint disease as well as disorders of the muscles of mastication. TMD is an extremely broad and nonspecific diagnostic term, encompassing both joint and muscle disorders of the masticatory system. To specify whether a diagnosis is primarily intra-articular (coming directly from the temporomandibular joint) or primarily extra-articular (coming from structures outside the temporomandibular joint) is far more useful in patient management.
Other extra-articular conditions beyond the common masticatory muscle disorders can mimic temporomandibular joint disease, for example, coronoid hyperplasia, neoplasia, deep space infections, and myositis ossificans. Here the authors focus on the most common temporomandibular joint and masticatory muscle conditions that the clinician is likely to encounter. The abbreviation TMJ should be avoided and, when used, should refer solely to the anatomic structure. The term TMJ is often inappropriately used by patients and some health professionals to include the variety of disorders of the musculoskeletal component of the head and neck affecting the temporomandibular joint and surrounding masticatory muscles.
Temporomandibular joint disorders are relatively common in the general population. Acute TMD symptoms such as pain, limitation of mandibular opening and impaired masticatory function are experienced in approximately 40% of the US population. LeResche reported that pain in the temporomandibular region occurs in 10% of the adult US population, involves mostly young and middle-aged adults, and has a female predilection. Another study reported that over a 6-month period, 10.8 million adults (6.0% of the US adult civilian population) experienced jaw joint and facial pain. Women reported these symptoms 2.1 times more frequently than men. TMD symptoms have a peak occurrence between ages 20 and 40 years and are reported to be more prevalent in women than in men. Studies show that approximately 5% of people with symptoms seek treatment.
Pathogenesis of Inflammatory/Degenerative Temporomandibular Joint Disorders
Internal derangement theory: a flawed approach to temporomandibular joint disorders
Internal derangement refers to a displaced position of the articular disk (usually anteriorly) of the temporomandibular joint. This condition was once considered to be central in the pathogenesis of temporomandibular joint disorders. Anterior disk displacement was believed to be the major cause of intra-articular symptoms. The progression from anterior disk displacement to osteoarthritis and disk perforation was erroneously believed to be inevitable; therefore, conservative and surgical treatments were designed to reposition a displaced disk. Acceptance of the internal derangement theory led to flawed treatments without a valid research basis. As disk displacement is extremely common in asymptomatic individuals, our current understanding of temporomandibular joint pathogenesis does not support therapeutic interventions designed to reposition or replace a diseased disk.
Current research has presented overwhelming evidence that temporomandibular joint disk displacement is the end result of changes in biochemistry and tissues caused by external factors such as overload and lack of movement. Ultimately, these external factors lead to tissue failure and altered joint biomechanics.
Patients with disk displacement presenting as a clicking joint, without significant symptoms of pain or altered range of motion, do not require surgical treatment. The clinician should view disk displacement as a flaw in joint biomechanics, which has occurred as a result of joint overloading. Disk displacement may be totally asymptomatic without any pain or limitation of function. Much research has been performed on temporomandibular joint pathology over the past 2 decades. The results of findings from clinical studies, magnetic resonance imaging (MRI) studies and synovial fluid analyses have provided compelling evidence that internal derangement theory as a major pathologic entity is flawed. Research performed by Stegenga and colleagues has furthered our understanding of temporomandibular joint pathogenesis, resulting in cartilage degradation. These studies concluded that abnormal disk position is the end result of degenerative changes that occur within the articular tissues.
Synovial fluid analysis research has provided great insight into the pathogenesis of inflammatory and degenerative conditions involving the temporomandibular joint. Studies involving obtaining synovial fluid samples and correlating the biochemical changes in the fluid with the morphologic alterations seen with arthroscopy have been extremely valuable. Biochemical changes and alteration in the structure and function of the synovial joint tissues occur in response to joint overloading and immobilization. Elevations in levels of inflammatory mediators and proteoglycan degradation products occur in the synovial fluids of pathologic temporomandibular joints. These biochemical abnormalities result in morphologic changes in the tissues including synovial inflammation and cartilage degradation (fibrillation). Osteoarthritis results in breakdown of the articular cartilage, which also impairs the sliding ability of opposing articular surfaces. Synovial inflammation causes pain and impaired lubrication leading to reduction in joint mobility. The combination of synovial inflammation and immobilization leads to temporomandibular joint adhesions, resulting in a further decrease in mobility. Orthopedic studies have shown that joint immobilization leads to adhesions, impaired cartilage nutrition, and cartilage degradation. Therefore, in patients with painful limitation of mandibular opening due to synovitis and osteoarthritis, there is a cycle of joint overloading leading to synovitis and osteoarthritis and reduced joint mobility. This condition leads to further adhesions, decreases in joint motion, pain, and more cartilage degradation ( Fig. 4 ).
Maladaptive changes in synovial joints
Successful management of temporomandibular joint pathology must be based on reducing the external factors that lead to the underlying tissue abnormalities. The 2 major factors that contribute to the loss of structure and function of the temporomandibular joint are joint overloading and joint immobilization. Joint overloading, is usually caused by parafunctional masticatory habits such as clenching or bruxism. When excessive joint loading exceeds the adaptive capacity of the tissue, cartilage degradation occurs. Cartilage degradation products in the synovial fluid lead to synovitis.
Decreased joint mobility also leads to maladaptive tissue responses. Because movement is necessary for the diffusion of synovial fluid through cartilage to provide nutrition of chondrocytes, failure of this movement leads to chondrocyte death, leading to a failure of matrix production and a further breakdown of the articular cartilage. Reduced mobility, as well as the pain from synovial inflammation, leads to the formation of intra-articular adhesions, which further reduces mobility. These factors ultimately lead to a self-perpetuating cycle of reduced range of motion, synovitis, adhesions, and osteoarthritis (see Fig. 4 ).
Maladaptive changes in the tissues can be seen arthroscopically. Osteoarthritis ( Fig. 5 A), synovitis (see Fig. 5 B), and adhesions (see Fig. 5 C) are the major tissue pathologies that lead to altered joint biomechanics, pain, and limitation of function. These maladaptive tissue changes are not independent of each other and often coexist within the same damaged joint.
