Gerodontology. 2011 Nov 2. [Epub ahead of print]

Prevalence of temporomandibular disorders in a population of complete denture wearers. Complete tooth loss among the elderly is still frequent in developing countries and the incidence of temporomandibular disorders is a common finding in complete denture wearers. The aim of this study was to evaluate the prevalence of temporomandibular disorders in a population of complete denture wearers. The data were collected by four examiners for the diagnosis of use and need for complete dentures followed by the World Health Organization standards and interviews for temporomandibular disorders signs and symptoms evaluation. Exploratory variables included demographic, socio-economic status and temporomandibular disorders prevalence.

The prevalence of temporomandibular disorders among denture wearers was 55.12%. Chi-squared test showed no statistical difference between subjects with or without temporomandibular disorders for gender, geographical location and skin colour. The number of subjects with temporomandibular disorders increased as the period of complete denture wear increased, although no statistical difference between groups were found. There is a need of educational programmes aiming at the importance of health care and periodical change of a complete denture, and strategies with a preventive approach to quality general dental care.

From: Clin J Pain. 2011 Jun 14. [Epub ahead of print]

To determine whether patients with myogenous and mixed temporomandibular disorders have greater fatigability of the cervical extensor muscles while performing a neck extensor muscle endurance test when compared with healthy controls.

A total of 151 individuals participated in this study. Of these 47 were healthy controls, 57 patients had myogenous temporomandibular disorders, and 47 patients had mixed temporomandibular disorders. All patients performed the neck extensor muscle endurance test. The patients were instructed to maintain a prone lying position with the neck unsupported as long as possible, stopping at signs of fatigue or any discomfort.

Electromyographic activity of the cervical extensor muscles during the neck extensor muscle endurance test and the holding time were collected for all patients and were compared across groups. A 1-way analysis of variance was used to evaluate the differences in holding time between patients with temporomandibular disorders and healthy controls. A mixed model analysis was used to evaluate the differences in normalized median frequency at different times (fatigue index) for the cervical extensor muscles while performing the neck extensor muscle endurance test between patients with temporomandibular disorders and controls.

There were statistically significant differences in the slopes of the normalized median frequency between patients with temporomandibular disorders and healthy controls at 10, 30, 40, 50, 60, 70, 80, 90, and 100 seconds of the neck extensor muscle endurance test. Holding time was significantly reduced in both patients with myogenous temporomandibular disorders and mixed temporomandibular disorders when compared with healthy controls.

These results highlight the fact that alterations of endurance capacity of the extensor cervical muscles could be implicated in the neck and shoulder disturbances presented in patients with temporomandibular disorders.

Related Source: Neck Muscle Endurance Self Report and Range of Motion Data From Subjects with Treated and Untreated Neck Pain

From: Phys Ther. 2011 Jun 9. [Epub ahead of print]

Most patients with temporomandibular disorders have been shown to have cervical spine dysfunction. However, this cervical dysfunction has been evaluated only qualitatively through a general clinical examination of the neck.

The purpose of this study was to determine whether patients with temporomandibular disorders had increased activity of the superficial cervical muscles when performing the craniocervical flexion test compared with a control group of individuals who were healthy. Design A cross-sectional study was conducted.

One hundred fifty individuals participated in this study: 47 were healthy, 54 had myogenous temporomandibular disorders, and 49 had mixed temporomandibular disorders. All participants performed the craniocervical flexion test. Data for electromyographic activity of the sternocleidomastoid and anterior scalene muscles were collected during the craniocervical flexion test for all participants. A 3-way mixed-design analysis of variance for repeated measures was used to evaluate the differences in electromyographic activity for selected muscles while performing the craniocervical flexion test under 5 incremental levels. Effect size values were calculated to evaluate the clinical relevance of the results.

Although there were no statistically significant differences in electromyographic activity in the sternocleidomastoid or anterior scalene muscles during the craniocervical flexion test in patients with mixed and myogenous temporomandibular disorders compared with the control group, those with temporomandibular disorders tended to have increased activity of the superficial cervical muscles. Limitations The results obtained in this research are applicable for the group of individuals who participated in this study under the protocols used. They could potentially be applied to people with temporomandibular disorders having characteristics similar to those of the participants of this study.

This information may give clinicians insight into the importance of evaluation and possible treatment of the deep neck flexors in patients with temporomandibular disorders. However, future research should test the effectiveness of this type of program through a randomized controlled trial in people with temporomandibular disorders in order to determine the real value of treating this type of impairment in this population.

From: BMC Ear Nose Throat Disord. 2011 May 25;11(1):5.

The temporomandibular joint is critical for normal mouth function, and thus plays a role in chewing, swallowing, speaking, oral health and nutrition. The temporomandibular joint is a synovial joint containing an articular disc which allows for hinge and sliding movements. The articular surfaces are covered by avascular andnon-innervated fibrocartilage which has a high regenerative capacity. The temporalis and masseter muscles control the joint’s motion.

The term temporomandibular disorders is a collective one, representing a sub-classification of muscle-skeletal disorders, and more specifically a number of signsand symptoms involving the masticatory muscles, the temporomandibular joint and associated structures. It is estimated that about one third of adults have temporomandibular disorders symptoms. Temporomandibular disorders has been related to stress, age, gender, personality and other systematic factors.

The maximum mouth opening distance is a generally accepted measurement to estimate temporomandibular joint mobility and function. Mouth opening can be measured using gauges or calipers, and while the normal range differs between populations, the critical functional opening is 35-40mm.

Aural symptoms such as tinnitus, otalgia, dizziness or vertigo, otic fullness sensation, hyperacousia or hypoacousia are thought to be associated with temporomandibular disorders, while their incidence reaches 85% in temporomandibular disorders patients. A causative role of temporomandibular disorders in otic symptomatology remains a matter of debate. Several studies have shown that aural symptoms may have no otic origin. Theories on the etiology of aural symptoms are based mainly on the common embryologic origin of the temporomandibular joint and the middle ear from Meckel cartilage, the presence of structures that connect the middle ear with the temporomandibular joint and the common innervation of the masticatory muscles and the ear.

The present study examined 464 healthy young Greek adults for the presence of temporomandibular disorders signs and symptoms. The study analyzed data for probable correlations between temporomandibular disorders severity and range of mouth opening, aural and joint symptoms and hearing loss. A feature of the study was the use of audiography to objectively assess the co-existence of hearing loss and temporomandibular disorders.

The present study examined the relationship between temporomandibular disorders symptoms and signs and mouth opening, gender, aural symptoms, temporomandibular joint pain, temporomandibular joint ankylosis, bruxism and hearing loss. The authors found that 73.3% of the young Greek adult population examined in this study had temporomandibular disorders symptoms and signs. This finding is consistent with previous studies involving college students. Compared to previous studies on young populations, the present population had fewer subjects with mild temporomandibular disorders and more with moderate and severe temporomandibular disorders.

Ethnicity is believed to affect the degree of mouth opening. The present study is the first focused on a young Greek adult population. The overall mean mouth opening recorded was 45.09 mm. The only previous study of a Greek population took place in 1989 and involved participants aged between 18 and 70 years. The average maximum mouth opening was 52.85 mm for males and 48.34 mm for females. Studies of other ethnicities found that the average mouth opening was 49.10 mm in Chinese, 49.8 mm in Americans aged 16-70 years, 47.1 mm in Nepalese population aged 18-68 years, 50.77 mm in French aged 18-84 years, and 55.9 mm in Swedes aged 18-25 years. It ranged between 41-43 mm in Irish and 35-61 mm in Croatians.

The authors found that temporomandibular disorders was more prevalent and severe in women than men. This observation is consistent with previous studies, as it has been reported that women present an increased risk of 1.5-2 or 2-9 times compared to men to develop temporomandibular disorders.

The current study found that pain in the temporomandibular joint was the most common symptom of temporomandibular disorders as reported elsewhere. Temporomandibular joint pain is caused by the pathological contraction of the masticatory muscles which stimulates extravascular production of inflammation associated substances around the temporomandibular joint. The incidence of pain in the present study is in accordance with the theory that temporomandibular disorders is more prevalent in early adulthood.

Joint sounds are regarded as the commonest sign of temporomandibular disorders, and are more frequent and severe in older populations. Joint sounds, such as clicks and friction, indicate temporomandibular joint derangement or joint disc displacements.

The authors found that bruxism was present in 27.02% of those with temporomandibular disorders and in none of the non-temporomandibular disorders subjects. Others reported that bruxism was present in 7.4%-27.2% of temporomandibular disorders subjects. Bruxism, as clenching or grinding, may be a source or a perpetuating factor for temporomandibular disorders. Some investigators reported that non-temporomandibular disorders and temporomandibular disorders patients have different electromyographic patterns while others failed to find a difference.

Head and neck ache may be of neurological, vascular, muscular, ligamental or bony origin. The temporomandibular joint has muscular and ligamentary connections to the cervical region forming a functional complex. Headache is regarded as the most common symptom of temporomandibular disorders patients, while 55% of chronic headache patients referred to a neurologist had signs or symptoms of temporomandibular disorders. The muscles of the neck and trunk are reported to have a greater electromyographic activity in temporomandibular disorders subjects sensitizing the sympathetic nerves of the autonomous nervous system and leading to headache via the trigeminal nerve.

The authors found that temporomandibular disorders severity is correlated with the number of aural symptoms. Costen, in 1934, firstly associated aural and craniosinusal symptoms with temporomandibular disorders, and named it Costen’s or Otognathic Syndrome. There are four main theories concerning the co-existence of aural and temporomandibular joint dysfunction symptoms.

The first one suggests that disposition of the joint disc during jaw movement increases pressure in the Eustachian tube, the ear structures, the auriculotemporal and masseteric nerve and some branches of the deep posteriortemporal nerve. The auriculotemporal nerve innervates the temporomandibular joint, the tympanic membrane, the anterosuperior part of the external ear and the tragus, and its stimulation gives the sense of otalgia. The authors observed that 10.8% of temporomandibular disorders subjects reported ear pain, and that 75% of those temporomandibular disorders subjects had severe temporomandibular disorders. A number of series report ear pain in 35% of temporomandibular disorders patients, while 70% of temporomandibular joint pain cases are described as otalgia particularly during acute or subacute inflammation of the temporomandibular joint. Additionally, the authors found that the rarely investigated symptom of ear itching was more common in temporomandibular disorders than non-temporomandibular disorders subjects, as reported elsewhere.

The second theory involves the tiny ligament called the discomalleolar or Pinto’s ligament, which originates from the anterior malleolar process, passes through the petrotympanic fissure and inserts in the medial and posterosuperior part of the articular capsule and the disc. In displacement of the temporomandibularjoint disc, the discomalleolar ligament can lead to traction of the malleus, the ossicular chain and the tympanic membrane. Furthermore, in disc displacement,the intralaminal vascular tissue moves forward and is trapped between the head of the condyle and the roof of the fossa, leading to edema, leakage and fibrosis. The petrotympanic fissure plays an important role in hosting the anterior malleolar ligament, the anterior tympanic artery and the chorda tympani nerve. Additionally, the petrotympanic fissure brings in contact the temporomandibular joint with the middle ear. Thus, beginning from the joint capsule, inflammation can spread to the origin of the levator and the tensor palatini muscles, and finally to the cul-de-sac over the vulnerable isthmus of the Eustachian tube, causing obstruction of the tube. A closed Eustachian tube may be responsible for the feeling of ear fullness, otalgia and serousotitis media. This fissure’s length and position may influence the development of otalgia, tinnitus, hearing loss and vertigo.

The third theory proposes that common innervation of the tensor veli palatini, tensortympani, masseter, temporalis and pterygoid muscles by the motor nucleus of the trigeminal nerve is the underlying cause of the aural symptomatology in temporomandibular disorders patients. Tensor tympani, tensor veli palatini and stapedial muscles are called auditory muscles, while the tensor veli palatini and the tensor tympani muscles are also called accessory mastication muscles. Strong sounds cause stapedial muscle contraction, which improves auditory discrimination, while tensor tympani muscle plays a role in the discrimination of low tones. Tensor tympani muscle also contracts in strong sounds, protecting from sound trauma, and vocalization, chewing, swallowing and facial muscle contraction. Malcontraction of the tensor tympani muscle pulls the ossicular chain medially in the middle ear and thus may alter the aural conductive system causing hyperacousia or hypoacousia even with normal audiometric values. It has also been shown that the tensor tympani muscle is dysfunctional in temporomandibular disorders patients, leading to subjective hearing loss. The tensor tympani and stapedial are antagonistic muscles, and with the tympanic membrane are responsible for the appropriate balance and function of the ossicular chain in themiddle ear (malleus, incus and stapes). If the tensor tympani or stapedial contract inappropriately, then the perilymphatic and endolymphatic pressures in the inner ear are changed via the oval window, causing vestibular and cochlear impulse imbalance. Changes in endolymph pressure affect the hair cells of the inner ear, which also results in aural symptoms.

Electromyographical studies show that the tensor tympani and tensor and tensor veli palatini work simultaneously during swallowing, leading to ventilation of the Eustachian tube raising the intratympanic pressure. The Eustachian tube is actively opened by the tensor palatini and passively opened by the levator palatini muscle. In temporomandibular disorders, the tensor tympani muscle is hypertonic, impeding this normal mechanism. Such a pathological state may lead to hypoacusia, tinnitius, vertigo, otalgia, otic fullness sensation and otitis media. Additionally, temporomandibular disorders patients cannot open their mouths wide to yawn, which leads to poor Eustachian tubefunction as well. One study reported that ear fullness was experienced by 13.5% of temporomandibular disorders and 4.7% of non-temporomandibular disorders patients, while in other series involving older populations the relative risk ratio was 14.0. Objective tinnitus is caused by the palatine and middle ear myoclonus producing rhythmic movement of the tympanic membrane to the tension of the stapedial and tensor tympani muscle. Tinnitus related to temporomandibular disorders is thought to be produced by the lateral pterygoid muscles and the discomalleolar ligament.

Furthermore, every movement of the neck or jaw exerts tension on the carotid sheath, increasing the endolymphatic pressure of the hair cells in the cochlea via impedance of the saccus endolymphaticus’ pressure-regulating mechanism, causing tinnitus and vertigo. In bruxism and temporomandibular disorders, the tensor veli palatini dysfunctions and may change the position of tympanic membrane and malleus due to its anatomical association with the tensor tympani. Thus, the velopharyngeal, neck and face movements play a major role in otic-temporomandibular disorders symptomatology. The results of a previous study suggested that temporomandibular disorders peripherally sensitizes the V and VII pairs, leading to tonic spasm of these middle ear muscles. This process may cause low tones hearing loss. The authors found that severe temporomandibular disorders was associated with low tones hearing loss, while moderate temporomandibular disorders correlated with median tones hearing loss. Furthermore, the degree of hearing loss increased with temporomandibular disorders severity. In a study of 44 temporomandibular disorders patients, ear fullness was recorded in 13.6%, vertigo in 13.6% and hearing loss in 6.8% of the subjects. In that same study, audiometry revealed a sensorineural hearing loss in only one subject, at 28-30dB. Other studies reported no difference in audiographic findings between temporomandibular disorders and non-temporomandibular disorders patients, and that hearing loss was not correlated to temporomandibular disorders severity. It has also been previously reported that temporomandibular disorders symptoms are more common in subjects who present with sudden sensorineural hearing loss.

Finally, the fourth theory proposes that psychosocial disorders are responsible for the co-existence of aural symptoms in temporomandibular disorders patients. The limitation of this study is the absence of clinical diagnosis of temporomandibular disorders. No clinical examination or other laboratory findings confirmed or rejected each participants score according to his anamnestic questionnaire. The tool employed only describes signs and symptoms of temporomandibular disorders which may not be seen as a synonym of temporomandibular disorders presence. Thus, many volunteers of this study could not be diagnosed as temporomandibular disorders patients. For the convenience of the results’ interpretation the authors stratified the subjects in four temporomandibular disorders severity groups referring to the number of temporomandibular disorders signs and symptoms. Nevertheless,the results of several studies based on such data verify the utility of evaluation via only an anamnestic questionnaire.

The present study found that temporomandibular disorders severity was associated with gender (more common and severe in women), range of mouth opening, the number of aural symptoms, ear itching, temporomandibular joint ankylosis, temporomandibular jointpain, bruxism and qualitative and quantitative hearing loss. The close embryological, anatomical and functional relationships between the temporomandibular joint and the middle ear may explain the link between aural symptoms and temporomandibular disorders severity. A feature of the present study was the use of audiometry to assess hearing loss in temporomandibular disorders.

Temporomandibular disorders signs and symptoms were more common and severe in females than males. Temporomandibular disorders severity is correlated with the degree of mouth opening and the number of aural symptoms. The absence or presence of mild temporomandibular disorders are associated with normal audiograms while moderate and severe temporomandibular disorders are related to hearing loss in median andlow tones respectively. Bruxism, joint ankylosis, joint pain and ear itching were more common in temporomandibular disorders than non-temporomandibular disorders patients.

From: J Orofac Pain. 2011 Spring;25(2):99-106

The aim of this study was to use magnetic resonance imaging and voxel-based morphometry to search for evidence of altered brain morphology in patients with temporomandibular disorders using voxel-based morphometry, regional gray and white matter volume was investigated in nine temporomandibular disorder patients and nine carefully matched healthy controls.

A decrease in gray matter volume occurred in the left anterior cingulate gyrus, in the right posterior cingulate gyrus, the right anterior insular cortex, left inferior frontal gyrus, as well as the superior temporal gyrus bilaterally in the temporomandibular disorders patients. Also, white matter analyses revealed decreases in regional white matter volume in the medial prefrontal cortex bilaterally in temporomandibular disorder patients.

These data support previous findings by showing that temporomandibular disorders, like other chronic pain states, is associated with changes in brain morphology in brain regions known to be part of the central pain system.

In Pain. 2010 May;149(2):222-8. Epub 2010 Mar 16. Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems. The chronic myofascial temporomandibular pain group evidenced decreased or increased gray matter volume compared to controls in several areas of the trigeminothalamocortical pathway, including brainstem trigeminal sensory nuclei, the thalamus, and the primary somatosensory cortex. In addition, chronic myofascial temporomandibular pain individuals showed increased gray matter volume compared to controls in limbic regions such as the posterior putamen, globus pallidus, and anterior insula. Within the chronic myofascial temporomandibular pain group, jaw pain, pain tolerance, and pain duration were differentially associated with brain and brainstem gray matter volume. Self-reported pain severity was associated with increased gray matter in the rostral anterior cingulate cortex and posterior cingulate. Sensitivity to pressure algometry was associated with decreased gray matter in the pons, corresponding to the trigeminal sensory nuclei. Longer pain duration was associated with greater gray matter in the posterior cingulate, hippocampus, midbrain, and cerebellum. The pattern of gray matter abnormality found in chronic myofascial temporomandibular pain individuals suggests the involvement of trigeminal and limbic system dysregulation, as well as potential somatotopic reorganization in the putamen, thalamus, and somatosensory cortex.

In Neurology. 2009 Sep 22;73(12):978-83. Gray matter changes related to chronic posttraumatic headache. Patients who developed chronic headache revealed decreases in gray matter in the anterior cingulate and dorsolateral prefrontal cortex after 3 months. These changes resolved after 1 year, in parallel to the cessation of headache. The same patients who developed chronic headache showed an increase of gray matter in antinociceptive brainstem centers, thalamus, and cerebellum 1 year after the accident.

In Schmerz. 2009 Dec;23(6):569-75. Chronic pain alters the structure of the brain. Local morphologic alterations of the brain in areas ascribable to the transmission of pain were recently detected in patients suffering from phantom pain, chronic back pain, irritable bowl syndrome, fibromyalgia and frequent headaches. These alterations were different for each pain syndrome, but overlapped in the cingulate cortex, the orbit frontal cortex, the insula and dorsal pons. As it seems that chronic pain patients have a common “brain signature” in areas known to be involved in pain regulation, the question arises whether these changes are the cause or the consequence of chronic pain. The in vivo demonstration of a loss of brain gray matter in patients suffering from chronic pain compared to age and sex-matched healthy controls could represent the heavily discussed neuroanatomical substrate for pain memory.

In Arthritis Rheum. 2008 Dec;58(12):3960-9. White and gray matter abnormalities in the brain of patients with fibromyalgia: a diffusion-tensor and volumetric imaging study. Increased fatigue was correlated with changes in the left superior frontal and left anterior cingulate gyrus, and self-perceived physical impairment was correlated with changes in the left postcentral gyrus. Higher intensity scores for stress symptoms were correlated negatively with diffusivity in the thalamus and fractional anisotropy in the left insular cortex.

In Pain. 2008 Jul;137(1):7-15. Epub 2008 Apr 14. Chronic pain may change the structure of the brain. Local morphologic alterations of the brain in areas ascribable to the transmission of pain were detected in patients suffering from phantom pain, chronic back pain, irritable bowl syndrome, fibromyalgia and two types of frequent headaches. These alterations were different for each pain syndrome, but overlapped in the cingulate cortex, the orbitofrontal cortex, the insula and dorsal pons. These regions function as multi-integrative structures during the experience and the anticipation of pain. As it seems that chronic pain patients have a common “brain signature” in areas known to be involved in pain regulation, the question arises whether these changes are the cause or the consequence of chronic pain. The author suggests that the gray matter change observed in chronic pain patients are the consequence of frequent nociceptive input and should thus be reversible when pain is adequately treated.

In Pain. 2007 Nov;132 Suppl 1:S109-16. Epub 2007 Jun 22. Striatal grey matter increase in patients suffering from fibromyalgia–a voxel-based morphometry study. Fibromyalgia is associated with structural changes in the CNS of patients suffering from this chronic pain disorder. They might reflect either a consequence of chronic nociceptive input or they might be causative to the pathogenesis of fibromyalgia. The affected areas are known to be both, part of the somatosensory system and part of the motor system.

In Pain. 2006 Nov;125(1-2):89-97. Epub 2006 Jun 5. Affective components and intensity of pain correlate with structural differences in gray matter in chronic back pain patients. Although chronic back pain is one of the most frequent reasons for permanent impairment in people under 65, the neurobiological mechanisms of chronification remain vague. Evidence suggests that cortical reorganisation, so-called functional plasticity, may play a role in chronic back pain patients. In the search for the structural counterpart of such functional changes in the CNS, the authors examined 18 patients suffering from chronic back pain with voxel-based morphometry and compared them to 18 sex and age matched healthy controls. We found a significant decrease of gray matter in the brainstem and the somatosensory cortex. Correlation analysis of pain unpleasantness and the intensity of pain on the day of scanning revealed a strong negative correlation (i.e. a decrease in gray matter with increasing unpleasantness/increasing intensity of pain) in these areas. Additionally, the authors found a significant increase in gray matter bilaterally in the basal ganglia and the left thalamus. These data support the hypothesis that ongoing nociception is associated with cortical and subcortical reorganisation on a structural level, which may play an important role in the process of the chronification of pain.

In J Neurosci. 2004 Nov 17;24(46):10410-5. Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic chronic back pain. Theur results imply that chronic back pain is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.

From: J Pain. 2011 Jan;12(1):101-7.

Pain sensitivity varies substantially among humans. A significant part of the human population develops chronic pain conditions that are characterized by heightened pain sensitivity. The association of COMT polymorphism with human pain perception and persistent pain conditions is of considerable importance. One of the genes in which variability is believed to contribute to differences in pain sensitivity and response to analgesics is the catechol-O-methyltransferase (COMT) gene. The COMT enzyme metabolises catecholamines such as dopamine, noradrenaline and adrenaline. Genetic variation contributes to differences in pain sensitivity and response to different analgesics. Catecholamines are involved in the modulation of pain and are partly metabolized by the catechol-O-methyltransferase (COMT) enzyme. It is shown that a polymorphism in the COMT gene, influence pain sensitivity in human experimental pain and the efficacy for morphine in cancer pain treatment.

A pathological pain condition that appears to be associated with COMT activity is myogenous temporomandibular joint disorder. This condition is characterized by persistent facial pain, impaired oral function and heightened sensitivity to pain-evoking stimuli (e.g. mechanical, thermal and ischemic) at numerous body sites. Myogenous temporomandibular joint disorder impacts 5–15% of the adult population and incurs billions of dollars in health care costs. In 1976, Marbach and Levitt reported that patients with facial pain conditions comparable to myogenous temporomandibular joint disorder show increased urinary levels of catecholamine metabolites and express diminished erythrocytic COMT activity, suggesting a role for COMT in this persistent pain condition. There is a relationship between COMT polymorphism, pain sensitivity and the risk of TMD development.

This article looks at the association of neck pain and psychological symptoms after a motor vehicle accident in relation to COMT haplotype, with interesting implications.

We know that widepspread pain occurrs early in the course of whiplash associated disorders. Even though the cumulative incidence was 21%, continuous widespread pain was rare. Subjects with whiplash associated disoreders who report early depressive symptoms and more severe neck injury symptoms are at risk of developing widespread pain after a motor vehicle collision.

Significant risk factors for persistant problems following whiplash injury are: no postsecondary education, female gender, history of previous neck pain, baseline neck pain intensity greater than 55/100, presence of neck pain at baseline, presence of headache at baseline, catastrophizing, whiplash associated disorder grade 2 or 3, and no seat belt in use at time of collision.

Additinal studies identify the prognostic factors associated with a poor response to treatment in the early stages of a whiplash-associated disorder. Multivariable analysis revealed eight prognostic factors associated with a negative outcome: 1) older age, 2) female gender, 3) increasing lag time between injury date and presentation for treatment, 4) initial pain location, 5) province of injury, 6) higher initial pain intensity, 7) lawyer involvement, and 8) at work at entry to the clinic. The effect of lawyer involvement was stronger for patients with less intense pain on initial visit. Similarly, the effect of work status was stronger for patients with less intense pain on initial visit.

The Neck Pain Task Force undertook a best evidence synthesis to establish a baseline of the current best evidence on the course and prognosis for whiplash associated disorder. Recovery of whiplash associated disorder seems to be multifactorial. The evidence suggests that approximately 50% of those with whiplash associated disorder will report neck pain symptoms 1 year after their injuries. Greater initial pain, more symptoms, and greater initial disability predicted slower recovery. Few factors related to the collision itself (for example, direction of the collision, headrest type) were prognostic; however, postinjury psychological factors such as passive coping style, depressed mood, and fear of movement were prognostic for slower or less complete recovery. There is also preliminary evidence that the prevailing compensation system is prognostic for recovery in whiplash associated disorder.

While analyzing factors for prognosis, treatment plan and ongoing assessment, this new article gives us some new insights to factors related to musculoskeletal pain and psychological factors. Genetic variations in the catechol-O-methyltransferase (COMT) gene have been associated with experimental pain and risk of chronic pain development, but no studies have examined genetic predictors of neck pain intensity and other patient characteristics after motor vehicle collision.

In Catechol O-methyltransferase haplotype predicts immediate musculoskeletal neck pain and psychological symptoms after motor vehicle collision, the authors evaluated the association between COMT genotype and acute neck pain intensity and other patient characteristics in 89 Caucasian individuals presenting to the emergency department (ED) aftermotor vehicle collision. In the ED in the hours after motor vehicle collision, individuals with a COMT pain vulnerable genotype were more likely to report moderate-to-severe musculoskeletal neck pain, moderate or severe headache, and moderate or severe dizziness. Individuals with a pain vulnerable genotype also experienced more dissociative symptoms in the ED, and estimated a longer time to physical recovery and emotional recovery.

These findings suggest that genetic variations affecting stress response system function influence the somatic and psychological response to motor vehicle collision, and provide the first evidence of genetic risk for clinical symptoms after motor vehicle collision. The association of COMT genotype with pain symptoms, psychological symptoms, and recovery beliefs exemplifies the pleiotropic effects of stress-related genes, which may provide the biological substrate for the biopsychosocial model of post-motor vehicle collision pain. The identification of genes associated with post-motor vehicle collision symptoms may also provide new insights into pathophysiology.

The question is, should genetic testing be done with persons seeking treatment for motor vehicle collisions? If positive, should this become a part of clinical reasoning or treatment planning? Does this provide evidence for a multi-disciplinary approach to treatment? Does this provide evidence for continued passive therapies, active treatment or a more biopsychosocial approach? Further studies should shed some light in this direction.

From: J Orofac Pain. 2011 Winter;25(1):56-67.

To compare kinematic parameters (ie, amplitude, velocity, cycle frequency) of chewing and pain characteristics in a group of female myofascial temporomandibular disorder patients with an age-matched control female group, and to study correlations between psychological variables and kinematic variables of chewing.

Twenty-nine female participants were recruited. All participants were categorized according to the Research Diagnostic Criteria for temporomandibular disorder (RDC/temporomandibular disorder) into control (n = 14, mean age 28.9 years, SD 5.0 years) or temporomandibular disorder (n = 15, mean age 31.3 years, SD 10.7) groups. Jaw movements were recorded during free gum chewing and chewing standardized for timing. Patients completed the Depression, Anxiety, and Stress Scales (DASS-42), the Pain Catastrophizing Scale (PCS), the Fear of Pain Questionnaire-III (FPQ-III), and the Pain Self-Efficacy Questionnaire (PSEQ). Statistical analyses involved evaluation for group differences, and correlations between kinematic variables and psychological questionnaire scores (eg, depression, anxiety, stress) and pain intensity ratings.

Velocity and amplitude of standardized (but not free) chewing were significantly greater in the temporomandibular disorder group than the control group. There were significant positive correlations between pain intensity ratings and velocity and amplitude of standardized chewing but not free chewing. There were significant positive correlations between depression and jaw amplitude and stress and jaw velocity for standardized but not free chewing.

This exploratory study has provided data suggesting that psychological factors, manifesting in depression and stress, play a role in influencing the association between pain and motor activity.

From: Cranio. 2011 Jan;29(1):43-56.

The present study was comprised of 43 patients (16 men) with cervicogenic headaches for over three months, diagnosed according to the International Classification of Diagnostic Criteria of Headaches (ICDH-II). The patients were randomly assigned to receive either manual therapy for the cervical region (usual care group) or additional manual therapy techniques to the temporomandibular region to additionally influence temporomandibular disorders. All patients were assessed prior to treatment, after six sessions of treatment, and at a six-month follow-up. The outcome criteria were: intensity of headaches measured on a colored analog scale, the Neck Disability Index (Dutch version), the Conti Anamnestic Questionnaire, noise registration at the mandibular joint using a stethoscope, the Graded Chronic Pain Status (Dutch version), mandibular deviation, range of mouth opening, and pressure/pain threshold of the masticatory muscles.

The results indicate in the studied sample of cervicogenic headache patients, 44.1% had temporomandibular disorders. The group that received additional temporomandibular manual therapy techniques showed significantly decreased headache intensities and increased neck function after the treatment period. These improvements persisted during the treatment-free period (follow-up) and were not observed in the usual care group. This trend was also reflected on the questionnaires and the clinical temporomandibular signs. Based on these observations, we strongly believe that treatment of the temporomandibular region has beneficial effects for patients with cervicogenic headaches, even in the long-term.

In The effects of manual therapy and exercise directed at the cervical spine on pain and pressure pain sensitivity in patients with myofascial temporomandibular disorders. J Oral Rehabil. 2009 Sep;36(9):644-52. Epub 2009 Jul 14.

Treatments were directed at the cervical spine in patients with temporomandibular disorders. Our aim was to investigate the effects of joint mobilization and exercise directed at the cervical spine on pain intensity and pressure pain sensitivity in the muscles of mastication in patients with temporomandibular disorders.

It was concluded, The application of treatment directed at the cervical spine may be beneficial in decreasing pain intensity, increasing pain pressure thresholds over the masticatory muscles and an increasing pain-free mouth opening in patients with myofascial temporomandibular disorders.

In, Cervicogenic headaches: a critical review. Spine J. 2001 Jan-Feb;1(1):31-46. The review indicated: Hilton described the concept of headaches originating from the cervical spine in 1860. In 1983 Sjaastad introduced the term “cervicogenic headache”. Diagnostic criteria have been established by several expert groups, with agreement that these headaches start in the neck or occipital region and are associated with tenderness of cervical paraspinal tissues. Prevalence estimates range from 0.4% to 2.5% of the general population to 15% to 20% of patients with chronic headaches. cervicogenic headache affects patients with a mean age of 42.9 years, has a 4:1 female disposition, and tends to be chronic. Almost any pathology affecting the cervical spine has been implicated in the genesis of cervicogenic headache as a result of convergence of sensory input from the cervical structures within the spinal nucleus of the trigeminal nerve.

The main differential diagnoses are tension type headache and migraine headache, with considerable overlap in symptoms and findings between these conditions. No specific pathology has been noted on imaging or diagnostic studies which correlates with cervicogenic headache. cervicogenic headache seems unresponsive to common headache medication. Small, noncontrolled case series have reported moderate success with surgery and injections. A few randomized controlled trials and a number of case series support the use of cervical manipulation, transcutaneous electrical nerve stimulation, and botulinum toxin injection.

From: Quintessence Int. 2011 Jan;42(1):e1-e14.

Recent research has shown that temporomandibular symptoms may be associated with or occur independently of whiplash associated disorders related to motor-vehicle collisions. A PubMed/Medline search was conducted using the terms “temporomandibular disorders,” “orofacial pain,” “temporomandibular joint,” “whiplash,” and “whiplash associated disorders and motor vehicle accidents and motor vehicle collisions” for the years 1995 to 2009. Systematic reviews, meta-analyses, and clinical studies were included if they addressed temporomandibular disorders, whiplash epidemiology, diagnosis, and prognosis. References in the selected articles were also reviewed (including those prior to 1995) if the articles specifically addressed the topic. An evidence base was established for general outcomes using the Oxford Centre for Evidence-Based Medicine Levels of Evidence. Temporomandibular symptoms may develop following motor vehicle collisions and be more complex, representing a component of a symptom cluster of potentially regional and widespread pain impacted by psychosocial factors. Oral health care providers must be aware of the relationship between temporomandibular symptoms, whiplash-associated disorders, and trauma and the more complex nature of the symptoms for appropriate diagnosis and management.

From: J Can Dent Assoc. 2010 Oct;76:a115

Despite continuing research, which is providing an increasing evidence base, the dental profession still does not have a standard of care for diagnosing or managing temporomandibular disorders. Although guidelines have been published by organizations including the American Academy of Orofacial Pain and the American Academy of Oral Medicine, which has published a handbook for managing various orofacial conditions causing pain, these are not officially recognized as authoritative documents by national associations. The Canadian Dental Association and American Dental Association have not established clinical guidelines for this segment of dental practice. To our knowledge, the only North American dental organization that has published temporomandibular disorder guidelines—in 1999, revised in 2009—is the Royal College of Dental Surgeons of Ontario.

In 1996, the American Association of Dental Research published a science information statement on temporomandibular disorders, based on recommendations submitted by its Neuroscience Group. This document, which was based on evidence at that time, provided guidelines for the diagnosis and management of temporomandibular disorders. In 2010, the statement was revised in light of continuing research and the strengthened evidence base. After a broad literature review by the American Association of Dental Research’s Neuroscience Group and a lengthy process of administrative review and revision, the updated official American Association of Dental Research temporomandibular disorder statement was approved in March 2010.

The American Association of Dental Research recognizes that temporomandibular disorders encompass a group of musculoskeletal and neuromuscular conditions that involve the temporomandibular joints, the masticatory muscles, and all associated tissues. The signs and symptoms associated with these disorders are diverse, and may include difficulties with chewing, speaking, and other orofacial functions. They also are frequently associated with acute or persistent pain, and the patients often suffer from other painful disorders (comorbidities). The chronic forms of temporomandibular disorder pain may lead to absence from or impairment of work or social interactions, resulting in an overall reduction in the quality of life.

Based on the evidence from clinical trials as well as experimental and epidemiologic studies:

• 1.It is recommended that the differential diagnosis of temporomandibular disorders or related orofacial pain conditions should be based primarily on information obtained from the patient’s history, clinical examination, and when indicated temporomandibular joint radiology or other imaging procedures. The choice of adjunctive diagnostic procedures should be based upon published, peer-reviewed data showing diagnostic efficacy and safety. However, the consensus of recent scientific literature about currently available technological diagnostic devices for temporomandibular disorders is that, except for various imaging modalities, none of them shows the sensitivity and specificity required to separate normal subjects from temporomandibular disorder patients or to distinguish among temporomandibular disorder subgroups. Currently, standard medical diagnostic or laboratory tests that are used for evaluating similar orthopedic, rheumatological and neurological disorders may also be utilized when indicated with temporomandibular disorder patients. In addition, various standardized and validated psychometric tests may be used to assess the psychosocial dimensions of each patient’s temporomandibular disorder problem.
• 2.It is strongly recommended that, unless there are specific and justifiable indications to the contrary, treatment of temporomandibular disorder patients initially should be based on the use of conservative, reversible and evidence-based therapeutic modalities. Studies of the natural history of many temporomandibular disorders suggest that they tend to improve or resolve over time. While no specific therapies have been proven to be uniformly effective, many of the conservative modalities have proven to be at least as effective in providing symptomatic relief as most forms of invasive treatment. Because those modalities do not produce irreversible changes, they present much less risk of producing harm. Professional treatment should be augmented with a home care program, in which patients are taught about their disorder and how to manage their symptoms.

The main question regarding the diagnosis of temporomandibular disorders was related to the use of electronic diagnostic devices, such as electromyography, jaw movement trackers and sound recorders. Although various imaging modalities have been developed and validated for their use in diagnostic assessment of the temporomandibular joint, their value is mainly limited to the discovery of intracapsular pathologic conditions. Most technological devices proposed for temporomandibular disorder diagnosis have failed to meet standards of reliability and validity: they do not satisfy the sensitivity and specificity requirements or produce the positive and negative predictive values required for individual diagnosis in a clinical setting.

In terms of management of temporomandibular disorders, controversy has been primarily related to structural and mechanistic issues, such as occlusal relationships, condylar positions, neuromuscular balance and similar mechanistic concepts. Based on various concepts of “ideal,” many dentists believed these variations to be essential etiologic factors in the development of temporomandibular disorders. These beliefs and opinions have resulted in the delivery of extensive and invasive treatment plans to manage temporomandibular disorders.

The current literature has clearly shown that the use of adjunctive diagnostic devices (except for various imaging procedures) does not contribute to the ability to correctly diagnose orofacial pain problems (including temporomandibular disorders) beyond that arising from a thorough history and comprehensive examination. Instead, their use poses a relatively high risk of false-positive findings, which may lead the provider to mechanistic therapies. In addition, patients with non-temporomandibular disorder orofacial pain may be wrongly classified as temporomandibular disorder patients, and their real diagnosis may be obscured by subsequent management for temporomandibular disorders.

Management of temporomandibular disorders by conservative and reversible interventions has been shown to be both appropriate and successful. Controlled studies have revealed little or no evidence of a need to change occlusal relationships or condylar positions permanently. In addition, internal derangements of the temporomandibular joint usually do not need to be “corrected”; instead, most symptomatic patients with internal derangements will respond well to pain management and physical medicine approaches.

Furthermore, the importance of biopsychosocial variables, which tend to be minimized when focusing on mechanistic approaches, has been emphasized throughout the medical pain management literature. Because temporomandibular disorders are similar to other musculoskeletal pain conditions (e.g., low back pain, knee problems), it is obvious that dentists should incorporate this perspective into patient care. This is especially true when pain becomes chronic, because of the increasing recognition of the impact of psychosocial factors on persisting pain, and vice versa.

The 1996 American Association of Dental Research statement was updated based on the evidence-based scientific findings of the past 14 years, and the revised version includes a number of new elements. The concept of comorbid pain disorders has been added, reflecting current knowledge about pain susceptibility, neuroplasticity and psychosocial consequences of pain. Recognition of these phenomena has changed the field of pain management in general and has affected our understanding of temporomandibular disorders.

The original language regarding the use of adjunctive tests and devices has been modified, based on data from continuing research.temporomandibular disorders are now recognized as a subset of orthopedic and rheumatologic musculoskeletal disorders and, therefore, require similar approaches in diagnostic testing as is conducted in other similar medical disciplines. In addition, the biopsychosocial perspective about temporomandibular disorders and many other chronic pain disorders has become widely accepted, which means that assessing the psychosocial issues as they relate to temporomandibular disorder patients must be part of the diagnostic process.

Modifications regarding temporomandibular disorder management approaches are included in the new statement, with emphasis on the need for conservative and reversible strategies as supported by recent treatment literature. In-clinic cognitive behavioural therapy and structured home-care programs, in which patients learn to understand their condition and engage in self-management strategies, are an important part of that approach.

The 2010 American Association of Dental Research statement reflects current best knowledge, but undoubtedly it will be reviewed over time and adapted to conform to new evidence as this is developed. Within the scientific community, the new statement reflects widely accepted concepts and is essentially noncontroversial; however, the practitioner community may have mixed reactions to it. We urge all clinicians to read the statement carefully and look at the supporting references to benefit both patients and professionals in the diagnosis and management of problems causing orofacial pain.