986 resultados para Temporomandibular joint dysfunction
Resumo:
1. The present study compared the duration of the electromyographic silent period (SP) of the masseter muscles elicited by chin-tapping in normal asymptomatic adults (N = 39) and in a group with symptoms of temporomandibular joint dysfunction (TMJD) (N = 31).2. EMG activity was recorded from right (RM) and left (LM) masseter muscles using bipolar surface electrodes coupled to a DISA 1500 EMG-System. During maximal clenching, ten taps were applied downwards to the chin with a reflex hammer.3. The mean SP durations obtained for the normal group were 25.45 +/- 4.20 ms (RM) and 25.33 +/- 4.18 ms (LM), whereas the TMJD group presented significantly greater values (P < 0.01, Student t-test) of 41.89 +/- 12.94 ms (RM) and 42.40 +/- 12.99 ms (LM). The upper limits of normality calculated for RM and LM were 32.36 ms and 31.21 ms, respectively. Eighty-four percent of patients with TMJD showed SP durations above these limits.4. The results indicate that the measurement of masseteric SP duration may be used as an objective diagnostic method of TMJ disorders, provided that borderline values are interpreted with caution along with clinical impressions.
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Purpose: The aim of this study was to test the association between quality of sleep and stress in individuals with temporomandibular disorder (TMD). Methods: The study sample consisted of 354 adult subjects (males and females) from the municipality of Piacatu, São Paulo state, in the Southeast region of Brazil. Data were collected using the Fonseca’s Questionnaire to record the level of TMD, the Pittsburgh Sleep Quality Index (PSQI) to assess quality of sleep and the Social Readjustment Rating Scale (SRRS) to record stress level. The data were analyzed by the software Epi Info 2000 version 3.2 using a chi-square test at the 0.05 level of significance. Results: One hundred and eighty (50.8%) subjects had some level of TMD. The statistical analysis showed a significant relationship between the three stress scores and the presence or absence of sleep disorders, considering an overall PSQI score > 5 as an indicator of a subject with sleep problems (P<0.01). Conclusion: Both quality of sleep and stress levels were associated with TMD in this sample.
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INTRODUCTION: Little explanation is given to patients with temporomandibular disorders and muscles dysfunction on the mechanism and the expected results of conservative treatment. The purpose of this prospective study was to evaluate the efficacy of specific physical therapy prescribed after this explanation was given and also after using a flat occlusal splint adapted only if muscle pain remained after physical therapy. MATERIAL AND METHOD: Twenty-seven patients with temporomandibular joint dysfunction of muscular origin were evaluated after a mean of six sessions of specialized physical therapy with professionals. Patients were treated by oral and facial massages and were trained for self-reeducation. They were also trained for a specific exercise named the "propulsive/opening maneuver". Every patient was questioned on the subjective evolution of pain and the current maximal pain was evaluated with the Visual Analogical Scale (VAS). Clinical evaluation focused on tenderness of masticator muscles and also assessed the changes in the amplitude of mouth opening. RESULTS: Ninety-three percent of the patients treated by specific physical therapy had a significant reduction of their maximal pain feeling (p<0.05). The recovery of an optimal mouth opening without deviation was also improved as was the protrusion. For 33% of the patients a flat nighttime occlusal splint was necessary as a complementary treatment. Twenty-two percent of the patients decided to change their treatment for alternative therapies (osteopathy, acupuncture, etc.). Fifty percent of the patients were convinced of the efficacy of the prescribed treatment. DISCUSSION: Patients who undertake the specific physical therapy and who regularly practice self-physical therapy succeed in relaxing their masticator muscles and in decreasing the level of pain. Explanations given by the doctor concerning the etiology of pain, during temporomandibular joint dysfunction of muscular origin, and the purpose of specific physical therapy increase the capacity of self-relaxation. A flat occlusal splint is indicated for patients who grind their teeth and for those whose pain resists to physical therapy.
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Temporomandibular joint disorder (TMJD) is known for its mastication-associated pain. TMJD is medically relevant because of its prevalence, severity, chronicity, the therapy-refractoriness of its pain, and its largely elusive pathogenesis. Against this background, we sought to investigate the pathogenetic contributions of the calcium-permeable TRPV4 ion channel, robustly expressed in the trigeminal ganglion sensory neurons, to TMJ inflammation and pain behavior. We demonstrate here that TRPV4 is critical for TMJ-inflammation-evoked pain behavior in mice and that trigeminal ganglion pronociceptive changes are TRPV4-dependent. As a quantitative metric, bite force was recorded as evidence of masticatory sensitization, in keeping with human translational studies. In Trpv4(-/-) mice with TMJ inflammation, attenuation of bite force was significantly less than in wildtype (WT) mice. Similar effects were seen with systemic application of a specific TRPV4 inhibitor. TMJ inflammation and mandibular bony changes were apparent after injections of complete Freund adjuvant but were remarkably independent of the Trpv4 genotype. It was intriguing that, as a result of TMJ inflammation, WT mice exhibited significant upregulation of TRPV4 and phosphorylated extracellular-signal-regulated kinase (ERK) in TMJ-innervating trigeminal sensory neurons, which were absent in Trpv4(-/-) mice. Mice with genetically-impaired MEK/ERK phosphorylation in neurons showed resistance to reduction of bite force similar to that of Trpv4(-/-) mice. Thus, TRPV4 is necessary for masticatory sensitization in TMJ inflammation and probably functions upstream of MEK/ERK phosphorylation in trigeminal ganglion sensory neurons in vivo. TRPV4 therefore represents a novel pronociceptive target in TMJ inflammation and should be considered a target of interest in human TMJD.
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Temporomandibular disorder (TMD) is characterized by a combination of symptoms affecting the temporomandibular joint and/or chewing muscles. The two most common clinical TMD symptoms are pain and dysfunction. Pain is usually caused by dysfunction, and emergency therapy has focused on controlling it. Recent investigations into TMD have led to the recommendation of antidepressants as a supporting treatment against constant neuralgic pain. The aim of this double-blind study was to verify the efficiency of antidepressants (amitriptyline) as a support in the treatment of chronic TMD pain. Twelve female volunteers presenting chronic TMD pain were divided into two groups and treated for 14 days: Group 1 with 25 mg/day of amitriptyline and Group 2 with a placebo. The intensity of pain and discomfort was evaluated daily, using a visual analog scale (VAS), over a period of seven days preceding the treatment (baseline), during the 14-day treatment, and for seven days after the treatment. The results revealed a significant reduction of pain and discomfort in Group 1 (75%) compared to Group 2 (28%) during the three weeks beginning at baseline (p< 0.01). Amitriptyline proved to be an efficient alternative treatment for chronic pain in TMD patients. Copyright © 2003 by CHROMA, Inc.
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The aim of this study was to verify possible relationships between global body posture and temporomandibular joint internal derangement (TMJ-id), by comparing 30 subjects presenting typical TMJ-id signs to 20 healthy subjects. Body posture was assessed using the analysis of muscle chains on several photographs. Results show a higher frequency of lifted shoulders (p=0.04) and of changes in the antero-internal hip chain (p=0.02) in the test group, but no further differences were found significant between the control and test groups. The test group was then divided into three subgroups according to the Helkimo index of temporomandibular disorder severity. Again, no significant differences were found between the subgroups. However, there was a trend noticed in the group with the most severe dysfunction, to present a forward head and shoulders posture. Results are discussed in light of previous studies using the same sample.
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Objective: The objective of this study was to determine the frequency of signs and symptoms of temporomandibular disorder (TMD) in fibromyalgic patients. Methods: Sixty subjects of both sexes (mean age, 49.2 +/- 13.8 years) with fibromyalgia (FM) diagnosis were included in this study. All patients were examined by a calibrated investigator to identify the presence of TMD using the Research Diagnostic Criteria for TMD. Results: The most common signs (A) and symptoms (B) reported by FM patients were (A) pain in the masticatory muscles (masseter, 80%; posterior digastric, 76.7%), pain in the temporomandibular joint (83.3%), and 33.3% and 28.3%, respectively, presented joint sounds when opening and closing the mouth; (B) headache (97%) and facial pain (81.7%). In regard to the classic triad for the diagnosis of the TMD, it was found that 35% of the FM patients presented, at the same time, pain, joint sounds, and alteration of the mandibular movements. It was verified that myofascial pain without limitation of mouth opening was the most prevalent diagnosis (47%) for the RDC subgroup I. For the subgroup II, the disk displacement with reduction was the most prevalent diagnosis (21.6%). For the subgroup III, 36.7% of the subjects presented osteoarthritis. Conclusions: Thus, there is a high prevalence of signs and symptoms of TMD in FM patients, indicating the need for an integrated diagnosis and treatment of these patients, which suggest that the FM could be a medium- or long-term risk factor for the development of TMD.
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Background: The presence of body posture changes among patients with temporomandibular disorders (TMD) has been a controversial issue in the literature, in which it supporters point out the muscular origin as the main etiological factors, mainly associated with postural changes in head. Due to this controversy, it is pertinent to check whether this relationship exists on the most common etiology of TMD, the disk displacement, which translates a biomechanical internal disorder of the temporomandibular joint (TMJ). Objectives: Assess body posture changes in subjects with internal derangement of the TMJ when compared to subjects without this biomechanical dysfunction, characterize the patterns of the jaw movements and assess to the muscle activation during jaw movements. Methods: 21 subjects with TMJ disc displacement (DD) (test group) and 21 subjects without any TMD (control group) was assessed for body posture changes through evaluation of several body segments by posturography and also was evaluated the postural balance reactions through the center of mass during jaw movements using a balance platform. For the characterization of the jaw movement patterns it was done a kinematic analysis during jaw movements (active ROM and path of the jaw). For the muscle activation during jaw movements it was evaluated the masseter, sternocleidomastoid and spinae erector muscles by surface electromyography (EMG). Results Discussion: Both groups show forward head posture and extension of the cervical spine, not noticing any other significant body posture changes in subjects with DD, and if we had to see in detail, in general, subjects without TMD shows more body posture changes than subjects with DD. The pattern of jaw movements is similar in both groups, but in subjects with DD the closing movements are more instable than the opening movements, related to a less effective movement control to counteract the force of gravity and the disk displacement. The bilateral muscle activation during jaw movements is higher in subjects with DD, likely related to a less stable pattern of movement which leads in a higher muscle activation to guide the movement and ensure the best as possible articular stability. Conclusion: The disk displacement with reduction should be viewed as part of a set of signs and symptoms that require an accurate musculoskeletal and psychosocial assessment towards an earlier diagnosis for reduction and control of the functional limiting factors. In this direction, it seems that the relevant set of limiting signs and symptoms deserve a particular attention by health care practitioners involved in the assessment and treatment of TMD, in order to define effective therapeutic options.
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BACKGROUND: The temporomandibular joint (TMJ) cartilage consists of condylar cartilage and disc and undergoes continuous remodeling throughout post-natal life. To maintain the integrity of the TMJ cartilage, anti-angiogenic factors play an important role during the remodeling process. In this study, we investigated the expression of the anti-angiogenic factor, chondromodulin- 1 (ChM-1), in TMJ cartilage and evaluate its potential role in TMJ remodeling. METHODS: Eight TMJ specimens were collected from six 4-month-old Japanese white rabbits. Safranin-O staining was performed to determine proteoglycan content. ChM-1 expression in TMJ condylar cartilage and disc was determined by immunohistochemistry. Three human perforated disc tissue samples were collected for investigation of ChM-1 and vascular endothelial growth factor (VEGF) distribution in perforated TMJ disc. RESULTS: Safranin-O stained weakly in TMJ compared with tibial articular and epiphyseal cartilage. In TMJ, ChM-1 was expressed in the proliferative and hypertrophic zone of condylar cartilage and chondrocyte-like cells in the disc. No expression of ChM-1 was observed in osteoblasts and subchondral bone. ChM-1 and VEGF were both similarly expressed in perforated disc tissues. CONCLUSIONS: ChM-1 may play a role in the regulation of TMJ remodeling by preventing blood vessel invasion of the cartilage, thereby maintaining condylar cartilage and disc integrity.
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1.Pre-assessment data of the patient A 2-year-old boy, weighing 15 kg was admitted with a history of limited mouth opening(inter-incisor distance of 6 mm), hypoplastic and retrognathic mandible (bird face deformity) and facial asymmetry from left temporomandibular joint ankylosis (TMJA). He was born at term, after an uneventful pregnancy, and there was no report of trauma during caesarean section. No other possible aetiologies were identified. He was scheduled for mandibular osteotomy. Preoperative ENT examination revealed adenotonsillar hypertrophy. 2. Anaesthetic Plan A fiberoptic nasal intubation was performed under deep inhalation anaesthesia with sevoflurane, with the patient breathing spontaneously. Midazolam (0.05 mg.kg-1) and alfentanil (0.03 mg.kg-1) were given and anaesthesia was maintained with O2/air and sevoflurane. No neuromuscular blocking agent was administered since the surgical team needed facial nerve monitoring. 3. Description of incident During surgery an accidental extubation occurred and an attempt was made to reintubate the trachea by direct laryngoscopy. Although the osteotomy was nearly completed, the vocal cords could not be visualized (Cormack-Lehane grade IV laryngoscopic view). 4. Solving the problem Re-intubation was finally accomplished with the flexible fiberscope and the procedure was concluded without any more incidents. Extubation was performed 24 hours postoperatively with the patient fully awake. After surgery mouth opening improved to inter-incisor gap of 15 mm. 5. Lessons learned and take home message Two airways issues present in this case can lead to difficultventilation and intubation: TMJA and adenotonsillar hypertrophy. These difficulties were anticipated and managed accordingly. The accidental extubation brought to our attention the fact that, even after surgical correction, this airway remains challenging. Even with intensive jaw stretchingexercises there is a high incidence of re-ankylosis, especially in younger patients. One should bear that in mind when anaesthetizing patients with TMJA.
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The proteinase-activated receptor 2 (PAR(2)) is a putative therapeutic target for arthritis. We hypothesized that the early pro-inflammatory effects secondary to its activation in the temporomandibular joint (TMJ) are mediated by neurogenic mechanisms. Immunofluorescence analysis revealed a high degree of neurons expressing PAR(2) in retrogradely labeled trigeminal ganglion neurons. Furthermore, PAR(2) immunoreactivity was observed in the lining layer of the TMJ, co-localizing with the neuronal marker PGP9.5 and substance-P-containing peripheral sensory nerve fibers. The intra-articular injection of PAR(2) agonists into the TMJ triggered a dose-dependent increase in plasma extravasation, neutrophil influx, and induction of mechanical allodynia. The pharmacological blockade of natural killer 1 (NK(1)) receptors abolished PAR(2)-induced plasma extravasation and inhibited neutrophil influx and mechanical allodynia. We conclude that PAR(2) activation is proinflammatory in the TMJ, through a neurogenic mechanism involving NK(1) receptors. This suggests that PAR(2) is an important component of innate neuro-immune response in the rat TMJ.
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In order to investigate a putative role for nitric oxide (NO) in the central nociceptive processing following carrageenan-induced arthritis in the rat temporomandibular joint (TMJ), we analyzed the immunoreactivity, gene expression and activity of nitric oxide synthases (NOS) in the caudal part of the spinal trigeminal nucleus (Sp5C) during the acute (24 h), chronic (15 days) and chronic-active (14 days-24 h) arthritis. In addition, evaluation of head-withdrawal threshold was carried out in all phases of arthritis under chronic inhibition of nNOS with the selective inhibitor 7-nitroindazole (7-NI). Neurons with nNOS-like immunoreactivity (nNOS-LI) were concentrated mainly in the lamina II of the Sp5C, showing no significant statistical difference during arthritis. Only a discrete percentage of nNOS-LI neurons expressed Fos immunoreactivity. The mRNA expression for both nNOS and endothelial nitric oxide synthases (eNOS) presented no noticeable differences among the groups. No expression of inducible nitric oxide synthase (iNOS) was detected in the Sp5C by either immunohistochemistry or reverse-transcription polymerase chain reaction (RTPCR). Ca(2+)-dependent NOS activity in the ipsilateral Sp5C was significantly higher (108.3 +/- 49.2%; P<0.01) in animals during the chronic arthritis. Interestingly, this increased activity was completely abolished 24 h later, in the chronic-active arthritis. Finally, head-withdrawal threshold decreased significantly in the chronic arthritis in animals under 7-NI chronic inhibition. In conclusion, nNOS immunoreactivity and mRNA expression are stable in the Sp5C during TMJ arthritis evolution, but its activity significantly increases in the chronic-phases supporting an antinociceptive role of the nNOS as evidenced by pain threshold experiment. (C) 2009 Elsevier B.V. All rights reserved.
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Temporomandibular disorders represent one of the major challenges in dentistry therapeutics. This study was undertaken to evaluate the time course of carrageenan-induced inflammation in the rat temporomandibular joint (TMJ) and to investigate the role of tachykinin NK(1) receptors. Inflammation was induced by a single intra-articular (i.art.) injection of carrageenan into the left TMJ (control group received sterile saline). Inflammatory parameters such as plasma extravasation, leukocyte influx and mechanical allodynia (measured as the head-withdrawal force threshold) and TNF alpha and IL-1 beta concentrations were measured in the TMJ lavages at selected time-points. The carrageenan-induced responses were also evaluated after treatment with the NK(1) receptor antagonist SR140333. The i.art. injection of carrageenan into the TMJ caused a time-dependent plasma extravasation associated with mechanical allodynia, and a marked neutrophil accumulation between 4 and 24 h. Treatment with SR140333 substantially inhibited the increase in plasma extravasation and leukocyte influx at 4 and 24 h, as well as the production of TNF alpha and IL-1 beta into the joint cavity, but failed to affect changes in head-withdrawal threshold. The results obtained from the present TMJ-arthritis model provide, for the first time, information regarding the time course of this experimental inflammatory process. In addition, our data show that peripheral NK(1) receptors mediate the production of both TNF alpha and IL-1 beta in the TMJ as well as some of the inflammatory signs, such as plasma extravasation and leukocyte influx, but not the nociceptive component. 2008 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved.
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Previous studies that have used retrograde axonal tracers (horseradish peroxidase alone or conjugated with wheat germ agglutinin) have shown that the temporomandibular joint (TMJ) is supplied with nerve fibers originating mainly from the trigeminal ganglion, in addition to other sensory and sympathetic ganglia. The existence of nerve fibers in the TMJ originating from the trigeminal mesencephalic nucleus is unclear, and the possible innervation by parasympathetic nerve fibers has not been determined. In the present work, the retrograde axonal tracer, fast blue, was used to elucidate these questions and re-evaluated the literature data. The tracer was deposited in the supradiscal articular space of the rat TMJ, and an extensive morphometric analysis was performed of the labeled perikaryal profiles located in sensory and autonomic ganglia. This methodology permitted us to observe labeled small perikaryal profiles in the trigeminal ganglion, clustered mainly in the posterior-lateral region of the dorsal, medial and ventral thirds of horizontal sections, with some located in the anterior-lateral region of the ventral third. Sensory perikarya were also labeled in the dorsal root ganglia from C2 to C5. No labeled perikaryal profiles were found in the trigeminal mesencephalic nucleus. on the other hand, autonomic labeled perikaryal profiles were distributed in the sympathetic superior cervical and stellate ganglia, and parasympathetic otic ganglion. Our results confirmed those of previous studies and also demonstrated that: (i) there is a distribution pattern of labeled perikaryal profiles in the trigeminal ganglion; (ii) some perikaryal profiles located in the otic ganglion were labeled; and (iii) the trigeminal mesencephalic nucleus did not show any retrogradely labeled perikaryal profiles.