José Tadeu Tesseroli de Siqueira

Evaluation of Body Posture in Individuals With Internal Temporomandibular Joint Derangement

Abstract Temporomandibular dysfunctions (TMD) comprise a great number of disruptions that may affect the temporomandibular joint (TMJ), the masticatory muscles, or both. TMJ internal derangement is a specific type of TMD, of which the etiology and physiopathology are broadly unknown, but have been suggested to be linked to head, neck, and body posture factors. This study aimed at verifying possible relationships between body posture and TMJ internal derangements (TMJ-id), by comparing 30 subjects presenting typical TMJ-id signs to 20 healthy subjects. Subjects’ clinical evaluations included anamnesis, stomatognatic system evaluation, and plotting analysis on body posture photographs. No statistically significant differences were found between the groups. Results do not support the assertion that body posture plays a role in causing or enhancing TMD; however, these results should be cautiously considered because of the small number of subjects evaluated and the many posture variables submitted to statistical procedures that lead to high standard deviations.

Clinical study of patients with persistent orofacial pain

OBJECTIVE [corrected] To evaluate a sample of patients with persistent facial pain unresponsive to prior treatments. METHODS Hospital records of 26 patients with persistent facial pain were reviewed (20 female and 6 male). RESULTS Patients were classified into three groups according to their presenting symptoms: a)Group I, eight patients (30.7%) with severe, diffuse pain at the face, teeth or head; b)Group II, eight patients (30.7%) with chronic non-myofascial pain and; c)Group III, ten patients with chronic myofascial pain (38.4%). We find 11 different diagnoses among the 26 patients: pulpitis(7), leukemia(1), oropharyngeal tumor(1), atypical odontalgia(1), Eagles syndrome(1), trigeminal neuralgia(4), continuous neuralgia(1), temporomandibular disorders (9), fibromyalgia (2), tension-type headache(1), conversion hysteria(2). After the treatment program all patients had a six-month follow-up period with pain relief, except the patient with tumor. CONCLUSION The wide variability of orofacial pain diagnosis (benign to life-threatening diseases) indicates the necessity to reevaluate patients presenting recurrent pain that is refractory to the usual treatments.

Sleep bruxism increases the risk for painful temporomandibular disorder, depression and non‐specific physical symptoms

To explore the relationship between sleep bruxism (SB), painful temporomandibular disorders (TMD) and psychologic status in a cross-sectional study. The sample consisted of 272 individuals. The Research Diagnostic Criteria for TMD (RDC/TMD) was used to diagnose TMD; SB was diagnosed by clinical criteria proposed by The American Academy of Sleep Medicine. The sample was divided into four groups: (1) patients without painful TMD and without SB, (2) patients without painful TMD and with SB, (3) patients with painful TMD and without SB and (4) patients with painful TMD and with SB. Data were analysed by Odds Ratio test with a 95% confidence interval. Patients with SB had an increased risk for the occurrence of myofascial pain (OR = 5·93, 95% CI: 3·19-11·02) and arthralgia (2·34, 1·58-3·46). Group 3 had an increased risk for moderate/severe depression and non-specific physical symptoms (10·1, 3·67-27·79; 14·7, 5·39-39·92, respectively), and this risk increased in the presence of SB (25·0, 9·65-64·77; 35·8, 13·94-91·90, respectively). SB seems to be a risk factor for painful TMD, and this in turn is a risk factor for the occurrence of higher depression and non-specific physical symptoms levels, but a cause-effect relationship could not be established.

Abnormal expression of voltage-gated sodium channels Nav1.7, Nav1.3 and Nav1.8 in trigeminal neuralgia.

Voltage-gated sodium channels have been implicated in acute and chronic neuropathic pain. Among subtypes, Nav1.7 single mutations can cause congenital indifference to pain or chronic neuropathic pain syndromes, including paroxysmal ones. This channel is co-expressed with Nav1.8, which sustains the initial action potential; Nav1.3 is an embrionary channel which is expressed in neurons after injury, as in neuropathic conditions. Few studies are focused on the expression of these molecules in human tissues having chronic pain. Trigeminal neuralgia (TN) is an idiopathic paroxysmal pain treated with sodium channel blockers. The aim of this study was to investigate the expression of Nav1.3, Nav1.7 and Nav1.8 by RT-PCR in patients with TN, compared to controls. The gingival tissue was removed from the correspondent trigeminal area affected. We found that Nav1.7 was downregulated in TN (P=0.017) and Nav1.3 was upregulated in these patients (P=0.043). We propose a physiopathological mechanism for these findings. Besides vascular compression of TN, this disease might be also a channelopathy.

Persistent Periodontal Disease Hampers Anti-Tumor Necrosis Factor Treatment Response in Rheumatoid Arthritis

ObjectiveThis study aimed to evaluate prospectively the influence and the evolution of periodontal disease (PD) in rheumatoid arthritis (RA) patients submitted to anti–tumor necrosis factor (TNF) therapy. MethodsEighteen patients with RA (according to the American College of Rheumatology criteria) were assessed for PD before (BL) and after 6 months (6M) of anti-TNF treatment: 15 infliximab, 2 adalimumab, and 1 etanercept. Periodontal assessment included plaque and gingival bleeding indices, probing pocket depth, cementoenamel junction, and clinical attachment level. Rheumatologic evaluation was performed blinded to the dentist’s assessment: demographic data, clinical manifestations, and disease activity (Disease Activity Score using 28 joints [DAS28], erythrocyte sedimentation rate [ESR], and C-reactive protein [CRP]). ResultsThe median age and disease duration of patients with RA were 50 years (25–71 y) and 94% were female. Periodontal disease was diagnosed in 8 patients (44.4%). Comparing BL to 6M, periodontal parameters in the entire group remained stable (P > 0.05) throughout the study (plaque and gingival bleeding indices, probing pocket depth, cementoenamel junction, and clinical attachment level), whereas an improvement in most analyzed RA parameters was observed in the same period: DAS28 (5.5 vs. 3.9, P = 0.02), ESR (21 vs. 12.5 mm/first hour, P = 0.07), and CRP (7.8 vs. 2.8 mg/dL, P = 0.25). Further analysis revealed that this improvement was restricted to the group of patients without PD (DAS28 [5.5 vs. 3.6, P = 0.04], ESR [23.0 vs. 11.5 mm/first hour, P = 0.008], and CRP [7.4 vs. 2.1, P = 0.01]). In contrast, patients with PD had lack of response, with no significant differences in disease activity parameters between BL and 6M: DAS28 (5.2 vs. 4.4, P = 0.11), ESR (17.0 vs. 21.0, P = 0.56), and CRP (9.0 vs. 8.8, P = 0.55). ConclusionsThis study supports the notion that PD may affect TNF blocker efficacy in patients with RA. The possibility that a sustained gingival inflammatory state may hamper treatment response in this disease has high clinical interest because this is a treatable condition.

Diferential diagnosis in atypical facial pain: a clinical study

OBJECTIVE To evaluate a sample of patients with atypical facial pain (AFP) in comparison to patients with symptomatic facial pain (SFP). METHOD 41 patients with previous diagnostic of AFP were submitted to a standardized evaluation protocol, by a multidisciplinary pain team. RESULTS 21 (51.2%) were considered AFP and 20 (48.8%) (SFP) received the following diagnosis: 8 (40.0%) had temporomandibular disorders (TMD); 3 (15.0%) had TMD associated to systemic disease (fibromyalgia, systemic erythematosus lupus); 4 (20.0%) had neuropathy after ear, nose and throat (ENT) surgery for petroclival tumor; 2 (10.0%) had Wallenberg syndrome; 1 (5.0%) had intracranial tumor; 1 (5.0%) had oral cancer (epidermoid carcinoma), and 1 (5.0%) had burning mouth syndrome (BMS) associated to fibromyalgia. Spontaneous descriptors of pain were not different between AFP and SFP groups (p=0.82). Allodynia was frequent in SFP (p=0.05) and emotion was the triggering factor most prevalent in AFP (p=0.06). AFP patients had more traumatic events previously to pain (p=0.001). CONCLUSION AFP patients had more: a) traumatic events previously to pain onset, and b) emotions as a triggering factor for pain. These data support the need of trained health professionals in multidisciplinary groups for the accurate diagnosis and treatment of these patients.

Radiographic evaluation of cervical spine of subjects with temporomandibular joint internal disorder

Although the etiopathophysiology of internal temporomandibular joint internal disorders (TMJ ID) is still unknown, it has been suggested that head and body posture could be related to its initial onset, development and perpetuation. The purpose of the present study was to observe the relationship between cervical spine X-ray abnormalities and TMJ ID. This investigation evaluated 30 subjects with internal TMJ disorder symptoms (test group) and 20 healthy subjects (control group). Subjects were submitted to clinical and radiographic evaluation. Clinical evaluation comprised anamnesis and stomatognathic system physical examination. Radiographic evaluation comprised analysis of lateral cervical spine X-rays by three physical therapists and tracing on the same images. The test group presented twice as much cervical spine hyperlordosis as the control group (20.7% versus 10.5%), but almost half of rectification prevalence (41.4 versus 79.0%, p = 0.03). After that, the test group was divided into three subgroups according to TMJ dysfunction severity, evaluated by Helkimos index. These subgroups were not significantly different, but the subgroup with more severe TMD showed a tendency to cervical spine hyperlordosis prevalence. Results showed a tendency for subjects with more severe TMD to exhibit cervical spine hyperlordosis. Nevertheless, studies with a larger number of subjects suffering from severe TMD are encouraged in order to corroborate the present findings.

Trigeminal pain and quantitative sensory testing in painful peripheral diabetic neuropathy.

OBJECTIVE To evaluate patients with Diabetes Mellitus type 2 and painful peripheral neuropathy in order to investigate oral complaints and facial somatosensory findings. RESEARCH DESIGN AND METHODS Case-control study; 29 patients (12 women, mean age 57.86 yo) with Diabetes Mellitus type 2 and 31 age-gender-matched controls were evaluated with a standardized protocol for general characteristics, orofacial pain, research diagnostic criteria for temporomandibular disorders, visual analogue scale and McGill Pain questionnaire, and a systematic protocol of quantitative sensory testing for bilateral facial sensitivity at the areas innervated by the trigeminal branches, which included the thermal detection by ThermoSensi 2, tactile evaluation with vonFrey filaments, and superficial pain thresholds with a superficial algometer (Micromar). Statistical analysis was performed with Wilcoxon, chi-square, confidence intervals and Spearman (p<0.05). RESULTS Orofacial pain was reported by 55.2% of patients, and the most common descriptor was fatigue (50%); 17.2% had burning mouth. Myofascial temporomandibular disorders were diagnosed in 9 (31%) patients. The study group showed higher sensory thresholds of pain at the right maxillary branch (p=0.017) but sensorial differences were not associated with pain (p=0.608). Glycemia and HbA(1c) were positively correlated with the quantitative sensory testing results of pain (p<0.05) and cold (p=0.044) perceptions. Higher pain thresholds were correlated with higher glycemia and glycated hemoglobin (p=0.027 and p=0.026). CONCLUSIONS There was a high prevalence of orofacial pain and burning mouth was the most common complaint. The association of loss of pain sensation and higher glycemia and glycated hemoglobin can be of clinical use for the follow-up of DM complications.

Dental and facial characteristics of patients with juvenile idiopathic arthritis

OBJECTIVE It has been shown that the temporomandibular joint is frequently affected by juvenile idiopathic arthritis, and this degenerative disease, which may occur during facial growth, results in severe mandibular dysfunction. However, there are no studies that correlate oral health (tooth decay and gingival diseases) and temporomandibular joint dysfunction in patients with juvenile idiopathic arthritis. The aim of this study is to evaluate the oral and facial characteristics of the patients with juvenile idiopathic arthritis treated in a large teaching hospital. METHOD Thirty-six patients with juvenile idiopathic arthritis (26 female and 10 male) underwent a systematic clinical evaluation of their dental, oral, and facial structures (DMFT index, plaque and gingival bleeding index, dental relationship, facial profile, and Helkimos index). The control group was composed of 13 healthy children. RESULTS The mean age of the patients with juvenile idiopathic arthritis was 10.8 years; convex facial profile was present in 12 juvenile idiopathic arthritis patients, and class II molar relation was present in 12 (P =.032). The indexes of plaque and gingival bleeding were significant in juvenile idiopathic arthritis patients with a higher number of superior limbs joints involved (P =.055). Anterior open bite (5) and temporomandibular joint noise (8) were present in the juvenile idiopathic arthritis group. Of the group in this sample, 94% (P =.017) had temporomandibular joint dysfunction, 80% had decreased mandibular opening (P = 0.0002), and mandibular mobility was severely impaired in 33% (P =.015). CONCLUSION This study confirms that patients with juvenile idiopathic arthritis a) have a high incidence of mandibular dysfunction that can be attributed to the direct effect of the disease in the temporomandibular joint and b) have a higher incidence of gingival disease that can be considered a secondary effect of juvenile idiopathic arthritis on oral health.

A Known SOST Gene Mutation Causes Sclerosteosis in a Familial and an Isolated Case from Brazilian Origin

Sclerosteosis is a severe, rare, autosomal recessive bone condition that is characterized by a progressive craniotubular hyperostosis. The main features are a significant sclerosis of the long bones, ribs, pelvis, and skull, leading to facial distortion and entrapment of cranial nerves. Clinical features include a tall stature, nail dysplasia, cutaneous syndactyly of some fingers, and raised intracranial pressure. The sclerosteosis gene has been mapped to chromosome 17q12-21 and is currently known as the SOST gene encoding the sclerostin protein. Here, we report on one familial and one isolated case of Brazilian origin with the clinical and molecular diagnosis of sclerosteosis. The radiological and clinical features are described, and the diagnosis of sclerosteosis was confirmed in both cases by mutation analysis of the SOST gene showing a homozygous nonsense mutation (Trp124X) in the two patients. We reported this mutation previously in other sclerosteosis patients from a consanguineous Brazilian family. Interestingly, all three families were from the same state in Brazil, but they denied familial relationship. These patients confirm the clinical picture as found in other cases with a loss of function mutation in the SOST gene.