Occlusal Trauma Induces Neuroimmune Crosstalk for a Pain State.

Temporomandibular joint (TMJ) disorder caused by occlusal trauma is one of the most controversial topics in dentistry. Experimental traumatic occlusion (ETO) induced by metal crowns cemented to mandibular first molars in rats causes a long-lasting nociceptive response. This study aimed to elucidate whether ETO generates an increase in inflammatory mediators in the TMJ. In addition, the impact of ETO on trigeminal ganglia, neurotransmitter release, and satellite glial cell (SGC) activation was investigated. ELISA revealed enhanced inflammatory mediators, including TNF-α, IL-1ß, IL-6, CX3CL1, and ADAM-17 by Western blotting, in periarticular TMJ tissue after 28 d of ETO. In the trigeminal ganglia, ETO groups increased the release of the neurotransmitters substance P and glutamate. Overexpression of the AMPA receptor and upregulation of NMDA were observed in the 0.4- and 0.7-mm ETO groups, respectively, highlighting enhanced neuronal excitation. Increased IL-1ß and COX-2 mRNA levels in the 0.7-mm ETO group confirmed trigeminal ganglia SGC activation. Immunofluorescence and electrophoresis of SGC revealed increased pERK expression in the 0.7-mm ETO group. ERK phosphorylation was shown to be nociceptive specific, with its upregulation occurring in cases of chronic inflammatory pain. Increased PKA mRNA levels were observed in the 0.4-mm ETO group, while CREB mRNA levels were upregulated for both ETO groups. Electrophoresis showed overexpression of sodium channel Nav 1.7 in the 0.7-mm ETO group, while immunofluorescence revealed that Nav 1.7 is expressed in sensory trigeminal ganglia cells. The results of this study suggest that occlusal trauma induces neuroimmune crosstalk, with synthesis of proinflammatory/pronociceptive mediators, which increases neuronal activity in trigeminal ganglia via the activation of an inflammatory response cascade to develop a persistent neuroinflammatory state that leads to central sensitization.

Electromyographic evaluation during masticatory function, in patients with temporomandibular disorders following interocclusal appliance treatment.

The aim of this study was to evaluate the electromyographic activity during masticatory function, in patients with stomatognathic system dysfunctions, treated with interocclusal splints. Electromyography was carried out through a computer diagnostic system K6-l DIAGNOSTIC SYSTEM (Myo-Tronics, Inc.; Tukwila, WA; USA). Study sample involved 20 individuals, age 18-53 years, both genders. Electromyographic activity of the masticatory muscles (masseter and anterior temporalis) was measured before and 90, 120, and 150 days after treatment with interocclusal splints, which were modified at days 90 (in canine guidance) and 120 (in group function). Data were statistically analyzed through a simple linear regression model. There was no statistically significant difference (p > 0.05) among the 3 periods assessed. Bilateral equilibrium of electromyographic activity was observed for the masseter and anterior temporalis muscles during the treatment.

Tumour cell and stromal features in metastatic and non-metastatic non-small cell lung carcinomas.

AIMS: Tumour cell behaviour depends on the interactions between nuclear genetic changes in the malignant cells and a stroma favourable for growth, invasion and metastasis. To evaluate such interactions, we studied the relationship between tumour cell and stromal features for proliferative factors, p53, microvessel density and metalloproteinases, controlled for the extent of the primary lesion (T1 to T4), in early (non-metastatic) and late (metastatic) non-small cell lung carcinomas (NSCLC). METHODS AND RESULTS: Variables were examined for differences and correlations in the frequency of p53, AgNOR, CD34 and MMP-9 expression in primary lesions and metastases of NSCLC using a general linear model. The patients included 58 males and 22 females (mean age 62 +/- 9 years) with 19 T1 (23.8%), 40 T2 (50.0%), 14 T3 (17.5%) and seven T4 (8.8%). In late disease, AgNOR and p53 were statistically related to the extent of the primary lesion, whereas in early disease AgNOR tended to be increased in tumours without metastasis, while p53 expression tended to decrease progressively in tumours with metastasis. Microvessel density in late disease was of no statistical significance, whereas in early disease strong CD34 expression was seen in tumours with metastasis, being at its maximum in T3 primary lesions. The best marker for the extent of the lesion and its progression was MMP-9, with greater expression by tumours with metastasis than those without. CONCLUSIONS: Different tumour cell and stromal interactions control metastasis and therefore the biological risk of NSCLC. A panel of molecular markers, such as p53, MMP-9 and CD34 could help to identify subgroups of patients that could benefit from adjuvant therapy.

Soldering and remelting influence on fatigue strength of cobalt-chromium alloys.

STATEMENT OF PROBLEM: For laboratory production, it would be economically advisable to reuse excess cobalt-chromium alloys in manufacturing partial denture frameworks. Furthermore, discrepancies in fit, modifications, repairs, and also economic factors could lead to soldering procedure on the metal framework. PURPOSE: This study evaluated the influence of soldering and remelting procedures on the fatigue strength of Steldent, Dentorium, and Biosil cobalt-chromium alloys, as new alloys and in a mixture of new and previously casted alloy and when submitted or not submitted to conventional soldering procedure. MATERIAL AND METHODS: The soldering procedure was conducted in rod specimens 1.7 mm in diameter made with new, or with a mixture of new and reused alloy (n = 10 per group). The results were compared with those of intact rods. The fatigue strength was carried out with a cyclic testing machine simulating the insertion and the removal of partial dentures. After failure, the fracture surface was examined with a scanning electron microscope. RESULTS: The soldered specimens revealed 1119 loading cycles before fracture. These means differed statistically from those of intact alloys, which disclosed 2733 cycles before failure (p < 0.05). Statistical analysis indicated that the soldering procedure reduced fatigue strength of all new alloys or those in a mixture of new and previously casted alloys. It was also found that the soldering procedure may cause premature failure of a removable partial denture. Photomicrographs from fracture surfaces revealed the presence of inclusions and voids. Conversely, there were no significant differences between new and reused specimens, soldered or not (p > 0.05), which suggested that it may be possible to reuse excess cobalt-chromium alloys without compromising the fatigue strength of the framework.