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1.
Front Pain Res (Lausanne) ; 3: 956117, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36093390

RESUMO

Although most cases of pain-related temporomandibular disorders (TMD) are mild and self-limiting, about 10% of TMD patients develop severe disorders associated with chronic pain and disability. It has been suggested that pain intensity contributes to the transition from acute to chronic pain-related TMD. Therefore, the aims of this current prospective cohort study were to assess if pain intensity, pain always being present, pain or stiffness on awakening, jaw activities, and interference, were associated with the transition from acute to chronic pain-related TMD at 3 months of follow-up. One hundred and nine participants, recruited from four clinics in Montreal and Ottawa, received examinations and completed the required instruments at baseline and at the 3rd month of follow-up. In a multivariable analysis including sex, age, characteristic pain index (CPI) (OR = 1.03, 95%CI = 1.01-1.06, P = 0.005), moderate to severe average pain intensity (OR = 3.51, 95%CI = 1.24-9.93, P = 0.02), disability points score (OR = 1.29, 95%CI = 1.06-1.57, P = 0.01), interferences (ORs = 1.30-1.32, P = 0.003-0.005), screening score (OR = 1.37, 95%CI = 1.08-1.76, P = 0.01), and pain always present (OR = 2.55, 95%CI = 1.08-6.00, P = 0.03) assessed at first-visit were related to the transition outcome at the 3rd month of follow-up. Further, we found that if 4 patients with acute pain-related TMD on average were exposed to these risk factors at baseline, 1 would have the transition from acute to chronic pain at 3 months of follow-up. Results indicate that these factors are associated with the transition from acute to chronic pain-related TMD, and therefore should be considered as important factors when evaluating and developing treatment plans for patients with pain-related TMD.

2.
J Oral Rehabil ; 49(3): 362-372, 2022 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-34800343

RESUMO

AIMS: The aims of this critical review were to: (i) assess the factors that differentiate acute from chronic temporomandibular disorders (TMD) pain; (ii) assess the risk factors associated with the transition from acute to chronic TMD pain; and (iii) summarize and appraise the studies. METHOD: The databases used were MEDLINE, Embase, and Cochrane Database of Systematic Reviews. Eligible studies included articles comparing acute to chronic TMD pain, and cohort studies assessing the risk factors implicated in the transition from acute to chronic TMD pain. RESULTS: Seven articles were selected: one case-control study, three cross-sectional studies, and three cohort studies. These studies found that psychological factors were more common in chronic than acute TMD pain patients; however, these factors did not increase the transition risk in the multivariable model. Myofascial and baseline pain intensity were associated with the transition from acute to chronic TMD pain at a 6-month follow-up. Due to methodological weaknesses in the available literature, more research is required to establish the risk factors implicated in the transition from acute to chronic TMD pain. CONCLUSION: This review found some evidence that myofascial pain is associated with the transition risk from acute to chronic TMD pain at a 6-month follow-up and that pain intensity at baseline is associated with more intense TMD pain 6 months later. There is insufficient evidence to draw conclusions about the role of demographics and psychological disorders as independent risk factors.


Assuntos
Dor Crônica , Transtornos da Articulação Temporomandibular , Estudos de Casos e Controles , Dor Crônica/etiologia , Estudos Transversais , Dor Facial/etiologia , Humanos , Revisões Sistemáticas como Assunto , Transtornos da Articulação Temporomandibular/complicações , Transtornos da Articulação Temporomandibular/epidemiologia
3.
J Dent Educ ; 85(3): 349-358, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33098113

RESUMO

Dentists stand in an optimal position to prevent and manage patients suffering from chronic orofacial pain (OFP) disorders, such as temporomandibular disorders, burning mouth syndrome, trigeminal neuralgia, persistent idiopathic dentoalveolar pain, among others. However, there are consistent reports highlighting a lack of knowledge and confidence in diagnosing and treating OFP among dental students, recent graduates, and trained dentists, which leads to misdiagnosis, unnecessary costs, delay in appropriate care and possible harm to patients. Education in OFP is necessary to improve the quality of general dental care and reduce individual and societal burden of chronic pain through prevention and improved quality of life for OFP patients. Our aims are to emphasize the goals of OFP education, to identify barriers for its implementation, and to suggest possible avenues to improve OFP education in general, postgraduate, and continuing dental education levels, including proposed minimum OFP competencies for all dentists. Moreover, patient perspectives are also incorporated, including a testimony from a person with OFP. General dentists, OFP experts, educators, researchers, patients, and policy makers need to combine efforts in order to successfully address the urgent need for quality OFP education.


Assuntos
Dor Crônica , Dor Crônica/terapia , Competência Clínica , Dor Facial/terapia , Humanos , Assistência ao Paciente , Qualidade de Vida
4.
Spec Care Dentist ; 39(2): 208-213, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30768727

RESUMO

AIMS: This study describes a novel nerve block directed at the maxillary (V2) division of the fifth cranial nerve as treatment for medication-refractory trigeminal neuralgia (TN). METHODS AND RESULTS: The authors present three cases of TN treated with V2 nerve block using commonly available local anesthetics injected through the greater palatine foramen. Patients' medications were noted before and after the procedure. Following the injection, patients were followed over time and outcome was assessed. Patients experienced rapid and long-lasting pain relief allowing for significant reduction in antineuralgia medications. This was done with the objective of breaking the pain cycle with subsequent discontinuation or reduction of analgesic medications. CONCLUSION: This technique may be an effective treatment for medication-refractory V2 TN. By interrupting the pain cycle, this renders the condition amenable to long-term control using diminished doses of standard antineuralgia pharmaceuticals. The practical implications of the described procedure are that it is simple, safe, and well-tolerated with few or no adverse effects. This novel technique is a diagnostic feature for the dentist to differentiate between sources of facial pain.


Assuntos
Bloqueio Nervoso/métodos , Palato Duro , Neuralgia do Trigêmeo/terapia , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Medição da Dor , Neuralgia do Trigêmeo/tratamento farmacológico
5.
Biochim Biophys Acta ; 1783(5): 770-8, 2008 May.
Artigo em Inglês | MEDLINE | ID: mdl-18328269

RESUMO

Rac1 and Cdc42 are members of the Rho family of small GTPases and have been shown to induce lamellipodia and filopodia formation, respectively. This leads to changes in cytoskeleton organization and as a consequence affects cell migration. In the present work we demonstrate that endogenous Rac1 and Cdc42 interact with calmodulin (CaM) in a Ca(2+)-dependent fashion. The interaction of Rac1 and Cdc42 with CaM was shown to be direct. This novel interaction was further confirmed in platelets using co-immunoprecipitation studies. Using CaM database analysis and in vitro peptide competition assays we have identified a 14 amino acid region in Rac1 that is essential for CaM binding. The scrambled form of the peptide did not bind CaM demonstrating specificity of the predicted CaM binding region in Rac1. A similar region capable of binding CaM exists in Cdc42. Furthermore, using the optimal activation time-point for each GTPase, the role of CaM in the function of Rac1 and Cdc42 was examined. Results demonstrate that in human platelets, thrombin caused maximal activation of Rac1 and Cdc42 at ~60 s and ~25 s respectively. The potent CaM antagonist W7 abolished thrombin-mediated activation of Rac1. However, addition of W7 resulted in the activation of Cdc42 over basal and W7 did not inhibit thrombin-mediated activation of Cdc42. The less potent CaM inhibitor, W5, did not have any effect on Rac1 and Cdc42 activation. The results demonstrate that in platelets, binding of CaM to Rac1 increases its activation while its binding to Cdc42 reduces the activation of this GTPase. This suggests an important role for CaM in coordinating Rac1 and Cdc42 activation and in the regulation of cytoskeleton remodeling.


Assuntos
Plaquetas/enzimologia , Calmodulina/metabolismo , Proteína cdc42 de Ligação ao GTP/metabolismo , Proteínas rac1 de Ligação ao GTP/metabolismo , Animais , Sítios de Ligação , Ligação Competitiva , Calmodulina/fisiologia , Bovinos , Ativação Enzimática , Inibidores Enzimáticos/farmacologia , Humanos , Peptídeos/metabolismo , Sulfonamidas/farmacologia , Proteínas rac1 de Ligação ao GTP/química
6.
Can J Physiol Pharmacol ; 85(3-4): 444-54, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17612654

RESUMO

Na+/K+-ATPase functions as both an ion pump and a signal transducer. Cardiac glycosides partially inhibit Na+/K+-ATPase, causing activation of multiple interrelated growth pathways via the Na+/K+-ATPase/c-Src/epidermal growth factor receptor complex. Such pathways include Ras/MEK/ERK and Ral/RalGDS cascades, which can lead to cardiac hypertrophy. In search of novel Ral-GTPase binding proteins, we used RalB as the bait to screen a human testes cDNA expression library using the yeast 2-hybrid system. The results demonstrated that 1 of the RalB interacting clones represented the C-terminal region of the beta1 subunit of Na+/K+-ATPase. Further analysis using the yeast 2-hybrid system and full-length beta1 subunit of Na+/K+-ATPase confirmed the interaction with RalA and RalB. In vitro binding and pull-down assays demonstrated that the beta1 subunit of Na+/K+-ATPase interacts directly with RalA and RalB. Ral-GTP pull-down assays demonstrated that short-term ouabain treatment of A7r5 cells, a rat aorta smooth muscle cell line, caused activation of Ral GTPase. Maximal activation was observed 10 min after ouabain treatment. Ouabain-mediated Ral activation was inhibited upon the stimulation of Na+/K+-ATPase activity by Ang II. We propose that Ral GTPase is involved in the signal transducing function of Na+/K+-ATPase and provides a possible molecular mechanism connecting Ral to cardiac hypertrophy during diseased conditions.


Assuntos
Ouabaína/farmacologia , ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores , ATPase Trocadora de Sódio-Potássio/metabolismo , Proteínas ral de Ligação ao GTP/metabolismo , Angiotensina II/farmacologia , Animais , Linhagem Celular , DNA Complementar/genética , Glutationa Transferase/metabolismo , Humanos , Masculino , Plasmídeos , Ratos , Proteínas Recombinantes/metabolismo , ATPase Trocadora de Sódio-Potássio/genética , Testículo/metabolismo , Técnicas do Sistema de Duplo-Híbrido , Leveduras/genética , Proteínas ral de Ligação ao GTP/genética
7.
Biochem Biophys Res Commun ; 336(1): 105-9, 2005 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-16125679

RESUMO

Ral, a member of the Ras-p21 superfamily of small GTPases, has been shown to require the calcium-signaling protein calmodulin (CaM) for activation. In the present work, we investigated the properties of the Ral-CaM interaction. Using CaM affinity binding assay with lysates from mammalian cells overexpressing various Ral mutants, we found that RalB(V23, DeltaCAAX) lacking the C-terminal isoprenylation region bound significantly less efficiently to CaM. Binding of other mutants containing critical amino acid changes in the nucleotide or substrate binding regions (residues 23, 28, and 49) was not affected. In addition, all mutants bound significantly better in the presence of calcium versus the calcium chelator EGTA. Using in vitro transcription-translation in the presence of geranylgeranyl pyrophosphate, we demonstrate enhanced Ral binding to CaM. Inhibition of isoprenylation in cells in culture with lovastatin resulted in decreased binding of CaM to Ral. The present results show that post-translational isoprenylation of Ral is important in Ral-CaM interaction.


Assuntos
Calmodulina/metabolismo , Proteínas ral de Ligação ao GTP/metabolismo , Células HeLa , Humanos , Ligação Proteica , Prenilação de Proteína
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