Risk factors associated with injury to the inferior alveolar and lingual nerves following third molar surgery-revisited.

OBJECTIVE: Earlier reports, including a preliminary study within our unit, have shown that the surgeon's experience is one of the most influential factors in determining the likelihood of both permanent inferior alveolar nerve (IAN) and lingual nerve (LN) paresthesia, following third molar surgery. The effect of this and other factors influencing such prevalence are assessed in this study. STUDY DESIGN: This prospective study involved 3236 patients who underwent surgical removal of impacted third molars. Patients' demographics and radiological parameters were recorded along with the grade of the treating surgeon. The prevalence of inferior alveolar and lingual nerves paresthesia at 1 month, 6 months, and 18 to 24 months postoperatively were also traced. RESULTS: At 1 month postoperatively, the incidence of IAN paresthesia was 1.5% and the LN was 1.8%. These figures decreased over time and 18 to 24 months postoperatively, the incidence of permanent dysfunction of the IAN was 0.6% and LN was 1.1%. With regard to inferior alveolar nerve paresthesia, risk factors included the patient's age (26-30 years), horizontally impacted teeth, close radiographic proximity to the inferior alveolar canal (IAC), and treatment by trainee surgeons. With regard to the lingual nerve, risk factors included male patients, distoangular impactions, close radiographic proximity to the IAC, and treatment by trainee surgeons. CONCLUSION: One of the main risk factors of developing permanent sensory dysfunction in the distribution of these nerves is related to the surgical skills/experience of the operator. Other factors are associated with the type of impaction and the radiographic proximity of the tooth to the inferior alveolar nerve. Such long-term complications can affect the patient's quality of life; the impact on profession, education, and research is unknown.

Third molar surgery: the patient's and the clinician's perspective.

BACKGROUND: In this report, the problems of third molar surgery have been reviewed from the perspective of both patient and clinician; additionally an overall analysis of preoperative imaging investigations was carried out.Specifically, three main areas of interest were investigated: the prediction of surgical difficulty and potential complications; the assessment of stress and anxiety and finally the assessment of postoperative complications and the surgeon's experience. FINDINGS: In the first study, the prediction of surgical difficulty and potential injury to the inferior alveolar nerve was assessed. This was achieved by examining the patient's orthopantomograms and by using the Pederson Difficulty Index (PDI). Several radiological signs were identified and a classification tree was created to help predict the incidence of such event.In the second study, a prospective assessment addressing the patient's stress and anxiety pre-, intra- and postoperatively was employed. Midazolam was the active drug used against placebo. Objective and subjective parameters were assessed, including measuring the cortisol level in saliva. Midazolam was found to significantly reduce anxiety levels and salivary cortisol was identified as an accurate anxiety marker.In the third study, postoperative complications and the surgeon's experience were examined. Few patients in this study suffered permanent nerve dysfunction. Junior surgeons reported a higher complication rate particularly in trismus, alveolar osteitis, infection and paraesthesia over the distributions of the inferior alveolar and lingual nerves. In apparent contrast, senior surgeons reported higher incidence of postoperative bleeding. DISCUSSION: These studies if well employed can lead to favourable alteration in patient management and might have a positive impact on future healthcare service.

Muscle disorders and dentition-related aspects in temporomandibular disorders: controversies in the most commonly used treatment modalities.

This review explores the aetiology of temporomandibular disorders and discusses the controversies in variable treatment modalities.Pathologies of the temporomandibular joint (TMJ) and its' associated muscles of mastication are jointly termed temporomandibular disorders (TMDs).TMDs present with a variety of symptoms which include pain in the joint and its surrounding area, jaw clicking, limited jaw opening and headaches. It is mainly reported by middle aged females who tend to recognize the symptoms more readily than males and therefore more commonly seek professional help.Several aetiological factors have been acknowledged including local trauma, bruxism, malocclusion, stress and psychiatric illnesses. The Research Diagnostic Criteria of the Temporomandibular Disorders (RDC/TMD) is advanced to other criteria as it takes into consideration the socio-psychological status of the patient.Several treatment modalities have been recommended including homecare practices, splint therapy, occlusal adjustment, analgesics and the use of psychotropic medication; as well as surgery, supplementary therapy and cognitive behavioural therapy. Although splint therapy and occlusal adjustment have been extensively used, there is no evidence to suggest that they can be curative; a number of evidence-based trials have concluded that these appliances should not be suggested as part of the routine care.Surgery, except in very rare cases, is discouraged since it is the most invasive alternative; recent studies have shown healthier outcome with cognitive behavioural therapy.

Nitric oxide-dependent beta2-adrenergic dilatation of rat aorta is mediated through activation of both protein kinase A and Akt.

Vasorelaxation to beta(2)-adrenoceptor stimulation occurs through both endothelium-dependent and endothelium-independent mechanisms, and the former is mediated through Ca(2+)-independent activation of endothelial-type nitric oxide synthase (NOS-3). Since Ca(2+)-independent NOS-3 activation may occur through its serine phosphorylation via protein kinase A (PKA) or Akt, we determined the PKA and Akt dependency of beta(2)-adrenergic relaxation of rat aorta. Rat aortic rings were pre-incubated with the PKA inhibitor H-89 (10(-7) m), the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin (5 x 10(-7) m), Akt inhibitor (10(-5) m), or vehicle, in the absence or presence of the NOS inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME, 10(-4) m). Rings were then contracted with phenylephrine (10(-7) m), and concentration-relaxation responses determined to the beta(2)-adrenoceptor agonist albuterol. Rings exhibited a concentration-dependent relaxation to albuterol: pEC(50) 6.9+/-0.2, E(max) 88.2+/-4.0%. l-NAME attenuated E(max) to 60.2+/-3.5% (P<0.001). In the presence of l-NAME, wortmannin or Akt inhibitor did not influence albuterol responses, whereas H-89 reduced E(max) further, to 27.5+/-2.2% (P<0.001). In the absence of l-NAME, E(max) to albuterol was reduced by H-89, wortmannin or Akt inhibitor, to 56.2+/-2.2, 56.0+/-1.6 and 55.4+/-1.8%, respectively (P<0.001 for each); the combinations H-89 plus wortmannin or H-89 plus Akt inhibitor reduced E(max) further still. Western blotting of NOS-3 immunoprecipitates from rat aortas confirmed that albuterol increased serine phosphorylation of NOS-3, and this increase was attenuated by H-89 or Akt inhibitor. Our results indicate that beta(2)-adrenoceptor stimulation relaxes rat aorta through both NO-dependent and independent mechanisms. The latter is predominantly PKA-mediated, whereas the former occurs through both PKA and PI3K/Akt activation.