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Many psychological factors may have a significant bearing on an individual's oral health and success of dental treatments. Overall, these factors may result in the avoidance of dental visits, emergency-based dental appointments, noncompliant dental behavior, the utilization of multiple oral health care providers, and poor oral health. These factors may affect the quality of life of individuals and may lead to patient dissatisfaction, poor prognosis, and failure of dental treatment. Multiple psychological factors may affect the dentist and the patient. Those factors may alter the prognosis for successful dental treatment. Physician empathy is fundamental in developing long-term physician-patient trust.

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Throughout the recorded history in the literature of temporomandibular disorders (TMD) there have been a variety of opinions as to its primary cause. Those supporting an occlusal basis of TMD opined that occlusal dysfunction is either the primary cause for or a significant etiopathogenic factor in the causation of TMD. Most of the current literature, however, points to evidence in another direction and questions the causal role of occlusion and occlusal disharmony in TMD etiopathogenesis. Recognition of this evidence-based literature is paramount in eliminating and preventing the chances of overtreatment of patients with TMD.

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Comprehending orofacial referred pain requires an understanding of the neuroanatomy of the trigeminal nerve and associated cranial nerves. It also requires knowledge of the concept of neuronal convergence as well as the recognition that the caudalis is laminated and is therefore responsible for sensory receptive fields-that one interneuron may receive multiple sensory inputs and that structures within a lamina have sensory neurons which project into the caudalis and may share the same interneuron.

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OBJECTIVE: The aim of this study was to evaluate the effect of topical treatment with pregabalin and diclofenac on neuropathic orofacial pain induced by infraorbital nerve injury in the rat. STUDY DESIGN: Sixty-four Sprague-Dawley rats underwent infraorbital nerve injury. Seven days after surgery, pain was verified and the rats randomly assigned to topical or systemic treatment with pregabalin or diclofenac, or to no treatment. Pain intensity and motor coordination were assessed at baseline, after surgery, and daily after treatment for 4 consecutive days. Medication plasma levels were assessed at the end of the study. RESULTS: Topical treatment with 10% pregabalin or 5% diclofenac reduced the pain significantly. A significant decrease in motor coordination was found in the systemic pregabalin. The medications' plasma levels were significantly higher in the systemic treatment compared with the topical. CONCLUSIONS: Topical treatment with pregabalin or diclofenac can reduce neuropathic orofacial pain induced by nerve injury.

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In the present study, we assessed IL-17 levels at 3 and 8 days following various forms of injuries to the sciatic nerve and related the cytokine levels to the pain behaviors associated with the injuries. The four experimental models employed were chronic constriction injury (CCI), partial sciatic ligation (PSL), complete sciatic transection (CST) and perineural inflammation (Neuritis). Behavior withdrawal thresholds for mechanical stimulus and withdrawal latency for thermal stimulation were used to measure mechanical allodynia and thermal hyperalgesia. IL-17 levels of the affected, contralateral and naïve rats' sciatic nerve were assessed employing enzyme-linked immunosorbent assay (ELISA). Rats exposed to CCI and Neuritis displayed significant mechanical allodynia and thermal hyperalgesia 3, 5 and 8 days following the procedure, rats exposed to PSL displayed significant mechanical allodynia 5 and 8 days following the procedure and rats exposed to CST developed significant hypoesthesia. Three days following the procedure, IL-17 levels increased significantly compared to naïve rats only in the PSL model. Eight days following the procedure, IL-17 levels in nerves exposed to CCI, CST, PSL and Neuritis were significantly elevated compare to intact nerve levels. It is likely that IL-17 has a limited role in the acute phase of nerve injury and the associated acute pain, but may have a role in later phases of the processes of the development of neuropathic pain.

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A 50-year-old white woman was referred to the emergency room of the University of Medicine and Dentistry of New Jersey with a major complaint of right facial pain of 3 months' duration. A comprehensive intraoral and extraoral examination was performed. She reported a limited mandibular opening and the need for a soft diet for approximately 1 month. Her medical history was noncontributory. The examiner, suspecting a lesion because of the lack of response to masseteric injection and the patient's ongoing report of facial numbness, referred the patient for imaging. A CT scan and MRI revealed a large mass in the right nasopharyngeal submucosa that extended into the nasopharyngeal space. The magnitude of the finding was not anticipated. This case demonstrates several important aspects relative to dental care: Orofacial pain is complex; evaluation of the history of a patient with orofacial pain is quite different from evaluating a patient with dental pain; and more training is required to treat patients with unusual oral and facial pain complaints.

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The dental profession is devoted to treating and preventing dental pain. Such pain can be referred from teeth in one jaw to teeth in the opposing jaw, and the origin of the pain a patient describes may not be the same as the source of that pain. As a result, dental procedures often produce no relief for the patient. This article discusses the neural mechanisms involved in referred pain from one tooth to another and from muscles to teeth.

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In order for the neuropathic pain associated with AO to occur in the oral or facial area, a deafferentation process must be initiated as previously explained. Deafferentation happens when there is a trauma to tissues including, but not limited to, endodontic therapy, a surgical extraction or even a simple one, a deep scaling, an injurious dental injection, and even the placement of a crown. Thankfully, most patients heal uneventfully. Apparently a small percentage of patients have a genetic predisposition to deafferentation pain. In reviewing articles on this subject, there is often material about the inadvertent dental treatment of patients with AO. Many patients often have undergone numerous invasive procedures in an effort to ameliorate pain. It is not possible to read a research paper about AO without reading about the recurrent theme of either overtreatment or unnecessary treatment. Caution should be exercised when performing endodontic therapy solely for the relief of pain without objective need for such therapy. It is common for the AO patient to undergo many other irreversible dental treatments with no resolution of pain symptoms. When the dentist encounters a patient in pain for which there is no dental connection, he or she should strongly consider referring the patient to a facility or practitioner who has expertise in dealing with the non-dental source of dental pain.

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