Simultaneous Occurrence of Myofascial Pain Referred to Tooth and Endodontic Lesions in Patient with Toothache: A Case Report

Toothache is almost always caused by odontogenic toothache, but diagnosis is more difficult in the case of nonodontogenic toothache. We report a case of simultaneous occurrence of odontogenic and nonodontogenic toothache. This manuscript presents a case report for a 35-year-old woman who visited our Orofacial and Head Pain Clinic with the chief complaint of continuous dull pain in left maxillary molar teeth region. It was concluded to be a case of simultaneous odontogenic toothache and nonodontogenic toothache. It was successfully treated by an endodontist and an orofacial pain specialist. The endodontist performed root canal treatment against odontogenic toothache caused by apical periodontitis using a dental operating microscope. The presence of a trigger point (TP) resulting in tooth pain was inferred. A trigger point injection (TPI) was administered by orofacial pain specialist, and toothache relief was confirmed. Myofascial pain was diagnosed definitively. After confirming that the toothache had resolved at multiple TPIs, a crown prosthesis was placed. Following the application of crown prosthesis, we were concerned but did not find recurrence of toothache from myofascial pain due to increased occlusal force. This case suggests that there is no single cause of chronic pain and that multiple causes must be considered for diagnosis, suggesting the need for treatment by multiple specialists.

The relationship between multiple clinicopathological features and nerve invasion in pancreatic cancer

BACKGROUND:Nerve invasion is a specific type of tumor expansion and characteristic manifestation of pancreatic cancer(PC),with an incidence rate ranging from 50% to 100%.It is an important prognostic factor for pancreatic cancer,and its early detection is helpful in the management of the disease.This study was undertaken to analyze retrospectively the relationship between neural invasion and multiple clinicopathological features and to provide evidences for clinicians in the management of neural invasion in patients with PC.METHODS:Formalin-fixed paraffin-embeded specimens of PC taken from 215 patients were examined for the presence of neural invasion under a light microscope.Analyzed was the relationship between neural invasion and multiple clinicopathological feature including preoperative fasting blood glucose level,amylase level,serum CA19-9 level,abdominal pain,lumbar and back pain,and the expressions of p53 and Ki67 in tumor tissues.RESULTS:Preoperative fasting blood glucose level,serum CA19-9 level and p53 positive cells in cancer tissue were increased with the rise of pathological grade(P【0.05).These indices were significantly higher in patients with neural invasion than in those without(P【0.05).Further analysis revealed a positive correlation between p53 and Ki67 overexpression and lymphatic metastasis(P【0.05).Referred pain was positively correlated with neural invasion(P【0.05).Patients with PC perineural invasion were more likely to have a higher pathological grade(P【0.05).CONCLUSIONS:Our data indicated that the preoperative fasting blood glucose level,serum CA19-9 level,and referred pain are novel predictive markers for neural invasion in patients with PC.p53 and Ki67 play important roles in neural invasion of PC.Management of hyperglycemia may serve as an auxiliary treatment to curb neural invasion in PC.

Medial Pterygoid Myositis Complicated by Numbness of the Tongue and Nonodontogenic Toothache: A Case Report

A 34-year-old woman visited our clinic with complaints of trismus, numbness in the left half of the tongue, and pain in tooth 34. At the patient’s initial visit to our clinic, the maximum assisted jaw opening movement was 20 mm, pointing to severe trismus. The patient complained of spontaneous pain in tooth 34 but did not evince percussion pain. Her pain remained unchanged even under local anesthesia. Radiography showed no pathological findings. A tenderness test of masticatory muscles failed to induce pain. The presence of severe trismus argued against temporomandibular disorders, resulting in suspicion of other inflammatory disease. In view of numbness of the tongue, other diseases such as inflammation or neoplastic disease in the head and neck region were considered. The patient was referred to the departments of neurosurgery and otolaryngology for examination. The results of MRI and CT diagnosis led to the identification of acute myositis of the left medial pterygoid muscle requiring the prescription of nonsteroidal anti-inflammatory drugs, and relaxation of mandibular muscles. With time, maximum unassisted jaw opening improved and pain in tooth 34 ceased, but tongue numbness persisted. The condition was attributed to compression of lingual nerve (LN) and mandibular nerve (MN) resulting from medial pterygoid muscle inflammation.

Referred Somatic Hyperalgesia Mediates Cardiac Regulation by the Activation of Sympathetic Nerves in a Rat Model of Myocardial Ischemia

Myocardial ischemia(MI)causes somatic referred pain and sympathetic hyperactivity,and the role of sensory inputs from referred areas in cardiac function and sympathetic hyperactivity remain unclear.Here,in a rat model,we showed that MI not only led to referred mechanical hypersensitivity on the forelimbs and upper back,but also elicited sympathetic sprouting in the skin of the referred area and C8–T6 dorsal root ganglia,and increased cardiac sympathetic tone,indicating sympathetic-sensory coupling.Moreover,intensifying referred hyperalgesic inputs with noxious mechanical,thermal,and electro-stimulation(ES)of the forearm augmented sympathetic hyperactivity and regulated cardiac function,whereas deafferentation of the left brachial plexus diminished sympathoexcitation.Intradermal injection of the α_(2) adrenoceptor(α_(2)AR)antagonist yohimbine and agonist dexmedetomidine in the forearm attenuated the cardiac adjustment by ES.Overall,these findings suggest that sensory inputs from the referred pain area contribute to cardiac functional adjustment via peripheral α_(2)AR-mediated sympathetic-sensory coupling.