Purpose: This study aimed to develop a Japanese version of the Tampa Scale for Kinesiophobia （TSK） for temporomandibular disorders （TSK-TMD） and to investigate its benefits.
Methods: We translated the original 12-item version of TSK-TMD into a tentative Japanese version by referring to the Japanese version of TSK with permission from the original authors. The original author of TSK-TMD also validated the quality of a reverse-translation of the tentative Japanese version of TSK-TMD back into English. Subsequently, we developed the final Japanese version of TSK-TMD （TSK-TMD-J）. Thirty-eight patients with temporomandibular disorders were enrolled to answer the TSK-TMD-J. For each patient, we calculated the total score and the subscale scores, which were activity avoidance （AA） and somatic focus （SF）. We also calculated the mean, maximum, and minimum values of the total and subscale scores. We assessed the frequency distribution and calculated Cronbach’s alpha to measure the internal validity. For patients with no subjective change in the pathological condition between the first and second visits, we assessed the test-retest reliability of the questionnaire by calculating the intraclass correlation coefficient （ICC）. The statistical significance was set at p＜0.05.
Results: The mean ± SD and maximum and minimum values of the total score of TSK-TMD-J were 26.7 ± 4.7, 36, and 14, respectively; those of AA were 14.8 ± 3.1, 21, and 9, respectively; and those of SF were 11.8 ± 2.6, 17, and 5, respectively. Cronbach’s alpha was 0.76. The ICC was 0.89 （95％ confidence interval ranged from 0.65 to 0.97）.
Conclusions: The TSK-TMD-J exhibited neither a ceiling nor floor effect. The results of this study also indicate that the TSK-TMD-J is an acceptable psychological scale with high internal validity and test-retest reliability.

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Purpose: Although chronic pain might affect to sleep, there is no clearly defined relation between orofacial pain and sleep. The aim of this study was to illustrate the quality of sleep for the patients with glossodynia as oral chronic pain using sleep questionnaire.
Methods: Thirteen primary glossodynia and nineteen secondary glossodynia patients were compared with nineteen healthy control subjects （HC） matched for age and sex. Especially, secondary glossodynia was decided as oral candida disease. The Japanese version of Pittsburgh sleep quality index （PSQI） and the visual analog scale （VAS） for glossalgia were administrated. The evaluated items contained the seven sleep-related components, PSQI global score （PSQIG）, illness duration and VAS for sleep disturbance. Furthermore, PSQIG was divided into sleep disturbance or non-sleep disturbance to indicate quality of sleep.
Results: There were not significant differences between sleep conditions and illness duration or VAS in glossodynia patients in comparison with HC. However, primary glossodynia patients had higher score of subjective sleep quality than HC （P＝0.03）. Secondary glossodynia patients had higher scores of subjective sleep quality than HC （P＝0.02, respectively）. Furthermore, sleep disturbance of each glossodynia patients was significant worse than HC （P＝0.04）.
Conclusion: Glossodynia patients complained sleep disturbance as compared with healthy control subjects. Glossalgia as oral chronic pain might reduce quality of sleep.

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Idiopathic bizarre bodily sensations are referred to as cenesthopathy, which was originally proposed by Dupré and Camus in 1907. Most patients with cenesthopathy who visit dentists are elderly, and their complaints are usually monosymptomatic and limited to within or around the oral cavity. Although cenesthopathy is traditionally considered refractory, some reports indicate that pharmacotherapy can improve about 50％ of cenesthopathic sensations. The present report describes cenesthopathy that was very much improved by psychotropic agents in three patients.
Patients: Case 1 was a 65-year-old man who described cenesthesic symptoms of threads and metal coils emerging from his gums. These symptoms disappeared after taking aripiprazole（6 mg/day）for 9.5 months. Case 2 was a 60-year-old man who described cenesthesic symptoms of his chest and left upper incisor being tied with a spinning, thread-like nerve. He was already under amitriptyline（50 mg/day）treatment for depression. Adding risperidone（1 mg/day）gradually improved these symptoms and they finally disappeared after one year. Case 3 was a 45-year-old woman who described cenesthesic symptoms of an electrical current circulating within her four left lower back teeth. These symptoms disappeared after taking amitriptyline（75 mg/day）for three months.
Discussion: Patients with oral cenesthopathy might comprise two groups within the spectrum of schizophrenia, or depression. Organic, age-related changes in the brain might also influence bodily sensations.
Conclusion: The first-line treatment for oral cenesthopathy should be psychotropic agents such as antipsychotics and/or antidepressants.

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Purpose: In the international classification of headache disorders 3rd edition （ICHD-3β）, trigeminal neuralgia （13.1） is classified into 2 categories; classical trigeminal neuralgia （13.1.1） and painful trigeminal neuropathy （13.1.2） （previously referred to as symptomatic trigeminal neuralgia）. We aimed to clarify features of trigeminal neuralgias by investigating clinical statistics of patients at orofacial pain clinics.
Methods: The clinical data of 69 patients with trigeminal neuralgia who visited the orofacial pain clinic of dentistry and oral surgery at Keio University Hospital, Kawasaki Municipal Ida Hospital and Hino Municipal Hospital between April 2014 - April 2017 were analyzed retrospectively. The ratio of each pathological diagnosis and therapeutic responses of treatment were evaluated.
Results: Painful post-traumatic trigeminal neuropathy （13.1.2.3）, a subclass of a painful trigeminal neuropathy was most commonly observed （51％）. Classical trigeminal neuralgia, purely paroxysmal （13.1.1.1） was 28％, and classical trigeminal neuralgia with concomitant persistent facial pain （13.1.1.2） was 6％. Tooth extraction at 66％ was the most common cause of painful post-traumatic neuropathy. As treatment, pregabalin was prescribed for painful post-traumatic trigeminal neuropathy with improvement of pain in 51％ of patients. Carbamazepine was prescribed in patients with classical trigeminal neuralgia. The treatment was effective in 63％ of patients of pure paroxysmal type and 25％ of patients with persistent facial pain type.
Conclusions: It was clarified some differences in some features of progress and efficacy of pharmacotherapy for each subtype of trigeminal neuralgia （in Orofacial pain outpatient clinic）.

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Purpose: Tumor-associated trigeminal neuralgia is classified under ‘painful trigeminal neuropathy attributed to space-occupying lesion’ according to the International Classification of Headache Disorders, 3rd edition beta version （ICHD3β: 13.1.2.5: hereinafter ‘PTN-SOL’）. Many trigeminal neuralgia patients are diagnosed by dentists. However, some clinicians have reported that PTN-SOL accounts for 10％ of trigeminal neuropathy cases. For this reason, it’s important we have to also consider PTN-SOL when making the diagnosis for early diagnosis. In this paper, we report a case of PTN-SOL diagnosed early by cranial nerve examination.
Case: A female patient in her seventies presented at our hospital department due to pain in her right mandibular tooth. She had consulted a dental practitioner beforehand because she had felt phasic strong pain in her right mandibular premolar teeth region while eating in December 2012 years. The doctor suspected it was trigeminal neuropathy and referred the patient to our hospital, but she did not present because the pain had subsided. However, she came to our hospital on July 2013 years due to recurrence of the pain. The pain was caused by brushing teeth or eating meals, and there were two types of pain resembling numbness. One was a paroxysmal attack with middle to severe intensity and the other was persistent pain for 20 minutes with mild intensity. We conducted a detailed medical interview with the patient because it was not a typical condition for classical trigeminal neuralgia. We determined that the numb-like feeling was hyperesthesia in the right mental region. She had dysfunctional eye movements, diplopia and hyperethesia in the right trigeminal nerve, 3rd branch, by cranial nerve examination. Furthermore, there was a neoplastic lesion around the tuberculum sellae and cavernous sinus on MRI. For this reason, we consulted the neurosurgery department in our hospital.
Results: It was considered a case of painful trigeminal neuropathy attributed to space-occupying lesions by meningioma around the tuberculum sellae and cavernous sinus.
Conclusion: In our report, we have showed the importance of conducting a cranial nerve examination for early diagnosis.

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Patient: A 69-year-old woman had experienced the paroxysmal pain around the left periorbital and temporal area approximately a month ago. Computed tomography（CT） and magnetic resonance imaging（MRI） of the head performed at the Neurosurgery clinic had revealed that there was no problem. Suspected of the pain caused by dental disease, she visited our hospital. The attack was electric pain （Visual Analogue Scale: 75） with autonomic symptoms, such as lacrimation, for few minutes about 10 times per day. We diagnosed possible trigeminal autonomic cephalalgias（TACs）, and she was prescribed Indometacin farnesyl （400mg/day） for 7 days. Subsequently, because the pain persisted, we excluded episodic paroxysmal hemicrania and diagnosed short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing（SUNCT） or short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms（SUNA）. At the Neurology, she was definitely diagnosed with SUNCT and prescribed Clonazepam and Gabapentin. Subsequently, the pain improved.
Discussion: SUNCT is TACs characterized by the paroxysmal pain around unilateral orbital, superior orbital, and temporal area with ipsilateral conjunctival injection and lacrimation. It is important for diagnosis of TACs type to evaluate the duration of the paroxysmal pain and the effect of Indometacin. It is recommended that general dentists should have knowledge of headache because headache patients such as TACs may visit a dental department. In particular, orofacial pain clinicians need to have knowledge to correctly diagnose TACs type.
Conclusions: We consider it is important that dentists have knowledge of headache.

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Patient: A 45-year-old man had experienced intense left facial pain at the beginning of and after meals. No apparent abnormal finding was detected by the clinical examination, panoramic radiography, CT and MRI except for tenderness of left masseter and temporal muscles, and we diagnosed trigeminal neuralgia and myofascial pain. However, neither oral administration of carbamazepine nor injection of local anesthetic to the lesion suppressed the pain. His familiar pain was reproduced just by looking at pickled plum. Moreover, sialography revealed that the duct of parotid gland was narrowed. This suggested the disturbance of natural saliva ejection caused the intense pain during the meal time.
After parotid sialography, his pain has completely disappeared.
Discussion: Trigeminal neuralgia and narrowing of parotid ducts cause transient pain in the face at the beginning of meal. Similarity in the characteristic features of these conditions sometimes makes the diagnosis challenging. Sialography is the only intervention that helps in diagnosing parotid duct stenosis, which should be considered to differentiate this condition and trigeminal neuralgia.
Conclusions: This case suggests that a disturbance of saliva ejection causes trigeminal neuralgia-like intense pain.

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Case summary: The patient was a 42-year-old man. His chief complaint was sharp pain in the left temporal region, masseter, and neck. When he became busy and exhausted with work, the frequency of his tension-type headaches and pain intensity were exacerbated. No abnormalities were found in a thorough neurosurgical examination, and he was referred by his primary dentist to an oral surgeon for examination for suspected temporomandibular disorder. At that hospital he was diagnosed as headache caused by temporomandibular disorder, and underwent jaw exercise and splint treatment. However, his headaches continued to worsen and he was referred to our department for examination. Because the headaches occurred on consecutive days, he had been taking 3-4 tablets of 60mg loxoprofen sodium each day for 3 months prior to the examination. From the transition of episodic tension-type headaches to daily headaches and other findings, he was diagnosed as medication overuse headache; MOH. First, he was immediately taken off of loxoprofen sodium. At the same time amitriptyline was started to prevent tension-type headaches and diazepam was started to ease anxiety. The following day his headache was alleviated to less than one third. The dose of amitriptyline was gradually increased to 50mg/day, and his severe headaches nearly disappeared.
Discussion: MOH was diagnosed from the fact that the headaches began to occur daily as he started taking a daily dose of analgesic. The pain was also thought to be exacerbated by strong anxiety toward the pain.
Conclusion: This patient had been diagnosed as headache attributed to temporomandibular disorder, but he had both MOH and strong anxiety. For accurate diagnosis, it is necessary to have knowledge of not only toothache and temporomandibular disorder but also headache disease.

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Patients: A 72-year-old man presented with a history of bilateral masseter muscle fatigue aggravated by mastication and jaw claudication, and other manifestations included trismus, diplopia, dizziness, a 4-kg weight loss over a month, and intermittent pain over the scalp. A diagnosis of giant cell arteritis （GCA） complicated by polymyalgia rheumatica （PMR） was confirmed via a carotid artery ultrasonographic examination and superficial temporal artery biopsy. After immediate steroid administration, his symptoms markedly improved.
Discussion: The most common presenting symptom of GCA is headache; however, a wide range of general symptoms have also been observed. Some of the symptoms such as jaw claudication, trismus, and tongue pain may result in the patient consulting a general dental practitioner. Early urgent referral is required in suspected cases, especially in those manifesting jaw claudication, diplopia, and temporal artery abnormalities because the positive likelihood ratio in cases with these symptoms is high and any delay in diagnosis and treatment may result in blindness in severe cases involving the ophthalmic artery. Dental clinicians may play a role in the early diagnosis of GCA. Therefore, dental clinicians should be aware of the possibility of GCA.
Conclusion: This is a report of a case of GCA with jaw claudication, trismus, diplopia, dizziness, weight loss, and PMR. Dental clinicians need to be aware of the possibility of GCA in patients presenting with the typical symptoms.

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Patient: A 74-year-old female was referred to our department with symptoms of unpleasant dull aching on bilateral cheek, teeth and gum. The patient had been suffering from cheek and teeth pain from several months after two-years-treatment for 14 teeth at the dental clinic A. However, her pain had not been properly treated at this clinic A. One year later, although endodontic therapy was performed at the dental clinic B, her symptoms did not improve. Then the patient was referred to several hospitals, and these hospitals repeated endodontic therapy and extraction for neighboring teeth felt pain. Accordingly, 10 teeth were extracted for approximately two years before her visiting our clinical department. At the first visiting our hospital referred pain at #12 from a trigger point on the left masseter, and allodynia at gingiva corresponding to #12, #13, #14, #15, #18, #19, and #20 were observed. Thus, our clinical diagnosis is as follow: non-odontogenic tooth pain at #14, neuropathic pain at maxillary and mandibular gingiva where teeth were extracted and temporomandibular disorder with masticatory muscle myalgia. Therefore, based on a cognitive behavior model, the evaluation and intervention for her pain problem were performed by physical, emotional, cognitive, and behavioral aspects. As a result, two months after the intervention, the allodynia of gingiva were alleviated to dysesthesia.
Discussion: Besides physical treatments for pain, it has been reported that multi-dimensional countermeasures based on cognitive behavioral models such as attention to emotion, modification of non-functional cognition, and intervention to pain behavior and/or pain avoidance behavior is effective. In this case, providing not only physical care but also psychological interventions were beneficial for the patient with chronic non-odontogenic toothache.
Conclusion: We experienced the patient with non-odontogenic tooth ache who had lost 10 teeth during the past two years and psychological interventions were beneficial.

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