Peripheral nerves are often subjected to various forces such as surgical invasion, trauma, disease infiltration, and drug action. These attacks cause the peripheral nerve fibers to be pulled, pressed, damaged, or ruptured, resulting in a decline in peripheral function or loss of function. This symptom is often expressed in various ways such as numbness, palsy, paralysis, neuropathy, and nerve abnormality. Paralysis in the oral and facial areas includes motor palsy associated with efferent peripheral neuropathy such as the facial and hypoglossal nerves and sensory palsy associated with afferent peripheral neuropathy such as the inferior alveolar nerve and the lingual nerve. In addition, dysgeusia, taste disorders, dysfunction of autonomic nerves, and autonomic neuropathy may occur in the oral cavity and the facial region as one of paralysis. If these symptoms or disorders recover within days to weeks, it is temporary loss of motor and sensory function due to blockage of nerve conduction, and the diagnosis is neurapraxia. On the other hand, if the symptoms of paralysis persist and the aftereffects remain, or if the function does not recover at all, it can be diagnosed as axonotmesis or neurotmesis. Paralysis is exceedingly difficult to diagnose the prognosis and degree of disability only by the initial symptoms. In particular, the sensory function is more difficult to evaluate than the motor function because the sensory cannot be visualized, and therefore the diagnostic criteria cannot be determined, and inaccurate diagnosis causes confusion in the course of treatment. As a result, despite the definitive diagnosis being Neurapraxia, there is the possibility of giving unnecessary medication, surgical treatment, or wrong physical therapy. Not only that, but for axonotmesis and neurotmesis, which must be treated early, there is a possibility that the start of treatment will be delayed. A quantitative and objective, reproducible and accurate diagnosis is needed to determine the prognosis of paralysis and to make treatment decisions. Accurately grasping the cause of external force applied to the peripheral nerves and the timing of damage, it is possible to cure peripheral functions if the amount and duration of drug therapy and physical therapy and the timing of surgical treatment can be correctly determined. The purpose of this review is to explore preventive and diagnostic methods for peripheral neuropathy during dental treatment. Therefore, we considered the need for a Precision tactile function test for painful trigeminal neuropathy and neuropathic pain, considering the time to fix the symptoms of neuropathy. In addition, we discussed the treatment experience of hyperalgesia and allodynia caused by disorders of the somatosensory nervous system.
Trigeminal neuropathy is characterized by numbness in the skin or mucosa in the distribution of the trigeminal nerves, sometimes in association with pain. Sensory deficits in the lower lip and tongue frequently causes difficulties with speech and eating. Thus, numbness in the trigeminal distribution is more distressin than numbness involving spinal dermatomes.
The differential diagnosis of the causative diseases underlying the trigeminal neuropathy is difficult, because a spectrum of pathophysiological conditions may affect the trigeminal nerves, including traumatic, vascular, inflammatory, demyelinating, infectious, and neoplastic disorders. Moreover, trigeminal neuropathy develops in isolation or in combination with other neurological deficits of nearby cranial nerves or extremity. Trigeminal neuropathy may also be the presenting manifestation of malignancy, autoimmune disease, or vascular hemorrhage or ischemia of the brainstem. Thus, the findings of orofacial numbness necessitate a comprehensive assessment of all aspects of the trigeminal pathways, which may include neurophysiological, radiographic, and laboratory evaluation in addition to the careful medical interview. In this review, we illustrated some of the principal pathological conditions causing trigeminal neuropathy.
A malignant tumor that occurs in the tongue is histologically squamous cell carcinoma in many cases, and a salivary gland malignant tumor originating from the lingual gland, especially the anterior lingual salivary gland, is very rare. We report a case of adenocarcinoma, not otherwise specified (NOS) occurring from the anterior lingual salivary gland. The patient was a 52-year-old woman with a spherical, elastic hard and painless mass in the right side of the submucosa of the tongue. The results of diagnostic imaging indicated the possibility of a tumor derived from a gland. Since it was not possible to determine whether the mass was benign or malignant, an incisional biopsy was performed. However, the pathological diagnosis was a malignant epithelial tumor derived from a minor salivary gland, which did not lead to a definitive diagnosis. Following a clinical diagnosis of tongue carcinoma (cT1N0M0), the tumor was surgically resected under general anesthesia. The histological features and immunohistochemical profiles did not match those of known epithelial salivary gland carcinomas. Consequently, the resected tumor was pathologically diagnosed as adenocarcinoma, NOS. There was no recurrence for 3 years after the operation.
The prevalence of syphilis has increased in Japan since 2010. Its rapid increase among women in their 20s is of particular concern because it is associated with an increase in the prevalence of congenital syphilis. We report a case of primary syphilis diagnosed from a tongue ulcer in a pregnant woman who did not receive antenatal care. A 29-year-old pregnant woman, who did not receive antenatal care, presented with a tongue ulcer at our hospital. She had a history of being a commercial sex worker. Laboratory tests revealed elevated C-reactive protein levels (5.56 mg/dL) and positive TPLA and RPR. We referred the patient to the department of infectious diseases as well as to the department of obstetrics and gynecology. She was treated with benzylpenicillin potassium (24 MU/day) for 14 days. Later, the tongue ulcer disappeared and RPR showed negative results. She gave birth to a boy who did not have congenital syphilis. The number of patients with syphilis presenting with oral symptoms is increasing, and it is expected that more of such cases will be examined by dentists. Therefore, it is crucial to consider syphilis as a differential diagnosis of oral mucosal disease and establish coordination among specialists who can be consulted and referred to when syphilis is initially suspected.
Calcium hydroxide formulation is frequently used in the treatment of root canals. We report a case where this formulation caused maxillary vascular embolism. A patient received an injection of calcium hydroxide formulation in to the right maxillary lateral incisor in a dental clinic. Immediately after, he presented with swelling of the surrounding gingiva, right cheek swelling, pain, and malaise. Necrosis of the right palate mucosa was observed. A CT image showed calcium hydroxide formulation confirmed to running from the greater palatal artery to the maxillary artery. We diagnosed maxillary vascular embolism caused by calcium hydroxide. On day 32, necrotic tissue of the palate mucosa was removed as much as possible under local anesthesia. On Day 233, the right upper 2 teeth were extracted and a radicular cyst was removed. On day 335, the redness on the right cheek skin almost disappeared, and the opening increased to 42 mm. The right oral and extraoral hypoesthesia remained, but was improving, and the right palate mucosa was completely epithelialized.
Hemophilic pseudotumor causes hematoma mainly in the joints and muscles of hemophilia patients. It rarely occurs in the jawbone. We describe our experience with a hemophilic pseudotumor in the maxilla of an infant aged 1 year, 4 months. The patient was being followed-up for severe hemophilia B in our hospital’s department of pediatrics. At the initial visit, swelling of the buccal gingiva of the maxilla second deciduous molar was observed, and CT images showed a tumor in the maxillary left molar region. After the examination, repeated bleeding from the gingival sulcus due to mobility of the maxillary second deciduous molar occurred. Therefore, following the guidelines, we administered a blood coagulation factor IX preparation and extracted the maxillary second deciduous molar under local anesthesia. About 1 month later, we removed the maxillary lesion with the patient under general anesthesia. The lesion was covered with a thin capsule and filled with blood, and the crown of the maxillary first molar was contained within the lesion. The histopathological findings showed internal blood retention and reactive granulation augmentation. The lesion was diagnosed as a hemophilic pseudotumor. The postoperative course has been good with no recurrence of the lesion for 2 years.
We report a case in which the manifestation of fasciculations in the tongue led to a diagnosis of amyotrophic lateral sclerosis (ALS)-associated disease. An 80-year-old man visited our department with chief complaints of tongue discomfort and swallowing difficulty. The patient had been aware of dysarthria for 2 years and had visited several physicians without receiving an accurate diagnosis. Intraoral examination in our department showed fasciculations in the tongue; therefore, ALS was suspected. He was referred to the Department of Neurology where a definite diagnosis of ALS was made. Our experience suggests that dentists can contribute to the diagnosis of ALS, as well as the assessment of dysphagia and management of oral health.