Unilateral atrophy of the masticatory muscles and mandibular ramus due to pure trigeminal motor neuropathy: a case report.

Pure trigeminal motor neuropathy is a very unusual disease that is characterized by trigeminal motor paralysis without trigeminal sensory disturbances and without the involvement of the other cranial nerves. We report a case of pure trigeminal motor neuropathy in a 70-year-old woman. The diagnosis was based on the results of clinical, electromyographic, and radiologic examinations. Only the motor branch of the left trigeminal nerve was damaged. Atrophy of the left-side masticatory muscles and jaw resulted in facial asymmetry. Magnetic resonance imaging (MRI) of the head and face did not detect any pathologic lesion, with the exception of atrophy and fatty infiltration of the muscles innervated by the left trigeminal motor nerve. The etiology of the patient's pure trigeminal motor neuropathy was undetermined. Patients with suspected trigeminal motor neuropathy should undergo MRI of the head and face to evaluate the sequelae of denervation and to detect an intracranial or extracranial lesion.

Decoration of fibrinogen γ-chain peptide on adenosine diphosphate-encapsulated liposomes enhances binding of the liposomes to activated platelets.

For the purpose of efficient hemostasis, we previously developed ADP-encapsulated liposomes modified with a dodecapeptide (HHLGGAKQAGDV, H12), H12-(ADP)Lipo. This liposome actually enhanced platelet aggregation in vitro, and showed significant hemostatic effect in vivo. Since fibrinogen (Fbg) is abundant in the bloodstream, it is unclear why this liposome binds platelets so efficiently, overcoming the competition with Fbg. Therefore, we investigated the relationship between H12 density on the liposome and the binding ability to platelets, and evaluated the inhibitory effect of Fbg on the binding of H12-(ADP)Lipo to platelets. As a result, the binding ability to platelets steeply increased depending on H12 density until it reached about 3×10(15) H12 molecules/m(2). The 50% inhibition concentration of Fbg on the binding of H12-(ADP)Lipo to platelets was about 25-fold over the concentration of H12 molecules on the liposome. Moreover, almost no inhibition by Fbg was observed at the physiological concentration of it. This result suggests that the ability of H12 to bind to GPIIb/IIIa increased overwhelmingly by the anchoring to the liposome that enabled the cooperative binding of H12 peptides to the platelets.

Long-term cigarette smoking increases the prevalence of carotid artery calcification seen on panoramic dental radiographs in male patients.

Panoramic dental radiographs are commonly used in general dentistry and oral and maxillofacial surgery to examine upper and lower teeth, maxilla, mandible and the surroundings simultaneously. Carotid artery calcification, a specific indicator of atherosclerotic change of the carotid arteries, can be seen on the radiographs. Many studies have suggested that cigarette smoking is a risk factor of atherosclerotic change as well as cerebral infarction. We hypothesized that smoking could increase the prevalence of carotid artery calcification, and compared the radiographs of smokers and non-smokers aged 50 years and over: 146 male smokers, 165 male non-smokers, 42 female smokers and 422 female non-smokers. This is the first study to focus on carotid artery calcification seen on panoramic dental radiographs to show the connection between smoking and atherosclerotic change. In male patients, carotid artery calcification was seen in 18 (14.1%) of the smokers, and in 8 (4.8%) of the non-smokers, which clearly shows that male patients aged 50 years old or over are more likely to develop carotid artery calcification if they smoke. However, there is no significant difference between female smokers and female non-smokers in the same age group. Dentists are in a good position to find carotid artery calcification on radiographs. When this is found on a radiograph, the patient should be advised to stop smoking and be referred to a physician for further tests. Clinicians should be aware that this radiographic finding indicates the presence of atherosclerotic change of the carotid arteries.

Clinical study on eruption of permanent canines after secondary alveolar bone grafting.

OBJECTIVE: Eruption of cleft-associated permanent canines was studied in 190 patients with unilateral cleft lip/palate and whose permanent canines had not erupted at the time of alveolar bone grafting. In 162 of these patients, width of bone defect was compared between patients who underwent surgical exposure of canines and those whose canines erupted naturally. RESULTS: Cleft-associated canines naturally erupted after bone grafting in 150 patients (78.9%) and required surgical exposure in 36 patients (18.9%). Cleft-associated canines had not yet erupted in two patients. Two patients were lost to follow-up. Nasal-side bone defects were significantly wider in patients who underwent surgical exposure of cleft-associated permanent canines than in those whose cleft-associated permanent canines erupted naturally. CONCLUSIONS: The present results suggest that nasal-side cleft width is related to the need for surgical exposure of permanent canines in children with cleft lip/palate.