An updated review on pathophysiology and management of burning mouth syndrome with endocrinological,psychological and neuropathic perspectives

Burning mouth syndrome (BMS) is a chronic oro‐facial pain disorder of unknown cause. It is more common in peri‐ and post‐menopausal women, and sex hormone dysregulation is believed to be an important causative factor. Psychosocial events often trigger or exacerbate symptoms, and persons with BMS appear to be predisposed towards anxiety and depression. Atrophy of small nerve fibres in the tongue epithelium has been reported, and potential neuropathic mechanisms for BMS are now widely investigated. Historically, BMS was thought to comprise endocrinological, psychosocial and neuropathic components. Neuroprotective steroids and glial cell line–derived neurotrophic factor family ligands may have pivotal roles in the peripheral mechanisms associated with atrophy of small nerve fibres. Denervation of chorda tympani nerve fibres that innervate fungiform buds leads to alternative trigeminal innervation, which results in dysgeusia and burning pain when eating hot foods. With regard to the central mechanism of BMS, depletion of neuroprotective steroids alters the brain network–related mood and pain modulation. Peripheral mechanistic studies support the use of topical clonazepam and capsaicin for the management of BMS, and some evidence supports the use of cognitive behavioural therapy. Hormone replacement therapy may address the causes of BMS, although adverse effects prevent its use as a first‐line treatment. Selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs) may have important benefits, and well‐designed controlled studies are expected. Other treatment options to be investigated include brain stimulation and TSPO (translocator protein 18 kDa) ligands.     

Genetic variations of HSD11B2 in hypertensive patients and in the general population, six rare missense/frameshift mutations.

Mutations in the gene encoding 11beta-hydroxysteroid dehydrogenase type 2, HSD11B2, cause a rare monogenic juvenile hypertensive syndrome called apparent mineralocorticoid excess (AME). In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Here, we have studied whether genetic variations in HDS11B2 are implicated in essential hypertension in Japanese hypertensives and the general population. By sequencing the entire coding region and the promoter region of HDS11B2 in 953 Japanese hypertensives, we identified five missense mutations in 11 patients (L14F, n = 5; R74H, n = 1; R147H, n = 3; T156I, n = 1; R335H, n = 1) and one novel frameshift mutation (4884Gdel, n = 1) in a heterozygous state, in addition to 19 genetic variations. All genetic variations identified were rare, with minor allele frequencies less than 0.005. Four of 12 patients with the missense/frameshift mutations showed renal failure. Four missense mutations, L14F, R74H, R147H, and R335H, were successfully genotyped in the general population, with a sample size of 3,655 individuals (2,175 normotensives and 1,480 hypertensives). Mutations L14F, R74H, R147H, and R335H were identified in hypertensives (n = 6, 8, 3, and 0, respectively) and normotensives (n = 8, 12, 5, and 0, respectively) with a similar frequency, suggesting that these missense mutations may not strongly affect the etiology of essential hypertension. Since the allele frequency of all of the genetic variations identified in this study was rare, an association study was not conducted. Taken together, our results indicate that missense mutations in HSD11B2 do not substantially contribute to essential hypertension in Japanese.     

Psychiatric symptoms associated with oculogyric crisis: a review of literature for the characterization of antipsychotic-induced episodes.

Antipsychotics have been found to induce recurrent psychotic episodes lasting minutes to hours, mostly accompanied by oculogyric crisis (OGC). To characterize this side effect, antipsychotic-induced and postencephalitic OGCs that were reported in the literature were compared to find out common characteristics of OGCs and their associated symptoms. Both postencephalitic and antipsychotic-induced OGCs were found to occur late in the day and at regular intervals, and were associated with autonomic symptoms such as profuse sweating, facial flushing, transitory hypertension and difficulty in micturition. They were often associated also with transient psychiatric episodes: visual hallucinations and illusions, auditory hallucinations, delusions, catatonic phenomena, obsessive thoughts and panic attacks. These (OGC) characteristics will be useful in recognizing antipsychotic-induced psychiatric episodes. The associated psychiatric episodes were noted to recur occasionally also without OGC in a few postencephalic cases, and during gradual dose reduction or after a switch to a novel or low-potency antipsychotic in drug-induced cases. These findings suggest that episodes with the OGC characteristics but without OGC per se, may be less severe reactions to antipsychotic medication than those with OGC, and may represent manifestations of subclinical OGC.     

Myosin heavy chain composition of tongue muscle in microphthalmic (mi/mi) mice before and after weaning.

To elucidate the effects of teeth on muscle fibers in the tongue during the developmental process, we examined the expression of muscle contractile proteins and the genes for those proteins in normal mice and microphthalmic (mi/mi) mice with impaired tooth eruption. The mice were observed during the growth period, including weaning, which is when feeding movements undergo major changes. Expression of the myosin heavy chain (MyHC)-2a protein, whose contraction speed is relatively slow, disappeared after weaning in normal mice, while it remained in high concentrations even after weaning in mi/mi mice. The presence of MyHC-2a after weaning in mice with no tooth eruption was attributed to a compensation for lack of proper masticatory function and sucking-like movements, as MyHC-2a is necessary for these movements.     

Fit and fill analysis of a newly designed femoral stem in cementless total hip arthroplasty for patients with secondary osteoarthritis

The fit and fill of the femoral canal are critical to the success of cementless femoral stems in total hip arthroplasty. It is difficult for conventional stems to provide a good fit and fill for the femora of patients with secondary osteoarthritis. Based on measurements of 100 femora of these patients, we designed two types of Fukui Medical School (FMS) stems with a proximal lateral flare that differed in the medial radius. We compared the fit and fill of the FMS stems with those of four conventional stems, using computer simulation. The mean proximal fit and total fit of the FMS stems were 46% and 53% respectively, a significant improvement compared with the other stems examined. The mean fill of FMS stems was 82% at the lower end of the lesser trochanter and 84% at the upper end of the isthmus, values that were significantly higher than those of the other stems. Since September 1995, we have implanted FMS stems in 15 hips with secondary osteoarthritis. Radiographic evaluations showed that the canal fill of the FMS stems was significantly greater in the proximal femur compared with other stems previously inserted at our department. A summary of this paper was presented at the 9th Symposium on Computer-Assisted Radiology; June 1995, Berlin, and at the 8th International Symposium on Technology in Arthroplasty; September 1995, Puerto Rico.     

系膜细胞α-平滑肌肌动蛋白表达与细胞表型的关系

目的：探讨增殖性肾小球肾炎大鼠动物模型中系膜细胞α－平滑肌肌动蛋白（α－SMA）表达与细胞表型的关系。方法：应用单克隆抗体1－22－3（MoAb1-22-3)及Habu蛇毒素分别诱导大鼠增殖性肾小球肾炎动物模型。用免疫组化技术并结合计算机图像分析，检测两个不同诱因引起模型的各个阶段的系膜细胞内α－平滑肌肌动蛋白，SMeb的表达程度，系膜细胞增殖和细胞外基质（ECM）分泌的情况。结果：在MoAb1-22-3模型，随着系膜细胞增殖程度的加理，ECM积聚增多，α－SMA的表达程度也增加，三者平行变化并具有高度相关性，而Habu模型则系膜细胞增殖和ECM增加的同时α－SMA，SMemb表达不增加。结论：α－SMA不是系膜细胞被激活并处于增殖／分泌表型唯一标志。