密集型压痛点银质针治疗肩关节周围炎30例

目的:观察密集型压痛点银质针治疗肩关节周围炎的临床疗效。方法:选择2011年1月—2013年12月本院治疗的肩周炎患者90例,均为初次发病者,采用单盲法随机分为A组、B组和C组,每组30例。A组采用密集型压痛点银质针治疗,B组采用肩关节腔内注射玻璃酸钠治疗,C组采用局部封闭治疗。结果:A组治疗后1周、治疗后3个月VAS评分、Constant-Murley肩关节功能评分均优于B组、C组(P0.05)。结论:密集型压痛点银质针治疗肩关节周围炎疗效显著,减轻疼痛见效快,改善功能明显,疗效持久。     

Radiographic examination of ectopically erupting maxillary canines

This study analyzes the need for and possibility of obtaining further information from different radiographic procedures in 125 children with potential ectopic eruption of the maxillary canines. After clinical examination of 3,000 10 to 15-year-old children, it was found that 7% needed radiographic examinations for determination of the canine position. Eighty-four children (2.8%), with a total of 125 potential ectopically erupting maxillary canines diagnosed clinically and by means of periapical radiographs, were selected and a stepwise extended radiographic diagnostic procedure was used. Most canines in ectopic eruption were positioned palatally; the positions could be assessed with sufficient accuracy from conventional periapical films in 92% of the cases. Only in 37% of the cases, however, could the lateral incisor be projected free from the ectopic canine by the intraoral technique. The lamina dura of the lateral incisor facing the canine was often found to be interrupted. For 29% of the ectopic canines, the lateral incisors could neither be projected free nor judged free from resorptions and a supplementary polytomographic investigation was believed to be necessary. The number of resorbed teeth was doubled by polytomography and altogether 12.5% of the ectopic canines caused resorptions. A stepwise radiographic procedure including polytomography is described and recommended in cases of ectopic eruption of maxillary canines for determining the correct position and ruling out or confirming resorptions on incisors, thereby optimizing the orthodontic treatment planning.     

In situ localization of tenascin mRNA in developing mouse teeth

Tenascin is a large extracellular-matrix glycoprotein found in developing connective tissue. A cDNA probe to mouse tenascin, mTN2, was used to determine the cellular origins of this molecule in the murine tooth germ by in situ hybridization. At embryonic day 19, a hybridization signal significantly greater than background was detected with mTN2 in the subodontoblastic layer of the dental mesenchyme and in the inner enamel epithelium of the enamel organ. At postnatal day 1, a signal was detected over pre-odontoblasts and the strata intermedium and externum. No tenascin mRNA was detected in odontoblasts or the stellate reticulum at either age, and hybridization in ameloblasts was not significantly greater than background at postnatal day 1. Thus, much of the tenascin found throughout developing teeth appears to be synthesized by pre-odontoblasts and the inner enamel epithelium, the two populations of cells destined to generate mineralized matrix.     

Stimulation by carrageenan of arachidonate 12-lipoxygenase activity in dog gingival tissue

At 4 h after injection of carrageenan into the gingiva, the 12-lipoxygenase activity of the gingival homogenate was markedly increased. Activity in the cytosol and microsomal fractions was markedly increased when assessed as the specific activity based on nmol/min/mg of protein, and in the cytosol fraction as the percentage distribution of total activity. The 12-lipoxygenase activity in the homogenate from carrageenan-treated gingiva was not affected by either EDTA or calcium ion, or a combination of the two. 12-lipoxygenase activity in both carrageenan-treated and untreated gingiva was inhibited dose-dependently by AA861, a striking difference from its effect on platelet 12-lipoxygenase. There was a marked increase of 12-lipoxygenase activity in experimentally inflamed gingiva compared to the non-inflamed gingiva.     

In vivo and in vitro study of the effects of chlorpromazine on tooth mineralization in rats and mice

The effects of chlorpromazine (CPZ) on tooth mineralization were examined using incisor dentine in adult rats and cultured tooth germs of mandibular first molars dissected from mouse embryos. CPZ (10, 50 and 250 mg/kg, s.c.) substantially inhibited dentine mineralization as evaluated by contact microradiographs. Plasma calcium and phosphorus concentrations were not decreased by CPZ (10 and 50 mg/kg). Physicochemical effects were not involved in the action of CPZ on the mineralization. In vitro experiments showed that CPZ (1 and 10 μM) inhibited mineralization and alkaline phosphatase (ALP) activity in the tooth germs. As CPZ has the properties of a calmodulin antagonist, the calmodulin antagonists W-7 and W-5 were also examined. Both inhibited mineralization and ALP activity in tooth germs; W-5 had less effect than W-7. These in vivo and in vitro findings suggest that CPZ inhibited cell-mediated mineralization in dentine without affecting the calciumdashregulating system and physicochemical mineral deposition. In addition, calmodulin could be involved in cell-mediated mineralization.     

Immunohistochemical localization of very late activation integrins in healthy and diseased human gingiva

The β1-integrins (VLA family) are cellular adhesion molecules (CAM) that play a major role in cell-cell and cell-matrix interactions. The expression pattern of CAM was studied in 5 clinically normal volunteers with healthy gingiva and in 18 patients with clinically different stages of periodontitis. In healthy human gingiva α2. α3 and α6 integrin chains were found in a characteristic distribution, showing a broad continuous expression on the junctional and sulcular epithelium sites. The expression of these integrins was demonstrated primarily on the basal cell layers and in some cells of the stratum spinosum. Inflammatory stages of periodontitis revealed further upregulation of α2, α3 and α6 integrins into the junctional and sulcular epithelial cells, which correlated with the stage of the periodontitis and the extent of the cellular infiltration. α4 and α6 were found to be the predominant β1 integrin chains on inflammatory cells. The amount of δ4 and ş6 positive infiltrative cells increased with the number of inflammatory cells. VCAM-1. the corresponding cell-cell ligand of VLA-4 (α4) was present on the majority of subepithelial vessels in all stages of gingivitis and periodontitis. The α5 subunit was expressed on both endothelium and gingival connective tissue cells. Samples from advanced periodontitis cases showed a higher number of a5 positive mononuclear cells. In comparison to normal epidermis, a human gingival epithelial cells express higher levels of integrins. This expression is further upregulated in advanced stages of periodontitis, indicating changes of the β1 integrin organization.     

Effects of benzo(a)pyrene and nicotine on prostaglandin synthesis in buccal pouch and submandibular glands of the Syrian hamster

Adult male Syrian hamsters were treated by swabbing the apex of the buccal pouch with corn oil (control, C), 1 mM benzo(a)pyrene (BP), nicotine (NC), or BP + NC in corn oil, twice daily, 5 days a week. After a 4-week treatment, the pouches and submandibular glands were dissected and used for the determination of endogenous prostaglandin (PG) production and studies on in vitro PG synthesis. Of the three PGs analysed (PGE₂, PGF₂ and 6-keto-PGF₁), PGE₂ was predominant in the pouch and the glands. BP or NC alone had only a weak effect on PG synthesis in both tissues. However, the combination of BP and NC had a synergistic effect, causing diminished PG synthesis in both tissues. In buccal pouch, BP + NC significantly decreased the concentrations of endogenous PGE₂ and PGF₂ (PGE₂: 0.669 + 0.254 versus 1.698 + 0.460, PGF₂: 0.273 ± 0.090 versus 0.625 ± 0.272 ng/g tissue; BP + NC versus C; mean ± SD, n = 5, p < 0.05). Similarly significant results were also found for in vitro PG synthesis (PGE₂: 0.541 ± 0.249 versus 1.399 ± 0.340, PGF₂: 1.045 ± 0.428 versus 2.133 ± 0.510 ng/g tissue; BP + NC versus C; mean ± SD, n = 5, p < 0.05). In submandibular glands, BP + NC significantly diminished the concentration of endogenous PGE₂ (1.183 ± 0.175 versus 2.379 ± 0.488 ng/g tissue; BP + NC versus C; mean ± SD, n = 5, p < 0.05). The synthesis of 6-keto-PGF₁ in both tissues, and the synthesis of PGF₂ in submandibular gland, were slightly decreased with all treatments.     

Mineralized nodule formation by cultures of human dental pulp-derived fibroblasts

Pulp fibroblasts were isolated from human deciduous and supernumerary teeth and cultured in vitro. With continued culture in normal tissue-culture medium, six pulp fibroblast strains formed cell nodules after 10–15 days. By electron microscopy the nodules had matrix vesicles, and needle-shaped crystals associated with a dense network of collagen fibrils. The crystalline material exhibited a pattern consistent with hydroxyapatite when nodules were examined by X-ray diffractometry. Furthermore, the cells showed high levels of alkaline phosphatase activity, which could be increased more than seven-fold by the addition of 1,25(OH)₂D₃ (5 × 10⁻⁹−5 × 10⁻⁸M). In addition to the production of type I collagen, these cells also synthesized fibronectin and osteonectin. The formation of mineralized tissue nodules by pulp cells in vitro provides a useful system for study of the pathological calcification of pulp tissues.     

腕踝针对肩关节周围炎急性期的镇痛效果及其对血清P物质的影响

目的 观察腕踝针治疗急性期肩周炎的临床疼痛改善效果及体内血清P 物质的变化,并进行分析。方法 随机选取我科62 例肩周炎急性期患者,随机数字表法分为治疗组与对照组,每组各31 例,对照组予口服双氯芬酸钠缓释胶囊,治疗组予利多卡因行星状神经节阻滞后加腕踝针治疗,两组均连续治疗4 周后进行主动、被动功能锻炼,共治疗4 周。比较两组临床疗效、视觉模拟评分（Visual analogue scale score,VAS）及血清内P 物质水平变化。结果 ①疗程结束后,治疗组临床总有效率为100.00%,与对照组的77.42%比较,差异有统计学意义（χ2＝4.348,P＜0.05）;②治疗组治疗4 周后VAS 为（2.07±0.44）分,与治疗前（8.24±1.52）分比较,差异有统计学意义（P＜0.05）;对照组治疗后VAS 为（4.22±0.65）分,与治疗前（8.36±1.14）分比较,差异有统计学意义（P＜0.05）;治疗后治疗组VAS 评分低于对照组,差异有统计学意义（P＜0.05）。③治疗组治疗4 周后P 物质浓度为（33.07±6.74）pg/mL,与治疗前（69.24±7.52）pg/mL 比较,差异有统计学意义（P＜0.05）;对照组治疗后P 物质浓度是（40.22±6.65）pg/mL,与治疗前（70.36±8.02）pg/mL 比较,差异有统计学意义（P＜0.05）;治疗后治疗组P 物质浓度低于对照组,差异有统计学意义（P＜0.05）。结论 腕踝针治疗肩关节周围炎,可改善疼痛症状,且安全有效。     

重症肌无力的发病机制

重症肌无力(MG)是一种神经-肌肉接头传递功能障碍的自身免疫性疾病。MG的发病机制主要涉及免疫因素和遗传因素。免疫因素包括多种致病抗体、细胞免疫、细胞因子、补体及胸腺等。随着免疫学研究的不断进展,MG的发病机制也有了更深入的研究。