Vertical root fracture (VRF) is different from odontoclasis caused by trauma or injury. VRF is defined as a complete or incomplete fracture of roots caused by long-term and persistent stimulus, such as excessive forces from mastication or occlusion, improper tooth anatomy, and tooth treatment accident. Early diagnosis of VRF is essential to prevent the absorption of alveolar bone, thereby improving prognosis. Radiographic examination is the most common and effective evaluation method for VRF. Cone beam computed tomography can provide three-dimensional information for fracture details, which are more precise than traditional periapical films. In this paper, we present the radiographic features, differential diagnosis, and new treatment techniques for VRF.
Cone-Beam Computed Tomography ; Humans ; Tooth Fractures ; Tooth Root

The farnesoid X receptor(FXR)is a member of the nuclear receptor superfamily.It was studied extensively as a receptor for bile acids at first and found to control the metabolism of bile acids.In the past several years,FXR has been found that besides maintaining the homeostasis of bile acids,it also regulates the metabolism of lipid and carbohydrate,protects hepatocytes,promotes hepatic regeneration,inhibits hepatic fibrosis,regulates intestinal bacterial growth,etc.This article reviews the study progression of FXR,especially in the new discovery of FXR functions.

Objective To evaluate the mortality and survival time of war injuries, followed by seawater immersion. Methods Animal models of injuries including open chest injury, open abdominal injury, burn, hemorrhagic shock, were reproduced. The animals were divided into two groups: control group consisting simple injury without seawater immersion, and seawater immersion group consisting similar injuries followed by seawater immersion. The survival time of animals of the two groups were recorded. Results The mean survival time of the animals with open chest injury and open abdominal injury followed by seawater immersion was 45 minutes and 162 minutes, respectively. The mortality of 30% Ⅱ degree burn was 50% after seawater immersion for 4 hours, while it was 6% without seawater immersion. The mortality of moderate hemorrhagic shock with four-hour with seawater immersion was 90%, while all the animals survived without seawater immersion. Conclusions The experimental study showed that the mortality rate was significantly raised and the survival time significantly shortened when open wounds were exposed to seawater for a certain period of time. Hypertonicity of the seawater with high sodium content, and low temperature of seawater might play important roles in producing various pathophysiological changes which contributed to early death of the animals.

Objective To analyze the clinical and histological features of drug-induced autoimmune hepatitis (DI-AIH).Methods From January 2008 to June 2011,five patients with auto-immune hepatitis (AIH),having a definitive history of medicine taking prior to the onset of disease and accepted liver biopsy were retrospectively analyzed.The general information was collected,which included gender,age,onset of the disease,medication,clinical manifestations,treatment and follow-up.The laboratory findings were also collected,which included total bilirubin (TBil),direct bilirubin (DBil),alanine transaminase (ALT),aspartate transaminase (AST),alkaline phosphatase (ALP),gamma glutamyl transpeptidase (GGT),globulin,γ-globulin percentage,albumin (Alb),eosinophils,antinuclear antibodies,antimitochondrial antibodies,anti-smooth muscle antibodies and the type of live injury.The liver tissue sections of patients were stained with hematoxylin-eosinstaining (HE) and reticular fiber staining and then pathological changes were observed.Patients with DI-AIH were scored with AIH scoring scale.Results All five patients with DI-AIH were female,average age was 48.0--+7.5.Prior to the onset of disease,all patients had taken Chinese traditional medicine.Anorexia and fatigue were the most common clinical symptoms.Among laboratory findings,the level of ALT ((795.0+467.4) U/L),AST ((730.44-451.5) U/L),TBil ((80.3-+ 64.1) μmol/L) and DBil ((65.2 +_ 58.0) μmol/L) significantly increased.One patient was antinuclear antibody positive.One patient had drug-induced liver injury,pathological features were spotty necrosis of liver cells,liver tissue eosinophil infiltration and liver cell microbubble type degeneration.All the patients had interface hepatitis,periportal infiltration of lymphocytes or lymphocytes-plasma cells,liver cells adjacent to lesion showed rosette-like structure.All the patients received glucocorticoid treatment.After glucocorticoid withdrawal,the liver function was normal during the follow-up period.Conclusion There are no specificity of clinical manifestations,laboratory findings and histological features in patients with DI-AIH.

Objective:To evaluate the effects of resin infiltration in the treatment of post-orthodontic white spot lesions (WSLs)and compare it with microabrasion.Methods:1 0 subjects with 66 teeth with noncavitated and unrestored WSLs after multibracket treatment were recruited.A simple randomized,split-mouth and controlled design was used to allocate WSLs to the resin infiltration and micro-abrasion groups(n =33).The area of the WSLs were measured photographically by using image analysis software before treatment (T0),1 week(T2)and 3 months(T3)after treatment.Data were analyzed with multifactorial analysis of the variances with repeated measures at an a level of 5% and a power of 80%.Results:The area of the white spot lesions(R)decreased significantly in both groups(P <0.05).At T3 the success rate of resin infiltration group(88.68%)was significantly higher than that of microabrasion group (64.67%)(P <0.05).Conclusion:Resin infiltration is more effective than microabrasion in the treatment of post-orthodontic WSLs.

Objecfive To explore pathological mechanism and treatment of central hyponatrem-ia. Methods Synchronous assay was made to detect changes of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),endogenous digitalis-like substance(EDLS),antideuretic hormone (ADH),Na+ concentrations in blood and urine as well as osmotic pressure of plasma and urine in 68 pa-tients with traumatic brain injury(TBI). Results Of all,there were 27 patients with hyponatremia,mostly in patients with severe or critical TBI.There found syndrome of inappropriate secretion of antidi-uretic hormone(SIADH)in 7 patients and cerebral salt wasting syndrome(CSWS)in 20. Conclu-sions The central hyponatremia in patients with TBI may be related to the increased secretion of EDLS and ADH.The decrease of ANP and BNP in blood has no direct effect on Na+ concentration in blood.In-travenous injection of extrinsic thyrotropin releasing hormone(TRH)may inhibit dilutional hyponatremia resulted from increased secretion of ADH in TBI patients.

Objective:To evaluate the translucency,opalescence and fluorescence reflection of 6 light-cured resin composites. Methods:Disks of 6 resin composites including Filtek Supreme XT-YT(XT),Filtek Supreme XT-A3B(3M),Clearfil Majesty-A3 (MJ),Gradia Direct-A3(GC),Venus-A3(VE)and Charisma Diamond-A3(CA)were prepared in the diameter of 9 mm with the thickness 2.0 mm.PR-650 spectral scanning colorimeter was used to measure and caculate translucency parameters(TP),opal-escence parameter(OP)and fluorescence reflection(FL)and to draw the fluorescence reflection curves.Results:Except XT and MJ,TP value of other resin composites were in the range of natural tooth.Only OP value of XT was in the range of natural tooth en-amel.FL value of XT was close to that of natural tooth dentin.Fluorescent peak wavelength of GC,MJ,VE and CA were in the range of natural tooth,but fluorescent peak height was higher than that of natual tooth.TP was positively correlated with OP(r =0.85,P <0.05).There was no statistic correlation between TP and FL,between OP and FL.Conclusion:The 6 resin composites can simulate optical property of natual tooth,but the opalescence of resin composites is defective.

Objective To comprehensively evaluate the clinical and radiological features of patients with Klebsiella pneumonia liver abscess (KLA) in order to improve treatment. Methods Data of 197 patients with KLA (n=106) or non-KLA (n=56) between March 2001 and January 2009 were collected and retrospectively analyzed on the aspects of underlying diseases, clinical manifestations, laboratory tests, pathogenic and imaging examinations. Results In comparison with non-KLA patients, the underlying diseases such as diabetes (53. 77% vs 25.00%, P = 0. 001) and hepatic adipose infiltration (16. 04% vs 5, 36%, P<0.05) were more common in KLA patients.Whereas the clinical presentations including abdominal pain (57. 14% vs 40. 57%, P<0. 05),hypodynamia (46.43% vs 19.81%, P=0. 001) and hepatomegaly (14.29% vs 4.72%, P<0. 05)were more severe in non-KLA patients than in KLA patients, however, the fasting blood glucose was higher in KLA patients than in non-KLA patients [(7.84±0.36) mmol/L vs (5.76±0.30) mmol/L,P=0. 001] on the admission. In addition, the abscess of KLA often appeared alone in the right lobe of the liver and was liable to generate air cavity (32. 88% vs 13.51%, P<0.05), un-smooth rim (71.23% vs 40.54% ,P<0.05) and dynamic septum enhancement (41.10% vs 16.22% ,P<0.01) in comparison with non-KLA. Conclusions Klebsiella pneumonia has emerged as the main pathogen of pyogenic liver abscess. The patients with KLA are often complicated with diabetes and fatty liver, as well as high prevalence of air cavity. The CT findings may be helpful for prompt treatment of Klebsiella pneumonia liver abscess.

Objective To evaluate the frequency of mutations that occur in PHEX,FGF - 23 and DMP - I genes associated with familial hypophosphatemic vitamin D resistant rickets among 6 patients from 4 families in China. Methods The peripheral blood samples from 4 families were collected and other 10 persons from different families were selected as normal controls,and then the total gene DNA was extracted from the whole blood. Using polymerase chain reaction(PCR)amplication,sequences of the exons and flanking zones in PHEX,FGF - 23 and DMP - I genes were sequenced by direct DNA sequencing and TA cloning,and then the mutations found were analyzed. Results In exon 6 of DMP - I gene,c1218 C ﹥ T and c1230 G ﹥ A mutations were detected in lineage 1,as same sense mutation (propositus and its sister:homozygous mutation;mother:heterozygous mutation);c1333 - 1334 GC ﹥ TT mutation,as missense mutation,was found in exon 12 of PHEX gene on the propositus of lineage 2,determined as heterozygous muta-tion,but the same mutation was not found from their parents. In exon 3 of FGF - 23 gene,c716 C ﹥ T,p. T239M hetero-zygous mutation was found on the propositus and its mother. In exon 6 of the DMP - I gene,c205 A ﹥ T homozygous mutation was detected in lineage 3. In lineage 3,c716 C ﹥ T mutation of the FGF - 23 gene was detected,and the pro-positus and their father had the same mutation. No disease causing mutations of the PHEX,FGF - 23 and DMP - I genes were detected in the family members of lineage 1,3 and 4. Conclusions The mutation c1333 - 1334 GC ﹥ TT detected in exon 12 of PHEX gene might be the cause of disease for the propositus of lineage 2,as missense mutation, which needs further verification;c716 C ﹥ T,p. T239M mutation of the FGF - 23 gene detected in lineage 2 and 3 might not be the causes of the hypophosphatemic rickets and abnormal phenotype.

Objectives To study the molecular genetics of Niemann-Pick's disease (NPD), and its implication in the diagnosis of NPD. Methods The clinical data and blood samples of three unrelated families were collected. The genomic DNA was extracted from peripheral blood. The six coding exons and their lfanking intronic sequences of SMPD1 gene in all members of three pedigrees were ampliifed by polymerase chain reaction (PCR). The SMPD1 gene sequencing results were compared with the normal sequence from Genbank to identify possible causative mutations. The ampliifcation products of exons where mutations were located were cloned into TA vector for further conifrmation. Results Family 1 proband had homozygous T107C mutation and the parents had heterozygous T107C mutation. The homozygous delete mutation (c.108-113delGCTGGC) was detected and conifrmed by TA cloning in all members of family 2 and 3. The 20 normal control members did not have this delete mutation. Conclusions The genetic basis of NPD in the proband of family 1 is the homozygous T107C mutation in SMPD1 gene, while parents in family 1 are carriers of recessive T107C mutation. The homozygous mutation c.108-113delGCTGGC exists in SMPD1 gene in all members of the family 2 and 3. This delete mutation is considered to be genetic polymorphism.