Advanced atherosclerosis is associated with increased medial degeneration in sporadic ascending aortic aneurysms

Objective

The pathogenesis of non-familial, sporadic ascending aortic aneurysms (SAAA) is poorly understood, and the relationship between ascending aortic atherosclerosis and medial degeneration is unclear. We evaluated the prevalence and severity of aortic atherosclerosis and its association with medial degeneration in SAAA.

Methods and results

Atherosclerosis was characterized in ascending aortic tissues collected from 68 SAAA patients (mean age, 62.9 ± 12.0 years) and 15 controls (mean age, 56.6 ± 11.4 years [P = 0.07]) by using a modified American Heart Association classification system. Upon histologic examination, 97% of SAAA patients and 73% of controls showed atherosclerotic changes. Most SAAA samples had intermediate (types 2 and 3, 35%) or advanced atherosclerosis (types ≥ 4; 40%), whereas most control samples showed minimal atherosclerosis (none or type 1, 80%; P < 0.001 after adjusting for age). In a separate analysis, we examined the total incidence and grade distribution of medial degenerative changes among SAAA samples according to atherosclerosis grade. Advanced atherosclerosis was associated with higher grades of smooth muscle cell depletion (P < 0.001), elastic fiber depletion (P = 0.02), elastic fiber fragmentation (P < 0.001), and mucopolysaccharide accumulation (P = 0.04). Aortic diameter was larger in SAAA patients with advanced atherosclerosis than in patients with minimal (P = 0.04) or intermediate atherosclerosis (P = 0.04). Immunostaining showed marked CD3+ T-cell and CD68+ macrophage infiltration, MMP-2 and MMP-9 production, and cryopyrin expression in the medial layer adjacent to atherosclerotic plaque.

Conclusions

SAAA tissues exhibited advanced atherosclerosis that was associated with severe medial degeneration and increased aortic diameter. Our findings suggest a role for atherosclerosis in the progression of sporadic ascending aortic aneurysms.     

Neurotrophic Proteins in Dentin and Their Effect on Trigeminal Sensory Neurons

IntroductionA plethora of bioactive molecules present during tooth formation become sequestered in the mineralized dentin matrix and can be released into the pulp tissue after demineralization from carious lesions. However, neurotrophic factors are differentially expressed and secreted during various stages of odontogenesis. Thus, the aims of this study were(1) to investigate their presence and relative abundance in crown and root dentin and(2) to evaluate the bioactivity of dentin-derived proteins on neuronal cells.MethodsDentin matrix proteins (DMPs) were isolated from matched roots and crowns of extracted healthy human third molars. The total protein amount as well as the concentration of growth factors and neurotrophic proteins were quantified. The impact on neuritogenesis was determined with mouse trigeminal neurons in vitro and by a hydrogel implant model in vivo. Transient receptor potential cation channel subfamily V member 1 (TRPV1) sensitization of DMP-conditioned neurons was evaluated by single-cell calcium imaging.ResultsThe relative concentration of neurotrophic molecules revealed that nerve growth factor is the most abundant neurotrophin with 3-fold increased expression in radicular dentin. Similarly, brain-derived neurotrophic factor and neurotrophin 3 are more abundant in radicular than coronal dentin. Conversely, glial cell line–derived neurotrophic factor is more abundant in coronal dentin, whereas neurotrophin 4 is equally distributed. Dentin matrix proteins promoted neurite outgrowth in vitro and axonal targeting in vivo, with a greater effect observed by radicular dentin extracts. Furthermore, DMPs sensitized TRPV1 responses in mouse trigeminal neurons with greater activity seen with extracts from root dentin.ConclusionsNeurotrophic factors are differentially distributed between coronal and radicular dentin with different effects of dentin-derived proteins on axonal growth and targeting as well as the sensitization of TRPV1. Thus, extracellular proteins from the dentin matrix are likely involved in neurogenic responses to caries and could be exploited in clinical regenerative endodontics to promote reinnervation and enhance tissue regeneration.     

Regenerative Endodontic Procedures in Necrotic Mature Teeth with Periapical Radiolucencies: A Preliminary Randomized Clinical Study

IntroductionThis preliminary study compared clinical and radiographic outcomes of regenerative endodontic procedures (REPs) with that of conventional root canal treatment (CRCT) in necrotic mature teeth with periapical radiolucencies.MethodsFifty-six mature necrotic teeth with large periapical radiolucencies were distributed into 2 groups: group 1, REPs and group 2, CRCT (n = 28/group). Clinical and radiographic follow-up assessments were undertaken up to 12 months. Statistical analysis was performed using the independent samples t test and the chi-square test, and the level of significance was set at P = .05.ResultsWith a follow-up rate of about 73.4% of the total patients for 12 months, favorable clinical and radiographic outcomes were found in 92.3% and 80% in REPs and CRCT groups, respectively, and the difference was not statistically significant (P > .05). Half of the teeth treated with REPs responded to the electric pulp test.ConclusionsRegenerative endodontic procedures have the potential to be used as a treatment option for mature teeth with large periapical radiolucencies.     

Linear and volumetric gain after vertical bone augmentation in the posterior mandible using an autologous cortical tenting method

This study was performed to evaluate the linear and volumetric effects of a technique for reconstruction of the posterior atrophic mandible, including the final bone gain of the graft, by three-dimensional assessment. Thirteen individuals were recruited into the study and submitted to a total of 15 mandibular autogenous bone block surgeries. Cone beam computed tomography images were obtained at three different times. Bone graft length and thickness, and the volume, height, and width of the graft were measured. Data were compared statistically among the time points using the Friedman test, and cluster analysis was performed to identify the association between the study variables and the resorption rate (α = 0.05). Linear analysis of the width and height of the recipient area at the different time points revealed a statistically significant difference. The final average increase in height was 1.6 mm; all subjects showed an average volume gain of 3.412 mm³, and 77% of the subjects showed an average graft resorption of 0.688 mm³ construction of three-dimensional vertical defects of the posterior mandible resulted in good healing with minimal complications and minimal bone graft resorption, favouring vertical bone gain.     

浓缩生长因子对上颌前牙区种植骨增量术后反应的影响

目的 研究浓缩生长因子（CGF）对种植骨增量患者术后疼痛和肿胀的作用。方法 选择28例单颗上颌前牙缺失伴唇侧骨板缺损可同期植入种植体的患者,随机分为2组,每组14例,试验组应用CGF行引导骨再生术,对照组应用胶原膜行引导骨再生术,分析对比两组患者术后疼痛和肿胀程度。术后疼痛采用视觉模拟评分（VAS）法测定,肿胀程度根据肿胀范围划分4个等级。采用SPSS 23.0软件包对结果进行统计分析。结果 试验组和对照组患者疼痛VAS评分分别为35.1±22.5和47.0±20.3,术后疼痛持续时间分别为（2.1±1.5）、（2.8±1.0） d,组间差异无统计学意义（P>0.05）。试验组无肿胀、轻度肿胀、中度肿胀、重度肿胀的百分比分别为21.4%、57.1%、21.4%、0,对照组依次为7.1%、35.7%、35.7%和21.4%,术后肿胀持续时间分别为（2.4±1.4）、（4.2±2.2） d,差异存在统计学意义（P<0.05）。结论 CGF的应用可以减轻患者术后肿胀程度,缩短术后肿胀时间,但对疼痛无明显作用。     

血小板衍生生长因子对大鼠种植体周围神经再生影响的研究

目的 探讨血小板衍生生长因子（PDGF）对大鼠种植体周围神经再生的影响。方法 建立大鼠股骨植入种植体模型,愈合早期连续注射PDGF,采用免疫组化染色的方法分析PDGF对种植体周围神经再生的影响。结果 PDGF增加大鼠股骨种植体周围早期神经纤维数量,对种植体周围后期神经纤维数量无显著影响。同时,这些神经具有周围神经纤维的典型结构。结论 PDGF可以促进种植体周围早期神经再生。本研究为实现PDGF促进种植体周围神经再生,进而改善种植体感觉功能的临床应用,提供一定的实验依据。     

Nonsurgical Endodontic Treatment of Necrotic Teeth Resolved Apical Lesions on Adjacent Implants with Retrograde/Apical Peri-implantitis: A Case Series with 2-year Follow-up

Retrograde (or apical/periapical) peri-implantitis (RPI) presents with radiographic signs of bone loss at the periapical area of endosteal implants and may also present with clinical signs of abscess formation or a sinus tract traceable to the implant periapex. The lesion may form days up to several years after the initial implant placement. In contrast to marginal peri-implantitis, which has a prevalence of 19.83%, RPI may be underreported because many clinicians are currently not aware of this type of lesion. The etiology, although not fully understood, may be attributed to endodontic infection of an adjacent tooth or residual microorganisms present after the extraction of an infected tooth at the implant site. There are several treatment modalities available for the management of RPI. Nonsurgical root canal treatment may be an option if the implant RPI etiology is suspected to be related to an adjacent endodontically involved tooth. In a previous report, surgical treatment modalities to correct RPI were described. This current case series presents 2 cases of RPI in which nonsurgical treatment of the necrotic adjacent teeth resulted in full radiographic and clinical resolution of the adjacent apical peri-implant lesions with 18-month and 2-year follow-ups, respectively. RPI may be prevented by evaluating the endodontic status of natural teeth adjacent to the implants and by addressing endodontic infections near the implant sites. Certain types of implant RPI may successfully be resolved nonsurgically by addressing adjacent endodontic infections as shown by this case series.