Large platelet aggregates in endoscopic ultrasound‐guided fine‐needle aspiration of the pancreas and peripancreatic region: A clue for the diagnosis of intrapancreatic or accessory spleen

Intrapancreatic and intraabdominal accessory spleens (IPIASs) are rarely encountered in endoscopic ultrasound‐guided fine‐needle aspiration (EUS‐FNA) biopsies. However, as incidentally discovered IPIAS can mimic a benign or malignant pancreatic neoplasm on imaging studies, a definitive diagnosis made by EUS‐FNA can avert an unnecessary surgical intervention or additional radiologic follow‐up. We report five cases of intrapancreatic splenules and one case of accessory spleen (AS) in which a definitive diagnosis was made on EUS‐FNA. Previously recognized FNA cytomorphologic features of splenic tissue, including ASs and splenosis, are endothelial cells and polymorphous lymphocytes admixed with neutrophils, eosinophils, plasma cells, histiocytes, and lymphoglandular bodies. We describe the additional finding of abundant large platelet aggregates as another distinguishing feature of splenic tissue on FNA. In all six cases, large platelet aggregates were identified along with polymorphous lymphoid cells, lymphoglandular bodies, loose aggregates of endothelial cells and scattered or aggregated bland spindle cells. A review of 10 consecutive cases of EUS‐FNA‐sampled benign intraabdominal lymph nodes showed that the presence of large platelet aggregates, three‐dimensional aggregates of lymphoid cells and of bland slender spindle cells and the absence of follicular germinal cell components (tingible body macrophages and lymphohistiocytic aggregates) are useful in differentiating IPIASs from reactive lymph nodes. Immunoperoxidase stains were useful to confirm a suspected IPIASs by showing CD31‐positive acellular flocculent material, consistent with large platelet aggregates and a rich CD8‐positive endothelial cell network between CD45‐positive lymphoid cells and CD68‐positive histiocytes in all six cases. Diagn. Cytopathol. 2013;41:661–672. © 2013 Wiley Periodicals, Inc.     

Effect of Autologous Growth Factors in Maxillary Sinus Augmentation: A Systematic Review

Purpose: The aim of the present study was to systematically evaluate the effect of autogenous platelet concentrates on the clinical and histomorphometric outcomes of maxillary sinus augmentation. Materials and Methods: MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials were searched using a combination of specific search terms. Furthermore, a hand searching of the relevant journals and of the bibliographies of reviews was performed. Prospective comparative clinical studies were included. Implant survival and histomorphometric outcomes were evaluated. Results: Twelve studies were included. Four hundred forty‐five sinus floor augmentation procedures were considered. No difference in implant survival was reported between test and control groups. Six studies reported a beneficial effect of platelet concentrates based on histomorphometric outcomes, while another six studies found no significant effect. A large heterogeneity was found regarding study design, surgical techniques, graft materials, clinical and histomorphometric outcome variables, and methods for preparing platelet concentrates. Favorable effects on soft tissue healing and postoperative discomfort reduction were often reported but not quantified. Conclusions: A clear advantage of platelet concentrates could not be evidenced. Standardization in the experimental design is needed in order to detect the true effect of platelet concentrates in maxillary sinus augmentation procedure, especially regarding postoperative quality of life.     

Correlation of Platelet Growth Factor Release in Jawbone Defect Repair – A Study in the Dog Mandible

Background: Platelet concentrate/platelet‐rich plasma (PRP) has been studied extensively in various experimental models and there is some agreement among workers to its early effect in bone regeneration and healing. We have earlier showed in vitro that titanium in whole blood activates the thrombogenic response to a higher degree than PRP and that a fluoridated test surface augmented the effect compared with control. Purpose: We designed this study to evaluate the effect of PRP and whole blood on bone regeneration in a dog implant defect model and, in addition, the effect of a test surface modified in hydrofluoric acid. A correlation attempt between platelet count, release of growth factors, and bone regeneration was made. Materials and Methods: Six dogs were used and simultaneously with the experimental surgery and implant installation, autologous PRP was prepared. Defects were prepared (6 mm in diameter and 5 mm deep), and implants were installed (TiO₂ gritblasted and hydrofluoric acid treated [test] or TiO₂ gritblasted [control], 5 mm in diameter and 9 mm long) in defects filled with either PRP or whole blood. Randomization of sides between PRP and whole blood, and sites for test and control implants were made. Blood samples were collected from PRP and whole blood. The dogs were killed after 5 weeks of healing, and samples with implants and surrounding bone were collected and processed for analysis. Enzyme linked immunosorbent assays were used for detection of growth factors in PRP. Results: The mean increase of platelet count was 424% in PRP. A correlation for platelet counts and transforming growth factor β was found in each dog (r² = 0.857). Approximately 50% of the region of interest (ROI) in the defects was filled with new bone after 5 weeks. No difference could be observed in ROI by using PRP or whole blood in the defects regarding new bone formation, bone in contact with implant, or distance to first bone contact. However, the fluoridated implants exhibited more new bone formation (p = .03) compared with control, regardless of comparing PRP or whole blood, and also displayed a shorter distance from first bone contact to the margin of the bone envelope (p = .05). Conclusions: Platelet concentrate/PRP failed to show more new bone regeneration in a peri‐implant defect model compared with whole blood. Implants treated with hydrofluoric acid displayed higher percentages of bone fill in the defect.     

Bone Graft Healing in Reconstruction of Maxillary Atrophy

Purpose: Evaluate correlations between volume change for iliac crest bone grafts in maxillary reconstruction (graft volume change [GVC]) and bone mineral density (BMD), bone volume fraction (BVF), hematologic bone metabolic factors (I), and identify indicators of implant failure (II). Material and Methods: Forty‐six consecutive patients had their edentulous atrophic maxilla reconstructed with free autogenous bone grafts from anterior iliac crest. Endosteal implants were placed 6 months after graft healing. Computer tomography was performed after 3 weeks and 6 months after grafting. Bone biopsies were taken from the internal table of donor site for calculation (BVF), and blood samples were collected. Implant stability was measured at placement with resonance frequency analysis and expressed as implant stability quotient (ISQ). Implant failure was registered. Results: GVC in onlay bone graft was 37%. The BVF in iliac crest biopsies was 32%. Serum‐IGFBP3 differed with 79% of the samples over normal range. Fifteen patients had one or more implant failures prior to loading (early failures). Forty‐two patients were followed for a minimum of 3 years after implant loading and, in addition, 6/42 patients had one or more implants removed during the follow‐up (late failures). GVC correlated to decreased BMD of lumbar vertebrae L2‐L4 (Kruskal–Wallis test, p = .017). No correlation was found between GVC and hematologic factors (Pearson correlation test) or between GVC and BVF (Kruskal–Wallis test). No correlation was found between ISQ and GVC (Pearson correlation test, p = .865). The association between implant failures and the described factors were evaluated, and no significant correlations were found (unconditional logistic regression). Conclusion: Onlay bone grafts decrease 37% during initial healing period, which correlate to BMD of lumbar vertebrae L2‐L4. No other evaluated parameters could explain GVC. The evaluated factors could not explain implant failure.     

牙周炎与慢性阻塞性肺疾病关系的流行病学研究

目的通过流行病学调查及临床检查,探讨牙周炎与慢性阻塞性肺疾病（COPD）之间的相关性。方法收集中国医科大学附属第一医院、盛京医院、第四医院和沈阳市第八人民医院2008年10月至2009年4月确诊为COPD的患者266例,其中稳定期COPD患者160例,急性加重期COPD（AE—COPD）患者106例,检查并记录所有患者6颗指数牙（61 6、6 16）的简化1：7腔卫生指数（OHI—S）、龈沟出血指数（SBI）、牙周探诊深度（PD）、临床附着丧失（CAL）,同时对所有患者进行肺功能指标的检查,并进行口腔问卷调查。结果（1）AE—COPD组的吸烟率为47．2％,明显高于稳定期COPD组（P〈0．01）;（2）AE—COPD组的SBI、PD及CAL明显高于稳定期COPD组（P〈0．01）;（3）AE—COPD组的OHI—S、SBI、PD及CAL均与FEVl％呈负相关（r分别为-0．309、-0．333、-0．395、-0．702,均P〈0．01）,其中CAL与FEVI％的相关性最强;稳定期COPD组CAL与FEVI％呈负相关（r=-0．657,P〈0．01）。结论（1）吸烟作为牙周炎和COPD的共同危险因素,在牙周炎和COPD的发生和发展中发挥重要作用;（2）AE—COPD患者的牙周炎症程度均随着肺功能的减弱而加重,提示牙周炎与COPD之间存在一定相关性。     

Essentials of cell physiology

Cell physiology and molecular genetics now provide the basis for the fundamental understanding of the mechanisms involved in normal and pathological physiology, modes of drug action, and risks involved in surgical procedures. Some explanations, often involving a single mutation in a protein are straightforward (e.g. cystic fibrosis transmembrane conductance regulator (CFTR) in cystic fibrosis). Others may involve a constellation of effects (e.g. obesity) and surprisingly there still remain important areas lacking comprehensive explanation (e.g. the mode of action of general anaesthetics) or close to resolution but still lacking detail (aldosterone controlling both K and Na regulation in the kidney). The present article presents a concise summary of regulation of cell function, concentrating on the cell membrane and important organelles. Signalling and second messengers, together with the role of membrane channels and transporters constitute an important aspect of this, mediated via kinases and phosphatases. Cell volume regulation, reflecting swelling and oedema, are an important aspect of organ transplantation and brain function.     

Autoantibody-mediated complement activation on platelets is a common finding in patients with immune thrombocytopenic purpura (ITP)

Background: It is commonly accepted that antibody‐mediated removal of platelets represents a major mechanism of platelet destruction in immune thrombocytopenic purpura (ITP). Although complement activation may participate in platelet clearance, frequency and specificity of complement activation have not yet been studied systematically in ITP. Patients and methods: We examined blood samples from 240 patients with ITP. Samples were assessed for the presence of free and bound platelet autoantibodies by a standard glycoprotein‐specific assay (monoclonal antibody‐specific immobilization of platelet antigens). The ability of all sera to fix complement to a panel of human platelets was investigated in a complement fixation (CF) assay. Fixation of C1q to isolated GP IIb/IIIa was assessed by flow cytometry. Results: Glycoprotein‐specific autoantibodies were detected as platelet‐bound antibodies in 129 (54%) and as additional free antibodies in 26 (11%) and were undetectable in 111 (46%) patients. Assessing these subgroups for CF, 103 (65%), 21 (81%), and 33 (30%) sera gave positive results. If GP IIb/IIIa was absent from the test platelets, 81 (67%) lost their ability to fix complement; if GP Ib/IX was absent, 37 (30%) lost their ability to fix complement. C1q fixation to immunobeads coated with GP IIb/IIIa was observed in 50% of sera containing anti‐GP IIb/IIIa antibodies. Conclusions: In a significant number of patients with chronic ITP, platelet autoantibodies are capable of activating the classical complement pathway. CF is even present in ITP sera without detectable autoantibodies, indicating that current techniques for autoantibody detection may be insufficient. The major targets for complement‐fixing autoantibodies in ITP are GP IIb/IIIa and GP Ib/IX.