Biomaterials for promoting periodontal regeneration in human intrabony defects: a systematic review

Intrabony periodontal defects are a frequent complication of periodontitis and, if left untreated, may negatively affect long‐term tooth prognosis. The optimal outcome of treatment in intrabony defects is considered to be the absence of bleeding on probing, the presence of shallow pockets associated with periodontal regeneration (i.e. formation of new root cementum with functionally orientated inserting periodontal ligament fibers connected to new alveolar bone) and no soft‐tissue recession. A plethora of different surgical techniques, often including implantation of various types of bone graft and/or bone substitutes, root surface demineralization, guided tissue regeneration, growth and differentiation factors, enamel matrix proteins or various combinations thereof, have been employed to achieve periodontal regeneration. Despite positive observations in animal models and successful outcomes reported for many of the available regenerative techniques and materials in patients, including histologic reports, robust information on the degree to which reported clinical improvements reflect true periodontal regeneration does not exist. Thus, the aim of this review was to summarize, in a systematic manner, the available histologic evidence on the effect of reconstructive periodontal surgery using various types of biomaterials to enhance periodontal wound healing/regeneration in human intrabony defects. In addition, the inherent problems associated with performing human histologic studies and in interpreting the results, as well as certain ethical considerations, are discussed. The results of the present systematic review indicate that periodontal regeneration in human intrabony defects can be achieved to a variable extent using a range of methods and materials. Periodontal regeneration has been observed following the use of a variety of bone grafts and substitutes, guided tissue regeneration, biological factors and combinations thereof. Combination approaches appear to provide the best outcomes, whilst implantation of alloplastic material alone demonstrated limited, to no, periodontal regeneration.     

Increase in Skin Autofluorescence and Release of Heart‐Type Fatty Acid Binding Protein in Plasma Predicts Mortality of Hemodialysis Patients

Advanced glycation end‐products (AGEs) are uremic toxins that accumulate progressively in hemodialysis (HD) patients. The aim of this study was to assess the 1‐year increase in skin autofluorescence (ΔAF), a measure of AGEs accumulation and plasma markers, as predictors of mortality in HD patients. One hundred sixty‐nine HD patients were enrolled in this study. Skin autofluorescence was measured twice, 1 year apart using an AGE Reader (DiagnOptics Technologies BV, Groningen, The Netherlands). Besides routine blood chemistry, additional plasma markers including superoxide dismutase, myeloperoxydase, intercellular adhesion molecule 1 (ICAM‐1), C‐reactive protein (hs‐CRP), heart‐type fatty acid binding protein (H‐FABP), and von Willebrand factor were measured at baseline. The mortality of HD patients was followed for 36 months. Skin autofluorescence values of the HD patients at the two time points were significantly higher (P < 0.001) than those of healthy subjects of the same age. Mean 1‐year ΔAF of HD patients was 0.16 ± 0.06, which was around seven‐ to ninefold higher than 1‐year ΔAF in healthy subjects. Multivariate Cox regression showed that age, hypertension, 1‐year ΔAF, hs‐CRP, ICAM‐1, and H‐FABP were independent predictors of overall mortality. Hypertension, 1‐year ΔAF, hs‐CRP, and H‐FABP were also independent predictors of cardiovascular mortality. One‐year ΔAF and plasma H‐FABP, used separately and in combination, are strong predictors of overall and cardiovascular mortality in HD patients.     

Warren shunt combined with partial splenectomy for children with extrahepatic portal hypertension, massive splenomegaly, and severe hypersplenism

Purpose

To establish the importance of shunt surgery combined with partial resection of the spleen for selected pediatric patients with extra-hepatic portal vein obstruction (EHPVO), enormous splenomegaly and severe hypersplenism. Severe hypersplenism is often refractory to treatment with endoscopic sclerotherapy or band ligation and shunt surgery; however, to our knowledge, this is the first such study to be published.

Methods

Distal splenorenal shunt with partial resection of the spleen was performed in 16 of 60 children treated for EHPVO in the Gastroenterology Department of our hospital. Upper gastrointestinal endoscopy had shown esophageal varices of varying grade in all patients and band ligation or endoscopic sclerotherapy had been done for children with a history of bleeding. The indications for surgery were pain and discomfort caused by a large spleen (5–15 cm below the costal margin) and symptomatic hypersplenism with leucopenia, thrombocytopenia, and anemia. Partial resection of the spleen was performed, starting with ligation of the branches and tributaries of the caudal two-thirds. When an ischemic line demarcated the splenic parenchyma, it was transected using electrocautery or LigaSure, leaving 20–30 % of splenic tissue. After the spleen resection, a Warren shunt was performed. Platelet and white blood cell counts and liver function tests were performed before and after the operation. Growth was assessed using SD scores (z scores) for height, weight, and body mass index at the time of surgery and 1 year later.

Results

Postoperative recovery was uneventful and the leukocyte and platelet counts normalized. The shunt patency rate was 100 %. Two cases of shunt stenosis were treated successfully with percutaneous angioplasty. There was no postoperative mortality. During the follow-up period, from 1 to 7 years, all 16 children were asymptomatic, with improved quality of life, growth, and nutrition. No episodes of variceal bleeding, sepsis or encephalopathy occurred.

Conclusion

Our results demonstrate that shunt surgery with partial resection of the spleen is effective and safe for pediatric patients with massive splenomegaly and severe hypersplenism secondary to EHPVO.     

Human class I major histocompatibility complex alleles determine central nervous system injury versus repair

Background

We investigated the role of human HLA class I molecules in persistent central nervous system (CNS) injury versus repair following virus infection of the CNS.

Methods

Human class I A11⁺ and B27⁺ transgenic human beta-2 microglobulin positive (Hβ2m⁺) mice of the H-2 ^b background were generated on a combined class I-deficient (mouse beta-2 microglobulin deficient, β2m⁰) and class II-deficient (mouse Aβ⁰) phenotype. Intracranial infection with Theiler’s murine encephalomyelitis virus (TMEV) in susceptible SJL mice results in acute encephalitis with prominent injury in the hippocampus, striatum, and cortex.

Results

Following infection with TMEV, a picornavirus, the Aβ⁰.β2m⁰ mice lacking active immune responses died within 18 to 21 days post-infection. These mice showed severe encephalomyelitis due to rapid replication of the viral genome. In contrast, transgenic Hβ2m mice with insertion of a single human class I MHC gene in the absence of human or mouse class II survived the acute infection. Both A11⁺ and B27⁺ mice significantly controlled virus RNA expression by 45 days and did not develop late-onset spinal cord demyelination. By 45 days post-infection (DPI), B27⁺ transgenic mice showed almost complete repair of the virus-induced brain injury, but A11⁺ mice conversely showed persistent severe hippocampal and cortical injury.

Conclusions

The findings support the hypothesis that the expression of a single human class I MHC molecule, independent of persistent virus infection, influences the extent of sub frequent chronic neuronal injury or repair in the absence of a class II MHC immune response.