DESPITE THE WIDESPREAD use of the periodontal probe as a diagnostic tool to measure the depth of periodontal pockets, there is surprisingly little information available on the exact location of the probe tip during routine measurements of clinical pocket depth. Although Orban et al. 1 believed that the probe tip is generally located at the coronal end of the epithelial attachment, Waerhaug 2 favored the view that the tip passes between the epithe lium and the tooth to a level which corresponds to the apical end of the junctional epithelium. The present investigation was carried out to determine the most common location of the periodontal probe tip during routine measurements of periodontal pocket depth. MATERIALS AND METHODSThe sample consisted of 31 teeth which were scheduled for extraction in the Oral Surgery Clinic of the Univer sity of Pennsylvania School of Dental Medicine. The reasons for extraction included advanced periodontal disease, orthodontic or prosthetic indications. With the exception of two mandibular molars, all specimens were single-rooted teeth. Periodontal pocket depth level was measured with a calibrated No. 28 Glickman periodontal probe on the mesial and distal surfaces from the cemento-enamel junction (CEJ) or a reference groove located in the general location of the CEJ if the latter could not be clearly located. The mesial pocket depth level measure ment was obtained by averaging the most approximal mesio-oral and mesio-vestibular probe readings. The distal pocket depth levels were obtained in a similar fashion by averaging the most approximal disto-oral and disto-vestibular probe readings. The teeth were extracted without the use of elevators along the approximal surfaces. After extraction, the periodontal probe readings were used to mark the estimated location of the apical extent of the probe tip on the tooth surface by means of a fine diamond cutting disc, using the CEJ or the groove at the estimated CEJ as a reference point. The tooth was then immediately fixed in 10% neutral buffered formalin for 48 hours and was sectioned in an oro-vestibular plane into a mesial and distal segment. After demineralization in a mixture of formic acid and sodium citrate, the tooth fragments were routinely embedded in paraffin and sectioned in a mesio-distal plane.Step-serial sections were collected at intervals of approximately 70 and were stained with eosin and hematoxylin. Sections were selected which demonstrated the presence of the apical reference mark (P) as well as the CEJ or the groove located in the vicinity of the CEJ. Other landmarks sought included the most apical extension of bacterial plaque adherent to the tooth surface (API), the most coronal extent of the cellular remains of the junctional epithelium (CJE) and the most coronal level of gingival connective tissue fibers inserted in cementum (CCT). If two or more of these landmarks could not be identified, the specimen was not included in the sample. For the purpose of this study it was assumed that the most coronal insertion of the co...

No abstract

No abstract

Diabetic nephropathy (DN) as a kind of serious microvascular complication of Diabetes Mellitus (DM) usually causes the end‐stage of renal disease (ESRD). Studies have demonstrated that CD103+ dendritic cells (DCs) exhibited a renal pathogenic effect in murine chronic kidney disease (CKD). Mesenchymal stem cells (MSCs) can alleviate DN and suppress the DCs maturation. To explore the role of CD103+ DCs and the potential mechanisms underlying MSCs‐mediated protective effects in DN, we used bone marrow MSCs (BM‐MSCs) to treat DN rats. MSCs transplantation considerably recovered kidney function and diminished renal injury, fibrosis and the population of renal CD103+ DCs in DN rat. The MSCs‐treated DN rats had decreased mRNA expression levels of interleukin (IL)1β, IL6, tumour necrosis factor alpha (TNF‐α), monocyte chemotactic protein 1 (MCP‐1) and reduced CD8 T cell infiltration in the kidney. MSCs significantly down‐regulated the genes expression of transcription factors (Basic leucine zipper transcriptional factor ATF‐like 3, Batf3 and DNA‐binding protein inhibitor ID‐2, Id2) and FMS‐like tyrosine kinase‐3 (Flt3) which are necessary for CD103+ DCs development. The protective effect of MSCs may be partly related to their immunosuppression of CD8+ T cell proliferation and activation mediated by CD103+ DCs in the kidney of DN rats.

Acute kidney injury (AKI) is a clinical condition that is associated with high morbidity and mortality. Inflammation is reported to play a key role in AKI. Although the M2 macrophages exhibit antimicrobial and anti‐inflammatory activities, their therapeutic potential has not been evaluated for AKI. This study aimed to investigate the protective effect of peritoneal M2 macrophage transplantation on AKI in mice. The macrophages were isolated from peritoneal dialysates of mice. The macrophages were induced to undergo M2 polarization using interleukin (IL)‐4/IL‐13. AKI was induced in mice by restoring the blood supply after bilateral renal artery occlusion for 30 minutes. The macrophages were injected into the renal cortex of mice. The changes in renal function, inflammation and tubular proliferation were measured. The M2 macrophages were co‐cultured with the mouse primary proximal tubular epithelial cells (PTECs) under hypoxia/reoxygenation conditions in vitro. The PTEC apoptosis and proliferation were analysed. The peritoneal M2 macrophages effectively alleviated the renal injury and inflammatory response in mice with ischaemia‐reperfusion injury (IRI) and promoted the PTEC proliferation in vivo and in vitro. These results indicated that the peritoneal M2 macrophages ameliorated AKI by decreasing inflammatory response and promoting PTEC proliferation. Hence, the peritoneal M2 macrophage transplantation can serve as a potential cell therapy for renal diseases.

No abstract

Nowadays, biodegradable nanoscale preparations such as liposomes, micelles, nanoparticles (NPs), and solid lipid nanoparticles (SLN) have attracted increasing attention from major researchers. Meanwhile the biosafety of the nanomaterials brings more and more attention. Toxicity of the biodegradable nanoscale preparations varies depending on their particle size, shape, surface structure, etc. This article aims to review the toxicity of the above-mentioned nanoscale preparations and the relative methodology. It may be significant for successful use of more nanoscale preparations in clinical practice.

No abstract