BACKGROUND: Objective, reliable and easy screening for peripheral artery disease (PAD) is essential to confirm the diagnosis and initiate the respective treatment. Therefore, a new non-invasive hyperspectral camera (TIVITA ® Tissue) was tested in pat

Background: Periodontitis is a bacterial inflammatory disease leading to attachment loss with the consequence of tooth loss. There exists a multifactorial risk pattern including bacterial challenge, age, smoking, diabetes mellitus, as well as socioeconomic and genetic factors. An interleukin (IL)‐1 haplotype is associated with periodontitis. We report the relationship between type 2 diabetes, the IL‐1A/1B haplotype, and periodontitis in a population‐based study.Methods: In a cross‐sectional health survey in northeast Germany, we genotyped 1,515 subjects aged 40 to 60 years for the IL‐1 genotype, examined their periodontal status, and assessed diabetes, including the history of diagnosed diabetes, the use of antidiabetic medications, and hemoglobin A_1c (HbA_1c) measures.Results: Subjects with increased levels of HbA_1c had more widespread and severe periodontal disease than normoglycemic subjects. There is a gene–environmental interaction because diabetic subjects bearing a variant IL‐1 genotype C/T or T/T had an enhanced risk for periodontal disease in comparison with their IL‐1 wild‐type counterparts. Bleeding on probing (P = 0.007), attachment loss (P = 0.009), and number of teeth (P <0.001) were associated significantly with diabetes and the IL‐1 genotype. Logistic regression and a matched‐pair analysis confirmed these results.Conclusion: Subjects with type 2 diabetes have an increased risk for periodontitis, which is aggravated further if combined with the variant IL‐1A/1B genotype.

Polyetheretherketone (PEEK) has the potential to overcome some of the disadvantages of titanium interbody implants in anterior cervical and discectomy and fusion (ACDF). However, PEEK shows an inferior biological behavior regarding osseointegration and bioactivity. Therefore, the aim of the study was to create a bioactive surface coating on PEEK implants with a unique nanopore structure enabling the generation of a long-lasting interfacial composite layer between coating material and implant. Seventy-two PEEK implants—each thirty-six pure PEEK implants (PI) and thirty-six PEEK implants with a sprayed coating consisting of nanocrystalline hydroxyapatite (ncHA) embedded in a silica matrix and interfacial composite layer (SPI)—were inserted in the femoral condyles of adult rats using a split-side model. After 2, 4 and 8 weeks, the femur bones were harvested. Half of the femur bones were used in histological and histomorphometrical analyses. Additionally, pull-out tests were performed in the second half. Postoperative healing was uneventful for all animals, and no postoperative complications were observed. Considerable crestal and medullary bone remodeling could be found around all implants, with faster bone formation around the SPI and fewer regions with fibrous tissue barriers between implant and bone. Histomorphometrical analyses showed a higher bone to implant contact (BIC) in SPI after 4 and 8 weeks (p < 0.05). Pull-out tests revealed higher pull-out forces in SPI at all time points (p < 0.01). The presented findings demonstrate that a combination of a bioactive coating and the permanent chemical and structural modified interfacial composite layer can improve bone formation at the implant surface by creating a sustainable bone-implant interface. This might be a promising way to overcome the bioinert surface property of PEEK-based implants.

Chemical and physical processing of allografts is associated with a significant reduction in biomechanics. Therefore, treatment of tissue with high hydrostatic pressure (HHP) offers the possibility to devitalize tissue gently without changing biomechanical properties. To obtain an initial assessment of the effectiveness of HHP treatment, human osteoblasts and chondrocytes were treated with different HHPs (100–150 MPa, 250–300 MPa, 450–500 MPa). Devitalization efficiency was determined by analyzing the metabolic activity via WST-1(water-soluble tetrazolium salt) assay. The type of cell death was detected with an apoptosis/necrosis ELISA (enzyme-linked immune sorbent assay) and flow cytometry. Field emission scanning electron microscopy (FESEM) and transmission electron microscopy (TEM) were carried out to detect the degree of cell destruction. After HHP treatment, the metabolic activities of both cell types decreased, whereas HHP of 250 MPa and higher resulted in metabolic inactivation. Further, the highest HHP range induced mostly necrosis while the lower HHP ranges induced apoptosis and necrosis equally. FESEM and TEM analyses of treated osteoblasts revealed pressure-dependent cell damage. In the present study, it could be proven that a pressure range of 250–300 MPa can be used for cell devitalization. However, in order to treat bone and cartilage tissue gently with HHP, the results of our cell experiments must be verified for tissue samples in future studies.