Mouse Anti Chicken Collagen type II Hybridoma [JJ-JJ7C4]

Objectives: To highlight conditions that may cause early-onset degenerative joint disease, and to assess the possible impact of such diseases upon everyday life. Material: Four adults aged under 50 years from a medieval skeletal collection of Prague (Czechia). Methods: Visual, osteometric, X-ray, and histological examinations, stable isotope analysis of bone collagen. Results: All four individuals showed multiple symmetrical degenerative changes, affecting the majority of joints of the postcranial skeleton. Associated dysplastic deformities were observed in all individuals, including bilateral hip dysplasia (n = 1), flattening of the femoral condyles (n = 3), and substantial deformation of the elbows (n = 3). The diet of the affected individuals differed from the contemporary population sample. Conclusions: We propose the diagnosis of a mild form of skeletal dysplasia in these four individuals, with multiple epiphyseal dysplasia or type-II collagenopathy linked to premature osteoarthritis as the most probable causes. Significance: Combining the skeletal findings with information from the medical literature, this paper defines several characteristic traits which may assist with the diagnosis of skeletal dysplasia in the archaeological record. Limitations: As no genetic analysis was performed to confirm the possible kinship of the individuals, it is not possible to definitively assess whether the individuals suffered from the same hereditary condition or from different forms of skeletal dysplasia. Suggestions for further research: Further studies on premature osteoarthritis in archaeological skeletal series are needed to correct the underrepresentation of these mild forms of dysplasia in past populations.

Objective: The application of adjunctive mediators in Autologous chondrocyte implantation (ACI) techniques might be useful for improving the dedifferentiated chondrocyte phenotype, to support neocartilage formation and inhibit post-traumatic cartilage destruction. In this study we examined if (a) interleukin 10 treatment can cause chondrogenic phenotype stabilization and matrix preservation in mechanically injured cartilage and if (b) IL-10 can promote chondrogenesis in a clinically applied collagen scaffold for ACI treatment. Materials and methods: For (a) bovine articular cartilage was harvested, subjected to an axial unconfined injury and treated with bovine IL-10 (1-10,000 pg/ng/ml). For (b) a post-operatively remaining ACI graft was treated with human IL-10. Expression levels of type I/II/X collagen, SOX9 and aggrecan were measured by qPCR (a, b). After 3 weeks cell death was analyzed (nuclear blebbing and TUNEL assay) and matrix composition was determined by GAG measurements and immunohistochemistry (aggrecan, type I/II collagen, hyaluronic acid). Statistics: One way ANOVA analysis with Bonferroni's correction. Results: (a) IL-10 stabilized the chondrogenic phenotype after injurious compression and preserved matrix integrity. This was indicated by elevated expression of chondrogenic markers COL2A1, ACAN, SOX9, while COL1A1 and COL10A1 were reduced. An increased GAG content paralleled this and histological staining of type 2 collagen, aggrecan and toluidine blue were enhanced after 3 weeks. (b) IL-10 [100 pg/ml] improved the chondrogenic differentiation of human chondrocytes, which was accompanied by cartilaginous matrix formation after 3 weeks of incubation. Conclusion: Interleukin-10 is a versatile adjuvant candidate to control the post-injurious environment in cartilage defects and promote chondrogenesis in ACI grafts. (C) 2017 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.