Anne-Christine Bay-Jensen

TL;DR: This review of several ambitious but failed attempts to develop joint structure-modifying treatments for OA suggests that these failures arose from unrealistic hypotheses, sub-optimal selection of patient populations or drug dose, and/or inadequate sensitivity of the trial endpoints.

TL;DR: This review discusses the structural components of the matrix and the relevance of their mutations to the pathology of diseases such as fibrosis and cancer, and introduces the possibility that post-translational modifications (PTMs), such as protease cleavage, citrullination, cross-linking, nitrosylation, glycosylation, and isomerization, generated during pathology, may be unique, disease-specific biochemical markers.

TL;DR: The aims of this review are to explore key structural and functional components of the ECM as exemplified by monogenetic disorders leading to severe pathologies, and discuss selected pathological posttranslational modifications of ECM proteins resulting in altered functional (signaling) properties from the original structural proteins.

TL;DR: Known bone therapies, namely oestrogens, selective oestrogen receptor modifiers (SERMs), bisphosphonates, strontium ranelate, calcitonin and parathyroid hormone, might prove useful for treating two critical tissue components of the OA joint, the bone and the cartilage.

TL;DR: The generation and release of fragmented molecules could generate novel biochemical markers with the capacity to monitor disease progression, facilitate drug development and add to the existing toolbox for in vitro studies, preclinical research and clinical trials.