Glenoid component failure is the most common complication of total shoulder arthroplasty. Glenoid components fail as a result of their inability to replicate essential properties of the normal glenoid articular surface to achieve durable fixation to the underlying bone, to withstand repeated eccentric loads and glenohumeral translation, and to resist wear and deformation. The possibility of glenoid component failure should be considered whenever a total shoulder arthroplasty has an unsatisfactory result. High-quality radiographs made in the plane of the scapula and in the axillary projection are usually sufficient to evaluate the status of the glenoid component. Failures of prosthetic glenoid arthroplasty can be understood in terms of failure of the component itself, failure of seating, failure of fixation, failure of the glenoid bone, and failure to effectively manage eccentric loading. An understanding of these modes of failure leads to strategies to minimize complications related to prosthetic glenoid arthroplasty.

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Insulin treatment of mouse ATDC5 chondroprogenitors induces these cells to differentiate into mature chondrocytes. To identify novel factors that are involved in this process, we carried out mutagenesis of ATDC5 cells through retroviral insertion and isolated two mutant clones incapable of differentiation. Inverse PCR analysis of these clones revealed that the retroviral DNA was inserted into the promoter region of the Rab23 gene, resulting in increased Rab23 expression. To investigate whether an elevated level of Rab23 protein led to inhibition of chondrogenic differentiation, we characterized ATDC5 cells that either overexpress endogenous Rab23 or stably express ectopic Rab23. Our results revealed that up-regulation of Rab23 can indeed inhibit chondrogenic differentiation with a concomitant down-regulation of matrix genes such as type II collagen and aggrecan. In addition, stable small interfering RNA knockdown of Rab23 also resulted in inhibition of chondrogenic differentiation as well as down-regulation of Sox9, a master regulator of chondrogenesis. Interestingly, Sox9 expression has recently been linked to Gli1, and we found that Rab23 knockdown decreased Gli1 expression in chondrocytes. Because the phenotypes of Rab23 mutations in mice and humans include defects in cartilage and bone development, our study suggests that Rab23 is involved in the control of Sox9 expression via Gli1 protein.Chondrogenesis is a multi-step process that coordinately controls differentiation of mesenchymal cells into mature chondrocytes marked by expression of Type II collagen (Col2) and other extracellular matrix proteins. These mature cells could in turn become hypertrophic chondrocytes marked by expression of Type X collagen. Hypertrophic chondrocytes then undergo apoptosis, leaving behind a scaffold for invasion by osteoblasts/osteoclasts during endochondral ossification. Differentiation of chondrocytes is controlled by a signaling pathway involving Indian hedgehog and by transcription factors such as Sox9 (1).Chondrocyte differentiation can be mimicked in vitro by insulin treatment of the murine chondroprogenitor cell line ATDC5 (2). When cultured in insulin-containing medium over a period of 3-4 weeks, ATDC5 cells will condense to form nodules, and cells in these nodules will eventually differentiate into mature chondrocytes to produce a cartilage-like extracellular matrix that can be stained with Alcian blue. After prolonged culture in insulin medium, mature ATDC5 chondrocytes will enter into the hypertrophic phase characterized by the synthesis of Type X collagen and eventually die by apoptosis.Utilizing these properties of ATDC5 cells, we carried out a large scale screening of random retroviral insertions to identify novel regulators of chondrocyte differentiation. By random integration of a retroviral vector into the genome of ATDC5 cells, genes that are critical to chondrogenesis could potentially be disrupted or conversely activated. Alterations of these genes will lead to either spontaneous differentiation of ATDC5 c...

Temperatures sufficient to induce thermal necrosis of glenoid bone can be generated by glenoid preparation in shoulder arthroplasty in vivo. Frequent irrigation may be effective in preventing temperatures from reaching the threshold for bone necrosis during glenoid preparation.