Faculty Bibliography

There are several options available for management of the middle-aged arthritic knee. Arthroscopic techniques continue to evolve, but the true natural history of the arthritic process is probably not altered. Good to excellent short-term results can be expected with proper patient selection. Patient counseling is important in order to discuss the nature of the underlying disease process, the limited goals of the arthroscopic procedure, and the possible need for further surgery. Proximal tibial osteotomy for the treatment of medial compartment osteoarthritis can be effective for as long as 15 years. There is a deterioration of results over time that can often be correlated to the degree of correction achieved. Strict selection criteria can maximize success. Revision surgery to total knee replacement, albeit technically difficult, is a viable option with results similar to primary TKR. Unicompartmental knee arthroplasty remains a controversial procedure as its indications continue to evolve. Good to excellent results can be expected in 80% to 90% of patients at 10 years follow-up. Unicompartmental knee arthroplasty occupies a special niche in the treatment of unicompartmental osteoarthritis and supplements total knee replacement and high tibial osteotomy surgery

Hemangioma is the most common soft-tissue tumor of infancy. Despite the frequency of these vascular tumors, the origin of hemangioma-endothelial cells is unknown. Circulating endothelial progenitor cells (EPCs) have recently been identified as vascular stem cells with the capacity to contribute to postnatal vascular development. We have attempted to determine whether circulating EPCs are increased in hemangioma patients and thereby provide insight into the role of EPCs in hemangioma growth. METHODS AND RESULTS: Peripheral blood mononuclear cells (PBMCs) were isolated from hemangioma patients undergoing surgical resection (N = 5) and from age-matched controls (N = 5) undergoing strabismus correction surgery. PBMCs were stained with fluorescent-labeled antibodies for AC133, CD34, and VEGFR2/KDR. Fluorescent-labeled isotype antibodies served as negative controls. Histologic sections of surgical specimens were stained with the specific hemangioma markers Glut1, CD32, and merosin, to confirm the diagnosis of common hemangioma of infancy. EPCs harvested from healthy adult volunteers were stained with Glut1, CD32, and merosin, to assess whether cultured EPCs express known hemangioma markers. Hemangioma patients had a 15-fold increase in the number of circulating CD34 AC133 dual-staining cells relative to controls (0.78+/-0.14% vs.0.052+/-0.017%, respectively). Similarly, the number of PBMCs that stained positively for both CD34 and KDR was also increased in hemangioma patients (0.49+/-0.074% vs. 0.19+/-0.041% in controls). Cultured EPCs stained positively for the known hemangioma markers Glut1, CD32, merosin. CONCLUSIONS: This is the first study to suggest a role for EPCs in the pathogenesis of hemangioma. Our results imply that increased levels of circulating EPCs may contribute to the formation of this vascular tumor

TGFss signals belonging to the Nodal family set up the embryonic axes, induce mesoderm and endoderm, pattern the nervous system, and determine left-right asymmetry in vertebrates. Nodal signaling activates a canonical TGFss pathway involving activin receptors, Smad2 transcription factors, and FoxH1 coactivators. In addition, Nodal signaling is dependent on coreceptors of the EGF-CFC family and antagonized by the Lefty and Cerberus families of secreted factors. Additional modulators of Nodal signaling include convertases that regulate the generation of the mature signal, and factors such as Arkadia and DRAP1 that regulate the cellular responses to the signal. Complex regulatory cascades and autoregulatory loops coordinate Nodal signaling during early development. Nodals have concentration-dependent roles and can act both locally and at a distance. These studies demonstrate that Nodal signaling is modulated at almost every level to precisely orchestrate tissue patterning during vertebrate embryogenesis

Purpose of review: Osteoarthritis is the most common form of arthritis, affecting a large population of mostly elderly people. No cure for osteoarthritis currently exists. Ultimate treatment is joint replacement. Understanding the mechanisms causing onset and progression is critical. This review describes recent findings that provide new insights into changes of cellular phenotype in osteoarthritis as a possible reason for tissue failure. Recent findings: Recent findings suggest that articular chondrocytes, when stimulated, can undergo hypertrophic and terminal differentiation events similar to those occurring during endochondral bone formation. Interestingly, collagenase-3 (matrix metalloproteinase-13), a main matrix-degrading enzyme in osteoarthritis, is expressed only in terminally differentiated chondrocytes during normal development. Summary: Although terminal differentiation events are required for endochondral bone formation, they lead to cartilage destruction when occurring in articular chondrocytes. Maintaining the articular chondrocyte phenotype and preventing these cells from undergoing hypertrophic and terminal differentiation might provide novel therapeutic targets to prevent onset or progression of osteoarthritis