Assistant Professor of Orthopaedic SurgeryDr. Caycedo has two areas of investigation, the first is to study the tendon bone interface with regard to avulsion and the second to analyze extracellular matrix molecules in the fracture calcaneus in experimentally induced diabetes and their implication to non-unions.
- Tissue Modulation Due to Injury at the Tendon-Bone Interface: Experiments are under way to study the attachment of the chilles tendon to the calcaneus. The goal is to utilize histology, immunohistology and quantitative rt-PCR to lean about the appearance of Type II and Type X collagens as they are involved in tendon reattachment to bone, and the effect of growth factors on the junctional tissue. The overall hypothesis is that the repair mechanism for tendon-bone attachment has features which are similar to endochondral ossification and some features similar to periosteal new bone formation. The experiments will investigate matrix producing cells in the reparative shase of tendon attachment, similar to fracture calllus, and tendon and fibrocartilage stimulation with growth factors.
- Analysis of Extracellular Matrix Collagens in Fracture Non-Unions: Changes in collagen expression have been noted in fractures that were created and analyzed in streptozotocin-induced diabetes. Type II collagen produces a fibrous matrix and Type X collagen, while being associated with Type II collagen fibers, is involved in a lattice that is thought to support the enlarged cellular structures which are known as hypotrophic chondrocytes. Chondrocyte size increases between 4-and 10-fold during the process of hypertrophy and matrix mineralization, and decreased Type X collagen would be detrimental to the adequacy of support that is normally provided by the transient cartilaginous matrix which exists in fracture healing. The hypothesis is that non-union of fractures is a disease-like state in which there is deficient production of matrix.
Selected Publications:
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