Continuation: Fracture healing
is a highly specialized type of wound repair that involves a complex
array of both cellular and molecular events. These events involve
a host of different cell types (e.g. blood cells, fibroblasts, epithelial,
chondroblasts, osteoblasts, osteoblasts, etc.) and molecules (e.g.
matrix proteins, growth factors' etc.) that ultimately restore the
bone to its original structural and functional integrity. Considering
the complexity of the healing process, marked predominantly by cellular
adhesion, migration, proliferation, and differentiation, it is only
reasonable to expect hundreds, if not thousands' of molecules to
be present and to play significant roles at the appropriate time
and place. The presence of all the different molecules undoubtedly
reflects a robust modulation of gene expression achieved by the
different cells types found within the fracture callus. We believe
that differential gene expression underlies the essence of the bone
repair process, and therefore identifying fracture repair-specific
genes (both novel and known) will unveil the clinical key to accelerate
the healing of fractures. During our past funding periods (1997-1999),
we have identified and isolated a large number of differentially
expressed genes (cDNAs) from fracture calluses, many of which are
novel. The goal of the proposed study is to further characterize
two novel genes at the molecular level and determine their functional
significance during normal bone development and fracture healing.
This work will continue to contribute to our understanding of the
molecular mechanisms involved in the healing process and enhance
our ability to treat fractures. |
