| We're investigating why
cleft lip and palate develops in the first place by studying a set of
"master control genes" called homeobox genes, which are felt
to control how all of our bodies are formed. We have identified two
strains of mice with cleft lip and palate called AJ and Twirler, which
we hope will help us to unravel this mystery. The AJ mouse is
genetically predisposed to having a cleft lip and palate. So much so
that the addition of a teratogen like prednisone or Dilantin to a
pregnant mother causes all the offspring to be born with a cleft.
Twirler mice all develop cleft lip and palate spontaneously. We hope
to use these two models to identify differences seen in animals, which
cleft spontaneously vs. those that require the presence of a teratogen
to get a cleft phenotype. Once commonalties are identified, research
can be conducted to develop in utero gene therapies for the treatment
of this problem.
We are also looking at ways to decrease
the amount of scar seen following cleft repair. Lip scars are a
constant reminder that a patient had a cleft at birth. Their presence
can detract from facial appearance and in many ways hamper a patient's
psychologic development. Scar along the palate also can restrict
maxillary growth. In severe cases, this causes the cleft patient to
undergo jaw surgery in order to have a normal dental relationship and
bite.
Dr. Stelnicki has funding from the
National Institute of Health to develop new strategies of inducing
scarless wound repair. His research involves the manipulation of
several DNA transcription factors present in cells at the wound site
during fetal wound repair. The mammalian fetus is unique in that it is
able to heal its injures without scar, in a process more akin to
tissue regeneration than classic wound repair. It is our belief that
the precise manipulations of various DNA regulating factors will allow
us to replicate this process in newborn infants and adults. |
