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The research in the Everett lab is focused on understanding the genes
that play key roles during embryonic and postnatal development of craniofacial/oral/dental
structures. They are interested in how these genes contribute to congenital
and acquired disorders of craniofacial development as well as normal variation.
Two major ongoing projects include: Non-syndromic cleft palate-
During the morphogenesis of the secondary palate (palatogenesis), bilateral
extensions of the maxillary processes reorient from a vertical to horizontal
position where epithelial transformation and remodeling of the extracellular
matrix result in palatal fusion. Perturbations of this complex cascade
of events can lead to cleft palate. Using mouse models of autosomal
recessive non-syndromic cleft palate, our ultimate goal is to identify
and validate candidate and modifier genes that lead to cleft palate
in mice and to determine the normal roles of these genes in the complex
network of events of palatogenesis. Evolutionary conservation of this
morphogenetic process between mice and humans will allow identification
of human genes that contribute to an individual’s susceptibility
to develop cleft palate. This will provide insight into gene-gene and
gene-environment interactions required for palatogenesis. Dental fluorosis-
For more than half a century, fluoridated drinking water has benefited
public health by protecting against tooth decay. Recognized by the Centers
for Disease Control and Prevention as one of the top 10 public health
measures ever initiated, fluoridation has contributed to a decline in
tooth decay in North Carolina and elsewhere in the United States over
the last 25 years. Concurrent with the decline in tooth decay has been
an increase in dental fluorosis, a developmental condition of tooth
enamel. A strong correlation has been repeatedly demonstrated between
the amount of fluoride consumed and the incidence of dental fluorosis.
Only recently have we begun to appreciate how an individual’s
genetic background influences fluorosis susceptibility and resistance.
In addition to the environmental component, genetic determinants that
play a role in enamel formation also influence fluorosis susceptibility
or resistance. A gap of knowledge exists in understanding the molecular
mechanisms of fluoride action on tooth and bone development. Using inbred
strains of mice, the Everett lab has embarked on quantitative trait
locus (QTL) mapping as a means to identify fluorosis susceptibility
and resistance genes. Selected Publications:
Mousny M, Banse X, Wise L, Everett ET, Hancock R, Vieth R, Devogelaer JP, Grynpas MD. (2006) The genetic influence on bone susceptibility to fluoride. Bone. 39:1283-9.
Al-Qawasmi RA, Hartsfield JK Jr, Everett ET, Weaver MR, Foroud TM, Faust DM, Roberts WE. (2006) Root resorption associated with orthodontic force in inbred mice: genetic contributions. Eur J Orthod. 28:13-9.
Kubota K, Lee DH, Tsuchiya M, Young CS, Everett ET, Martinez-Mier
EA, Snead ML, Nguyen L, Urano F, Bartlett JD. (2005) Fluoride
induces endoplasmic reticulum stress in ameloblasts responsible
for
dental enamel formation. J Biol Chem 280:23194-202.
Yu
X, Chen S, Potter OL, Murthy SM, Li J, Pulcini JM, Ohashi N,
Winata T, Everett ET, Ingram D, Clapp WD, Hock JM.(2005)
Neurofibromin and its inactivation of Ras are prerequisites for
osteoblast functioning. Bone 36:793-802.
Vieira
AP, Hancock R, Eggertsson H, Everett ET and Grynpas MD (2004)
Tooth quality in dental fluorosis: genetic and environmental factors.
Calcif Tissue Int 76:17-25.
Hartsfield JK Jr, Everett ET, and Al-Qawasmi RA (2004) Genetic factors
in external apical root resorption and orthodontic treatment. Crit
Rev Oral Biol Med 15:115-122.
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