#  Francesca Gori 

Associate Professor of Oral Medicine, Infection, and Immunity

 

 

 



   ![gori_francesca.jpeg](/sites/g/files/omnuum5321/files/styles/hwp_4_5__480x600/public/bbsphd/files/gori_francesca.jpeg?itok=FJtZQVCQ) 

 



 

 location\_on Harvard School of Dental MedicineREB 307188 Longwood AvenueBoston, MA 02115 

 email [francesca\_gori@hsdm.harvard.edu](mailto:francesca_gori@hsdm.harvard.edu) 

 laptop\_windows [Lab Website](https://hsdm.harvard.edu/people/francesca-gori) 

 laptop\_windows [Additional Lab Website](https://hsdm.harvard.edu/baron-laboratory) 

 laptop\_windows [Publications](https://www.ncbi.nlm.nih.gov/myncbi/1T9O9vifjir5P/bibliography/public/) 

 

 



 

My longstanding interest is to study the molecular, cellular and genetic basis underlying cell fate and differentiation. My research focuses on the exploration of the skeleton, a “dynamic” tissue where cell interactions and crosstalk are numerous, complex and puzzling. In particular I am interested in the identification and characterization of genes that regulate bone development and homeostasis in health and disease with emphasis on the mechanisms by which Wnt signaling regulates these processes. Wnt signaling is one of the most important developmental signaling pathways that controls cell fate decisions and tissue homeostasis. Not surprisingly, the last decade has provided abundant data implicating the Wnt pathway in bone development and in the regulation of bone mass. Indeed, rare human mutations together with gain- and loss-of- function approaches in mice, have clearly demonstrated that flaws in this pathway lead to altered bone development and mass. Work from our lab, including the work on the role of Wnt16 in skeletal homeostasis is of great interest, in that it established that trabecular and cortical bone are differentially regulated. In addition, our recent work on Sfrp4, a WNT signaling inhibitor, and skeletal homeostasis strengthen the hypothesis of a differential regulation of these two bone compartments by Wnt signaling. In this context, our recent studies have established that loss of function mutations of SFRP4 lead to Pyle’s disease (OMIM 265900), a rare skeletal disease characterized by limb deformity and fragility fractures and several oral/dental manifestations. Ongoing studies on the role of WNT signaling in skeletal homeostasis and bone regeneration are one of the current focus of the lab. In the last few years, I have developed a line of research, focused to define the role of Sfrp4, on the periosteal surface of cortical bone. The periosteum plays a critical role in cortical bone expansion and homeostasis, has regenerative capabilities and responds to anabolic drugs. However, in spite of its clinical significance our basic understanding of periosteal cellular characteristics, local or paracrine regulatory factors as well as the specific mechanisms by which anabolic drugs regulate it, remain elusive. We hypothesize that Sfrp4 expressed in a discreet pool of periosteal progenitors influences periosteal stem/progenitor cell activities in cortical bone and contributes to their bone regenerative potential and to their response to anabolic drugs. With these studies, I hope to gain a greater understanding of the mechanism underlying cortical biology and therefore human diseases associated with cortical bone fragility, bone healing and regeneration.  
  
In addition, we have ongoing studies on the role of WNT signaling in craniofacial development and tooth development. Oral diseases constitute a major public health issue. There is an increasing need to understand the molecular mechanisms driving tooth formation, development and renewal. In mice, incisors grow continuously through a process depending on a pool of epithelial stem cells, the precursor of enamel-secreting ameloblasts, and mesenchymal stem cells, odontoblast progenitors. Thus, the mouse incisor provide a great model for stem cells study. We are currently exploring the role of Sfrp4 in tooth development, matrix deposition and mineralization. Our working hypothesis is that Sfrp4 influences tooth development and dental mineralized tissues by regulating dental pulp niche interactions and mesenchymal cell differentiation, and activities. The understanding gained from these studies will serve as the foundation for future studies in the local regulation of adult stem cells, tissue homeostasis and repair.



 

 

 





 

 

- ## People
    
     [Faculty](/people/faculty)
- ## Location
    
     [Harvard School of Dental Medicine](/location/harvard-school-dental-medicine)