Periodontal diseases – research group

Periodontal diseases are the most common infectious diseases amongst humans. In these diseases inflammation of the tooth supporting tissues (periodontium) is gradually destroying the attachment of tooth to the jaw bone.  Our research aims at finding out the pathological mechanism of these diseases. The main aim of our studies is on bacterial-host cell interactions which is the initial phase of the periodontal disease process. We culture epithelial cells in the presence of periodontopathogenic bacteria or their isolated products and measure the activity of the infected cells. We measure invasion of bacteria to epithelial cells, epithelial cell proliferation, cell migration, production of matrix metalloproteinases and cell viability of the infected cells. We also examine the cell signaling involved in these changes. A novel biofilm-organotypic tissue culture system is employed in these studies.

Another project deals with the role of leukocyte defensins in the epithelial defence against oral bacteria. 

In a third project we examine the relationship of oral health and gelsolin-related familial amyloidosis. The incidence and type of periodontitis are analysed and compared with the values in the general population. We observed that many of the amyloidosis patients have diminished salivary secretion and some had an aggressive type of periodontitis. We are currently trying to determine the pathogenic mechanisms behind these manifestations. 

Members of the group

Ulvi Gursoy, Pirjo Juusela, Laura Lakio, Minna-Maija Ahonen, Veli-Jukka Uitto

Figure. A periodontopathogenic bacterial species Fusobacterium nucleatum is stimulating epithelial cells to produce a destructive enzyme, collagenase, in cultured epithelial cells. Immunohistological staining using two antibodies (Uitto et al. Infect Immun 2006;73:1171).

Six recent references

Zhang L, Heino J, Uitto V-J. ”Bacterial heat shock protein 60 may increase epithelial cell migration through activation of MAP kinases and inhibition of a6β4 integrin expression.” Biochem Biophys Res Commun 2004;319:1088–1095. 

Zhang L, Pelech S, Uitto V-J. ”Bacterial GroEL-like heat shock protein 60 protects epithelial cells from stress-induced death through activation of ERK and inhibition of caspase-3.” Exp Cell Res 2004;292:231–240.

Uitto V-J, Baillie D, Wu Q, Gendron R, Grenier D, Putnins E, Kanervo A, Firth J D. ’Fusobacterium nucleatum increases collagenase-3 production and migration of epithelial cells.’ Infect Immun 2006;73:1171-1179.   

Firth JD, Uitto VJ, Putnins EE. Mechanical induction of an epithelial cell chymase associated with wound edge migration. J Biol Chem. 2008; 283:34983-34993.

Gursoy UK, Könönen E, Uitto VJ. Intracellular replication of fusobacteria requires new actin filament formation of epithelial cells. APMIS. 2008; 116:1063-1070.

Gursoy UK, Könönen E, Uitto VJ. Stimulation of epithelial cell matrix metalloproteinase (MMP-2, -9, -13) and interleukin-8 secretion by fusobacteria. Oral Microbiol Immunol. 2008; 23:432-434.

Contact

Veli-Jukka Uitto, D.D.S., Ph.D.
Professor of Oral Biology, Institute of Dentistry, and Chief Dental Officer, Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital

E-mail: jukka.uitto(at)helsinki.fi