Runx2 expression is associated with pathologic new bone formation around radicular cysts: an immunohistochemical demonstration.
BACKGROUND
Radicular cysts are the most common cysts in human jaw bones. These lesions induce bone remodeling of the surrounding alveolar bones, which was termed 'condensing osteitis', and was suggested to be related to cells of the osteoblastic lineage. The Runx2 (core-binding protein [cbfa]1/polyoma enhancer-binding protein [pebp]2alphaA) was shown to be a DNA-binding transcriptional molecule expressed in osteoprogenitor cells.


METHODS
We confirmed the specificity of anti-Runx2 antiserum, using Western blotting analysis. We investigated the expression and localization of Runx2 in 32 radicular cyst cases with bone tissue fragments, immunohistochemically.


RESULTS
Signals for Runx2 were seen in 18 cases (56.3%) of radicular cysts with bone formation. These signals were immunolocalized in the nuclei of the spindle-shaped osteoprogenitor cells in the cyst walls, whereas only a few signals were seen in the cuboidal osteoblastic cells near the fibrous bones. Signals for type I collagen were immunolocalized in the dense collagen fibers in the cyst walls and in the matrix of the fibrous bone around the radicular cysts, whereas no signals were seen on the inner portions with inflammatory cell infiltration of the cyst walls. Very weak signals for transforming growth factor (TGF)-beta1 were infrequently seen in the osteoblasts of the fibrous bone, whereas signals for TGF-beta2 were observed in young osteocytes in the fibrous bones, in B-cell lymphocytes infiltrating into the inner portions, and on the cellular membranes of the lining epithelium.


CONCLUSIONS
The nuclear expression of Runx2 in spindle-shaped cells in the outer portions may play an essential role in the induction of fibrous bone tissue around radicular cysts. TGF-beta2 may play a role in the production of type I collagen, which acts as a template for pathologic new bone formation, in radicular cysts.
Kusafuka
Kimihide
K
Pathology Division, Shizuoka Cancer Center, Nagaizumi-cho, Sunto-gun, Shizuoka, Japan.
Sasaguri
Kenichi
K
Sato
Sadao
S
Takemura
Tamiko
T
Kameya
Toru
T
D030201:Activin Receptors, Type I / Q000032:analysis; D000818:Animals; D018951:Antigens, CD20 / Q000032:analysis; D016723:Bone Remodeling / Q000502:physiology*; D024042:Collagen Type I / Q000032:analysis*; D050659:Core Binding Factor Alpha 1 Subunit / Q000032:analysis*; D005260:Female; D006801:Humans; D017493:Leukocyte Common Antigens / Q000032:analysis; D008297:Male; D051379:Mice; D008875:Middle Aged; D009999:Ossification, Heterotopic / Q000378:metabolism*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D017346:Protein Serine-Threonine Kinases; D011842:Radicular Cyst / Q000378:metabolism* / Q000473:pathology; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000032:analysis
D018951:Antigens, CD20; D024042:Collagen Type I; D050659:Core Binding Factor Alpha 1 Subunit; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D018125:Receptors, Transforming Growth Factor beta; D017346:Protein Serine-Threonine Kinases; D030201:Activin Receptors, Type I; D000077293:Receptor, Transforming Growth Factor-beta Type I; D000077294:Receptor, Transforming Growth Factor-beta Type II; D017493:Leukocyte Common Antigens