2 research outputs found
CO2 laser therapy accelerates the healing of ulcers in the oral mucosa by inducing the expressions of heat shock protein-70 and tenascin C
The treatment of ulceration or stomatitis with
laser therapy is known to accelerate healing and relieve
pain, but the underlying biological mechanism is not
fully understood. The present study used a mouse model
of ulceration to investigate the molecular mechanisms by
which CO2 laser therapy accelerated the wound healing
process. An ulcer was experimentally created in the
palatal mucosa of the mouse and irradiated with light
from a CO2 laser. Compared with controls (no
irradiation), laser irradiation induced the proliferation of
epithelial cells and faster re-epithelialization of the
wound area. Immunohistochemistry experiments showed
that heat shock protein-70 (HSP70) was expressed
mainly in the epithelium of normal palatal tissue,
whereas there was little tenascin C (TnC) expression in
the epithelium and mesenchyme under normal
conditions. Laser irradiation induced HSP70 mRNA and
protein expression in the lamina propria as well as TnC
expression in the mesenchyme underlying the renewing
epithelium. Epithelial cells and fibroblasts were exposed
to heated culture medium or laser irradiation to establish
whether hyperthermia mimicked the effect of laser
irradiation. Culture of fibroblasts in heated medium
increased the expressions of both TnC and TGF-β1,
whereas laser irradiation induced only TnC expression.
The present study indicates that CO2 laser irradiation
exerts a photobiogenic effect to up-regulate TnC
expression without inducing TGF-β1 expression. We
suggest that CO2 laser therapy has an advantage over
thermal stimulation