Abstract
BACKGROUND AND OBJECTIVE: As the interface between the oral cavity and the teeth, the junctional epithelial barrier is critical for gingival defense. The junctional epithelium is subject to mechanical stresses from biting force or external insults such as bacterial attacks, but little is known about the effects of mechanical stimuli on epithelial functions. Transient receptor potential vanilloid 4 (TRPV4) functions as a mechanosensitive nonselective cation channel. In the present study, based on marked expression of TRPV4 in the mouse junctional epithelium, we aimed to clarify the putative links between TRPV4 and junctional complexes in the junctional epithelium. METHODS AND RESULTS: Histological observations revealed that the junctional epithelium in TRPV4-deficient (TRPV4(-/-) ) mice had wider intercellular spaces than that in wild-type (TRPV4(+/+) ) mice. Exogenous tracer penetration in the junctional epithelium was greater in TRPV4(-/-) mice than in TRPV4(+/+) mice, and immunoreactivity for adherens junction proteins was suppressed in TRPV4(-/-) mice compared with TRPV4(+/+) mice. Analysis of a mouse periodontitis model showed greater bone volume loss in TRPV4(-/-) mice compared with TRPV4(+/+) mice, indicating that an epithelial barrier deficiency in TRPV4(-/-) mice may be associated with periodontal complications. CONCLUSION: The present findings identify a crucial role for TRPV4 in the formation of adherens junctions in the junctional epithelium, which could regulate its permeability. TRPV4 may be a candidate pharmacological target to combat periodontal diseases.