ORAL WOUND HEALING AND PREVENTION OF PERIODONTITIS BY MODULATION AND EXAMINATION OF WIT3.0 FUNCTION
UCLA Technology Available For Licensing

BACKGROUND:  Periodontal (gum) diseases (including periodontics) affect one-third of the population in the U.S. These diseases typically associate with "loose gum tissue" resulting in tooth mobility. The late stages of gum disease are difficult, costly, and limited to tooth extraction or surgical removal of inflamed gum tissue. Early diagnosis of gum disease, therefore, may improve both the effectiveness and cost of treatment.

It is currently believed that the "loose gum tissue" is due to bacterial infection causing the gum tissue inflammation. Recent studies demonstrate a substantial contribution of genetic factors in adult periodontitis, which together may account for over 30% of etiological involvements. These findings suggest two major issues: (1) in addition to the currently postulated bacterial infection theory, periodontal disease may involve malfunction of host cells; and (2) susceptibility and severity of periodontal diseases may be the result of an individual's genetic variations.

Single nucleotide polymorphisms (SNPs) are small genetic changes that can occur within a DNA sequence. These variations may greatly affect gene function and ultimately result in the susceptibility and/or onset of disease. Diagnostic tools analyzing SNPs provide a means for studying the genetic basis as well as the preventative and curative treatment of disease. To this end, finding the key gene(s) participating in periodontal health and diseases must facilitate the new diagnosis and treatment options.

INNOVATION:  UCLA researchers have recently isolated a unique gene from oral wounds, named wound inducible transcript-3.0 (wit3.0). Wit3.0 is induced in response to tissue damage, and facilitates fibroblast mediated wound healing. UCLA researchers have shown that wit3.0 increases the rate of wound closure and decreases the area of granulation formation. Additionally, UCLA researchers have shown that direct administration of wit3.0 ameliorates periodontitis in animal models and accelerates wound closure when over-expressed in in-vitro models. Finally, UCLA researchers have demonstrated that wit3.0 has at least two SNPs which modulate its function and affect wound healing in-vitro. These findings demonstrate that examination of the various SNPs of wit3.0 may be valuable for the diagnostic screening and treatment of gum disease.

POTENTIAL APPLICATIONS 

Reference: UCLA Case No. 2005-500 PCT Application: US06/008678

For additional technical details and current licensing
availability, please contact the following UCLA office:

UCLA Office of Intellectual Property
11000 Kinross Avenue, Suite #200
Los Angeles, CA 90095-7231
Tel: 310-794-0558 Fax: 310-794-0638
email: ncd@research.ucla.edu
NCD URL:   http://www.research.ucla.edu/tech/ucla05-500.htm

Lead Inventor: Ichiro Nishimura

UCLA Technologies Available for Licensing
http://www.research.ucla.edu/tech

Copyright © 2005 The Regents of the University of California.

keywords: therapeutics uclancd ucla technologies intellectual property patents technology transfer invention business card