| UCLA Technology Available For Licensing |
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 |
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