Furthermore,  cigarette smoke was discovered to increase COX-2 and PGE2 expression in fibroblasts, which could indicate the role of cigarette smoke in Reinkes edema.While smoking is a clear risk factor to Reinkes edema, other risk factors are being identified to explain Reinkes edema in nonsmokers. Research has suggested the role of bacterial colonies in non-neoplastic lesions such as Reinkes edema. Using pyrosequencing, strains of S. pseudopneumoniae were found as the dominant bacterial strain across most non-neoplastic lesions. Of all the sequences analyzed, streptococcus represented 72.9% of bacteria found within these lesions. While smoking, gastric reflux, and vocal abuse have been more widely agreed upon in literature as risk factors for Reinkes edema, the altered bacterial cultures could be developed as a diagnostic tool in the future.The majority of the research within the last ten years focuses on improving surgery for Reinkes edema. Due to the importance of the Reinkes space in speech, it is important that minimally invasive techniques be perfected that minimize the risk of complications. The CO2 laser has been successfully incorporated into the surgical technique, however, there are several other lasers being investigated for use in Reinkes edema. These include photoangiolytic lasers and potassium titanyl phosphate lasers. See also
List of voice disorders
Histology of the Vocal Folds

References
Notes"Benign Vocal Lesions - Nodules, Polyps, Cysts". The Center for Voice at Northwestern University. Archived from the original on August 17, 2007. Retrieved July 24, 2007. External links

"Illustration of Reinkes Edema". The Center for Voice at Northwestern University. Archived from the original on August 17, 2007.
While the imidazole antifungals are mainly used topically, fluconazole and certain other triazole antifungals are preferred when systemic treatment is required because of their improved safety and predictable absorption when administered orally.Fluconazoles spectrum of activity includes most Candida species (but not Candida krusei or Candida glabrata), Cryptococcus neoformans, some dimorphic fungi, and dermatophytes, among others. Common uses include:
The treatment of non-systemic Candida infections of the vagina ("yeast infections"), throat, and mouth. Certain systemic Candida infections in people with healthy immune systems, including infections of the bloodstream, kidney, or joints. Other antifungals are usually preferred when the infection is in the heart or central nervous system, and for the treatment of active infections in people with weak immune systems. The prevention of Candida infections in people with weak immune systems, such as those neutropenic due to cancer chemotherapy, those with advanced HIV infections, transplant patients, and premature infants. As a second-line agent for the treatment of cryptococcal meningoencephalitis, a fungal infection of the central nervous system. Resistance
Fungal resistance to drugs in the azole class tends to occur gradually over the course of prolonged drug therapy, resulting in clinical failure in immunocompromised patients (e.g., patients with advanced HIV receiving treatment for thrush or esophageal Candida infection).In C. albicans, resistance occurs by way of mutations in the ERG11 gene, which codes for 14α-demethylase. These mutations prevent the azole drug from binding, while still allowing binding of the enzymes natural substrate, lanosterol. Development of resistance to one azole in this way will confer resistance to all drugs in the class.