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Megan Lindsay Falsetta Wood, Ph.D.

Megan Lindsay Falsetta Wood, Ph.D.

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Contact

Office (585) 273-5462

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About Me

Faculty Appointments

Associate Professor - Department of Obstetrics and Gynecology (SMD)

Associate Professor - Department of Pharmacology and Physiology (SMD) - Joint

Credentials

Post-doctoral Training & Residency

Environmental Medicine, University of Rochester, School of Medicine and Dentistry 2013 - 2015

Center for Oral Biology, University of Rochester, School of Medicine and Dentistry 2010 - 2013

Education

PhD | University of Iowa Roy J. and Lucille A. Carver College of Medicine. Microbiology. 2009

BA | Alfred University. Biology. 2004

Awards

International Society for the Study of Women's Sexual Health Fernand Labrie Distinguished Investigator Award. 2023

International Society for the Study of Women's Sexual Health Executive Board Research Grants Chair. 2023

International Society for the Study of Women's Sexual Health Scientific Program Committee Member. 2023

International Society for the Study of Vulvovaginal Disease Best Member/Fellow Presentation. 2022

Ecosanoid Research Foundation Young Investigator Award. 2022

International Society for the Study of Women's Sexual Health Best Abstract Prize. 2022

International Society for the Study of Women's Sexual Health Advocacy Committee Member. 2022

International Society for the Study of Vulvovaginal Disease Vulvar Disease Impact Committee Co-Chair. 2022

National Vulvodynia Association Research Fund Award. 2017

International Society for the Study of Vulvovaginal Disease Best Candidate Abstract. 2015

Research

The Falsetta lab is committed to translational women’s health research. Our goal is to identify previously unknown mechanisms of disease for disabling vulvar conditions, namely vulvodynia and lichens. By understanding the mechanisms of disease we can 1) identify new targets for therapy, 2) better ad...
The Falsetta lab is committed to translational women’s health research. Our goal is to identify previously unknown mechanisms of disease for disabling vulvar conditions, namely vulvodynia and lichens. By understanding the mechanisms of disease we can 1) identify new targets for therapy, 2) better adapt current modalities of treatment for rapid improvements in care, and 3) create new metrics to identify disease at an early stage and objectively track disease progression and response to treatment. Our research focuses on the basic science of disease, while directly interfacing with the clinical experts delivering care.

Localized provoked vulvodynia (LPV) is characterized by acute and lasting pain in response to light touch of the vulvar vestibule (area immediately surrounding the vaginal opening), which is associated with a reduction in quality of life. Although women afflicted with LPV experience profound pain that negatively impacts their sexual, emotional, social, and relationship health, they show no overt signs of disease. The origins of vulvodynia are poorly understood, and no current therapy targets the root of the disease or is completely curative, perhaps save surgical amputation of the affected tissue. The goal of our research is to identify less invasive, ideally topical, therapies, while simultaneously uncovering the poorly understood mechanisms of disease.

We have determined that a persistent low level of inflammation, generally undetectable clinically, is a key contributor to vulvodynia. We have also discovered likely defects in the inflammation resolution machinery, which can be overcome with exogenous supplementation with specialized pro-resolving mediators (SPMs). SPMs could represent a highly promising, non-invasive therapy for vulvodynia. SPMs are naturally produced by the body through metabolism of omega-3 and omega-6 fatty acids and are safe. Although our work in this area is ongoing, our findings suggest vulvodynia is the product of “two hits.” The first hit involves exaggerated inflammatory signaling, rendering the vestibule hypersensitive to inflammatory stimuli, such that a woman’s own natural flora may elicit a response. We are currently focusing on investigating the second hit, involving dysregulation of the resolution machinery.

Lichen planus (LP) and lichen sclerosis (LS) are common inflammatory dermatoses of the vulva characterized by intense pruritus (itching), burning, and changes in the architecture of the vulvar anatomy. Architectural changes can cause a loss of plasticity of the vagina, loss of mobility of the clitoral hood and/or fusion to the clitoral glans, and urinary symptoms (e.g. incontinence, dysuria). Additional manifestations include ulcers, erosions, and pre-cancerous or cancerous lesions. The standard of care for patients with LP and LS is topical application of ultrapotent steroids, more frequently to start and tapering off to weekly maintenance dosing, increasing frequency with flares or complications. Therefore, these are lifelong disorders, requiring long term treatment and regular follow up. Currently, there are no curative treatments available, and any architectural changes occurring prior to or during treatment are irreversible. The causes of lichen dermatoses are not well understood. Although these diseases are considered scarring dermatoses and the architectural changes are referred to as “scars,” limited and conflicting information about the role of scarring is available. There is some evidence to implicate alterations in scarring/wound healing in lichenoid vulvar disease, and our research in this area aims to evaluate the role of scarring in lichenoid disease by identifying specific pathways and targets that may be aberrant.

Publications

Journal Articles

Inflammation, lipid dysregulation, and transient receptor potential cation channel subfamily V member 4 signaling perpetuate chronic vulvar pain.

Bekauri T, Fischer S, Honn KV, Maddipati KR, Love T, Little C, Wood RW, Bonham AD, Linder MA, Yule DI, Emanuelle C, Falsetta ML

Pain.. 2024 April 1165 (4):820-837. Epub 10/26/2023.

Inflammation, lipids, and pain in vulvar disease.

Falsetta ML, Maddipati KR, Honn KV

Pharmacology & therapeutics.. 2023 August 248 :108467. Epub 06/05/2023.

Dual transcriptome of and interplay in biofilms.

Xiao J, Zeng Y, Rustchenko E, Huang X, Wu TT, Falsetta ML

Journal of oral microbiology.. 2023 15 (1):2144047. Epub 11/09/2022.

Editorial: Vulvodynia and beyond: innate immune sensing, microbes, inflammation, and chronic pain.

Falsetta ML

Frontiers in cellular and infection microbiology.. 2023 13 :1338659. Epub 12/08/2023.

Specialized Pro-resolving Mediators Reduce Pro-nociceptive Inflammatory Mediator Production in Models of Localized Provoked Vulvodynia.

Falsetta ML, Wood RW, Linder MA, Bonham AD, Honn KV, Maddipati KR, Phipps RP, Haidaris CG, Foster DC

The journal of pain.. 2021 October 22 (10):1195-1209. Epub 04/01/2021.

Thy1 (CD90) expression is regulated by DNA methylation during adipogenesis.

Flores EM, Woeller CF, Falsetta ML, Susiarjo M, Phipps RP

FASEB journal : official publication of the Federation of American Societies for Experimental Biology.. 2019 March 33 (3):3353-3363. Epub 10/30/2018.

Key roles for lipid mediators in the adaptive immune response.

Duffney PF, Falsetta ML, Rackow AR, Thatcher TH, Phipps RP, Sime PJ

The Journal of clinical investigation.. 2018 July 2128 (7):2724-2731. Epub 07/02/2018.

Toll-Like Receptor Signaling Contributes to Proinflammatory Mediator Production in Localized Provoked Vulvodynia.

Falsetta ML, Foster DC, Woeller CF, Pollock SJ, Bonham AD, Piekna-Przybylska D, Maggirwar SB, Haidaris CG, Phipps RP

Journal of lower genital tract disease.. 2018 January 22 (1):52-57. Epub 1900 01 01.

A review of the available clinical therapies for vulvodynia management and new data implicating proinflammatory mediators in pain elicitation.

Falsetta ML, Foster DC, Bonham AD, Phipps RP

BJOG : an international journal of obstetrics and gynaecology.. 2017 January 124 (2):210-218. Epub 06/17/2016.

A Role for Bradykinin Signaling in Chronic Vulvar Pain.

Falsetta ML, Foster DC, Woeller CF, Pollock SJ, Bonham AD, Haidaris CG, Phipps RP

The journal of pain.. 2016 November 17 (11):1183-1197. Epub 08/18/2016.

Identification of novel mechanisms involved in generating localized vulvodynia pain.

Falsetta ML, Foster DC, Woeller CF, Pollock SJ, Bonham AD, Haidaris CG, Stodgell CJ, Phipps RP

American journal of obstetrics and gynecology.. 2015 July 213 (1):38.e1-38.e12. Epub 02/12/2015.

Site-specific mesenchymal control of inflammatory pain to yeast challenge in vulvodynia-afflicted and pain-free women.

Foster DC, Falsetta ML, Woeller CF, Pollock SJ, Song K, Bonham A, Haidaris CG, Stodgell CJ, Messing SP, Iadarola M, Phipps RP

Pain.. 2015 March 156 (3):386-396. Epub 1900 01 01.

Symbiotic relationship between Streptococcus mutans and Candida albicans synergizes virulence of plaque biofilms in vivo.

Falsetta ML, Klein MI, Colonne PM, Scott-Anne K, Gregoire S, Pai CH, Gonzalez M, Watson G, Krysan DJ, Bowen WH, Koo H

Infection and immunity.. 2014 May 82 (5):1968-81. Epub 02/24/2014.

Quantification of confocal images of biofilms grown on irregular surfaces.

Sommerfeld Ross S, Tu MH, Falsetta ML, Ketterer MR, Kiedrowski MR, Horswill AR, Apicella MA, Reinhardt JM, Fiegel J

Journal of microbiological methods.. 2014 May 100 :111-20. Epub 03/13/2014.

?-Mangostin disrupts the development of Streptococcus mutans biofilms and facilitates its mechanical removal.

Nguyen PT, Falsetta ML, Hwang G, Gonzalez-Begne M, Koo H

PloS one.. 2014 9 (10):e111312. Epub 10/28/2014.

The exopolysaccharide matrix: a virulence determinant of cariogenic biofilm.

Koo H, Falsetta ML, Klein MI

Journal of dental research.. 2013 December 92 (12):1065-73. Epub 09/17/2013.

Effect of neovestitol-vestitol containing Brazilian red propolis on accumulation of biofilm in vitro and development of dental caries in vivo.

Bueno-Silva B, Koo H, Falsetta ML, Alencar SM, Ikegaki M, Rosalen PL

Biofouling.. 2013 29 (10):1233-42. Epub 10/07/2013.

Novel antibiofilm chemotherapy targets exopolysaccharide synthesis and stress tolerance in Streptococcus mutans to modulate virulence expression in vivo.

Falsetta ML, Klein MI, Lemos JA, Silva BB, Agidi S, Scott-Anne KK, Koo H

Antimicrobial agents and chemotherapy.. 2012 December 56 (12):6201-11. Epub 09/17/2012.

Phenotypic characterization of a copA mutant of Neisseria gonorrhoeae identifies a link between copper and nitrosative stress.

Djoko KY, Franiek JA, Edwards JL, Falsetta ML, Kidd SP, Potter AJ, Chen NH, Apicella MA, Jennings MP, McEwan AG

Infection and immunity.. 2012 March 80 (3):1065-71. Epub 12/19/2011.

The exopolysaccharide matrix modulates the interaction between 3D architecture and virulence of a mixed-species oral biofilm.

Xiao J, Klein MI, Falsetta ML, Lu B, Delahunty CM, Yates JR, Heydorn A, Koo H

PLoS pathogens.. 2012 8 (4):e1002623. Epub 04/05/2012.

Proteomic analysis of Neisseria gonorrhoeae biofilms shows shift to anaerobic respiration and changes in nutrient transport and outermembrane proteins.

Phillips NJ, Steichen CT, Schilling B, Post DM, Niles RK, Bair TB, Falsetta ML, Apicella MA, Gibson BW

PloS one.. 2012 7 (6):e38303. Epub 06/06/2012.

Influences of trans-trans farnesol, a membrane-targeting sesquiterpenoid, on Streptococcus mutans physiology and survival within mixed-species oral biofilms.

Jeon JG, Pandit S, Xiao J, Gregoire S, Falsetta ML, Klein MI, Koo H

International journal of oral science.. 2011 April 3 (2):98-106. Epub 1900 01 01.

Natural products in caries research: current (limited) knowledge, challenges and future perspective.

Jeon JG, Rosalen PL, Falsetta ML, Koo H

Caries research.. 2011 45 (3):243-63. Epub 05/12/2011.

The Composition and Metabolic Phenotype of Neisseria gonorrhoeae Biofilms.

Falsetta ML, Steichen CT, McEwan AG, Cho C, Ketterer M, Shao J, Hunt J, Jennings MP, Apicella MA

Frontiers in microbiology.. 2011 2 :75. Epub 04/18/2011.

Anaerobic metabolism occurs in the substratum of gonococcal biofilms and may be sustained in part by nitric oxide.

Falsetta ML, McEwan AG, Jennings MP, Apicella MA

Infection and immunity.. 2010 May 78 (5):2320-8. Epub 03/15/2010.

Transcriptional profiling identifies the metabolic phenotype of gonococcal biofilms.

Falsetta ML, Bair TB, Ku SC, Vanden Hoven RN, Steichen CT, McEwan AG, Jennings MP, Apicella MA

Infection and immunity.. 2009 September 77 (9):3522-32. Epub 06/15/2009.

Esterase D is essential for protection of Neisseria gonorrhoeae against nitrosative stress and for bacterial growth during interaction with cervical epithelial cells.

Potter AJ, Kidd SP, Edwards JL, Falsetta ML, Apicella MA, Jennings MP, McEwan AG

The Journal of infectious diseases.. 2009 July 15200 (2):273-8. Epub 1900 01 01.

Phasevarions mediate random switching of gene expression in pathogenic Neisseria.

Srikhanta YN, Dowideit SJ, Edwards JL, Falsetta ML, Wu HJ, Harrison OB, Fox KL, Seib KL, Maguire TL, Wang AH, Maiden MC, Grimmond SM, Apicella MA, Jennings MP

PLoS pathogens.. 2009 April 5 (4):e1000400. Epub 04/24/2009.

Thioredoxin reductase is essential for protection of Neisseria gonorrhoeae against killing by nitric oxide and for bacterial growth during interaction with cervical epithelial cells.

Potter AJ, Kidd SP, Edwards JL, Falsetta ML, Apicella MA, Jennings MP, McEwan AG

The Journal of infectious diseases.. 2009 January 15199 (2):227-35. Epub 1900 01 01.

Metal binding specificity of the MntABC permease of Neisseria gonorrhoeae and its influence on bacterial growth and interaction with cervical epithelial cells.

Lim KH, Jones CE, vanden Hoven RN, Edwards JL, Falsetta ML, Apicella MA, Jennings MP, McEwan AG

Infection and immunity.. 2008 August 76 (8):3569-76. Epub 04/21/2008.

Characterization of the OxyR regulon of Neisseria gonorrhoeae.

Seib KL, Wu HJ, Srikhanta YN, Edwards JL, Falsetta ML, Hamilton AJ, Maguire TL, Grimmond SM, Apicella MA, McEwan AG, Jennings MP

Molecular microbiology.. 2007 January 63 (1):54-68. Epub 11/27/2006.