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Medical ProfessionalsMedical Research FundGrants made through NVA’s Medical Research Fund provide scientists with the opportunity to gather vital pilot data, which they need to secure funding from larger institutions, such as the National Institutes of Health (NIH). Many of our grant recipients have been successful in obtaining multi-million grants from the NIH and other institutions. (To view summaries of NIH-funded studies, click here.) To date, the NVA has awarded over $600,000 in research grants. Announcements of funding availability are disseminated by e-mail twice a year. To sign-up for these announcements and/or to obtain an application, please e-mail Chris Veasley. Studies funded through NVA’s Medical Research Fund are summarized below.
Maureen Basha, PhD – Drexel University College of Medicine (2009 - 2012)
Yitzchak Binik, PhD – McGill University (2006 - 2008)
Nina Bohm-Starke, PhD - Danderyd Hospital (Sweden) (2009 - 2013)
Jacob Bornstein, MD and Tzipora Falik, MD – Western Galilee Hospital (Israel) (2007 - 2010)
Theodore Fellenbaum, MD - Mid-Michigan Vulvar Care & Colposcopy Center (2009 - 2010)
David Foster, MD, MPH – University of Rochester (1998 - 1999, 2000 - 2001)
In 2000, NVA awarded a second grant to Dr. Foster to continue his work on the etiology of VVS. Through cell culture, Dr. Foster found that the fibroblast, a type of cell that produces scar tissue, acts in a peculiar way immunologically in VVS patients. Dr. Foster proposed to study this peculiarity by testing for differences in cytokine and melanin genes and relating his genetic findings to his observations of cell culture. Dr. Foster’s ultimate goal was to identify inflammatory substances released by the relevant fibroblast cells, thereby providing a target for drug therapy. Dr. Foster’s NVA grants enabled him to gather enough pilot data to receive a large-scale NIH grant to study a combination treatment for VVS.
Bernard Harlow, PhD - University of Minnesota School of Public Health (2007)
Catherine Leclair, MD and Terry Morgan, MD -
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Dr. Basha was awarded an NVA grant in 2009. In collaboration with Susan Kellogg-Spadt, CRNP, PhD, director of vulvar and sexual medicine at the Pelvic and Sexual Institute, Graduate Hospital, Philadelphia, and Kristene Whitmore, MD, medical director of the Pelvic and Sexual Institute and chair of urology at Drexel University School of Medicine, she will study the influence of the ovarian hormones, estrogen, progesterone and testosterone, on vulvar sensory processing in women with and without vulvar vestibulitis syndrome (VVS), or provoked vestibulodynia. There is a growing body of research evidence that indicates that ovarian hormones play a role in pain modulation. The goals of this project are to determine: (i) changes in vulvar and non-vulvar sensory processing across the menstrual cycle; (ii) the impact of oral contraceptives on vulvar and non-vulvar sensory processing; and (iii) how ovarian hormone levels contribute to altered vulvar pain thresholds in women with vulvodynia. This study will provide further insight into the role of ovarian hormones in causing and/or maintaining vulvodynia. 
Dr. Binik was awarded an NVA grant in 2006 to investigate the relationship between chronic Candida infection and vulvar vestibulitis syndrome (VVS) in an animal model. Many women with VVS report previous recurrent episodes of vulvovaginal Candida infection. This association has led some researchers to propose that chronic Candida infection, in which there is continued irritation of the vulvovaginal mucosa, may lead to the abnormal pain transmission experienced by women with VVS. In the present study, Dr. Binik will evaluate whether chronic Candida infection results in lowered vulvar pain thresholds and reduced mating behavior in mice. In addition, he will determine if the immunological profile associated with chronic Candida infection is similar to the immunological profile in VVS. Dr. Binik’s goal is to use an animal model to pursue novel therapeutic interventions for women with vulvar pain. 
Dr. Bohm-Starke will use her 2009 NVA grant, matched by her institution, to investigate whether certain genetic variations are associated with general pain hypersensitivity in women with VVS. Recent studies have found that women with VVS also have lower pain thresholds than controls in non-vulvar body sites (e.g., arm, leg), suggesting altered pain processing in the brain and/or spinal cord. Furthermore, some studies show a significant percentage of women with VVS suffer from more than one pain condition, i.e., they also have fibromyalgia, interstitial cystitis, temporomandibular joint and muscle disorders, and/or irritable bowel syndrome. This has led researchers to propose that some women with VVS may be genetically predisposed to develop pain conditions. In VVS patients and controls, Dr. Bohm-Starke will investigate alterations in several genes that are involved in pain modulation and inflammation. This study aims to: (i) increase our knowledge of the underlying mechanisms in VVS, and (ii) identify a subgroup of women with VVS at risk of developing other pain conditions.
Dr. Bornstein (left photo) and Falik (right photo) were awarded a grant in 2007 to investigate possible associations between VVS and genes that transcribe proteins found or hypothesized to be involved in the abnormal tissue changes seen in VVS. Specifically, they will study a number of polymorphisms, or variations, of three genes coding for molecules involved in the break down, or degradation, of vestibular mast cells and increased vestibular nerve fiber growth: heparanase, vanilloid receptor-1 (TRPV1), and nerve growth 
factor (NGF). The subjects for this pilot study will be women suffering from severe vulvar vestibulitis who have experienced pain since their first episode of sexual intercourse. This study is an important exploratory part of a larger-scale study that will help delineate genetic susceptibility to the condition and pave the way for individualized treatment. 
Dr. Fellenbaum will use his 2009 NVA grant, matched by Genesys Medical Regional Center, Grand Blanc, Michigan, to test the effectiveness of a potential new treatment for VVS. Dr. Fellenbaum will clinically test the proposed link between mast cells, which play a key role in the inflammatory process, and the development of VVS. When triggered, mast cells degranulate, releasing toxic substances, such as histamine and cytokines, into the surrounding tissue. Mast cell degranulation may lead to an increase in nerve growth factor (a molecule that stimulates the growth of certain sensory nerves) and excessive hypersensitivity of the nerve fibers in the vestibule. This hypersensitivity may account for the pain of vulvar vestibulitis. In this study, Dr. Fellenbaum is investigating the action of an oral medication that reduces mast cell degranulation to see whether it alleviates VVS pain. He will compare the degree of pain relief reported by women taking this oral medication to that of two other groups of women being treated with topical medications.
Dr. Foster first received an NVA grant in 1998 to further his work on the neuro-inflammatory mechanisms of Vulvar Vestibulitis Syndrome (VVS). Specifically, Dr. Foster studied the cytokine system that mediates inflammation and the neurokine system that mediates pain. The ultimate goal of this research is to develop a specific therapy that interferes with the cytokine-neurokine pathway, thereby relieving the pain of VVS. 
Dr. Harlow was awarded a 5-year grant from the National Institutes of Health in 2000 to study the prevalence of vulvodynia and delineate factors associated with an increased risk of developing the condition (
Drs. Leclair and Morgan were awarded a grant in 2007 to continue their work investigating the etiology, or underlying mechanism, responsible for increased vestibular nerve fiber density found in women with VVS. They also plan to determine if a mild chronic inflammation involving mast cells plays a role in the initiation and/or perpetuation of the condition. Recent research has shown that women with VVS have a decreased number of estrogen receptors in their vestibular tissue. According to Drs. Leclair and Morgan, one consequence of the reduced level of estrogen receptors may be an up-regulation of epidermal growth factor receptor (EGFR), a mediator of abnormal nerve cell growth and mast cell development. EGFR shows significant cross-signaling with steroid receptors, such as estrogen receptors, and is also up-regulated by androgen receptor (AR). They hypothesize that abnormal ER down-regulation and/or AR up-regulation may lead to an increase in EGFR expression and the cascade of events culminating in VVS. The long term goal of their research is to determine the underlying mechanisms responsible for the initiation of vestibulitis and develop treatment strategies that will eliminate the need for surgery.
Dr. MacNeill was awarded a grant in 2007 to investigate the role of surfactant proteins in the initiation of the inflammatory process in VVS. Surfactant proteins are produced locally in the vaginal and vestibular mucosa, and based on numerous studies of other mucosa, may play an important role in the immune response that protects the vulva and vagina from infection. These proteins are found elsewhere in the body, such as the lung. Mice that have been genetically altered not to produce these proteins die of infection unless housed in a sterile environment. Dr. MacNeill hypothesizes that variation in the genes that code for these proteins may be responsible for initiating or maintaining the early inflammatory process in VVS. In this study, he will test this hypothesis by measuring levels of surfactant proteins in vestibular tissue and assess eleven different polymorphisms in VVS patients and controls. Ultimately, he will test a novel therapy that modulates the activity of these proteins. He speculates that if this process can be detected and treated early, the development of VVS could be stopped. In 2007, Dr. MacNeill used the data collected with his NVA grant in an application to the National Institutes of Health.
Drs. McLean (left photo) and Pukall (right photo) were awarded a grant in 2007 to study pelvic floor muscle function in women with VVS. Specifically, the study's objectives are to determine if, as compared to healthy controls, women with VVS demonstrate: (1) heightened activity of the superficial pelvic floor muscles in response to vestibular pressure and/or stretching of the introitus, or vaginal opening; (2) heightened activity of the deep pelvic floor muscles in response to introital pressure; (3) anticipatory reactions of the superficial and/or deep pelvic floor muscles in response to introital pressure or stretching; and (4) heightened activity of remote muscles (biceps and trapezius muscles) in anticipation of, or in response to, introital pressure 
or stretching. This study will be the first to investigate whether there are differences in the tonic and reactive contractility of pelvic floor muscles in women with VVS as compared to healthy controls, and to differentiate between superficial and deep pelvic floor muscle responses. The outcome of this work will shed light of the etiology of the condition and guide clinical assessment and management, including the development of new physical therapy techniques and utility of medications, such as neuromuscular transmission blocking agents (e.g., Botox).
Dr. Moldwin (left photo) and medical student Amin Herati, (right photo) were awarded an NVA grant in 2009 to investigate myofascial trigger points in women with vulvodynia. Women who have myofascial dysfunction have multiple trigger points, or hyperirritable spots of taut skeletal muscle, throughout their bodies. When active, trigger points cause pain and other symptoms. Although patients with chronic pelvic and urogenital pain can have trigger points in their pelvic floor muscles, very little is known about their prevalence and distribution. The goal of this 
study is to determine whether the locations or pattern of pelvic trigger points differ among three pelvic pain disorders – vulvodynia, interstitial cystitis (painful bladder syndrome) and chronic prostatitis. If distinct trigger point patterns can be identified for vulvodynia and interstitial cystitis, clinicians could add trigger point evaluation to the diagnostic workup of women presenting with pelvic pain and be better-equipped to differentiate vulvodynia from interstitial cystitis.
Drs. Nackley-Neely (left photo) and Zolnoun (right photo) were awarded an NVA grant in 2009 to investigate possible common mechanisms in vulvodynia and temporomandibular joint/muscle disorders (TMD). Drs. Nackley and Zolnoun note that recent studies have demonstrated that persistent pain conditions occurring in isolation may result from local increases in peripheral nerve activity and proinflammatory cytokines (substances that trigger inflammation). Alternately, pain conditions occurring in concert may result from changes in both the central nervous system’s processing of pain and circulating proinflammatory cytokines. They hypothesize that vulvodynia and TMD share 
common central pathophysiology and will compare pain sensitivity and circulating cytokines in four groups: women with vulvodynia, women with TMD, women with concurrent vulvodynia/TMD and healthy controls. This study aims to provide: (i) a better understanding of the key mechanisms that drive vulvodynia and TMD, (ii) more accurate differentiation of distinct subgroups of vulvodynia and TMD patients, and (iii) the development of new therapeutic strategies tailored to these subgroups. Their ultimate goal is to uncover the underlying mechanisms and perpetuating factors for each subgroup and utilize treatments that target those factors. 
Drs. Rapkin and McDonald were awarded a grant in August 2007 to study the efficacy of sequential nerve blocks in women with generalized vulvodynia. 
Dr. Wesselmann was awarded a grant in 1997 to develop a basic science model of vulvodynia. Her aim was to advance the knowledge of the neural mechanisms underlying the disorder in order to develop specific treatment modalities. Dr. Wesselmann’s NVA grant enabled her to gather pilot data and receive large-scale funding from the National Institutes of Health in 2002. 
Drs. Witkin (left photo) and Ledger (right photo) from Cornell University received their first NVA research grant in 2000 and have published the results of seven studies in the past nine years. They have found the following genetic variations in women with VVS, aka provoked vestibulodynia: (i) a reduced capacity to terminate inflammation (IL-1ra gene), (ii) an increased capacity to initiate inflammatory responses (IL-1beta gene), and (iii) a reduced capacity to combat Candida albicans infections (MBL gene). Similarly, they've found reduced circulating levels of the anti-microbial compound, interferon-alpha, increased pro-inflammatory cytokine and decreased production of an anti-inflammatory mediator in women with VVS. They have attempted to differentiate patients on the basis of time of symptom onset, factors associated with onset, history of recurrent yeast infections, degree of vestibular pain and associations with an indicator of an allergic response to seminal fluid. Their findings have verified that more than one biological process is responsible for the initiation of VVS. 
Dr. Witkin was awarded a third NVA grant in 2007 to continue his work on the etiology of VVS. Because women with VVS report a variety of events that initially trigger their symptoms, including vulvovaginal infection, childbirth, hormonal alteration and chemical and laser treatment, researchers have been unable to identify the exact etiology of the condition. Since 2000, Dr. Witkin has published several studies showing that some women with VVS have gene alterations (polymorphisms) that make them more susceptible to developing the condition. Women with VVS are more likely to exhibit a reduced capacity to ‘turn-off’ inflammation (IL-1ra gene polymorphism), an increased capacity to initiate inflammation (IL-1beta gene polymorphism) and a reduced capacity to combat Candida albicans infections (MBL gene polymorphism). He now proposes that VVS, regardless of the initial trigger, may be due to vestibular peripheral nerve damage caused by prolonged exposure to reactive oxygen species (ROS). ROS are oxygen-containing molecules that can damage other cells and molecules in the body, i.e., nerve cells; they can be induced by a number of different infectious or non-infectious insults. Specifically, he suggests that ROS persistence, which is known to increase susceptibility to nerve damage and maximize regional sensitivity, may be due to the presence of polymorphisms in genes that either directly inactivate ROS or foster a prolongation of ROS production. With this grant, Dr. Witkin will test this novel and unifying hypothesis by comparing the DNA of women with VVS whose symptoms began after a defined event such as childbirth, vulvovaginal infection or surgery, with those whose symptoms were not associated with any specific event. In addition, he will collect blood samples from these two groups to measure immune responses to the yeast and hyphal forms of Candida. Evidence of a unifying mechanism to explain the diverse clinical observations in women with VVS will lead to an improved ability to identify women at risk for development of this syndrome, the testing of more effective preventative strategies and the formulation of novel treatments.
Ms. Kendell was awarded a grant in 2006 to develop a curriculum to train and evaluate ob-gyn residents in the treatment of women with chronic vulvar pain. The educational component of the curriculum includes traditional and web-based learning tools, as well as hands-on training in standardized exam techniques and vulvar colposcopy. To evaluate residents’ competency, the George Washington University School of Medicine utilizes a state-of-the-art Standardized Patient Testing center that allows students and residents to hone their skills. In this controlled environment, faculty can observe and record resident/patient interactions and provide real time feedback to residents on their patient care, medical knowledge, interpersonal skills, professionalism and systems based practice. Ms. Kendell’s initial goal is to develop a successful standardized curriculum that will improve medical residents’ competence and level of comfort in evaluating and treating vulvar pain disorders. Her ultimate goal is to establish a vulvar pain clinic at George Washington University School of Medicine. 
Danielle Tonelli, DO, a fellowship-trained women’s health specialist with board certification in family medicine, received a NVA grant in early 2010 to start a vulvar pain clinic in Milwaukee, Wisconsin. Dr. Tonelli currently serves as co-clinical director of the Center for Optimal Health and Wellness at the Aurora Women’s Pavilion (AWP) in Milwaukee. AWP showed its support of her work by matching the NVA’s grant. Dr. Tonelli will develop and implement educational programs for local women with vulvodynia as well as medical professionals. “With the establishment of the AWP Vulvar Pain Clinic, women in our community and their providers will now have a local center with a full range of services, from outreach and education to compassionate patient care,” says Dr. Tonelli. For more information, visit the