Introduction
Hello, hello, happy August! I cannot believe how quickly this year has flown by. Last month, I (Jaclyn) had the privilege and honor of attending the 2026 International Society for the Study of Vulvovaginal Disease (ISSVD) World Congress in Halifax, Canada.
For those unfamiliar with the International Society for the Study of Vulvovaginal Disease (ISSVD), it is an international, multidisciplinary organization dedicated to advancing knowledge about vulvar and vaginal diseases. The ISSVD brings together healthcare professionals and researchers from many disciplines. Its goal is to improve our understanding, diagnosis, and treatment of vulvovaginal conditions.
One of the things that makes the ISSVD particularly special is this multidisciplinary approach. Vulvovaginal health does not neatly belong to one medical specialty, and the World Congress reflects that. The meeting brings together clinicians, researchers, pathologists, gynecologists, dermatologists, pelvic-health professionals, sexual-health experts, and others working in vulvovaginal disease.
For a patient advocate like me, it is an incredible opportunity to learn directly from people studying these conditions from many different perspectives.
In this blog, I want to share some of what I learned at the 2026 ISSVD World Congress. Importantly, this is not a summary of every study or presentation from Halifax. Instead, I’ve pulled together the findings, conversations, emerging research, and ideas that stood out to me most as a patient advocate. In some cases, they also gave me a glimpse into where vulvar-health research may be headed next.
Some Important Notes Before We Dive In
And yes, before we get started: this is a long one!
If you’ve followed my work for any length of time, you probably know how passionate I am about vulvar-health research. After spending several days surrounded by new research, thoughtful conversations, and people who have dedicated their careers to these conditions, it was incredibly hard for me not to share everything that stood out to me.
If you’d prefer the quicker version, don’t worry! I’ll also be putting together a short, high-level YouTube recap covering my biggest takeaways from ISSVD 2026.
But for my fellow research nerds—or anyone who wants to dig a little deeper—grab a coffee and settle in. There’s a lot to talk about.
A quick disclaimer before we dive in: Scientific conferences can include everything from well-established evidence to preliminary findings, early-stage studies, and ongoing clinical trials. Just because researchers presented something at the ISSVD World Congress does not automatically mean they have proven it effective, incorporated it into clinical guidelines, or established it for routine clinical use. I’ll do my best throughout this blog to make those distinctions clear.
This blog is also intended for educational purposes only and does not constitute medical advice. Please speak with your healthcare provider before making changes to your treatment or healthcare plan.
Lichen sclerosus research is finally moving beyond simply asking, “What causes LS?”
Getting Closer to the Biology Behind Lichen Sclerosus
One piece of new research that really caught my attention came from Changji Xiao and colleagues. They presented Integrated Transcriptomic and Metabolomic Analysis Reveals IFNγ/JAK/STAT-Mediated Immune and Metabolic Dysregulation in Vulvar Lichen Sclerosus.
Now, this will get a bit sciency—but stay with us!
The researchers wanted to better understand what is happening at a molecular level within vulvar lichen sclerosus (VLS). Its underlying pathogenesis is still not fully understood. Pathogenesis simply means how and why a disease develops—what happens in the body as the disease begins and progresses.
This was a small exploratory study involving 10 paired samples that compared tissue from LS lesions with nearby vulvar tissue from the same patients.
Researchers examined two different layers of activity inside those tissues: gene activity (transcriptomics) and metabolism (metabolomics). Put simply, they looked for differences in the biological instructions the cells were following and the chemical processes those cells were carrying out.
An Immune-Signaling Pathway Stood Out
One of the most interesting findings involved an immune communication system called the interferon-gamma (IFN-γ)/JAK/STAT signaling pathway.
Think of pathways like this as chains of messages that immune cells use to communicate. A signal starts the process, other molecules pass that message along, and eventually the message can change how cells behave. In the LS tissue, researchers found significantly greater activity in this particular immune-signaling pathway.
Two molecules in particular—STAT1 and CXCL10—stood out.
*Image created using NotebookLM AI for illustrative purposes only. It was not an official ISSVD slide or used in an ISSVD presentation and may contain inaccuracies or errors.
STAT1 helps carry immune signals inside cells. CXCL10 helps attract certain immune cells to areas of inflammation. Researchers also found increased infiltration of certain T cells, which help coordinate and carry out immune responses, in the LS lesions.
The amount of these T cells was associated with STAT1 and CXCL10 levels. Together, the findings suggest that this immune-signaling network may help activate and recruit T cells into LS-affected tissue. However, this small study cannot tell us whether that process actually causes LS.
Researchers Also Found Metabolic Differences
The researchers found something beyond the immune system: LS tissue showed differences in metabolism.
In other words, they identified changes in some of the chemical processes cells use to function, produce energy, and build or break down molecules. These differences involved amino-acid, lipid (fat), energy, and purine/pyrimidine metabolism.
Researchers also found connections between some of these metabolic changes and their immune-signaling findings.
So what does all of that mean for patients?
We still don’t know one single cause of LS, and this study is much too small to establish one. But research like this moves us beyond simply saying that LS involves “inflammation” or an “overactive immune system.”
Scientists are beginning to zoom in on which immune signals, immune cells, and biological processes may actually be involved inside LS tissue. Understanding those pathways more precisely could eventually help researchers investigate treatments that target specific parts of the disease process rather than broadly suppressing inflammation across multiple pathways.
In plain language: we don’t have the full LS puzzle yet, but researchers are starting to identify some of the individual pieces—and where they might fit.
JAK inhibitors were one of the most exciting LS developments—but steroids aren’t disappearing
A Potential New Treatment for LS Reaches Phase 3 Research
This large, multinational clinical trial is evaluating delgocitinib cream, a topical medication that inhibits the Janus kinase (JAK) family of enzymes.
This is exciting because it moves the conversation from “What pathways might be involved in LS?” to “Can we actually target one of those pathways with treatment?”
If you just read “pan-JAK inhibitor” and your eyes glazed over, stay with me. The idea is actually pretty straightforward.
Remember the immune-signaling pathways we just talked about? Immune cells communicate through a series of chemical messages. JAK proteins help carry some of those inflammatory messages from the outside of a cell to the machinery inside it.
A JAK inhibitor interferes with that communication chain.
Delgocitinib is called a pan-JAK inhibitor because it inhibits all four members of the JAK family: JAK1, JAK2, JAK3, and TYK2. Researchers are interested in this approach partly because accumulating molecular research has implicated JAK/STAT-related inflammatory signaling in LS.
In very simple terms: if inflammation is partly driven by immune cells repeatedly sending certain “go, go, go” messages, JAK inhibition attempts to interrupt some of those messages and reduce inflammation.
Importantly, delgocitinib is topical. You apply the cream to the affected area rather than taking an oral medication that acts throughout the body.
Why Phase 3 Is Such a Big Deal
What made this presentation particularly exciting to me was the phrase Phase 3.
New medications generally progress through several stages of clinical research before they can potentially receive approval for a particular disease. By Phase 3, researchers are no longer simply asking whether a treatment has an interesting biological rationale.
They’re conducting much larger, controlled studies designed to determine whether it actually works and to further evaluate its safety.
DELTA CARE 1 aims to recruit up to approximately 650 adults with LS across roughly 80–90 sites in the United States, Canada, and several European countries. The trial began enrollment in May 2026.
Researchers are also doing more than simply asking whether patients feel better after using the cream.
*Image created using NotebookLM AI for illustrative purposes only. It was not an official ISSVD slide or used in an ISSVD presentation and may contain inaccuracies or errors.
During the initial treatment period, they are comparing delgocitinib with a vehicle cream—essentially the cream formulation without the active drug. At Week 12, the primary endpoint evaluates whether participants’ LS reaches clear or almost clear, together with at least a two-step improvement on a clinician-rated LS severity scale developed for the trial.
Researchers are also examining outcomes that patients care deeply about, including itch, pain, and vulvar quality of life. They’re assessing clinician-rated disease severity and safety as well. Some outcomes continue later in the study, providing information beyond that initial 12-week comparison.
The investigators emphasized that DELTA CARE 1 will be the first trial to assess the efficacy and safety of a topical pan-JAK inhibitor in patients with LS.
Exciting? Yes. Proven New LS Treatment? Not Yet.
This is where I want to put my patient-advocate hat firmly back on.
A Phase 3 trial is genuinely exciting. It means a potential new treatment for LS has progressed into serious late-stage clinical investigation. Considering how limited our evidence-based treatment options have historically been, that matters.
But researchers are still studying delgocitinib for LS. The existence of a Phase 3 trial does not tell us that the trial will succeed. It certainly doesn’t establish delgocitinib as a replacement for topical corticosteroids.
There are also bigger questions that matter enormously in a lifelong disease like LS.
Improving itch, pain, and visible inflammation is important. But patients also need to know whether a treatment can provide durable long-term control and protect against progressive scarring and architectural changes.
Appropriately treated LS is associated with a lower risk of vulvar squamous cell carcinoma. We therefore ultimately need to understand whether newer therapies provide comparable protection against the long-term complications that make disease control so important.
The current 52-week DELTA CARE trial can provide valuable longer-term efficacy and safety information. However, it is not designed to establish decades-long cancer prevention.
So my biggest takeaway from this presentation was both hopeful and cautious:
New treatment options may finally be entering serious late-stage clinical research for LS. But “promising” and “proven replacement for topical corticosteroids” are two very different things.
Not every shiny new LS treatment is ready for prime time
Regenerative Treatments: Interesting Innovation, but Not a Replacement for Established LS Care
Another presentation that stood out to me came from Eleonora Petra Preti, MD, of the European Institute of Oncology (IRCCS) in Milan, Italy. She presented Microfragmented Adipose Tissue Transplant: A New Regenerative Approach for Vulvar Lichen Sclerosus.
The presentation explored microfragmented adipose tissue transplantation (MFAT). Essentially, clinicians take a patient’s own fat tissue, process it in a way designed to preserve components of its natural structure, and inject the processed tissue into the vulvar area.
The biological idea is that adipose tissue is more than simply “fat.” It contains cells and signaling components that may have immunomodulatory, tissue-supporting, blood-vessel-promoting, and anti-scarring effects.
The presentation described adipose tissue as a potential “regenerative hub.”
How Is This Different From Other “Regenerative” Treatments?
It’s important to clarify that MFAT is not the same thing as PRP, and not all treatments involving a patient’s fat tissue are the same procedure.
An important part of the biological rationale for MFAT is how clinicians process the fat. Rather than simply isolating individual cells, MFAT uses mechanical processing intended to retain the tissue’s cells and natural microarchitecture, including components of its vascular and stromal environment—the tissue’s natural support system.
The theory is that preserving this local cellular “neighborhood” may help retain some of the adipose tissue’s regenerative and signaling functions.
Dr. Preti’s presentation compared MFAT with other fat-processing methods, including centrifugation, stromal vascular fraction (SVF) isolation, and emulsification. These approaches produce biologically different preparations.
For example, SVF isolates a mixture of cells from adipose tissue. MFAT instead retains cells within fragments of their original tissue structure. Therefore, when you see studies or clinics discussing “adipose-derived” or “fat-derived” treatments for LS, you cannot automatically assume they’re studying the same intervention as MFAT.
What About Platelet-Rich Plasma (PRP)
PRP comes from a patient’s blood rather than their fat and concentrates platelets and platelet-associated growth factors. MFAT, by contrast, is actual adipose tissue containing a much more complex cellular and structural environment.
That distinction matters when interpreting LS research. Evidence for one regenerative preparation cannot simply transfer to another. A study of PRP does not establish that MFAT works. Likewise, a study of one fat-processing method does not prove that another fat-derived procedure will produce the same results.
*Image created using NotebookLM AI for illustrative purposes only. It was not an official ISSVD slide or used in an ISSVD presentation and may contain inaccuracies or errors.
When patients hear broad terms such as regenerative medicine, fat injections, stem-cell therapy, or PRP for LS, my advice is to look beyond the label.
Ask: What exactly was used? How was it prepared? What clinical evidence exists for that specific intervention in LS?
So, What Did They Actually Study?
This is where context becomes incredibly important.
This was not a randomized controlled trial. Instead, researchers conducted a single-center, prospective observational study involving women with VLS that had not responded to standard first-line treatment.
They analyzed 45 patients from 56 enrolled, with a mean age of approximately 57 years. Follow-up extended as long as 40 months.
Researchers evaluated burning, itching, painful sex, and dryness. They also assessed vulvar examination findings, quality of life, sexual function, and tissue changes under the microscope.
The results were definitely interesting.
Following a single MFAT procedure, researchers reported significant reductions in several symptoms, including burning, itching, painful sex, and dryness. Clinical examination scores also improved. Patients reported improvements in quality of life and sexual-function measures during portions of follow-up.
But one finding in particular caught my attention: feeling better did not necessarily mean that the underlying LS had disappeared.
When researchers examined tissue under the microscope, some histological abnormalities persisted. They found persistent chronic inflammation in 74.4% of evaluated tissue and persistent hyperkeratosis in 57.9%. Hyperkeratosis means the outermost layer of the skin remained thicker than normal.
This is important because symptom improvement did not necessarily mean that the underlying LS-related tissue changes had resolved.
In other words, less itching, burning, or pain should not automatically be interpreted as the disease itself being inactive or “cured.” The authors specifically described symptom improvement alongside persistent histological changes. Many patients also resumed topical corticosteroid treatment during follow-up.
Innovation Is Not the Same Thing as Established Treatment
The researchers clearly acknowledged the study’s limitations. It took place at one center, involved a limited sample size, and had no control group. They also noted the procedure’s high cost and limited availability.
This was probably one of my biggest lessons from ISSVD: we have to be able to get excited about innovation without getting ahead of the evidence.
Studies like this give researchers a reason to continue investigating whether regenerative approaches could eventually play a role in LS care, particularly for people with difficult-to-treat symptoms.
But an observational study cannot tell us whether MFAT itself caused the improvements. It also cannot establish how MFAT compares with other treatments, which patients are most likely to benefit, or how reliably those benefits will persist.
Perhaps most importantly, Dr. Preti’s concluding model did not present MFAT as a replacement for topical corticosteroids.
Instead, the presentation proposed a multimodal approach. Topical corticosteroids remained the maintenance standard of care for controlling chronic inflammation and disease progression. MFAT was positioned as a potential regenerative intervention targeting tissue microarchitecture and symptoms in selected patients with refractory VLS.
For me, that’s an especially important distinction. Patients with vulvar disease increasingly encounter procedures described as regenerative or restorative.
It’s completely understandable to be interested in something new, especially when you’re still experiencing pain, sexual dysfunction, or other symptoms despite treatment. But new, biologically interesting, and commercially available are not the same thing as proven effective.
Before an emerging procedure can reasonably be considered an alternative to established LS treatment, we need stronger evidence. That includes controlled comparative trials, adequate participant numbers, longer-term follow-up, reproducible results, and safety data.
ISSVD reminded me how important it is to distinguish innovation from established treatment. Early regenerative research can absolutely be worth following, but people deserve to know how strong the evidence actually is before investing their money, hope, or health in an emerging procedure.
Children With LS Need Much More Than a Prescription
Another area of the Congress that I was really glad to see receive dedicated attention was pediatric vulvar lichen sclerosus (VLS).
Several presentations approached pediatric LS from very different angles. They examined the symptoms children experience, treatment, and what it is actually like to grow up with the condition.
One study, presented by Alla Vash-Margita and colleagues, followed 91 patients diagnosed with LS before their first menstrual period. The average age at diagnosis was 6.9 years, although children in the cohort received diagnoses anywhere from ages 3 to 13.
And the symptoms weren’t limited to itching.
In this group, 48.9% had vulvar whitening, 23.9% had soreness, 23.9% experienced incontinence, 15.2% had fissures, and 51% experienced constipation or encopresis (meaning constipation and/or stool leakage or soiling).
Some symptoms, including vulvar soreness and whitening, could persist for years after the initial diagnosis.
That’s an important reminder for parents and healthcare providers: LS in a child may show up through bowel or bladder problems as well as obvious vulvar symptoms. A child may not have the language—or feel comfortable enough—to say that their vulva hurts.
Researchers also looked at other health conditions occurring alongside LS. In this cohort, 29.4% had eczema and 23.9% had asthma. Smaller numbers had conditions including vitiligo, morphea, Hashimoto’s thyroiditis, and celiac disease.
The authors concluded that pediatric LS coincided with several atopic, skin, and gastrointestinal autoimmune conditions, although they did not find an association with every condition they examined.
What About Treatment?
Carlotta Caia, MD, and colleagues presented a separate study asking an important practical question: Pediatric Vulvar Lichen Sclerosus: Is a One-Size-Fits-All Prolonged Induction Regimen Effective?
Their retrospective study included 94 pediatric patients with clinically diagnosed VLS.
Patients received clobetasol propionate 0.05% ointment using a six-month tapering regimen. A multidisciplinary team followed them, including specialists in vulvar disease, pediatric gynecology, pediatric dermatology, and pediatric urology.
Symptoms improved substantially.
Researchers reported complete symptom remission in 83% of patients. Itching decreased from 80% at the beginning of treatment to 13% at six months. Burning also decreased. Painful urination, painful bowel movements, and nighttime waking had resolved by three months in this cohort.
Researchers reported mild side effects in 8% at the three-month assessment, with no severe adverse events observed. Side effects also became less frequent over time.
The authors concluded that prolonged induction treatment with an ultrapotent topical corticosteroid was effective and safe in their cohort.
However, this doesn’t necessarily mean every child should receive an identical regimen. The researchers called for randomized controlled studies to better establish long-term benefits and the optimal duration of treatment.
What Is It Actually Like to Grow Up With LS?
Perhaps the pediatric presentation that stayed with me most wasn’t primarily about medication at all.
Caroline Owen and colleagues presented preliminary findings from the CHILL Study, Understanding the Lived Experiences and Unmet Needs of Children With Vulval Lichen Sclerosus and Their Caregivers: A Qualitative Study.
Rather than measuring skin changes or treatment response, researchers actually talked to children and their caregivers.
At the time of the presentation, the study included 36 participants from 19 families: 17 children and young people and 19 caregivers. The children interviewed had an average age of approximately 12 years.
Three major themes emerged: the journey to diagnosis, the impact of LS on everyday life, and the need for better education and information.
Families described early misdiagnosis and parents feeling guilty that they hadn’t been able to get help sooner. LS also interfered with things children should ordinarily be able to take for granted, including sleep, school, concentration, sports, clothing, and going to the toilet.
The study also identified a need for reassurance and education around topics including treatment and cancer risk.
That last part really struck me.
When we talk about pediatric LS clinically, it’s easy to focus on whether the skin looks better or whether the child is applying their medication. But that child is also trying to understand why something is happening to such a private part of their body.
At the same time, their parent or caregiver is trying to manage treatment, find knowledgeable healthcare professionals, answer difficult questions, and decide how much information is appropriate at each age.
Those needs change as the child grows and moves into adolescence.
The researchers proposed several next steps. These included developing information specifically for children, a child-friendly treatment plan, resources for schools, continued education for healthcare professionals, and support for parents and caregivers seeking specialist care.
For me, that was the bigger message running through the pediatric research at ISSVD.
Treating childhood LS isn’t simply about handing a parent a tube of medication. It means recognizing symptoms early and treating the disease effectively. It also means addressing bowel and urinary problems when present, educating families, communicating in ways children can understand, and supporting young people as they gradually take greater responsibility for their own healthcare.
Pediatric LS isn’t simply “adult LS in a smaller body.” Children and their families have their own medical, practical, educational, and emotional needs. Good LS care needs to grow with the child.
Vulvodynia Is Not “Pain When Nothing Is Wrong”
Although vulvodynia isn’t LS, I wanted to flag one of my biggest takeaways from the discussions and presentations on vulvodynia at ISSVD.
Bernard Harlow’s 25-year overview reinforced an important distinction. Vulvodynia describes chronic vulvar pain or discomfort when clinicians have not found an identifiable cause after appropriate evaluation.
However, it does not mean that the pain isn’t real or that “nothing is wrong.”
Researchers are increasingly investigating biological and biopsychosocial mechanisms that may contribute to this pain. These include immune and inflammatory processes, changes involving nerves, and interactions with reproductive, gynecologic, environmental, and psychological factors.
Other presentations explored increased glial-cell activity in vulvodynia and the role of pelvic-floor rehabilitation in breaking cycles of pain.
Together, they reinforced a message I think patients need to hear:
No visible lesion does not mean no biological process.
I would also add something from my own advocacy experience: don’t let the word “vulvodynia” end the conversation.
The diagnosis should prompt careful evaluation and appropriate consideration of other possible causes of vulvar pain. I’ve spoken with patients whose pain was initially attributed to vulvodynia—and sometimes managed primarily with approaches such as CBT or mindfulness—who later received LS or LP diagnoses that helped explain their worsening symptoms.
That doesn’t mean everyone diagnosed with vulvodynia has an undiagnosed vulvar disease. Nor does it make CBT, mindfulness, or pelvic-floor therapy inappropriate. They can be valuable parts of pain management.
It means clinicians should keep their detective hats on, particularly when symptoms change, progress, or don’t respond as expected.
My takeaway: vulvodynia is a real pain condition, not a synonym for imaginary or unexplained-away pain. A diagnosis should never be used as a reason to stop listening, examining, and reassessing.
Pathology Isn’t Always Black and White
One of the most validating discussions for patients came from the Advanced Pathology Roundtable at ISSVD.
The cases highlighted just how complicated diagnosing inflammatory vulvar diseases such as lichen sclerosus (LS) and lichen planus (LP) can sometimes be.
One of my biggest takeaways was this: a biopsy isn’t necessarily a magical yes-or-no test.
Under the microscope, LS does not always show the classic changes a pathologist expects. Some biopsies from clinically apparent LS can instead show a more nonspecific pattern called lichenoid dermatitis. Essentially, this describes a particular pattern of inflammation that can occur with more than one condition.
LS and LP can also have overlapping features. Importantly, a person can have both LS and LP at the same time. If you aren’t sure, check out our post here.
More on Pathology
That means an inconclusive biopsy doesn’t necessarily translate to “you don’t have LS.”
The ISSVD’s own practical guidance emphasizes interpreting biopsy results alongside the clinical examination and history. A nondiagnostic biopsy should not automatically overturn a strong clinical diagnosis of LS.
In difficult cases, communication between the clinician and pathologist may help clarify what’s happening. Sometimes clinicians may also take additional biopsies from areas that look different.
This is especially relevant when distinguishing vulvar LS from vulvovaginal LP. While these diseases can overlap, important differences exist in how they can present and which areas they affect. We have a deeper breakdown of VLS versus VLP on our website for anyone navigating a confusing diagnosis.
And this is exactly why better LP research matters. If you live with cutaneous, oral, or genital lichen planus, we’re currently collecting patient experiences through our Global Lichen Planus Patient Experience Survey.
My patient takeaway: If your pathology report says “nonspecific,” “lichenoid dermatitis,” or doesn’t perfectly match what your clinician sees, it doesn’t necessarily mean you’ve reached a diagnostic dead end. Clinical appearance + history + pathology + how things evolve over time can all be pieces of the same puzzle.
“Natural,” “Clean,” and “Hypoallergenic” Don’t Necessarily Mean Vulvar-Safe
Another super practical presentation at the ISSVD World Congress came from Sydney Rivera Dixon, MD, MPH, who examined the contact-allergen burden of commercially available vulvar soothing products.
Researchers analyzed 65 products marketed as vulvar balms, moisturizers, and vaginal moisturizers. They compared the ingredients against the North American Contact Dermatitis Group allergen series.
The results were striking: 78% contained at least one common contact allergen, 20% contained three or more, and nearly half contained botanical allergens.
Botanical fragrance ingredients were the most common. Researchers also identified other allergens, including preservatives, propylene glycol, and lanolin alcohol.
Perhaps most importantly, marketing claims didn’t predict which products contained fewer allergens.
Terms such as natural, organic, clean, and hypoallergenic were not associated with a lower allergen burden. In fact, none of the 14 zero-allergen products carried a “hypoallergenic” label, while 13 products containing allergens did.
Expensive Doesn’t Necessarily Mean Better
Price wasn’t protective either. More expensive products didn’t contain fewer allergens.
Ointments tended to contain fewer allergens than creams, gels, lotions, oils, serums, and sprays. Plain petrolatum was the most cost-efficient zero-allergen option in the analysis. This continues to be the number-one recommendation I hear from dermatologists I speak with.
This doesn’t mean everyone will react to an ingredient classified as an allergen.
However, if you have a vulvar condition and experience persistent or changing itching, burning, or irritation, remember this: a product you’re using to soothe the vulva could sometimes be contributing to your symptoms.
Patient takeaway: Don’t assume natural, clean, organic, or hypoallergenic means allergy-free. With vulvar skin, simpler products may sometimes be the better choice.
Conclusion: What I Really Took Away From the 2026 ISSVD
*Top left photo including Dr. Rutherford, Dr. Simpson, myself, Dr. Mauskar, and Dr. Owen. Second photo top left is myself and Dr. McClure. Top right photograph is Dr. Selk, myself, and Dr. Mauskar. Bottom left is myself and Aakankshya (University of Alberta). Last photo is my badge and congress agenda.
If there was one overarching theme I took away from Halifax, it’s that vulvar-health research is becoming more sophisticated, and that gives me a tremendous amount of hope.
We’re moving beyond simply asking what causes LS? Researchers are identifying specific immune pathways and investigating potential new treatments in late-stage clinical trials. They’re also examining not only disease biology, but what it actually means to live with these conditions.
I also left Halifax reminded that scientific progress and better patient care aren’t always the same thing—and we desperately need both.
A new molecular discovery doesn’t help the person who spends years being misdiagnosed. A promising treatment doesn’t replace the need for clinicians who understand these diseases today. Better research also means little if patients aren’t included in deciding which outcomes actually matter.
Progress is expansive
So yes, I left ISSVD incredibly excited about where the science is going. But progress isn’t only a new drug, procedure, or laboratory discovery.
Progress is a child being diagnosed sooner. It’s a person with vulvar pain finally being believed. It’s a clinician continuing to investigate when the answer isn’t obvious. It’s researchers listening to patients. And it’s a person being treated as a whole human being—not simply a vulva.
There is still so much we don’t know and still so much we can do. But I came home genuinely hopeful about the questions researchers are asking, the direction the science is moving, and the growing recognition that patient voices belong in that progress.
I feel incredibly privileged to have been in Halifax representing that voice, and I can’t wait to see where we go from here.
Stay In The Loop! Never Miss A Blog Post, YouTube Video, Podcast Episode, Event, Or Product Launch By Getting On Our Newsletter!
Support Resources
P. S LSSN is Expanding Our Support: Introducing AboutLichenPlanus.com
At LichenS Support Network (LSSN), our mission has always been to provide trusted education, resources, and community support for people living with chronic vulvar and skin conditions. We’re excited to share that we’re expanding our efforts beyond lichen sclerosus to include other closely related conditions, including lichen planus (LP) and lichen simplex chronicus (LSC).
To support this growing community, we’ve launched AboutLichenPlanus.com — a dedicated resource designed to help patients and caregivers better understand and manage lichen planus.
On the site, you’ll find:
- Easy-to-understand information about lichen planus and its various forms
- Expert educational resources
- Patient stories and lived experiences
- Treatment and management information
- Videos, blogs, and downloadable resources
- Opportunities to get involved in research and advocacy initiatives
If you or someone you know has lichen planus, we encourage you to explore the site, share it with others who may benefit, and help us spread awareness.
We’re also inviting individuals living with lichen planus to participate in our patient survey. Your experiences can help identify unmet needs, improve educational resources, and guide future research and advocacy efforts.
Visit AboutLichenPlanus.com to learn more, and please share it with anyone affected by lichen planus or related conditions. Together, we can build a stronger, more informed, and more supported community.
