Welcome to this July 2026 review of Dermatologic Surgery. We've got four pieces from the Communications and Reconstructive Conundrum sections this month — a novel histology stain for thermal injury, a diagnostically tricky adnexal tumor case, a pediatric phototherapy case report, and a nasal reconstruction conundrum. Let's get into it.

First up is a technique-and-methods communication out of the Manstein group at Massachusetts General Hospital, introducing what they're calling the Ahn–van Gieson stain, or AVG, for direct visualization of thermally denatured collagen. This isn't a clinical study — it's a histochemistry methods piece, so there's no patient cohort or outcomes to report, just a description of a staining protocol and a proof-of-concept demonstration.

The background problem will be familiar to anyone who's dealt with energy-based devices or thermal wound histology: when collagen is thermally denatured, the triple helix unwinds and you lose birefringence, but visualizing exactly where that thermal damage zone begins and ends has always been a workaround. Birefringence imaging and nitroblue tetrazolium staining both infer damage indirectly, from loss of signal, rather than positively labeling denatured collagen itself. And the old standby stains — H&E, Masson's trichrome, even conventional Verhoeff–van Gieson — either lack contrast or are maddeningly inconsistent, particularly because the ferric chloride differentiation step in classic VVG is notoriously hard to standardize.

Their fix is elegant and almost entirely a reagent-substitution story. They kept the iron-hematoxylin backbone of Verhoeff's original 1908 stain — the same iron-mediated binding that makes elastic fibers show up so darkly — but they swapped out the finicky ferric chloride differentiation step for a brief one percent acid alcohol rinse, followed by sodium thiosulfate to clear residual iodine. The rationale, which they spell out directly, is chemical: thermal injury exposes previously buried basic residues in the collagen, and those residues bind ionically to the anionic hematein dye. Iron, with its accessible 3d orbitals, forms a much stronger complex with that dye than the aluminum mordant used in routine H&E — which is presumably why H&E gives you murky bundle coalescence but no real color discrimination between normal and denatured collagen.

For their demonstration, they used discarded abdominoplasty skin, hit it with a fractional CO2 laser to create a defined vertical thermal damage zone, and then compared horizontal sections stained with H&E, conventional VVG, and their new AVG protocol, cross-checked against birefringence imaging as the reference standard. The results were about as clean as a proof-of-concept gets: H&E showed only vague bundle coalescence with no real color separation; conventional VVG gave inconsistent, patchy decolorization depending on how long the ferric chloride differentiation ran; AVG, by contrast, stained denatured collagen a sharp dark blue-black while normal surrounding collagen stayed pink, and elastic fibers still stained dark just as they do in standard VVG. Importantly, the AVG-positive zones lined up with the birefringence signal-loss areas, which supports specificity — and AVG actually did the birefringence method one better, revealing structural detail like ablation craters and adnexal remnants within those signal-void zones that birefringence imaging couldn't resolve on its own.

There's no patient outcome data here and really no limitations section to speak of — this is a single-demonstration, ex vivo proof-of-concept, not a validated diagnostic assay, and the authors are appropriately modest, framing it as broadly applicable to burn pathology, energy-based device development, and tissue engineering research rather than claiming clinical diagnostic utility. For the practicing Mohs surgeon, this isn't practice-changing tomorrow, but it's a genuinely useful bench tool if you or your institution does any laser research, device validation work, or thermal injury histology — a simple, reproducible one-step swap into your existing VVG workflow that could meaningfully improve how thermal damage zones are characterized in that research context.

Second, a case report from UT Health Houston on a proliferating pilar tumor that gave everyone a diagnostic runaround. This is a straightforward case presentation, so we'll walk through presentation, management, and the teaching point rather than forcing it into a methods-and-results shape.

Proliferating pilar tumors arise from the outer root sheath, usually out of a pre-existing trichilemmal cyst — and remember, garden-variety pilar cysts are common, affecting something like five to ten percent of the population — but transformation into a true proliferating tumor is rare, and when it happens, it can look unnervingly like squamous cell carcinoma, especially the keratoacanthoma-type. That histologic and clinical overlap is exactly what plays out here.

The patient was a 31-year-old woman with a draining scalp lesion, initially treated empirically as an abscess with doxycycline. A month later it was excised as a presumed pilar cyst, and pathology called it a hybrid cyst with proliferative features — sitting somewhere between an epidermal inclusion cyst and a trichilemmal cyst, with verrucous hyperplasia of the lining. Nine months after that, she came back with a large, keratotic, exophytic nodule that grew rapidly over the following month — clinically worrisome enough that keratoacanthoma-type SCC was seriously on the differential. A shave biopsy showed persistence of the same hybrid cyst process, and she went to excision with frozen section margin control. Intraoperative pathology showed focal residual epidermal involvement, and the final debulking specimen showed an exo-endophytic squamous proliferation with trichilemmal features — consistent with a persistent, locally aggressive proliferating pilar tumor, not SCC. Closure was primary, and healing was uneventful.

The teaching point the authors emphasize is the histologic hallmark that should anchor your diagnosis when a scalp lesion looks like this: trichilemmal keratinization, that abrupt shift from nucleated to anucleated keratin without an intervening granular layer, distinguishing it from the keratinization pattern of SCC. They also flag that there's no standardized grading system separating benign from malignant PPT — the field still relies on the three-tier classification proposed by Ye and colleagues from a case series of seventy-six patients, splitting lesions into PPT, low-grade malignant PPT, and high-grade malignant PPT — and that diagnosis remains fundamentally clinicopathologic rather than criteria-driven. Notably, despite this lesion's aggressive clinical behavior — rapid regrowth, local recurrence in a young patient — the histology stayed benign-appearing throughout, which is the crux of the diagnostic tension the authors want you to sit with.

Practically, this is not a paradigm-shifting paper, but it's a useful pattern-recognition reminder for anyone doing Mohs or frozen section work on scalp lesions: a keratotic, rapidly growing scalp nodule with a cystic origin story deserves a high index of suspicion for PPT even when histology looks reassuringly bland, frozen section margin control is a reasonable approach when there's diagnostic ambiguity and recurrence risk, and you shouldn't let benign-sounding histology fully talk you out of aggressive clinical behavior — treat the whole picture, not just the slide.

Third is a brief case report on pediatric localized scleroderma treated with 308-nanometer excimer light therapy, out of a Fujian Medical University group with rheumatology co-authors. Again, this is a case report, not a trial, so we're covering presentation and management and the teaching point, with no statistics to translate.

The clinical problem: localized scleroderma management is tailored to disease activity and extent, and while UVA phototherapy has been the traditional workhorse, UVB approaches — including targeted 308-nanometer excimer light — have been gaining traction, though the authors note there's still no reliable biomarker to predict who will respond.

Their patient was a 5-year-old girl with erythematous, sclerotic plaques on the upper back, present for a month and unresponsive to topical corticosteroids. Anti-single-stranded-DNA antibodies were normal, and biopsy showed dermal collagen deposition with mild perivascular lymphocytic infiltrate — histology consistent with active disease, which was corroborated by an active disease-activity score using the Childhood Arthritis and Rheumatology Research Alliance criteria. She was started on weekly 308-nanometer excimer light at a low starting dose of 0.1 joules per square centimeter, titrated up to 0.2 based on tolerance, reaching a cumulative dose of about 1.2 joules per square centimeter. She had significant clinical improvement — reduced erythema, softening of the sclerotic plaques — with no adverse effects like hyperpigmentation or blistering.

The authors' discussion frames the rationale for excimer light as targeted UVB delivery to affected skin only, lower cumulative UV exposure than broader phototherapy, and shorter treatment courses, with the presumed mechanism being T-cell suppression and downregulation of proinflammatory cytokines. They're appropriately restrained in their conclusion — this is a single case, so there's no control for spontaneous improvement or concurrent care, and they explicitly call for further work to define optimal protocols and predictive markers of response.

For your practice, this is interesting-but-not-yet-actionable territory unless you're managing pediatric morphea directly — it's a reasonable option to keep in mind for early, inflammatory-phase localized scleroderma when topical steroids fail, particularly appealing in a pediatric patient given the lower cumulative UV burden, but it's a single case report and shouldn't be read as established first-line therapy.

Last, a Reconstructive Conundrum piece on repairing a defect of the nasal soft triangle — a technique and decision-making discussion built around a single illustrative case, so we'll walk through it the way the feature is designed: problem, options considered, and the chosen solution.

The patient was a 64-year-old man with a small nodular basal cell carcinoma — about 0.3 by 0.4 centimeters — right on the left nasal soft triangle, which as you know is disproportionately unforgiving for its size given its propensity to notch and its total lack of forgiving subcutaneous bulk. After Mohs clearance, the authors walk through the standard reconstructive toolkit for this location before landing on their choice. Composite auricular grafts get a mention for their excellent three-dimensional color and texture match and their suitability for alar or soft triangle defects up to one to two centimeters, especially where cartilage support is needed to prevent alar retraction. Bilobed and trilobed transposition flaps are discussed as the traditional workhorses, moving adjacent tissue with minimal tension, with the trilobed variant adding a third lobe for extra flexibility in this anatomically tight corner. The nasalis sling myocutaneous flap gets a nod too, valued for its robust vascularity in a zone that's prone to healing complications.

But the authors point out the shared Achilles' heel of these local flap options in the soft triangle specifically: the flap thickness needed to preserve vascularity tends to produce a trap-door effect in what is naturally a very thin anatomic zone, and any tension or retraction at the pivot point shows up as visible asymmetry in a highly conspicuous part of the nose.

Their solution here was a columellar banner transposition flap — not a traditional first-line choice for soft triangle defects, but one they argue is well-suited to patients with a broad columella and a small defect, since the tissue is a near-perfect color and texture match and helps conceal the scar while minimizing notching risk. Closure used fine polydioxanone and fast-absorbing gut sutures. At two months, healing was good, though the authors are candid that there was still some degree of notching at the repair site — an honest, unembellished outcome rather than a polished success story. They suggest that adding a small helical cartilage strut beneath the flap in future cases might provide the structural support needed to prevent that residual notching.

The practical takeaway here is squarely for your reconstructive decision tree: the columellar banner flap is a reasonable, tissue-matched alternative to keep in your back pocket for small soft triangle defects in patients with a broad columella, particularly when you want to avoid the trap-door risk that comes with thicker local flaps — but the authors' own result argues for pairing it with a structural cartilage graft if notching prevention is a priority, and this should be viewed as one option among several rather than a new gold standard.

That wraps up this July 2026 issue — a novel stain worth knowing about if you touch laser or thermal injury research, a sharp reminder to keep proliferating pilar tumor on your scalp differential even when histology looks tame, a promising but early phototherapy option for pediatric morphea, and a creative, if imperfect, solution to one of the nose's least forgiving subunits. Thanks for listening.