Welcome back to the journal review. This is our walkthrough of the March twenty twenty-six issue of Dermatologic Surgery, and we've got four pieces worth your time today — a systematic review on the histology behind laser treatment of pigmented lesions, two reconstructive conundrum case reports tackling gnarly facial and periauricular defects, and a systematic review on squamoid eccrine ductal carcinoma that has real implications for how you counsel patients on modality choice. Let's get into it.

First up is a systematic review looking at lasers and energy-based devices for pigmented lesions, specifically correlating what happens clinically with what's actually happening under the microscope — light microscopy, electron microscopy, reflectance confocal microscopy, and optical coherence tomography. The clinical gap here is one you've probably felt in your own practice: we use nanosecond and picosecond devices for lentigines, melasma, café-au-lait macules, and tattoos, and we have plenty of outcome data, but the mechanistic explanation for why one device outperforms another, or why one lesion type stubbornly resists treatment, has been scattered across a fairly obscure ultrastructural literature. This review's aim is to pull that mechanistic thread together.

Methodologically, the authors ran a straightforward systematic review through PubMed, screened with no date restriction, and supplemented the electronic search with reference-list screening — a reasonable move given this is a mechanistic, imaging-focused literature that's likely to be indexed inconsistently. Two reviewers screened independently with a third as tiebreaker, which is standard rigor for this design. Out of over a thousand initial hits, they whittled down to thirty-nine included studies after excluding in vitro work, reviews, non-cutaneous indications, and non-English publications. The end product isn't a meta-analysis — you can't pool ultrastructural imaging findings quantitatively — so this is really a structured narrative synthesis, which is the right call given the heterogeneity of imaging modalities and lesion types involved.

The findings break down by lesion type, and there are some genuinely useful clinical correlates here. For lentigines, picosecond lasers created smaller vacuoles with disrupted melanosomes but preserved surrounding cytosolic architecture and an intact basement membrane, whereas nanosecond lasers produced larger vacuoles, more collateral cytosolic damage, and separation at the dermoepidermal junction. That histologic distinction lines up neatly with the clinical observation that picosecond devices carry a lower rate of postinflammatory hyperpigmentation, particularly in darker skin types — and it gives you a mechanistic reason to believe that observation rather than just anecdote. There's also a nice practical pearl buried in here about clinical endpoints: for picosecond lasers the correlate of appropriate tissue effect is subtle whitening, not the more dramatic graying you'd chase with a nanosecond device — worth remembering when you're calibrating fluence intraoperatively, especially in higher Fitzpatrick skin types where overtreatment risk is real.

For café-au-lait macules, the imaging explains a clinical pattern you've probably already noticed — jagged, "coast of Maine" bordered lesions respond better to laser than smooth, "coast of California" bordered ones. Confocal microscopy showed that the smooth-bordered lesions have denser papillae and more elongated rete ridges, and the authors' working hypothesis is that laser energy simply doesn't penetrate adequately to the base of those elongated ridges. That's a useful thing to tell patients up front when they present with a smooth-bordered CALM and unrealistic expectations.

For melasma, electron microscopy after low-fluence Nd:YAG laser toning showed selective photothermolysis at the subcellular level — melanosomes are cleared without killing the melanocyte outright — but cumulative treatments appear to induce melanocyte malfunction, which the authors link to the confetti-pattern hypomelanosis we sometimes see clinically after aggressive toning regimens. That's a mechanistic warning shot for anyone doing repeated toning sessions: the melanocyte isn't indestructible just because it survives the first few passes.

On tattoos, picosecond lasers confined ink particles within lysosomal structures for orderly clearance, while nanosecond lasers scattered particles into surrounding tissue — again, a tidy explanation for why picosecond devices tend to outperform on both efficacy and safety for tattoo removal.

The obvious limitation here, which the authors are appropriately candid about, is that this is a mechanistic hypothesis-generating synthesis, not controlled comparative trial data — much of the underlying histologic and ultrastructural work comes from small case series and single time-point sampling, and correlating a tissue-level observation with a clinical outcome doesn't prove causation. Still, the practical takeaway for your practice is genuinely useful, if not exactly practice-changing in the sense of overturning current protocols: it reinforces device selection you're likely already leaning toward, gives you defensible mechanistic language for patient counseling on picosecond versus nanosecond choice by skin type, and should make you think twice about how aggressively you toner-laser melasma given the hypomelanosis risk. File it under confirmatory and clinically reassuring rather than paradigm-shifting.

Next, a reconstructive conundrum on a large multisubunit defect involving the cheek, nose, and lip. The setup: a seventy-five-year-old woman with a deeply indurated metatypical basal cell carcinoma on the left nasolabial fold required three stages of Mohs to clear, with lymphovascular invasion noted on a prior stage — handled with a multidisciplinary discussion and a decision to monitor clinically rather than pursue additional imaging, given the lack of outcome data specifically for lymphovascular invasion in basal cell carcinoma. The resulting defect was substantial — five and a half by three and a half centimeters, extending to muscle and focally to bone, spanning the cheek, nasal ala, nasal sidewall, and cutaneous lip, with resection of the levator labii superioris and levator anguli oris muscles required for clearance.

The reconstructive discussion here is really a masterclass in subunit-based thinking under constraint. Secondary intention and skin grafting were both ruled out because of the risk of distorting three separate free margins — lip, eyelid, and ala. The authors also seriously considered a staged approach with delayed subunit reconstruction after a period of granulation, and separately considered a Mustarde cheek rotation flap paired with a paramedian forehead flap for the ala — but the patient explicitly did not want an interpolation flap or a prolonged open wound, which shaped the final plan as much as the anatomy did. That's worth flagging as a reminder that patient preference is a genuine input into reconstructive algorithm, not just an afterthought.

What they landed on was a single-stage combination repair: two subcutaneous hinge flaps borrowed from the bulky lateral cheek tissue to restore volume at the nasal sidewall, medial cheek, and lip; a lip rotation flap along the remaining nasolabial fold; a V-Y advancement for the residual cheek and apical triangle; and a small full-thickness skin graft from Burow's tissue to resurface the alar-facial junction. The teaching point on the hinge flap is a nice one — it's doing double duty here, restoring bulk to a deep defect and simultaneously creating a vascularized recipient bed for the skin graft, which let them avoid cartilage grafting or a two-stage repair altogether.

At six weeks the flap had healed well, but there was noticeable dynamic asymmetry from ipsilateral lip elevator paralysis due to the muscle resection — an expected functional tradeoff of clearing a deep tumor in that location, not a technical failure of the reconstruction. The patient opted for a revision at five months, which was accomplished with simple crescentic excisions along the nasolabial fold and alar crease to redefine contour and restore symmetry — notably not a redo of the whole flap, just targeted debulking. One year out, symmetry was improved, though she developed persistent lower eyelid festooning, which oculoplastics attributed to lymphatic disruption from the depth of the original defect and CPAP mask use rather than to the hinge flaps themselves, given the hinge donor tissue was anatomically distant from the eyelid.

There's no results-and-limitations scaffold here since this is a single case, but the take-home points are concrete: multisubunit defects of this scale genuinely call for restoring each cosmetic unit separately rather than trying to force one large flap across all of them; the subcutaneous hinge flap is a likely underused tool for volume restoration in bulky facial tissue and pairs nicely with a spacer skin graft to keep subunit boundaries intact; and when a patient refuses interpolation flaps, a single-stage combination repair followed by a straightforward revision is a legitimate strategy that can deliver high patient satisfaction even when a motor deficit complicates the initial cosmetic result.

The third article is another reconstructive conundrum, this one on closing double defects around the ear. A sixty-year-old man had squamous cell carcinoma in situ on the left superior helix, cleared in one stage to a two by one-and-a-half centimeter defect, and elected to delay closure so it could be combined with a second Mohs case the following week — an acantholytic squamous cell carcinoma on the left central zygoma that took two stages and left a one-and-a-half by one-point-eight centimeter defect. So the reconstructive question is really about efficiently handling two adjacent defects that both abut the anterior ear margin.

The solution used two random pattern flaps designed to work together. An O-to-L advancement flap closed the zygoma defect, drawn vertically along the anterior ear margin with a Burow's triangle taken medially to avoid distorting the ear. A complementary rotation flap, recruiting the bridging tissue between the two defects, closed the superior helical wound — and critically, the two flaps' motion vectors were designed to assist each other, with the rotation flap's lift helping the superior pull of the advancement closure below. The authors are explicit that alternative single large flaps, skin grafts, or secondary intention were all considered and rejected: combining the defects into one flap would have meant more undermining and more risk of pain and bruising for no real benefit; a graft was avoidable donor-site morbidity the patient didn't want; and secondary intention, while reasonable for the shallow concave helical defect, would have left a poor scar on the more convex zygoma.

The technique point worth remembering here is the deliberate choice of delayed closure — not as a compromise, but as a strategic advantage. Waiting allowed the two defects to be combined into a single coordinated closure, may have improved vascular supply to the flaps through vascular ingrowth during the interim, and the authors specifically note that despite common concern, delayed closure has not been shown in the literature to increase infection risk. The only technical caveat is that wound edges typically need refreshing to remove granulation tissue before final closure. At six months, the flaps were well healed with a nicely reconstructed anterior helix and no ear distortion.

The teaching points to carry forward: when you're facing multiple defects in one anatomic region, look for flap designs whose motion vectors complement rather than compete with each other — that's really the crux of a clean result here. Where feasible, merging two closures into a single contiguous line is both tissue-sparing and cosmetically favorable. And delayed closure deserves more consideration in your own scheduling logic than it typically gets — it's not just a stopgap for patient convenience, it's a legitimate reconstructive strategy, especially in compromised-vascularity zones like the helix.

Last, a systematic review — really a focused communication — on the surgical treatment of squamoid eccrine ductal carcinoma, a rare eccrine malignancy that behaves like a wolf in squamous cell carcinoma clothing: superficial features resembling SCC with a deeper eccrine ductal component that's easy to miss, especially on a shallow biopsy. The clinical problem is straightforward — this is a rare tumor with high recurrence and metastatic potential, there's no consensus treatment guideline, and the existing literature is scattered across individual case reports, so nobody has actually pooled the surgical outcomes data to see which modality performs best.

Methodologically, this followed the twenty twenty-four PRISMA checklist across PubMed, Embase, and Scopus, with two independent screeners and a third for discrepancies — appropriate rigor for a systematic review even though, as the authors acknowledge upfront, the underlying evidence is entirely case reports and case series, meaning this is Level 4 evidence with a Grade C recommendation. That's an important framing to hold onto through the results: this is the best available synthesis of a rare-tumor literature, not a comparative trial.

They identified ninety-eight cases across thirty-four articles. Thirty were treated with Mohs, sixty-four with surgical excision, and four with digit amputation. Mean age at diagnosis was seventy-four, roughly half were male, and just over half the cases occurred in the head and neck region, with cheek and temporal scalp the most common sites. Here's the number that actually matters for practice: recurrence after Mohs was ten percent, compared to about twenty percent after standard excision — roughly a two-fold difference favoring Mohs. Metastasis occurred in about eleven percent of the excision group and in none of the Mohs cases, though follow-up durations were comparable, around twenty-one to twenty-two months for both groups. The amputation cohort was tiny — only four cases — but notable for a fifty percent metastasis rate and one disease-related death, suggesting amputation was likely reserved for more advanced or distally located disease rather than reflecting some inferior technique.

The authors' interpretation is that Mohs' advantage plausibly comes from complete margin assessment catching the infiltrative growth pattern and perineural invasion that make this tumor prone to incomplete excision with standard margins — and that tracks with what we know about the biology of eccrine ductal tumors generally. They're appropriately honest about the limitations: this is case-level data with no ability to adjust for confounders like tumor size, depth, or perineural invasion status between treatment groups, margins for excision cases were inconsistently reported, and follow-up windows vary in quality across included studies. So the excision group could simply represent a higher-risk population that happened not to get Mohs, and we can't fully disentangle that with this data.

Practically, this is about as actionable as Level 4 evidence gets: if squamoid eccrine ductal carcinoma lands on your table, and given its head-and-neck predilection and propensity for perineural invasion, Mohs should be your default recommendation over standard excision. It won't rewrite formal guidelines by itself, since there's no denominator control for confounders, but for a rare tumor where a randomized trial will never happen, this is the strongest signal you're going to get, and it aligns with what most of us would already intuitively favor for an infiltrative, PNI-prone adnexal malignancy in cosmetically sensitive sites.

That wraps our four articles this month — a mechanistic deep dive that sharpens your rationale for picosecond versus nanosecond device selection, two elegant reconstructive conundrums that reinforce subunit-based flap planning and the underappreciated value of hinge flaps and delayed closure, and a rare-tumor systematic review that gives you real numbers to back up a Mohs-first approach to squamoid eccrine ductal carcinoma. Thanks for listening, and we'll see you next month.