Welcome back to the journal review. This month we're working through the July 2026 issue of Dermatologic Surgery, and I've pulled four pieces worth your time — two reader communications responding to recent trials, one clever bench-top experimental study on wound tension, and a reconstructive conundrum case report on a large nasal defect. Let's get into it.

First up is a communications letter responding to a systematic review by Yii and colleagues on follicular unit graft survival after hair transplantation in primary cicatricial alopecia — so this isn't itself the primary systematic review, it's a critical commentary on it, and the authors add their own case to make the point. Some quick background on what they're responding to: Yii's review pooled eight observational studies, just over a hundred patients total, and concluded that follicular unit graft survival in inactive cicatricial alopecia tends to peak around the one-year mark and then decline afterward. The letter writers — a hair restoration group out of Brazil — say that tracks with their own clinical impression, but they want to push on why that decline happens, and they lay out three candidate explanations. One, ongoing subclinical disease activity at the time of transplant that nobody detected. Two, the intrinsically poor quality of fibrotic, poorly vascularized recipient skin in these patients, which is well accepted and not really controversial. And three — the more provocative point — that the donor area itself may harbor occult inflammatory infiltrate, even in a zone that looks completely uninvolved clinically. They cite prior work showing lichenoid infiltrates on occipital biopsies in frontal fibrosing alopecia patients with no clinical signs there at all. The core clinical problem they're highlighting is that clinical markers of disease activity — peripilar erythema, hair casts, symptoms, even careful dermoscopy — just don't reliably correlate with histologic inflammation. So your bedside assessment of "quiescence" may simply be wrong, and you have no great noninvasive way to know that.

To illustrate this, they present a single case: a thirty-six-year-old man with androgenetic alopecia and coexisting active lichen planopilaris on the anterior scalp. He was treated medically — hydroxychloroquine, oral minoxidil, dutasteride — and after eight months his symptoms resolved and dermoscopy normalized, so by all conventional criteria he was called stable. A year later he underwent follicular unit extraction to the frontal hairline, on the order of thirty-six hundred grafts, with an uneventful immediate postoperative course. But at the twelve-month follow-up, density was disappointing and dermoscopy now suggested lichenoid folliculitis; a punch biopsy confirmed perifollicular lymphocytic infiltrate consistent with reactivated lichen planopilaris. There's no formal methods section here, obviously — it's a letter with an illustrative case, not a study — but the teaching point is squarely aimed at your surgical decision-making. The takeaway is not that hair transplantation is contraindicated in cicatricial alopecia; the letter explicitly says it can be a viable option in selected patients. The practical message is one of humility about what "clinical quiescence" actually means — a year of clean dermoscopy and resolved symptoms did not prevent reactivation in this patient — and it argues for a low threshold for pre-transplant biopsy in borderline cases and for genuinely close postoperative surveillance rather than a one-time clearance visit. This is squarely in the "interesting and cautionary, not yet practice-changing in a protocol sense" category, since there's no validated biomarker or histologic threshold offered — just a reminder to keep your index of suspicion high.

Next, an original experimental piece — and it's a fun one, because it's entirely a bench-top physical model rather than a clinical or animal study. The question they're addressing: does the geometry of a surgical incision — straight versus angled versus zigzag — change the tension distributed along its edges, and does that relationship depend on incision length? This matters because we already know clinically that wound tension drives worse scarring, dehiscence, and altered cytokine release at the wound edge, and we already use tension-redistributing closures like W-plasty and geometric broken-line closures on the assumption that they help. But the authors point out nobody had actually modeled this quantitatively based on shape and length together, so that's the gap.

Their method is refreshingly simple: latex elastic bands standing in for human skin elasticity. They cut straight, L-shaped, and S-shaped incisions ranging from one to five centimeters, in half-centimeter increments, then applied a standardized one-kilogram-force traction to both incision edges using a symmetric weighted pulley system — a bag of salt on a string on each side, to keep the loading unbiased. They photographed the resulting gaps and measured the distance between the cut edges with ImageJ, then used Hooke's law — since displacement and tension are directly proportional in an elastic material — to back-calculate relative tension at the center of each incision type. The rationale for this design, which the authors state directly, is that no experimental data existed on this relationship at all, so a controlled, reproducible, inexpensive physical analog let them isolate shape and length as variables without the confounding of real tissue variability, patient anatomy, or wound healing biology — you're purely testing geometry and force here, which is exactly what you want as a first pass before moving to anything biological.

The results: for incisions under about two and a half centimeters, shape didn't matter much — tension behaved similarly across straight, L-shaped, and S-shaped cuts. But above that roughly two-and-a-half-centimeter threshold, the straight linear incisions showed meaningfully more tension at the wound center than either the L-shaped or S-shaped incisions, with the S-shape performing best — consistent with the idea that breaking a line into angled or curved segments redistributes the force vectors rather than letting them all concentrate along one axis. The authors are appropriately modest about what this means: it's a nonhuman model on a flat elastic substrate, tested only up to five centimeters, so you can't extrapolate to longer incisions or to the topographic complexity of actual anatomic sites with variable mobility and skin laxity. There's no biology in this model at all — no dermis, no collagen remodeling, nothing about healing. So the honest read for your practice is: this is a nice mechanistic reinforcement of something you already do — favoring curvilinear or geometric closures over long straight lines, particularly once you're past a couple of centimeters, especially in areas of dynamic tension. It's confirmatory and satisfying from a physics standpoint, but it's not new information that should change how you close a wound tomorrow; think of it as elegant support for existing dogma rather than a new practice trigger.

Third is another reader letter, this one responding to Elradi and colleagues' randomized trial comparing intralesional insulin, intralesional botulinum toxin-A, and intralesional corticosteroids for keloid treatment. Again, this letter isn't the primary study — it's a commentary — but it does a nice job summarizing the trial before critiquing it, so let's take both together. The underlying randomized trial enrolled just over sixty patients split three ways with reasonably balanced baseline characteristics. On keloid volume reduction, insulin got roughly two-thirds shrinkage, botulinum toxin got about one-quarter, and corticosteroids got about three-quarters — so steroids still won numerically, but insulin was closing in on steroid-level efficacy and clearly outperformed botulinum toxin. On the Patient and Observer Scar Assessment Scale, both insulin and steroids were statistically better than botulinum toxin for pigmentation, thickness, and symptom relief, and insulin essentially matched steroids across most of those parameters. The letter authors call out the dual patient-and-observer scoring as a genuine methodological strength, since it captures both the objective exam finding and what the patient actually experiences, which strengthens confidence in the result.

Where the letter adds value is in picking apart what's not yet answered. First, generalizability: the trial excluded diabetics and anyone on insulin or hypoglycemic agents, which is notable given the known association between diabetes and keloid formation — so a chunk of your real-world keloid population wasn't represented, and pediatric patients under sixteen, another high-risk group for pathologic scarring, weren't addressed with any dosing data either. Second, on safety methodology: dosing was fixed — ten international units per cubic centimeter for insulin, two and a half for botulinum toxin — with no dose-response testing, and no systematic long-term surveillance for things like altered systemic insulin sensitivity from repeated injections, or subtler botulinum toxin effects like local weakness that a single trial's follow-up might not catch. The letter proposes what more rigorous monitoring would look like going forward — oral glucose tolerance testing, glycated hemoglobin, high-frequency ultrasound to objectively quantify tissue change, and standardized neuromuscular exams — none of which existed in the original trial. Third, they flag combination therapy as an unexplored angle, floating the idea that botulinum toxin's tension-reducing, collagen-aligning effect could synergize with insulin's antifibrotic action, though this is entirely speculative and untested. Bottom line for your practice: intralesional insulin looks like a genuinely promising steroid-sparing option with a possibly better safety profile than we're used to worrying about with repeated corticosteroid injections — but this is one moderately sized trial with fixed dosing and no long-term safety data, filtered through a commentary that's explicitly asking for more before treating it as protocol. File it as promising and worth trying selectively, not yet a guideline-level change.

Finally, a reconstructive conundrum case report — a large full-thickness nasal ala and tip defect. A sixty-five-year-old woman had a recurrent sclerodermiform basal cell carcinoma on the right ala extending toward the tip. Complete excision took skin, mucosa, and cartilage of the nasal vestibule, leaving a four-by-three centimeter, full-thickness defect spanning the ala and tip — about as reconstructively unforgiving as nasal defects get. The standard teaching answer here is a paramedian forehead flap, given its reliable vascularity and its ability to independently provide both lining and external cover for exactly this kind of three-layer loss. But it's a multi-stage commitment, and this patient wasn't willing to go through multiple procedures, which forced the authors to a single-stage alternative.

Their solution was a cheek transposition flap extending into the nasolabial fold, but they found the standard version of that flap didn't reach far enough past the midline to cover the defect on its own, so they modified it by adding a triangular segment of tissue harvested at the upper lip. Technically, the flap was elevated in a deep subcutaneous plane just above the muscle, the distal portion was thinned by removing subcutaneous bulk, then folded onto itself and sutured to recreate the mucosal vestibular lining before being transposed into the defect — the main body covering the sidewall and ala, the triangular extension covering the tip, and the folded segment sutured to the residual vestibular mucosa. Notably, they chose to omit a cartilage graft, which would normally be standard for ala support to prevent collapse, reasoning that the adjacent semi-rigid tissue near the nasolabial fold provided enough structural backup in this particular case. The secondary defect at the nasolabial fold and lip was closed primarily in layers. Recovery was uneventful, sutures came out at one week, and at six months they report a genuinely good functional and aesthetic outcome, with symmetric nasal airways and no alar collapse.

There's no results or limitations section to walk through here in the traditional sense — it's a single case, and the authors are transparent that this is a case-based technical solution rather than a validated series. The teaching points they explicitly draw out are that this combined nasolabial transposition flap with an upper-lip triangular extension can serve as an effective single-stage alternative to the paramedian forehead flap for large combined tip-and-full-thickness-ala defects, essentially merging two previously described concepts — the fold-over nasolabial flap for vestibular lining, and the triangular lip extension for extra reach — into one design, and that cartilage grafting can potentially be skipped when there's adequate adjacent structural support. For your own practice, this is a nice addition to the reconstructive toolkit for patients who are anatomically similar but unwilling or unable to tolerate a staged forehead flap — genuinely useful as an option to keep in your back pocket, though as with any single case report, it's a demonstration of feasibility in one patient rather than validated across a series, so the usual caveats about case-based generalizability apply.

That wraps the four pieces for this issue. Two cautionary reader letters reminding us how much biologic uncertainty still sits underneath our clinical impressions of quiescence and treatment response, one clean mechanical proof-of-concept for something we already practice, and one elegant single-stage reconstructive option for a genuinely hard defect. Thanks for listening, and I'll see you next month.