Welcome back to the journal review. This is our walkthrough of Dermatologic Surgery, September twenty twenty-six, volume fifty-two, number nine. Four pieces on the docket today, all from the case-report and reconstructive-conundrum side of the journal — no big registry studies this month, so we'll spend our time on surgical decision-making and technique rather than statistics. Let's get into it.

First up is a case report titled "Five Primary Microcystic Adnexal Carcinomas in a Young Adult," out of Mayo Clinic Arizona. You already know microcystic adnexal carcinoma, or MAC, as the quiet menace of adnexal tumors — indolent-looking, slow-growing, usually on the head and neck, but riddled with subclinical extension and a strong tendency toward perineural invasion. The authors open by reminding us just how disproportionate that subclinical spread can be: in one study the post-Mohs defect averaged four times the size of the clinically apparent lesion. And the comparative outcome data they cite is worth keeping in your back pocket for patient conversations — wide local excision alone leaves positive margins in over half of cases, and across a systematic review pooling fifty-five studies, wide local excision carried roughly a fifty-five percent recurrence rate compared with about six percent for Mohs. That's not a subtle difference; that's the whole argument for Mohs in MAC in one sentence.

The reason this particular case earns a write-up is rarity of a different kind — not the tumor type, but the multiplicity. Only two prior reports describe more than one primary MAC in the same patient. This one blows past that: a previously healthy thirty-one-year-old woman who, over about ten months, was diagnosed with five histologically confirmed, anatomically distinct primary MACs — back, two on the chin, vulva, and right temple — occurring alongside an incidental papillary thyroid carcinoma picked up on PET-CT, that's positron emission tomography–computed tomography, done for staging. The index lesion was a plaque she'd actually had for over fifteen years on her upper back, finally biopsied and confirmed as MAC. That lesion required debulking followed by two-stage Mohs, sixteen plus three blocks, and left a nine-by-nine centimeter defect reconstructed by plastic surgery. Interestingly, the Mohs sections themselves were clear of perineural invasion, but the debulking specimen had shown it, at just over a tenth of a millimeter, which is what triggered adjuvant radiation. A separate temple lesion also showed perineural invasion and was handled with wide excision and a skin graft by ENT, that's ear, nose, and throat surgery, again with adjuvant radiation. The remaining lesions were split across Mohs and wide excision depending on site and specialty involved — vulvar by gynecology, some facial lesions by ENT.

Given the multifocality plus a synchronous thyroid cancer, they pursued a real genetic workup: a seventy-gene cancer panel, whole blood genome sequencing, mitochondrial genome analysis, and metabolomic profiling. All negative. No pathogenic mutations identified. So this remains, mechanistically, unexplained — the authors raise field cancerization, epigenetic influence, or postzygotic mosaicism as speculative explanations, and point to prior next-generation sequencing work implicating p53 and JAK-STAT pathway alterations in MAC generally as a place future molecular studies might look.

As with any single case report, the limitation is obvious and the authors don't pretend otherwise — this is one patient, mechanism unresolved, and generalizability is inherently limited. But the practical takeaway is genuinely useful even without a mechanism: if you're staring at an unusual MAC presentation — young patient, atypical location, or a second nodule showing up where you weren't looking — this case is permission to raise your index of suspicion for a second primary rather than assuming recurrence or coincidence, and it's a reminder to think about whether a broader skin exam or even systemic imaging is warranted in that scenario. It is not, however, a mandate to start reflexively screening every solitary MAC patient for occult malignancy or ordering genetic panels — that workup here was justified by the unusual multiplicity, not something the data support as routine.

Second article: "Multiple Familial Trichoepithelioma: A Staged Surgical Approach," from a Brazilian group at Santa Casa de Misericórdia de Porto Alegre. Multiple familial trichoepithelioma, MFT, is the autosomal dominant, multi-lesion form of trichoepithelioma — benign follicular germinative-cell tumors that classically start in childhood and skew toward women. Malignant transformation into basal cell carcinoma is exceedingly rare, first described back in 1959, and it's exactly that rare event that drives this case.

Their patient was a fifty-year-old man — notably male, against the usual demographic — with disfiguring facial nodules since age seven, centrifugally involving the nose, eyebrows, scalp, and retroauricular area, with a family history consistent with autosomal dominant inheritance. Initial biopsies confirmed garden-variety trichoepithelioma, but when they debulked the larger pedunculated lesions on the nasal sidewall, ala, and nasolabial folds, histology came back as basal cell carcinoma — confirming malignant transformation in a disease where that's still considered a rarity.

This is where the case becomes genuinely instructive from a surgical planning standpoint. Multidisciplinary tumor board first considered vismodegib given multiple synchronous basal cell carcinomas, but surgery was initially deemed prohibitive because of the anticipated reconstructive complexity — essentially, nobody wanted to commit to resecting this in one setting. The solution was a staged, facial-subunit-based approach spread across three separate operations, each done under local anesthesia. Stage one tackled the largest tumor complex on the nasal dorsum and tip, resected en bloc down to cartilage and musculature, deliberately preserving the alae as functional subunits and reconstructing with a full-thickness skin graft from the infraclavicular region — they specifically avoided a paramedian forehead flap because the forehead and glabella were themselves involved with trichoepitheliomas, and avoided preauricular donor skin for the same reason. Four months later, once the graft had taken, stage two addressed the left hemiface — upper lip and medial malar region — with a malar advancement flap and a V-Y advancement for the lip. Two months after that, stage three mirrored the approach on the right hemiface.

The authors frame this explicitly as a resource-conscious model: staged excision with graft and local flap reconstruction, done entirely under local anesthesia, achieving oncologic control while preserving nasal and perioral function within what they describe as a public health care system. There's no comparative data here, no denominator of similar cases to benchmark against — this is n of one, and as always with malignant transformation of MFT, the evidence base for any single approach is thin. But the teaching point is a planning principle you can actually use: when a field of disease looks reconstructively "prohibitive" as a single procedure, breaking oncologic resection into cosmetic-subunit-based stages, timed around graft and flap maturation, can convert an unresectable-feeling case into a sequence of manageable ones. That's a conceptually transferable strategy, even if the specific flaps chosen were dictated by this patient's unique pattern of involvement.

Third article, another case report: "Neuromodulator-Assisted Tension Reduction in Refractory Bilateral Mandibular Hypertrophic Scars." This one is conceptually interesting because it's really testing an idea about wound biology rather than a new surgical maneuver. The premise, well supported in the wound-healing literature the authors cite, is that mechanotransduction — mechanical tension across a healing or scarred dermis — is a driver of hypertrophic scar persistence, and the mandibular border sits in a uniquely high-tension zone thanks to mastication, facial expression, and platysmal pull.

Their patient was a thirty-four-year-old man with over a decade of progressive, strikingly symmetric, bilateral linear hypertrophic scars overlying the masseters along the mandibular border — no antecedent trauma, no acne or folliculitis history, no personal or family history of abnormal scarring, and a linear tension-line pattern that made the authors think mechanical forces, compounded by his history of chronic teeth grinding, were driving persistence rather than any discrete injury. Biopsy wasn't performed, reasonably, given a clinical picture with no suspicion for infection or alternative diagnosis.

Before he ever presented to this practice, he'd already been through seven years of conventional scar-directed therapy without durable benefit — pulsed dye laser, combined pulsed dye and Nd:YAG, that's neodymium-doped yttrium aluminum garnet laser, fractional resurfacing, intralesional steroid, intralesional five-fluorouracil, and subcision. Starting in 2023, the authors layered on an extensive multimodal regimen over three years: twenty-four pulsed dye laser sessions, ten fractional nonablative fifteen-fifty-nanometer sessions, and fourteen rounds of intralesional five-fluorouracil. All of that produced only gradual, modest change. The inflection point came in January 2024, when they added neuromodulator injections targeting the masseters and platysma specifically to reduce dynamic tension across the scar lines — repeated roughly every three to six months, eighteen units per masseter and twenty-four units per platysma. After that addition, they report the most substantial and sustained improvement in erythema, thickness, and contour, visible on side-by-side photographs from 2023 versus 2026, along with a secondary cosmetic bonus of reduced lower facial width from masseteric chemodenervation.

The authors are appropriately honest about what they can't prove: there's no standardized scar-scoring instrument used here, so the improvement is assessed qualitatively from photographs, and because neuromodulator was layered onto an already-ongoing multimodal regimen rather than tested in isolation, they cannot mathematically separate its contribution from cumulative effects of the laser and five-fluorouracil sessions happening in parallel. This is a single case, uncontrolled, with no formal outcome metric — so treat the causal claim skeptically even though the timeline is suggestive. The practical takeaway is not "add Botox to every refractory scar" — it's narrower and more useful than that: in a scar sitting over a highly mobile, muscularly active field, particularly one that's failed years of standard modalities, mechanical off-loading with a neuromodulator is a biologically plausible and low-risk adjunct worth considering before you assume you've exhausted your options. Interesting and mechanistically grounded, not yet practice-changing in any evidence-based sense.

Last piece is a Reconstructive Conundrum — the journal's case-based teaching format where they show you the defect, ask how you'd close it, and then walk through the reasoning. This one is titled "Reconstruction of an 80% Full Thickness Lower Lip Defect." A forty-two-year-old man had a five-year history of an enlarging, fungating lower lip plaque, cleared in three stages of Mohs, leaving a six-by-three centimeter full-thickness central lower lip defect extending down to the gingivolabial sulcus — roughly eighty percent of lower lip width.

The resolution section is essentially a size-based algorithm you already know the shape of, but it's worth having refreshed with their specific framing. Defects under about a third of the lip can generally be closed primarily, with the real technical priorities being accurate reapproximation of the orbicularis oris and precise realignment of the white roll. Centrally located full-thickness defects between roughly a third and two-thirds of the lip fall into lip-switch or local flap territory — Abbe flap centrally, Estlander if the commissure is involved, or the Gillies fan flap and Karapandzic flap. The authors flag that both the fan flap and Karapandzic can cause microstomia and commissure displacement when rotated medially for larger defects, but they favor the Karapandzic specifically because it preserves the orbicularis and its neurovascular bundle, translating into better oral competence and sensation postoperatively.

This defect, though, exceeded two-thirds of the lip, which pushes you into Gate flap or Bernard-Webster territory. The Gate flap, as originally described by Fujimori, is a full-thickness subcutaneous island pedicle based lateral to the marionette line and rotated ninety degrees into the defect from both sides — it reduces microstomia risk but does poorly on nerve preservation, so oral competence suffers. The Bernard-Webster flap is a bilateral full-thickness advancement that imports cheek skin into the defect while advancing the residual lip medially, with mucosal flaps needed to reconstruct the vermilion and dog-ears excised along the nasolabial folds and mental crease.

The technical contribution here is a modification of that Bernard-Webster design specifically to protect facial nerve branches. The authors made the superior incision of the advancement flap full-thickness, but kept the inferior incision only down to the level of the depressor anguli oris without transecting it — because the marginal mandibular nerve runs superior to the horizontal plane of the oral commissure while the buccal nerve runs medial and inferior to it, this asymmetric incision depth threads the needle and preserves innervation to the perioral musculature. Surgically, they performed bilateral mental nerve blocks, incised each commissure horizontally at full thickness for half the defect length, excised a standing cone superiorly along the nasolabial fold, undermined laterally in the subcutaneous plane, advanced the flaps medially, and closed in the three layers you'd expect — orbicularis and dermis with four-0 polyglactin, mucosa with four-0 silk, lateral vermilion reconstructed by advancing buccal mucosa. Their six-month result showed restored contour and functional closure.

Because this is a technique conundrum rather than an original study, there's no results-versus-limitations arithmetic to walk through — just the reasoning and the outcome in this one patient. The teaching points they close with are worth keeping as a mental checklist: preserve oral function over form once you're dealing with full-thickness defects; the modified Bernard-Webster is the workhorse for defects beyond two-thirds of the lower lip, with the Karapandzic reserved for the intermediate third-to-two-thirds range; mucosal advancement flaps at the commissures are what actually rebuild the vermilion, not the skin closure; and any full-thickness lip repair needs to be conceived as three discrete layers — mucosa, muscle, and skin — closed as three discrete layers, not fudged together. For anyone doing their own Mohs on lower lip tumors and inheriting the reconstruction, this asymmetric-depth nerve-sparing modification is a small technical adjustment with a plausible, anatomically sound rationale, and it's reasonable to consider adopting directly.

That closes out this month's four pieces — two rare-tumor case reports pushing the boundaries of what we thought MAC and MFT could look like, one mechanistically interesting but unproven adjunct for refractory scarring, and one concrete, adoptable technical refinement for major lower lip reconstruction. Thanks for listening, and we'll pick back up with the next issue.