Research criticism · Dermatopathology · Morgellons
Reactive Perforating Collagenosis and Morgellons share plug and collagen observations but diverge on anatomy and symptoms. An intact, elastic-stained lesion could distinguish their tissue routes.
In reactive perforating collagenosis, damaged collagen can be pushed out through skin—and a pathologist can see that route under the microscope. Some Morgellons lesions are described as cratered or plug-centered. Middelveen has sectioned attached callus material and reported follicular casts and comedo-like masses. Those observations justify testing whether some lesions fit the RPC or acquired perforating dermatosis pattern. They do not already establish that diagnosis.
Plain-language glossary
Open the tissue terms used in this article
Transepidermal elimination: material passes from deeper tissue through the epidermis to the surface. Folliculocentric: centered on a hair follicle.
Keratinocyte: an epidermal cell that produces keratin. Fibroblast: a connective-tissue cell that produces collagen and other matrix. Basal layer: the deepest epidermal layer. Stratum corneum: the outermost layer.
Hyperkeratosis: thickened surface keratin. Parakeratosis: surface keratin whose cells retain nuclei. Acanthosis: thickening of the living epidermal layers. Rete ridges: downward epidermal projections.
Trichrome: a tissue stain used to distinguish collagen from surrounding structures. Immunohistochemistry: antibody staining used to locate a target in tissue. Lineage marker: a marker used to identify a cell type. Birefringence: an optical response seen when material is examined under polarized light.
Competing tissue templates · not a shared diagnosis
What the tissue routes predict
A lesion can resemble one template clinically and still require intact histology to determine its route.
A fiber that vanished
A dermatologist examining a biopsy specimen saw a black fiber protruding from its dermal side. The structure was photographed. Then the specimen entered routine processing—and the fiber disappeared.
In the resulting sections, the clinicians found only mild superficial perivascular inflammation. PAS, Grocott methenamine silver, Warthin–Starry and Wright–Giemsa stains were negative. Tissue culture was negative. Masson’s trichrome stained ordinary dermal collagen, but no structure corresponding to the photographed fiber remained.
The authors of the 2017 Korean case report proposed that organic solvents used during processing could have dissolved it. They did not demonstrate dissolution. The report is internally inconsistent on another point: its abstract says serum B. burgdorferi PCR was negative, while the body describes negative serology.
The larger failure came first. Processing broke the link between a visible object and the tissue beneath it. Its composition, attachment and complete spatial course became unanswerable.
Related background: Review our guides to Morgellons fibers and what the research shows and what Morgellons skin histology has—and has not—established.
What patients describe
People using the name Morgellons describe fibers, threads, plugs or other material in or emerging from skin. Savely’s clinical and specimen photographs show cratered or deep circular sores, pore-centered material, and projections beneath removed scabs or calluses. Her captions put “plugs” in quotation marks and describe one filament as “growing down into the dermis.” Those are the author’s observations, not intact-lesion or time-resolved demonstrations. The author of this site reports plugs seated inside cratered lesions before extraction, followed by cup-like indentations after removal. The first observation strengthens the clinical comparison; the second does not identify the underlying process. These observations can guide photography and biopsy before the structure is disturbed, but they cannot establish diagnosis or origin.
Pearson’s 2012 case definition centered the report of fibers or materials “emerging from the skin or embedded in the skin.” It did not determine where the material began. The affirmative literature likewise defines the lesion partly through filaments that lie under, are embedded in or project from skin.
An umbilicated papule—essentially a raised lesion with a central depression—or a plug-centered nodule can appear in the Morgellons bucket. That gives some lesions the clinical look that should prompt consideration of a perforating dermatosis. Appearance alone cannot supply the diagnosis. Dermatology requires the intact tissue route.
The family of diseases where skin does push material out
A crater can be present before removal, with an adherent plug seated at its center. That genuinely resembles Faver’s clinical criterion: an umbilicated papule or nodule with a central adherent keratotic plug. The indentation left after extraction is less specific because many adherent structures leave a defect when removed. Neither surface observation is RPC’s diagnostic histologic cup. That cup appears in cross-section with the plug still seated: the epidermis dips inward, lines the crater and preserves the tissue beneath it.
Reactive perforating collagenosis has a simple core: damaged collagen is pushed through the epidermis and can be seen doing so under the microscope. This is transepidermal elimination. Acquired perforating dermatosis (APD) is the adult umbrella for RPC, Kyrle disease, elastosis perforans serpiginosa and perforating folliculitis. More than one pattern may occur in one patient.
The diagnosis is architectural. In RPC, the lined cup contains keratin, debris and altered collagen continuous with abnormal collagen below. Perforating folliculitis is folliculocentric—centered on a hair follicle—and uses a dilated follicle. Elastosis perforans serpiginosa places elastic fibers in the channel. Similar surfaces can conceal different routes.
RPC is the clean comparator for dermal collagen, not every specimen. A follicular cast points first toward perforating folliculitis; mixed adult disease may stay under APD until histology places it. Scratching, diabetes and chronic kidney disease provide context, not the diagnosis.
RPC was named in 1967. Savely, Leitao and Stricker mentioned perforating dermatoses in the Morgellons differential in 2006, and Mayne and colleagues noted the comparison in 2013. Neither performed a prespecified same-specimen test.
Technical panel · What earns a perforating diagnosis?
Criteria, tissue and the elastic-stain discriminator
Faver, Daoud and Su’s criteria for acquired RPC require adult onset, umbilicated papules or nodules with a central adherent keratotic plug, and elimination of necrotic collagen through an epithelium-lined crater. Surface resemblance alone is insufficient.
DermNet’s dermatopathology guide describes the RPC plug as continuous with altered dermal collagen. It also explains the practical role of elastic van Gieson staining: RPC should not show black elastic fibers crossing the elimination focus, whereas elastosis perforans serpiginosa does.
Rapini, Hebert and Drucker documented combined elimination of collagen and elastic fibers in acquired disease. That overlap is one reason the umbrella term is safer before the section is stained.
Shah, Tiwary and Kumar distinguish active transepidermal elimination of altered dermal material from relatively passive transmigration with epidermal turnover. Finding material in the epidermis is not enough; the organized tissue relationship matters.
A 2001 report by Theile-Oche and colleagues asked whether scratching damaged collagen in acquired perforating collagenosis. It posed the question; it did not answer it. Four APD cases reported with scabies likewise leave itching, scratching and inflammation as competing links.
Where the comparison converges—and what remains untested
A surface report, a plug-like form, an itch-and-scratch setting, and keratin or collagen recur in both literatures. Those four convergences have never been joined to the spatial axis that would adjudicate the proposed routes.
The comparison—and its missing axis
Each convergence survives a negative perforation stain. None is a diagnosis.
The missing axis: Is altered material crossing an organized epidermal or follicular channel, and do elastic fibers cross with it?
How close are the plugs, actually?
Three different structures have been called “plugs,” and they cannot be treated as one specimen class. Savely photographed material on removed scabs and calluses, but the pictured objects were not examined histologically. Middelveen’s 2018 review describes follicular casts with a keratin-rich exterior and collagen-rich interior, stained with Gömöri trichrome—a stain used to separate collagen from surrounding tissue—but no channel was mapped. The 2013 keratin projections were sectioned. They carry the closest comparison.
The short version: the structures overlap in ingredients and rough shape. Their position, collagen state and connection to the dermis either differ or were never preserved.
| Feature | RPC standard | What Morgellons studies document |
|---|---|---|
| Composition | Converges Keratinous plug containing altered collagen | Converges Keratin projections containing collagen-positive fibroblast masses in 2013; keratin-rich exterior and collagen-rich interior in 2018 follicular casts |
| Gross form | Converges Central adherent keratotic plug seated in an epidermal cup | Converges Conical or papillary keratin projections, follicular casts and photographed plug-like material |
| Position relative to skin | Diverges The plug sits in attached epidermis and opens toward the surface | Diverges The 2013 projections were on the internal, concave face of removed calluses from patients 2 and 3; photographed examples sit on the underside of removed material |
| Collagen state | Diverges Necrotic, altered or basophilic collagen—damaged material in transit | Diverges Collagen-positive masses described as proliferative fibroblasts; filaments stained predominantly for collagen |
| Dermal continuity | Decisive The plug remains continuous with abnormal collagen in the dermis below | Untested Detached specimens did not preserve the dermis needed to assess that continuity |
The clinical neighborhoods overlap
Perforating disease lives in an itch-and-scratch landscape. Pearson found lichen simplex chronicus or prurigo nodularis in 15 of 37 biopsied lesions. In 2025, Gipple and colleagues offered questionnaires to 54 Morgellons patients; 50 contributed quality-of-life and sleep data, and 42 contributed itch scores. Using prurigo nodularis as a comparator does not make it a Morgellons comorbidity.
Psychiatric labels overlap too, without making the cohorts interchangeable. In Savely and Stricker’s selected 122-patient cohort, 55—45.1%—carried a delusions-of-parasitosis diagnosis. Tampa and colleagues documented both Kyrle disease and delusions of parasitosis in one patient. They proposed, but did not demonstrate, that dermatosis-related pruritus triggered the belief.
Both literatures report keratin and collagen
APD is classified partly by what crosses the surface: collagen, elastic tissue, keratinous or inflammatory material, or follicular contents. The affirmative Morgellons literature reports keratin- and collagen-containing filaments and casts. Pearson’s broader investigation found surface material that was largely protein—considered likely superficial skin—or cellulose consistent with cotton. The material categories overlap enough to make composition important. They overlap too much for composition to settle the route.
Where the two pictures do not match
The routes nobody has adjudicated
A keratin-and-collagen structure can carry more than one mechanistic story. Perforating disease describes altered material being expelled. Morgellons papers propose production by keratinocytes—epidermal cells that make keratin—and fibroblasts, connective-tissue cells that make collagen. They also use BDD as an infectious-proliferative analog. Injury supplies a third route.
The 2013 findings bring the first two routes close. Some keratin projections contained collagen-positive proliferative fibroblast masses and “appeared to have ruptured” under pressure, more often toward the external face. Middelveen interpreted proliferation pressure. A perforating comparison asks whether material crossed a keratinized route toward the surface. The detached callus preserved no dermis, reported cup or continuity with altered dermal collagen.
The accounts are spatially opposed but not exclusive: produced material could later be damaged and eliminated, and different lesions could follow different routes. The test must be lesion-level. An RPC or APD finding would classify that target, not rename Morgellons.
Chemical and imaging tests can identify what material contains, but not how it arrived. Congo red and trichrome change color around particular tissue components. Polarized light tests optical behavior; infrared spectroscopy estimates molecular composition; electron microscopy reveals fine structure. All can describe a keratin-and-collagen object under more than one model. Only intact spatial architecture can show production, elimination or entrapment.
This is why results from separate specimen streams cannot decide the route of one structure. Middelveen’s 2016 review reports negative calcofluor-white testing for cellulose. Pearson found cotton-consistent cellulose in 43% of 23 material specimens. Both address composition; neither maps how the tested material sat in tissue.
Middelveen’s 2018 review reports apple-green birefringence—an optical response under polarized light—suggestive of amyloid but needing confirmation. Shah, Tiwary and Kumar list amyloid among materials that may cross the epidermis. The signal remains unconfirmed and unmapped.
The routine stain missing from the cited Morgellons literature is an elastic stain. Across the cited papers whose method lists were checked in full, none reports Verhoeff–Van Gieson, elastic van Gieson or orcein staining read within a mapped channel. The stain would not diagnose RPC by itself. It would help classify an intact channel after routine histology shows whether one exists.
Each literature used tools suited to its question. The unanswered question sits between them: no cited study combines composition, cell identity and complete spatial course in one preserved target within an intact lesion.
Interactive evidence check
Open each question to see why one cannot substitute for the other.
Question 1 · What is the material?
Endogenous: biological material with genuine tissue continuity. Environmental: external material on the surface without continuity or reaction. Composite: both categories in distinct relationships within one mapped specimen. These are ingredient findings, not route findings.
Question 2 · What tissue architecture put it there?
Cellular production: reproducible continuity with lineage-confirmed cells without a perforating channel. BDD-like proliferation: abnormal keratin in thickened epidermis and surface keratin; this does not establish infection.
Perforating elimination: altered dermal or follicular material reconstructed through a channel. Injury and entrapment: external material within ulcerated or repairing tissue without either route.
Negative or insufficient: no elimination in an adequate target, or no answer because the target or required layers were lost.
The architectural test and the checked method lists
The table’s point: composition cannot replace the intact spatial relationship.
| Architectural question | Cellular production predicts | Perforating elimination predicts | What must be examined |
|---|---|---|---|
| Epidermal or follicular channel | No perforating channel is required | Cup-shaped or follicle-centered elimination channel | Oriented serial sections through the complete lesion |
| Condition of collagen | Newly produced or aberrantly expressed; necrosis is not defining | Altered, degenerate or necrotic material in the channel | H&E and collagen staining in spatial context |
| Critical continuity | Continuity with cell type confirmed by a lineage marker | Continuity with abnormal dermal or follicular substrate below | Serial reconstruction; cell-identity markers when attachment survives |
| Elastic fibers | Not required by the proposed mechanism | Absent from an RPC channel; present in elastosis perforans serpiginosa; potentially mixed in APD | Elastic van Gieson or Verhoeff–Van Gieson stain |
The complete 2013 method list included CK AE1/AE3, CK AE5/AE6, Fontana–Masson, Gömöri trichrome, Warthin–Starry, Dieterle silver nitrate, scanning electron microscopy and transmission electron microscopy; BDD samples also received Warthin–Faulkner. Across the cited Morgellons papers whose method lists were checked in full, none reports Verhoeff–Van Gieson, elastic van Gieson or orcein staining read within a mapped channel. That absence favors neither route. It identifies the unperformed comparison.
What the studies actually found
Ohn 2017: the nearest test was negative—and the target was gone
Ohn’s Korean case applied a collagen stain to sectioned biopsy tissue, but the photographed target was gone. Masson’s trichrome stained only ordinary dermal collagen. The remaining sections showed no altered collagen in a channel, cup-shaped invagination or perforating architecture. The observed tissue was negative; the vanished fiber was unclassifiable.
This was one patient. The authors proposed that processing solvents could have dissolved the fiber; they did not demonstrate dissolution. The negative section weighs against perforation in the tissue that remained, not in the missing structure.
Middelveen 2013: the production model takes shape
A detached callus can preserve tissue relationships while losing the lesion beneath it. In 2013, Middelveen and colleagues sectioned nonbiopsy material from four selected women, ages 49 to 73. None had a reported psychotic or delusional disorder; all were RPR-negative for syphilis and B. burgdorferi-seropositive.
The filaments stained predominantly for collagen and rarely only for keratin; keratin staining was usually patchy. The authors judged the morphology more consistent with collagen. Retained nuclei and apparent continuity with keratinocytes or fibroblasts were interpreted as cellular proliferation and activation.
The plug anatomy is the hinge. Patients 2 and 3 had conical or papillary keratin projections on the internal, concave face of removed calluses. Some contained collagen-positive proliferative fibroblast masses and “appeared to have ruptured” under pressure toward both faces, more often externally. The paper therefore documents collagen-positive cellular material inside a keratin-walled projection with apparent rupture toward the external face. Middelveen interpreted proliferation; a perforating comparison asks whether material crossed a keratinized route.
It is not RPC. No epidermal cup, altered basophilic collagen or dermal continuity was reported. Patient 1 supplies a limited negative: sections contained every epidermal layer, from the outer stratum corneum to the deepest stratum basale, yet no cup was described. This was one specimen, without prespecified scoring or dermis.
All four showed hyperplasia, or increased cell number, and parakeratotic hyperkeratosis—thick surface keratin retaining nuclei. This partly supports a BDD-like proliferative template in human tissue. It establishes neither BDD, infection-driven production nor perforating elimination.
These were selected, detached specimens: no intact route, Faver scoring, time-resolved synthesis or independent replication.
Reading the 2013 sections precisely
Specimen anatomy, selection and spatial courses
Attached filaments were selected; unattached material was excluded. Convex and concave faces applied to patients 2 and 3, not every specimen. Patient 4 supplied a roughly 1-mm tissue fragment embedded with filaments rather than a substantial callus.
Patient 1 included all epidermal layers. The authors describe filaments from the basal layer with “evolution inward towards the dermis”; fixed sections establish a spatial course, not development over time. Patients 2 and 3 had fibroblast collections and filaments extending toward the outer surface. Patient 4 has no comparable reported course.
Filaments showed cortex-and-medulla organization. Cytokeratin immunohistochemistry—antibody staining locating keratin proteins—was combined with Gömöri trichrome and other stains. The methods did not reconstruct a complete route through intact skin.
Middelveen 2016 and 2018: proliferation becomes explicit—and follicular
Middelveen and Stricker’s 2016 review states the model directly: collagen- and keratin-containing filaments arise from proliferative keratinocytes and fibroblasts. The 2018 history review interprets them as overproduction in response to spirochetal infection. These are the authors’ interpretations of observed structures; neither review directly measures new protein synthesis over time.
The same literature reports a follicular route: filaments stemming from the root sheath, thickened follicular casts with keratin-rich exteriors and collagen-rich interiors, and comedo-like masses within pores or follicles. Those observations make perforating folliculitis a closer structural comparator than RPC for a follicular specimen. They do not show an elimination channel, and they do not make the two routes interchangeable.
BDD: Middelveen’s analog is proliferative, not perforating
A BDD lesion is not a perforating crater. It is an overgrown, inflamed hoof-skin lesion. Middelveen and Stricker’s 2011 comparison chose bovine digital dermatitis (BDD) as the animal analog for Morgellons because the cattle lesions contain abnormal keratin-producing cells and unusually long keratin filaments.
Treponemes have been repeatedly characterized in BDD lesions; the 2011 paper also reports spirochetes within necrotic and outer proliferating epidermal cells, while healthy tissue was not associated with spirochetes. That is organism-in-lesion localization in cattle and helps explain the choice of analog. Other bacteria were reported mainly in necrotic layers. It does not establish the same localization in human Morgellons tissue or within a mapped human filament.
BDD is not classic RPC. Its template is inflammatory hyperkeratosis and keratin proliferation in an infectious lesion. The RPC template is altered dermal collagen crossing an organized epidermal channel. The comparison supports asking whether a human lesion shows comparable keratin overgrowth; it does not prove that Morgellons is digital dermatitis, that Borrelia produces a filament or that the same specimen shows perforating collagenosis.
The cattle histology in the paper’s terms
What the BDD tissue actually showed
BDD sections showed parakeratotic hyperkeratosis, epidermal acanthotic hyperplasia, ulcerated dermal papillae tips and pronounced rete-ridge formation with broad-based tips. In plain terms: surface keratin retained nuclei, the epidermis was thickened and its downward projections were enlarged.
Other projections contained elongated, ballooned, necrotic or keratinized keratinocytes, with keratin filaments reported at macroscopic lengths. The paper does not use “perforating,” “transepidermal elimination” or “collagenosis” to describe that process.
Middelveen 2020: attachment described at cellular scale
Middelveen and colleagues’ selected 16-subject series reports basal-layer filament attachment in multiple cases. At 1000×, Figure 7C shows a nucleated base described as continuous with basal keratinocytes. This is cellular-scale histologic evidence supporting endogenous origin in those specimens.
Cell identity rested on position and appearance, not a lineage-specific marker. The same attached structure was not separately typed as keratin or collagen. Missing specimen, section and filament counts prevent a filament-level frequency, while the complete spatial course and matched injured-skin controls are absent.
The basal-attachment architecture has not been independently replicated. No human study reviewed here localizes a validated organism within one filament’s complete mapped architecture.
Reading the 2020 evidence precisely
Pattern, antibody limits and reporting context
At least nine subject-level entries describe basal origin or attachment; several recur in a second table. The unknown denominator is individual specimens, sections and filaments—not subjects.
The polyclonal anti-B. burgdorferi antibody was intentionally selected for broad spirochetal reactivity and cross-reacts with T. pallidum, B. hermsii and B. parkeri. Reactivity cannot identify B. burgdorferi specifically or show filament production.
Controls support staining behavior, not cellular lineage, composition or Morgellons-specificity. Figure 7A says “origin in subcutaneous tissue” and Figure 7C “basal origin”; the legend does not establish that both show one filament, so this is an ambiguity rather than a contradiction.
The paper stages Morgellons in parallel with syphilis; this article does not adopt that analogy. The Lindorf Family Foundation funded the study; disclosures report Jyotsna Shah as President and a stock owner of IGeneX and Raphael Stricker as owner of Union Square Medical Associates. These facts are context, not a substitute for evaluating methods and results.
Pearson 2012: a broader study, but separate specimen streams
The CDC-funded investigation identified 115 case-patients. Forty-one received a clinical evaluation, and 31 had either a lesion suitable for biopsy or material available to collect. From there the units fork: the paper reports biopsies and separately reports loose material collected from intact skin. It does not state how many of the 31 participants were biopsied.
Pearson’s sampling flow
The top line counts people. The fork counts specimen types, so neither branch is another cohort step.
Among the 23 material specimens collected from intact skin, the material was reported as largely protein (83%), considered likely superficial skin, or cellulose consistent with cotton fibers (43%). The paper gives percentages, not counts, and does not present the categories as mutually exclusive.
Among the 37 biopsied lesions, solar elastosis appeared in 19 (51%). Fifteen (40%) showed lichen simplex chronicus or prurigo nodularis, interpreted as evidence of excoriation or chronic irritation. Six (16%) had features consistent with arthropod bite or drug allergy. Birefringent material appeared in 16 (43%) lesions; in all but two it was superficial, at a tissue edge, separate from tissue or on the biopsy surface and produced no tissue reaction.
Two lesions contained foreign-body-type giant cells around embedded material. One contained cellulose most consistent with cotton fragments; the other contained silicon-bearing material likely to be silicates. Both also had features suggestive of prior ulceration or trauma at the biopsy site.
Findings among 37 biopsied lesions
The findings are not mutually exclusive; the bars should not be added to 100%.
Pearson’s two giant-cell biopsies support a narrow injury-and-entrapment model: external material sat deeply enough to provoke a reaction at sites with features suggestive of prior ulceration or trauma. That is injury and entrapment in the same specimen. It is also only two of 37 lesions, does not show that perforation placed the material there and establishes no population pattern.
The question the debate keeps skipping
Before a lesion is picked, scraped or removed, is it an umbilicated papule or nodule with a central adherent plug? That is the shared surface question. Patients say plug. Middelveen reports calluses, follicular casts and comedo-like masses. Faver’s criterion specifies a central adherent keratotic plug. The words and images overlap enough to require scoring. They are not interchangeable, and the surface sign is insufficient without the tissue channel.
The table’s point: the studies recorded lesions or detached material, but none prespecified and scored the complete Faver pattern in an intact target with dermis attached.
| Paper | Lesion morphology recorded | APD hallmarks specifically scored? | What can be concluded |
|---|---|---|---|
| Pearson 2012 | Papules, scars, plaques, patches, macules and one cyst; many crusted, ulcerated or eroded | No systematic scoring of umbilication, crateriform shape or a central adherent keratotic plug | Heterogeneous lesions; the presence or absence of Faver’s surface pattern cannot be recovered |
| Savely & Stricker 2010 | Spontaneously appearing, slowly healing lesions and hyperpigmented scars after healing | No systematic scoring of umbilication, a central adherent plug or an elimination channel | The cohort documents chronic lesions, not RPC morphology or histopathology |
| Savely 2016 gallery | Photographs captioned as deep circular lesions, follicular casts, keratin “plugs,” underside projections and a gelatinous “plug” | No; this is a self-published clinical-image source, not a scored histopathology series | Some pictured specimens have a plug-centered look that warrants an intact biopsy |
| Middelveen 2013 | Patient 1 retained all epidermal layers; patients 2 and 3 had detached calluses with convex outer faces, concave dermal-facing surfaces and keratin projections | No; patient 1 could show an epidermal cup but had no dermis, while the other calluses were detached | No cup was reported in patient 1—a limited negative; dermal continuity was untestable in every specimen |
| Middelveen 2016/2018 | Filaments under, embedded in or projecting from lesions; follicular casts, pore-associated wads and comedo-like masses | No; the follicular structures were not tested as perforating plugs | The descriptions warrant RPC/APD and follicular comparisons, not a diagnosis |
| Middelveen 2020 | Calluses, ulcerative lesions, papules, scars, excoriations and slowly healing lesions; proposed follicular and vesicular subtypes | No reported systematic scoring of Faver’s features | Morphology was recorded, but not the features needed to test this comparison |
This is mostly missing data, not negative data. Patient 1 is the narrow exception: full-thickness epidermis with no reported cup. Without prespecified scoring or dermis, that observation cannot settle the route. No source preserves a scored target intact from surface through dermis.
The subset hypothesis remains testable: score umbilicated or plug-centered lesions individually. Diagnose a positive accurately without using it to relabel other lesions or the whole population.
The experiment—and it is small
The first experiment may be sitting in paraffin blocks. Inventory surviving blocks and slides from Pearson’s lesion biopsies and Middelveen’s sections, then re-cut every adequate candidate. Score intact lesions for a cup-shaped epidermal or follicular channel, altered collagen crossing it, continuity below and—with Verhoeff–Van Gieson—elastic fibers in the channel.
Read the same sections for BDD-like hyperkeratotic proliferation without an RPC-type collagen channel. The archive is useful only if the target and enough surface, epidermis, follicle and dermis survive. Missing anatomy is uninterpretable, not negative, and calls for a prospective same-structure protocol.
The table’s point: each result answers only the route actually preserved in that lesion. Negative, mixed and uninterpretable findings must remain separate.
| Result | Reading | What it settles | What it does not settle |
|---|---|---|---|
| Altered collagen crosses an organized epidermal channel; no black elastic fibers in it | Perforating collagenosis pattern | A collagen-elimination route in that specimen | Prevalence, upstream cause or every reported fiber |
| Black elastic fibers cross the channel | Elastic-fiber elimination; consider elastosis perforans serpiginosa or mixed APD | Elastic tissue participates in the mapped channel | Whether the lesion represents a pure subtype |
| Elimination occurs through a dilated follicle, with or without collagen or elastic fibers | Perforating folliculitis pattern | A folliculocentric elimination route in that specimen | Whether all follicular casts share it |
| Parakeratotic hyperkeratosis, acanthotic hyperplasia or pronounced rete-ridge formation with abnormal keratin formation; no RPC-type collagen channel | BDD-like proliferative template | The lesion fits a proliferative rather than RPC-elimination architecture | BDD identity, infection or microbial cause |
| Ordinary dermal collagen; no organized channel in an adequate mapped specimen | No perforating process in that specimen | Closes the APD explanation for the adequately sampled target | Cellular production unless lineage and continuity are separately shown |
| Target absent, orientation lost or required layers missing | Uninterpretable | The archive cannot answer the question | Either proposed route |
A compact archive-first protocol
What the dermatopathology team would actually do
Inventory first: link clinical photographs to lesion IDs where possible; report participants, lesions, blocks, levels and recognizable targets available from each archive.
Re-cut serially: follow each candidate through consecutive levels rather than selecting one favorable plane.
Stain compactly: H&E for architecture, a collagen stain and Verhoeff–Van Gieson for elastic tissue. Add lineage markers only when an attachment survives across levels.
Read blindly: score Faver/Rapini architecture and BDD-like hyperkeratotic proliferation using preregistered criteria. Include confirmed APD, comparably excoriated skin, prurigo nodularis, lichen simplex chronicus and normal skin as controls.
Report per lesion: keep production-compatible, perforating, BDD-like proliferative, injury-and-entrapment, mixed, negative in an adequate specimen and uninterpretable as distinct outcomes.
If the archives fail, photograph untreated plug-centered lesions before sampling and preserve one attached structure with its surface, epidermis, follicle and dermis. Divide matched tissue between routine and solvent-sparing processing. Tie composition, cell lineage, spatial architecture and microbial testing to that same target.
Keep outcomes specimen-specific. Adequate sections without a channel close perforation for that target. Lineage-confirmed attachment without perforation supports production. Hyperkeratotic proliferation without an RPC channel fits the BDD-like template, not infection by itself. Injured tissue around external material supports entrapment. A lost target remains uninterpretable.
If you have these lesions
The most useful thing you can do is leave one suitable lesion alone. Extraction severs the connection that matters. One intact, untreated, plug-centered lesion can answer more than many specimens photographed after removal.
Ask whether a punch or excisional biopsy through the dermis is appropriate. Target an untreated plug-centered lesion, not a scratched-open site, and keep the plug seated. The requisition can request assessment for perforating architecture with H&E and Verhoeff–Van Gieson.
Photograph before sampling, but keep the image in its proper role. It records surface form; only tissue can show the lined cup, altered collagen and continuity below.
Symptoms that do not fit are useful. Stabbing, stinging or prickling pain is not typical of RPC, which is dominated by intense itch. Raise those sensations with a clinician on their own merits, not as proof for or against one mechanism.
A positive, an adequate negative and an uninterpretable specimen are different answers. No study has prospectively obtained one from a preserved Morgellons target using this protocol.
Back to the fiber
The black fiber should not have ended as a photograph followed by blank sections. Preserved with the tissue beneath it, a channel containing altered collagen would support elimination; lineage-confirmed attachment without that channel would support production; injured tissue around external material would support entrapment. Missing structure remains missing evidence.
RPC may explain some plugs. It does not explain the whole filament picture. Colored filaments around nails, feather-like structures, non-uniform spatial courses and BDD-style keratin overgrowth require their own tests. A lesion-level RPC diagnosis would be a useful answer for that lesion, not a universal theory of Morgellons.
That is what the acquired perforating dermatoses contribute to the Morgellons debate: not a borrowed diagnosis, but a mature method for separating what a structure contains from the process that placed it there.
References
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- Gipple MO, Dhami RK, Latour E, Keller JJ. Patients with Morgellons disease have a lower quality of life than patients with psoriasis, atopic dermatitis and prurigo nodularis. British Journal of Dermatology. 2025;192(1):163–165. doi:10.1093/bjd/ljae335.
- Mehregan AH, Schwartz OD, Livingood CS. Reactive perforating collagenosis. Archives of Dermatology. 1967;96(3):277–282. doi:10.1001/archderm.1967.01610030055009.
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