ArticleExperimental dermatology2021
Histologic progression of acne inversa/hidradenitis suppurativa: Implications for future investigations and therapeutic intervention.
Article in Experimental dermatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pooled it
- Post-Transcriptional Regulators of Inflammation: The Role of microRNAs in Acne Inversa Pathogenesis.Journal of biochemical and molecular toxicology · 2026Review
- Spatial transcriptomics maps early B-cell and T-cell activation in hidradenitis suppurativa.The Journal of investigative dermatology · 2026Article
- Single-cell spatial profiling identifies a mucosal-like epithelial signature in Hidradenitis suppurativa tunnels.JCI insight · 2026Article
- Dissecting Cellulitis of the Scalp: Linking Pathogenesis to Therapy.Biomedicines · 2026Review
- The polygenic architecture of hidradenitis suppurativa reveals signaling mechanisms that implicate epithelial remodeling.medRxiv : the preprint server for health sciences · 2025Article
- Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity.JID innovations : skin science from molecules to population health · 2025Review
- Propolis-Based Nanostructured Lipid Carrier of α-Mangostin for Promoting Diabetic Wound Healing in Alloxan-Induced Mice.Journal of inflammation research · 2025Article
- The impact of innate immunity and epigenetics in the pathogenesis of hidradenitis suppurativa.Frontiers in immunology · 2025Review
- Tissue comparability and bias in hidradenitis suppurativa transcriptomic studies.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-cell transcriptomics suggest distinct upstream drivers of IL-17A/F in hidradenitis versus psoriasis.The Journal of allergy and clinical immunology · 2023Article
- Inborn Errors of Immunity in Hidradenitis Suppurativa Pathogenesis and Disease Burden.Journal of clinical immunology · 2023Review
- Bone Metabolism in Patients with Hidradenitis Suppurativa: A Case-control Study.Acta dermato-venereologica · 2022Article
- Advances in molecular pathogenesis of hidradenitis suppurativa: Dysregulated keratins and ECM signaling.Seminars in cell & developmental biology · 2022Review
- Holistic health record for Hidradenitis suppurativa patients.Scientific reports · 2022Article
- [Clinical, pathology-associated and molecular biomarkers of hidradenitis suppurativa/acne inversa].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Since first recognized in 1839, the pathogenesis of acne inversa (AI) has undergone repeated revisions. Although there is agreement that AI involves occlusion of hair follicles with subsequent inflammation and the formation of tracts, the histologic progression of this disease still requires refinement. The objective of this study was to examine the histologic progression of AI based on the examination of a large cohort of punch biopsies and excisional samples that were examined first by hematoxylin and eosin staining. The most informative of these samples were step-sectioned and stained by immunohistochemistry for epithelial and inflammatory markers. Based on this examination, the following observations were made: 1) AI arises from the epithelium of the infundibulum of terminal and vellus hairs; 2) These form cysts and epithelial tendrils that extend into soft tissue; 3) Immunohistochemical staining demonstrates the epithelium of AI is disordered with infundibular and isthmic differentiation and de novo expression of stem cell markers; 4) The inflammatory response in AI is heterogeneous and largely due to cyst rupture. The conclusions of this investigation were that AI is an epithelial-driven disease caused by infiltrative, cyst forming tendrils and most of the inflammation is due to cyst rupture and release of cornified debris and bacteria. Cyst rupture often occurs below the depths of punch biopsy samples indicating their use for analysis may give an incomplete picture of the disease. Finally, our data suggest that unless therapies inhibit tendril development, it is unlikely they will cause prolonged treatment-induced remission in AI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.