Archimetrosis: the evolution of a disease and its extant presentation : Pathogenesis and pathophysiology of archimetrosis (uterine adenomyosis and endometriosis)

other OA: green CC0 ⤵ 3 in-corpus citations
AI-generated summary by gemini-2.5-flash-lite, 2026-06-07

This paper proposes the term "Archimetrosis" for uterine adenomyosis and endometriosis, suggesting its pathogenesis evolved from the uterine stratum vasculare in haplorrhine primates, leading to tissue injury and repair mechanisms.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text

The paper proposes a novel evolutionary concept of “archimetrosis” to explain the pathogenesis and pathophysiology of uterine adenomyosis and peritoneal/peripheral endometriosis, using an extensive literature search on primate evolution and comparative functional morphology of birthing processes, then correlating these with the authors’ human archimetrosis pathophysiology findings and published clinical data. It argues that haplorrhine primates developed specific reproductive features (including fusion of Müllerian ducts and a new myometrial layer derived from the stratum vasculare) that supports expulsion and externalization of menstrual debris in non-conceptive cycles, with hypercontractility potentially causing tissue injury/ischemia and extra-uterine lesion maintenance via biomechanical stress; the authors frame tissue injury and repair as the most parsimonious mechanism. A stated limitation is that the clinical implications depend on analyses of published data and on a “yet to be defined” latency phase after biomechanical injury in a uterine hypercontractility risk population. This paper is centrally about endometriosis and adenomyosis—specifically proposing “archimetrosis” as an evolutionary tissue-injury-and-repair framework unifying their development.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Purpose This article presents a novel concept of the evolution and, thus, the pathogenesis of uterine adenomyosis as well as peritoneal and peripheral endometriosis. Presently, no unifying denomination of this nosological entity exists. Methods An extensive search of the literature on primate evolution was performed. This included comparative functional morphology with special focus on the evolution of the birthing process that fundamentally difers between the haplorrhine primates and most of the other eutherian mammals. The data were correlated with the results of own research on the pathophysiology of human archimetrosis and with the extant presentation of the disease. Results The term Archimetrosis is suggested as a denomination of the nosological entity. Archimetrosis occurs in human females and also in subhuman primates. There are common features in the reproductive process of haplorrhine primates such as spontaneous ovulation and corpus luteum formation, spontaneous decidualization and menstruation. These have fused Müllerian ducts resulting in a uterus simplex. Following a usually singleton pregnancy, the fetus is delivered in the skull position. Some of these features are shared by other mammals, but not in that simultaneous fashion. In haplorrhine primates, with the stratum vasculare, a new myometrial layer has evolved during the time of the Cretaceous–Terrestrial Revolution (KTR) that subserves expulsion of the conceptus and externalization of menstrual debris in non-conceptive cycles. Hypercontractility of this layer has evolved as an advantage with respect to the survival of the mother and the birth of a living child during delivery and may be experienced as primary dysmenorrhea during menstruation. It may result in tissue injury by the sheer power of the contractions and possibly by the associated uterine ischemia. Moreover, the lesions at extra-uterine sites appear to be maintained by biomechanical stress. Conclusions Since the pathogenesis of archimetrosis is connected with the evolution of the stratum vasculare, tissue injury and repair (TIAR) turns out to be the most parsimonious explanation for the development of the disease based on clinical, experimental and evolutionary evidence. Furthermore, a careful analysis of the published clinical data suggests that, in the risk population with uterine hypercontractility, the disease develops with a yet to be defned latency phase after the onset of the biomechanical injury. This opens a new avenue of prevention of the disease in potentially afected women that we consider to be primarily highly fertile.
Full text 4,133 characters · extracted from oa-html · click to expand
Please use this identifier to cite or link to this item: doi:10.22028/D291-44061 | Title: | Archimetrosis: the evolution of a disease and its extant presentation : Pathogenesis and pathophysiology of archimetrosis (uterine adenomyosis and endometriosis) | | Author(s): | Leyendecker, Gerhard Wildt, Ludwig Laschke, Matthias W. Mall, Gerhard | | Language: | English | | Title: | Archives of Gynecology and Obstetrics | | Volume: | 307 (2023) | | Issue: | 1 | | Pages: | 93-112 | | Publisher/Platform: | Springer Nature | | Year of Publication: | 2022 | | Free key words: | Endometriosis Adenomyosis Archimetrosis Pathogenesis Primate evolution Primary dysmenorrhea Tissue injury and repair | | DDC notations: | 610 Medicine and health | | Publikation type: | Journal Article | | Abstract: | Purpose This article presents a novel concept of the evolution and, thus, the pathogenesis of uterine adenomyosis as well as peritoneal and peripheral endometriosis. Presently, no unifying denomination of this nosological entity exists. Methods An extensive search of the literature on primate evolution was performed. This included comparative functional morphology with special focus on the evolution of the birthing process that fundamentally difers between the haplorrhine primates and most of the other eutherian mammals. The data were correlated with the results of own research on the pathophysiology of human archimetrosis and with the extant presentation of the disease. Results The term Archimetrosis is suggested as a denomination of the nosological entity. Archimetrosis occurs in human females and also in subhuman primates. There are common features in the reproductive process of haplorrhine primates such as spontaneous ovulation and corpus luteum formation, spontaneous decidualization and menstruation. These have fused Müllerian ducts resulting in a uterus simplex. Following a usually singleton pregnancy, the fetus is delivered in the skull position. Some of these features are shared by other mammals, but not in that simultaneous fashion. In haplorrhine primates, with the stratum vasculare, a new myometrial layer has evolved during the time of the Cretaceous–Terrestrial Revolution (KTR) that subserves expulsion of the conceptus and externalization of menstrual debris in non-conceptive cycles. Hypercontractility of this layer has evolved as an advantage with respect to the survival of the mother and the birth of a living child during delivery and may be experienced as primary dysmenorrhea during menstruation. It may result in tissue injury by the sheer power of the contractions and possibly by the associated uterine ischemia. Moreover, the lesions at extra-uterine sites appear to be maintained by biomechanical stress. Conclusions Since the pathogenesis of archimetrosis is connected with the evolution of the stratum vasculare, tissue injury and repair (TIAR) turns out to be the most parsimonious explanation for the development of the disease based on clinical, experimental and evolutionary evidence. Furthermore, a careful analysis of the published clinical data suggests that, in the risk population with uterine hypercontractility, the disease develops with a yet to be defned latency phase after the onset of the biomechanical injury. This opens a new avenue of prevention of the disease in potentially afected women that we consider to be primarily highly fertile. | | DOI of the first publication: | 10.1007/s00404-022-06597-y | | URL of the first publication: | https://doi.org/10.1007/s00404-022-06597-y | | Link to this record: | urn:nbn:de:bsz:291--ds-440611 hdl:20.500.11880/39417 http://dx.doi.org/10.22028/D291-44061 | | ISSN: | 1432-0711 | | Date of registration: | 21-Jan-2025 | | Faculty: | M - Medizinische Fakultät | | Department: | M - Chirurgie | | Professorship: | M - Prof. Dr. Michael D. Menger | | Collections: | SciDok - Der Wissenschaftsserver der Universität des Saarlandes | Files for this record: | File | Description | Size | Format | | |---|---|---|---|---| | s00404-022-06597-y.pdf | 1,57 MB | Adobe PDF | View/Open | This item is licensed under a Creative Commons License

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-html

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosisadenomyosisdysmenorrhea

Citation neighborhood (sparse)

Too few in-corpus citations on either side for a chart; here are the lists.

Cited by (3)

Cited by (3)

Source provenance

openalex
last seen: 2026-05-11T04:09:40.449411+00:00
License: CC0 · commercial use OK