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name: Endometriosis
creation_date: '2025-12-18T17:01:35Z'
updated_date: '2026-02-17T21:53:14Z'
category: Complex
parents:
- Reproductive Disease
disease_term:
preferred_term: endometriosis
term:
id: MONDO:0005133
label: endometriosis
pathophysiology:
- name: Ectopic Endometrial Tissue
description: >
Endometrial-like tissue grows outside the uterus, commonly on
ovaries, fallopian tubes, and pelvic peritoneum. Responds to
hormonal cycling with bleeding and inflammation.
cell_types:
- preferred_term: Endometrial Stromal Cell
term:
id: CL:0002255
label: stromal cell of endometrium
biological_processes:
- preferred_term: Cell Proliferation
term:
id: GO:0008283
label: cell population proliferation
evidence:
- reference: PMID:16166933
reference_title: "Immunology of endometriosis."
supports: PARTIAL
snippet: "Endometriosis is classically described as the presence of both endometrial
glandular and stromal cells outside the uterine cavity, mainly in the pelvis."
explanation: Defines endometriosis as ectopic presence of endometrial
glandular and stromal cells outside the uterus
- name: Retrograde Menstruation
description: >
Menstrual blood flows backward through fallopian tubes into
pelvic cavity. Most women have retrograde menstruation, but only
some develop endometriosis, suggesting other factors involved.
evidence:
- reference: PMID:16166933
reference_title: "Immunology of endometriosis."
supports: SUPPORT
snippet: "Although multiple theories have been put forth to explain the pathophysiology
and pathogenesis of endometriosis, the retrograde menstruation theory of Sampson
is the most widely accepted. However, since retrograde menstruation occurs in
most of the reproductive age women, it is clear that there must be other factors
which may contribute to the implantation of endometrial cells and their subsequent
development into endometriotic disease."
explanation: Retrograde menstruation is the most widely accepted theory but
insufficient alone to explain disease development
- name: Chronic Inflammation
description: >
Ectopic lesions trigger chronic pelvic inflammation with elevated
cytokines and prostaglandins. Inflammatory milieu contributes to
pain and adhesion formation.
biological_processes:
- preferred_term: Inflammatory Response
term:
id: GO:0006954
label: inflammatory response
evidence:
- reference: PMID:16166933
reference_title: "Immunology of endometriosis."
supports: SUPPORT
snippet: "Increased levels of several cytokines and growth factors which are secreted
by either immune and endometrial cells seem to promote implantation and growth
of ectopic endometrium by inducing proliferation and angiogenesis."
explanation: Supports inflammatory cytokine/growth-factor milieu, but not
the full downstream pain and adhesion statement.
- name: Estrogen Dependence
description: >
Endometriotic lesions produce their own estrogen via aromatase
and are highly estrogen-responsive. Progesterone resistance
impairs normal tissue regression.
biological_processes:
- preferred_term: Estrogen Response
term:
id: GO:0043627
label: response to estrogen
evidence:
- reference: PMID:10731122
reference_title: "Estrogen production in endometriosis and use of aromatase inhibitors to treat endometriosis."
supports: SUPPORT
snippet: "Estrogen is the most important known factor that stimulates the growth
of endometriosis. Estrogen delivery to endometriotic implants was classically
viewed to be only via the circulating blood in an endocrine fashion. We recently
uncovered an autocrine positive feedback mechanism, which favored the continuous
production of estrogen and prostaglandin (PG)E2 in the endometriotic stromal
cells."
explanation: Estrogen drives endometriosis growth through both systemic
delivery and local autocrine production
- reference: PMID:10731122
reference_title: "Estrogen production in endometriosis and use of aromatase inhibitors to treat endometriosis."
supports: SUPPORT
snippet: "The enzyme, aromatase, is aberrantly expressed in endometriotic stromal
cells and catalyzes the conversion of C19 steroids to estrogens, which then
stimulate cyclooxygenase-2 to increase the levels of PGE2. PGE2, in turn, is
a potent inducer of aromatase activity in endometriotic stromal cells. Aromatase
is not expressed in the eutopic endometrium."
explanation: Aromatase expression in endometriotic stromal cells creates a
positive feedback loop with PGE2 for local estrogen production
- reference: PMID:10731122
reference_title: "Estrogen production in endometriosis and use of aromatase inhibitors to treat endometriosis."
supports: SUPPORT
snippet: "In addition, we find that endometriotic tissue is deficient in 17beta-hydroxysteroid
dehydrogenase type 2, which is normally expressed in eutopic endometrial glandular
cells and inactivates estradiol-17beta to estrone. This deficiency is another
aberration that favors higher levels of estradiol-17beta in endometriotic tissues
in comparison with the eutopic endometrium."
explanation: Deficiency of 17beta-HSD type 2 prevents estradiol
inactivation, contributing to local estrogen dominance
- name: Immune Dysfunction
description: >
Immune system alterations enable ectopic endometrial cells to evade
clearance. Includes increased peritoneal macrophages, reduced NK cell
cytotoxicity, T cell dysfunction, and elevated inflammatory cytokines.
Crosstalk between endometrial stromal cells and macrophages impairs
NK cell function via IL-10 and TGF-beta secretion.
biological_processes:
- preferred_term: Inflammatory Response
term:
id: GO:0006954
label: inflammatory response
evidence:
- reference: PMID:16166933
reference_title: "Immunology of endometriosis."
supports: NO_EVIDENCE
snippet: "Increased number and activation of peritoneal macrophages, decreased
T cell and natural killer (NK) cell cytotoxicities are the alterations in cellular
immunity and result in inadequate removal of ectopic endometrial cells from
the peritoneal cavity."
explanation: Immune cell dysfunction leads to impaired clearance of ectopic
endometrial cells
- reference: PMID:28971893
reference_title: "The crosstalk between endometrial stromal cells and macrophages impairs cytotoxicity of NK cells in endometriosis by secreting IL-10 and TGF-β."
supports: SUPPORT
snippet: "The dysfunction of NK cells in women with endometriosis (EMS) contributes
to the immune escape of menstrual endometrial fragments refluxed into the peritoneal
cavity."
explanation: NK cell dysfunction is a key mechanism enabling immune escape
of refluxed endometrial fragments
- reference: PMID:28971893
reference_title: "The crosstalk between endometrial stromal cells and macrophages impairs cytotoxicity of NK cells in endometriosis by secreting IL-10 and TGF-β."
supports: SUPPORT
snippet: "After incubation with ESCs and macrophages, the expression of CD16,
NKG2D, perforin and IFN-γ, viability and cytotoxicity of NK cells were significantly
downregulated. The secretion of interleukin (IL)-1β, IL-10 and transforming
growth factor (TGF)-β in the co-culture system of ESCs and macrophages was increased."
explanation: Interaction between endometrial stromal cells and macrophages
suppresses NK cell cytotoxicity through IL-10 and TGF-beta
- name: Hypoxia and Angiogenesis
description: >
Ectopic lesions experience hypoxia which stabilizes HIF-1alpha,
upregulating VEGF and promoting angiogenesis. Neovascularization
supports lesion survival and growth. Ovarian endometriomas show
particularly high expression of hypoxic and angiogenic factors.
biological_processes:
- preferred_term: Response to Hypoxia
term:
id: GO:0001666
label: response to hypoxia
- preferred_term: Angiogenesis
term:
id: GO:0001525
label: angiogenesis
evidence:
- reference: PMID:26408396
reference_title: "Different Expression of Hypoxic and Angiogenic Factors in Human Endometriotic Lesions."
supports: SUPPORT
snippet: "Endometriosis is associated with local angiogenic and hypoxic mechanisms.
Indeed, peritoneal fluid of women with endometriosis generates a specific microenvironment
to support the growth and development of ectopic endometrial tissues."
explanation: Angiogenic and hypoxic mechanisms create a supportive
microenvironment for ectopic lesion growth
- reference: PMID:26408396
reference_title: "Different Expression of Hypoxic and Angiogenic Factors in Human Endometriotic Lesions."
supports: SUPPORT
snippet: "Ovarian endometrioma expresses high levels of HIF-1/2α, PAR-1/4, and
VEGF-A, while DIE did not show significantly different gene expression compared
to endometrium from unaffected women. A positive correlation between the expression
of HIF-1/2α and VEGF-A mRNA was observed in OMA."
explanation: Ovarian endometriomas specifically show elevated
hypoxia-inducible factors and VEGF with correlated expression
- reference: PMID:30074218
reference_title: "Expression of MMIF, HIF-1α and VEGF in Serum and Endometrial Tissues of Patients with Endometriosis."
supports: SUPPORT
snippet: "The results showed that serum concentrations of MMIF, HIF-1α, and VEGF
were significantly higher in EM patients than in controls (P<0.05). The expression
of all three proteins in both serum and endometrial tissues increased significantly
with the R-AFS stage (P<0.05) and with dysmenorrheal severity (P<0.05)."
explanation: HIF-1alpha and VEGF expression correlates with disease stage
and dysmenorrhea severity
- name: Adhesion Formation
description: >
Chronic inflammation leads to fibrous adhesions distorting pelvic
anatomy. Adhesions contribute to pain and infertility.
phenotypes:
- name: Pelvic Pain
category: Reproductive
frequency: VERY_FREQUENT
diagnostic: true
notes: Chronic, cyclical
phenotype_term:
preferred_term: Pelvic Pain
term:
id: HP:0030016
label: Dyspareunia
- name: Dysmenorrhea
category: Reproductive
frequency: VERY_FREQUENT
phenotype_term:
preferred_term: Dysmenorrhea
term:
id: HP:0100607
label: Dysmenorrhea
evidence:
- reference: PMID:30074218
reference_title: "Expression of MMIF, HIF-1α and VEGF in Serum and Endometrial Tissues of Patients with Endometriosis."
supports: SUPPORT
snippet: "The expression of all three proteins in both serum and endometrial tissues
increased significantly with the R-AFS stage (P<0.05) and with dysmenorrheal
severity (P<0.05)."
explanation: VEGF and HIF-1alpha expression correlates with dysmenorrhea
severity, linking hypoxia and angiogenesis to pain
- name: Dyspareunia
category: Reproductive
frequency: FREQUENT
notes: Deep dyspareunia
phenotype_term:
preferred_term: Dyspareunia
term:
id: HP:0030016
label: Dyspareunia
- name: Infertility
category: Reproductive
frequency: FREQUENT
phenotype_term:
preferred_term: Infertility
term:
id: HP:0000789
label: Infertility
evidence:
- reference: PMID:16166933
reference_title: "Immunology of endometriosis."
supports: SUPPORT
snippet: "Increased levels of several cytokines and growth factors which are secreted
by either immune and endometrial cells seem to promote implantation and growth
of ectopic endometrium by inducing proliferation and angiogenesis."
explanation: Snippet supports inflammatory lesion growth mechanisms but does
not directly support infertility frequency.
- name: Heavy Menstrual Bleeding
category: Reproductive
frequency: FREQUENT
phenotype_term:
preferred_term: Menorrhagia
term:
id: HP:0000132
label: Menorrhagia
- name: Painful Bowel Movements
category: Gastrointestinal
frequency: OCCASIONAL
notes: With rectovaginal disease
phenotype_term:
preferred_term: Dyschezia
term:
id: HP:0002027
label: Abdominal pain
- name: Fatigue
category: Systemic
frequency: FREQUENT
phenotype_term:
preferred_term: Fatigue
term:
id: HP:0012378
label: Fatigue
biochemical:
- name: CA-125
presence: Elevated
context: Nonspecific, may be elevated in severe disease
- name: Estradiol
presence: Normal to Elevated
context: Local estrogen production in lesions
genetic:
- name: WNT4
association: Risk Factor
- name: VEZT
association: Risk Factor
- name: GREB1
association: Risk Factor
- name: ID4
association: Risk Factor
environmental:
- name: Early Menarche
notes: Increases lifetime estrogen exposure
- name: Short Menstrual Cycles
notes: More frequent retrograde menstruation
- name: Nulliparity
notes: Risk factor
- name: Low BMI
notes: Associated with increased risk
treatments:
- name: NSAIDs
description: First-line for pain management.
- name: Combined Oral Contraceptives
description: Suppress ovulation and reduce menstruation.
- name: Progestins
description: Create hypoestrogenic state (dienogest, medroxyprogesterone).
- name: GnRH Agonists
description: Induce medical menopause, add-back therapy needed.
- name: GnRH Antagonists
description: Elagolix with dose-dependent estrogen suppression.
- name: Aromatase Inhibitors
description: Reduce local estrogen production in lesions.
- name: Laparoscopic Surgery
description: Excision or ablation of lesions, adhesiolysis.
- name: Hysterectomy
description: Definitive surgery for completed childbearing.
classifications:
harrisons_chapter:
- classification_value: ENDOCRINOLOGY_METABOLISM
datasets:
references:
- reference: DOI:10.3389/fphar.2023.1155558
title: Targeting the formation of estrogens for treatment of hormone dependent
diseases–current status
findings: []
- reference: DOI:10.3390/ijms25147624
title: Pathogenesis of Endometriosis and Endometriosis-Associated Cancers
findings: []
- reference: DOI:10.69622/28227977
title: Molecular and cellular landscape of endometriosis
findings: []
- reference: DOI:10.7759/cureus.87091
title: "Exploring the Immune System's Role in Endometriosis: Insights Into Pathogenesis,
Pain, and Treatment"
findings: []
Endometriosis is an estrogen‑dependent, chronic inflammatory condition in which endometrial‑like glands and stroma establish at ectopic sites, most commonly on the peritoneum and ovary. Current models integrate retrograde menstruation with permissive host factors—genetic susceptibility, altered endometrial biology, immune dysregulation, hypoxia‑driven angiogenesis, neuroangiogenesis, and progressive fibrotic remodeling. The disease affects about 10% of reproductive‑aged women worldwide, with a diagnostic delay of approximately 7–9 years, contributing to substantial pain and infertility burden (papandreouUnknownyearinterinstitutionalinterdepartmentalmasterof pages 7-15). Lesions display estrogen dominance and progesterone resistance, supported by local estrogen biosynthesis (aromatase/CYP19A1; reductive HSD17B1 with reduced oxidative HSD17B2) and diminished progesterone receptor signaling; hypoxia and HIF‑1α amplify VEGF‑mediated angiogenesis and inflammatory circuits. Immune alterations include macrophage reprogramming, reduced NK cytotoxicity, T‑cell imbalance, and elevated pro‑inflammatory cytokines (e.g., IL‑6, TNF‑α), enabling immune evasion and lesion persistence. Warburg‑like metabolic reprogramming, EMT/TGF‑β‑driven fibrosis, and extracellular matrix (ECM) remodeling consolidate chronicity. Somatic alterations (ARID1A, PIK3CA, KRAS, PTEN) occur in some lesions and are implicated in the small but real risk of malignant transformation to endometriosis‑associated ovarian cancer. Single‑cell/spatial transcriptomics and large‑scale genetics highlight disease‑relevant stromal and immune cell states and suggest polygenic risk acting through immune regulation, cell differentiation, and hormone pathways (sarsenova2025molecularandcellular pages 10-14, adilbayeva2024pathogenesisofendometriosis pages 14-15, sarsenova2025molecularandcellular pages 14-17).
| Axis | Key genes/proteins (HGNC) | Perturbed processes (GO / plain text) | Primary cell types (CL / plain text) | Anatomical locations (UBERON / plain text) | Chemical entities (CHEBI / plain text) | Representative evidence |
|---|---|---|---|---|---|---|
| Estrogen dominance & progesterone resistance | ESR1, ESR2, PGR | Steroid hormone signaling; altered receptor expression (progesterone response) | Endometrial epithelial cells, stromal cells | Uterine endometrium; peritoneum (ectopic sites) | Estradiol (E2), Progesterone (P4) | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 14-17) |
| Local estrogen biosynthesis (aromatase / HSD17B / sulfatase) | CYP19A1, HSD17B1, HSD17B2, STS | Local steroid biosynthesis and activation/inactivation of estrogens | Stromal cells, epithelial cells | Endometriotic lesions, eutopic endometrium | Androstenedione/testosterone → estrone/estradiol; estrogen-sulfates | https://doi.org/10.3389/fphar.2023.1155558 (sarsenova2025molecularandcellular pages 10-14) |
| Hypoxia / HIF-1 / VEGF angiogenesis & neuroangiogenesis | HIF1A, VEGFA, EPAS1 | Hypoxia response, angiogenesis, vascular development | Endothelial cells, stromal fibroblasts, perivascular cells | Lesion microenvironment, peritoneum, ovary (endometrioma) | VEGF (growth factor); hypoxia-induced metabolites | https://doi.org/10.3390/ijms25147624 (adilbayeva2024pathogenesisofendometriosis pages 14-15) |
| Immune dysregulation (macrophages, NK, T cells, cytokines, checkpoints) | IL6, TNF, CCL2, PDCD1 (PD-1), CTLA4 | Inflammatory signaling, immune evasion, cytokine-mediated recruitment | Macrophages (M1/M2-like), NK cells, CD4+/CD8+ T cells, Tregs | Peritoneal cavity, lesion stroma | Pro-inflammatory cytokines (IL-6, TNF-α), chemokines | https://doi.org/10.7759/cureus.87091 (ahmed2025exploringtheimmune pages 15-16) |
| Fibrosis / EMT / TGF-β / ECM remodeling | TGFB1, TGFBI, MMP1, MMP2 | Extracellular matrix organization, epithelial–mesenchymal transition, fibrosis | Stromal fibroblasts, myofibroblasts, mesenchymal cells | Lesions, adhesions, affected peritoneum | Collagen, fibronectin; TGF-β signaling molecules | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 10-14) |
| Metabolic reprogramming (Warburg-like) | SLC2A1 (GLUT1), HK2, PDK1 | Glycolysis upregulation, altered mitochondrial function, ROS metabolism | Lesion stromal/epithelial cells, macrophages | Ectopic lesions (hypoxic niches) | Glucose, lactate, reactive oxygen species (ROS) | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 10-14) |
| Somatic driver mutations & malignant transformation risk | ARID1A, PIK3CA, KRAS, PTEN | DNA repair/PI3K signaling / oncogenic activation | Epithelial cells of lesions (clonal populations) | Ovarian endometrioma → risk for EAOC (clear cell, endometrioid) | DNA damage products; ROS | https://doi.org/10.3390/ijms25147624 (adilbayeva2024pathogenesisofendometriosis pages 14-15) |
| GWAS / germline risk architecture | Multiple risk loci (incl. loci near ESR1) | Genetic susceptibility; regulation of immune, hormonal, proliferative pathways | Decidualized stromal cells, macrophages (cell-context from atlas) | Uterine tissues; systemic genetic risk | — (polygenic risk) | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 10-14) |
| Microbiome / estrobolome contributions | Bacterial β-glucuronidase (functional) | Estrogen recycling (deconjugation), modulation of inflammation | Gut microbiota; reproductive-tract microbiota | Gut, vagina, endometrium | Microbial metabolites (SCFAs), estrogen-sulfates | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 10-14) |
| Single-cell & spatial niche insights | CXCL12, MRC1, APOE (cell-state markers) | Cell–cell signaling, immune–stromal interactions, angiogenic niches | Stromal subtypes, epithelial subtypes, lesion-resident macrophages | Lesion microenvironment (spatially organized niches) | Chemokines (CXCL12), lipids (ApoE-associated) | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 10-14) |
| Disease progression sequence (mechanistic) | — (process-level) | Retrograde menstruation → implantation → immune evasion → angiogenesis & innervation → fibrosis | Shed endometrial epithelial & stromal cells; recruited immune cells | Peritoneal surfaces, ovary, pelvic organs | Hemoglobin/iron (from bleed) → ROS; prostaglandins (PGE2) | https://doi.org/10.69622/28227977 (sarsenova2025molecularandcellular pages 10-14) |
| Clinical phenotypes & burden | — (clinical manifestations) | Pain signaling, impaired fertility, systemic comorbidity | N/A (multicellular) | Pelvis, reproductive organs; systemic symptoms | Analgesics, hormonal modulators (therapeutics) | Prevalence ~10%; diagnostic delay median ~7–9 yrs — https://doi.org/10.69622/28227977 (papandreouUnknownyearinterinstitutionalinterdepartmentalmasterof pages 7-15) |
Table: Compact, ontology-style summary linking major pathophysiology axes to genes, processes, cell types, anatomical sites, chemical entities and representative evidence (DOI + context ID); useful as a knowledge-base import or quick reference for mechanistic claims.
Metabolic reprogramming: hypoxia‑adapted glycolysis/Warburg‑like metabolism in lesions (sarsenova2025molecularandcellular pages 10-14).
Dysregulated molecular pathways: estrogen biosynthesis and signaling (CYP19A1/HSD17B1/HSD17B2; ESR1/ESR2; PGR), hypoxia/HIF‑1/VEGF, NF‑κB‑mediated inflammation, TGF‑β/EMT/ECM, PI3K/AKT from somatic drivers, and immune checkpoint axes (PD‑1/CTLA4) in immune suppression (adilbayeva2024pathogenesisofendometriosis pages 14-15, sarsenova2025molecularandcellular pages 14-17, ahmed2025exploringtheimmune pages 15-16).
Affected cellular processes: implantation/adhesion, angiogenesis and neurogenesis, aberrant stromal–epithelial signaling and decidualization, ECM deposition, immune cell recruitment and polarization, altered glycolysis/ROS handling (sarsenova2025molecularandcellular pages 10-14, adilbayeva2024pathogenesisofendometriosis pages 14-15, ahmed2025exploringtheimmune pages 15-16).
Somatic drivers: ARID1A, PIK3CA, KRAS, PTEN (adilbayeva2024pathogenesisofendometriosis pages 14-15).
Chemical entities (CHEBI): estradiol (E2), progesterone (P4), prostaglandin E2 (PGE2), VEGF as growth factor ligand, ROS/iron byproducts (adilbayeva2024pathogenesisofendometriosis pages 14-15, sarsenova2025molecularandcellular pages 14-17).
Cell types (CL): endometrial epithelial and stromal cells; endothelial cells; peritoneal/lesion‑resident macrophages (M2‑like, scar‑associated); NK cells; CD4+/CD8+ T cells; Tregs (ahmed2025exploringtheimmune pages 15-16, sarsenova2025molecularandcellular pages 10-14).
Anatomical locations (UBERON): uterine endometrium, peritoneum, ovary (endometrioma), pelvic peritoneal surfaces; adhesions across pelvic organs (sarsenova2025molecularandcellular pages 10-14, papandreouUnknownyearinterinstitutionalinterdepartmentalmasterof pages 7-15).
Where possible, peer‑reviewed 2023–2024 articles were prioritized. Some 2025 narrative reviews provide context but were downweighted in drawing mechanistic conclusions. Further primary single‑cell and GWAS fine‑mapping studies are continually refining cell‑type‑specific mechanisms, especially in stromal decidualization failure and macrophage phenotypes.
References
(papandreouUnknownyearinterinstitutionalinterdepartmentalmasterof pages 7-15): P PAPANDREOU. Interinstitutional/interdepartmental master of science<< application of endoscopic surgical techniques in. Unknown journal, Unknown year.
(sarsenova2025molecularandcellular pages 10-14): Meruert Sarsenova. Molecular and cellular landscape of endometriosis. Mar 2025. URL: https://doi.org/10.69622/28227977, doi:10.69622/28227977.
(adilbayeva2024pathogenesisofendometriosis pages 14-15): Altynay Adilbayeva and Jeannette Kunz. Pathogenesis of endometriosis and endometriosis-associated cancers. International Journal of Molecular Sciences, 25:7624, Jul 2024. URL: https://doi.org/10.3390/ijms25147624, doi:10.3390/ijms25147624. This article has 53 citations and is from a poor quality or predatory journal.
(sarsenova2025molecularandcellular pages 14-17): Meruert Sarsenova. Molecular and cellular landscape of endometriosis. Mar 2025. URL: https://doi.org/10.69622/28227977, doi:10.69622/28227977.
(ahmed2025exploringtheimmune pages 15-16): Rania S Ahmed, Mohamed Sherif, Majd A Alghamdi, Salah N El-Tallawy, Omar K Alzaydan, Joseph V Pergolizzi, Giustino Varrassi, Zaina Zaghra, Ziad S Abdelsalam, Mahmoud T Kamal, and Flaminia Coluzzi. Exploring the immune system's role in endometriosis: insights into pathogenesis, pain, and treatment. Cureus, Jul 2025. URL: https://doi.org/10.7759/cureus.87091, doi:10.7759/cureus.87091. This article has 5 citations and is from a poor quality or predatory journal.