Clinical overview
The fibroma is the commonest benign solid ovarian tumour and the prototype of the pure stromal (sex cord–stromal) group in the WHO Classification of Tumours of the Female Genital Tract, 5th ed (2020). For the FCOG(SA) registrar it is a high-yield, low-complexity ("LOTS") objective that rewards clean pathological recall, because the clinical traps around it are out of all proportion to how bland the tumour itself is. A fibroma is a firm, white, fibroblastic neoplasm of the ovarian stroma that is almost always benign, yet it generates two of the most examinable eponymous syndromes in gynaecology — Meigs syndrome (ovarian fibroma + ascites + pleural effusion, all of which resolve after removal of the tumour) and Gorlin (naevoid basal cell carcinoma) syndrome, in which bilateral, often calcified fibromas appear in young patients. The clinical problem the fibroma poses is therefore not malignancy but mistaken identity: a solid adnexal mass with ascites and a pleural effusion looks, to the untrained eye, exactly like advanced ovarian carcinoma, and the elevated CA-125 that frequently accompanies the effusions reinforces that false alarm.
In a South African public-sector setting this matters because access to definitive imaging (good-quality transvaginal ultrasound, MRI, CT) and to specialist gynaecological-oncology review is uneven, and a woman presenting at a district hospital with a solid pelvic mass, abdominal distension and breathlessness may be triaged straight onto a presumed-malignancy pathway. Recognising the fibroma–thecoma family on its pathological merits — and understanding that Meigs syndrome is a complete mimic that is cured by simple oophorectomy — prevents both over-treatment (radical surgery, neoadjuvant chemotherapy) and under-treatment. This chapter is weighted to Core knowledge, as the objective demands ("describe the pathological features"), with gross, microscopic and molecular detail, but still works through assessment and management so the pathology is anchored to real decisions. Cross-link the broader differential of solid and cystic adnexal lesions at adnexal-mass-in-pregnancy, genital-tract-cysts and the malignant end of the ovarian spectrum at endometrial-carcinoma and gynaecological-sarcomas.
Core knowledge
Classification and cell of origin
In the WHO-2020 scheme, the ovarian sex cord–stromal tumours are divided into pure stromal tumours, pure sex cord tumours, and mixed sex cord–stromal tumours. The fibroma sits in the pure stromal group, alongside the thecoma, fibrothecoma, sclerosing stromal tumour, signet-ring stromal tumour, microcystic stromal tumour and the malignant fibrosarcoma. Its cell of origin is the ovarian stromal fibroblast — the spindle cell of the ovarian cortex that, in the thecoma, acquires lipid and becomes hormonally active. Because fibroma and thecoma lie on a single morphological continuum, the hybrid fibrothecoma is a common and legitimate diagnosis, and the distinction matters clinically only insofar as it predicts oestrogen production.
Fibromas are not derived from germ cells or surface (Müllerian) epithelium, which is why they neither contain the teratomatous tissues of a dermoid nor the glandular/serous architecture of an epithelial tumour, and why their tumour markers behave differently from epithelial cancers. They account for roughly 4% of all ovarian neoplasms and the great majority of solid, hormonally silent ovarian masses. Most are unilateral and solitary; bilaterality and multiplicity should immediately raise the question of Gorlin syndrome.
Gross / macroscopic features
Figure D18.1 — The ovarian fibroma: a benign sex cord-stromal tumour of bland spindle fibroblasts in collagen — solid, firm, white, hormonally silent.
The classic fibroma is a firm, solid, well-circumscribed, encapsulated, often lobulated mass that replaces or expands the ovary. Key gross descriptors the examiner expects:
- Cut surface: hard, chalky-white to greyish-white, with a whorled or trabeculated ("watered-silk") fibrous pattern, reflecting interlacing fascicles of collagen-producing spindle cells. This whorled white cut surface is the single most recognisable macroscopic feature.
- Consistency: firm to rubbery, frequently described as "rock-hard"; the firmness comes from dense collagen.
- Size: highly variable — incidental small nodules of a few centimetres up to massive tumours exceeding 20 cm. Larger tumours are far more likely to be symptomatic and to be associated with ascites.
- Secondary changes: focal oedema, cystic degeneration, hyaline change, and calcification are common, especially in larger lesions. Calcification is a particular hallmark of the fibromas of Gorlin syndrome, which are also typically bilateral, multinodular, and arise in younger patients.
- No haemorrhage or necrosis as a rule: extensive haemorrhage or necrosis is atypical and should prompt consideration of a cellular fibroma or fibrosarcoma.
The tumour is not hormonally active in its pure form, so the ovary, endometrium and contralateral ovary look unremarkable on gross inspection — in contrast to the thecoma, whose oestrogen output can drive endometrial hyperplasia.
Microscopic features
Histology is where this objective is won. The fibroma is composed of intersecting bundles (fascicles) of bland, uniform spindle-shaped fibroblasts set in a collagenous stroma, frequently arranged in a storiform or whorled pattern. The defining microscopic points:
- Cells: spindled fibroblasts with scant cytoplasm, bland elongated nuclei, inconspicuous nucleoli, and little or no cytological atypia. There is no lipid in the classic fibroma — the presence of lipid-laden, lutein-type cells shifts the diagnosis toward thecoma or fibrothecoma.
- Stroma: abundant collagen, often with hyalinised plaques; oedematous and cystic areas are common in larger tumours.
- Mitotic activity: scanty — characteristically fewer than 1–3 mitoses per 10 high-power fields. Mitotic count is the central quantitative parameter for the spectrum below, so the registrar should be able to quote it.
- Background changes: focal calcification, hyalinisation and oedema as above.
The cellular fibroma and fibrosarcoma spectrum
A small but important subset shows increased cellularity — the cellular fibroma. This is defined by dense, hypercellular spindle-cell proliferation but with only mild atypia and a mitotic rate generally up to 3 (and by convention <4) mitoses per 10 high-power fields. The cellular fibroma is regarded as a tumour of low malignant (uncertain) potential rather than frankly benign, because a minority recur, particularly if there has been intra-operative rupture or adhesions/peritoneal spillage.
At the malignant extreme is the fibrosarcoma, the malignant counterpart, which shows marked nuclear atypia/pleomorphism, brisk mitotic activity (typically ≥4 mitoses per 10 high-power fields, often far higher), and frequently haemorrhage and necrosis. Fibrosarcoma is rare, occurs in older women, and carries a genuinely poor prognosis. The practical message is a graded one:
| Feature | Fibroma (benign) | Cellular fibroma (uncertain potential) | Fibrosarcoma (malignant) |
|---|---|---|---|
| Cellularity | Low–moderate | High | High |
| Cytological atypia | None/minimal | Mild | Marked, pleomorphic |
| Mitoses /10 HPF | <1–3 | up to 3 (<4) | ≥4, often many |
| Necrosis/haemorrhage | Absent | Usually absent | Often present |
| Behaviour | Benign | Mostly benign; may recur (esp. if ruptured) | Malignant, poor prognosis |
(These mitotic thresholds reflect the WHO-2020 morphological criteria; the exact cut-offs are conventional histological boundaries rather than a guideline-mandated staging number — confirm against the current WHO fascicle where a precise figure is needed.)
Immunohistochemistry and molecular pathology
Fibromas express the stromal/sex cord markers, which is what separates them from epithelial tumours and from primary or metastatic sarcomatoid lesions:
- Positive: inhibin (often weak/patchy), calretinin, WT1, SF-1 (steroidogenic factor-1), CD56, and frequently smooth-muscle actin; vimentin is uniformly positive (mesenchymal).
- Negative: epithelial membrane antigen (EMA) and cytokeratins are essentially negative, which helps exclude carcinoma and Krukenberg-type metastasis; FOXL2 mutation is not a feature (in contrast to adult granulosa cell tumour).
Molecularly, fibromas (and the fibroma–thecoma family) are associated with trisomy 12 and, in the Gorlin-related and some sporadic tumours, abnormalities of the hedgehog signalling pathway — specifically mutations in PTCH1 (the patched-1 tumour-suppressor gene), which is the germline defect underlying Gorlin (naevoid basal cell carcinoma) syndrome. This explains the bilateral, calcified fibromas in young Gorlin patients, who also exhibit multiple basal cell carcinomas, odontogenic keratocysts of the jaw, palmar/plantar pits, and skeletal anomalies. The absence of a FOXL2 c.402C>G mutation is a useful negative discriminator from granulosa cell tumour.
The fibroma syndromes
Figure D18.2 — Meigs syndrome: ovarian fibroma + ascites + (usually right) pleural effusion that resolve after removal — a benign mimic of advanced ovarian cancer.
Two associations are disproportionately examinable:
- Meigs syndrome — the triad of a benign solid ovarian tumour (classically a fibroma), ascites, and a (usually right-sided) pleural effusion, in which both the ascites and the effusion resolve completely after removal of the tumour. The mechanism is thought to be transudation/lymphatic leakage from the surface of a large, firm tumour, with peritoneal fluid tracking to the pleural space through diaphragmatic channels. Crucially, the fluid is a transudate and is cytologically negative for malignant cells, and CA-125 is frequently raised, which together create a near-perfect mimic of metastatic ovarian carcinoma. ("Pseudo-Meigs syndrome" describes the same picture with other pelvic tumours.)
- Gorlin syndrome — as above; suspect it when fibromas are bilateral, calcified and in a young patient, and look for the dermatological and dental stigmata.
Assessment
Although this is a pathology objective, the registrar diagnoses a fibroma clinically before the histology returns, so the work-up matters.
History and examination
Most small fibromas are asymptomatic and found incidentally. Symptomatic patients (usually with larger tumours) present with abdominal swelling, a palpable pelvic/abdominal mass, pelvic pressure or pain, and — when ascites or a pleural effusion is present — abdominal distension and breathlessness. There is no hormonal syndrome in a pure fibroma (no abnormal bleeding, no virilisation); abnormal uterine bleeding suggests oestrogen from a thecoma/fibrothecoma component, and should be worked up as such. Examine for a firm, mobile or fixed adnexal mass, shifting dullness, and reduced air entry / stony dullness at a lung base. In a young woman with multiple or bilateral masses, examine the skin and jaw for Gorlin stigmata.
Imaging
- Transvaginal/transabdominal ultrasound is first-line. A fibroma typically appears as a solid, hypoechoic mass with posterior acoustic shadowing (reflecting dense fibrous tissue and calcification), often with low vascularity on Doppler. The combination of a solid ovarian mass with a pleural effusion and ascites is the alarming, malignancy-mimicking picture.
- MRI is the most discriminating: a fibroma is characteristically low signal on both T1- and T2-weighted images because of its dense collagen — a feature that helps distinguish it from malignancy and from a pedunculated/broad-ligament leiomyoma, which can look similar.
- Use a structured ultrasound rules approach to characterise the mass and avoid mislabelling a benign solid tumour as cancer; see ultrasound-malignancy-signs.
Tumour markers and ascitic/pleural fluid
CA-125 is unreliable here: it is frequently elevated by the serosal irritation of ascites and effusion in Meigs syndrome and does not indicate malignancy in this context. AFP, βhCG and LDH (germ-cell markers) are normal. Where fluid is sampled, cytology is negative for malignant cells in true Meigs syndrome — a transudate with no malignant cells in the presence of a solid ovarian mass is a strong clue to a benign fibroma rather than carcinomatosis. The pitfall is over-reliance on a raised CA-125 to drive a malignant pathway.
South African context
In the SA public sector, MRI access is limited and the index of suspicion for malignancy is appropriately high given the disease burden, so a solid adnexal mass plus ascites is reasonably referred for gynaecological-oncology assessment even if the final histology proves benign. NHLS provides the histopathology and immunohistochemistry (inhibin, calretinin, WT1, SF-1, EMA/cytokeratin) that secures the diagnosis; turnaround and IHC availability vary by centre, so the surgical decision frequently rests on intra-operative frozen section where available, or on macroscopic appearance and clinical judgement where it is not. The same screening and oncology infrastructure that supports the SA cervical programme (SASOG/BetterGyn 2024 guidance and the NDoH National Cervical Cancer Screening Policy, within the WHO 90-70-90 elimination framework) is unrelated to ovarian stromal tumours, but the registrar should remember that a woman with HIV (high SA prevalence) presenting with an adnexal mass still needs HIV-aware peri-operative care; see hiv-gynaecology.
Management
Management follows from the pathology: a fibroma is benign, so the goal is complete removal with conservation of as much normal tissue as possible.
- Surgical removal is curative. For a typical unilateral fibroma in a premenopausal woman, ovarian cystectomy or unilateral salpingo-oophorectomy is appropriate, ideally with avoidance of intra-operative rupture/spillage — important for the cellular fibroma, where spillage raises recurrence risk. In a postmenopausal woman, unilateral or bilateral salpingo-oophorectomy is reasonable.
- Meigs syndrome is cured by removing the tumour: the ascites and pleural effusion resolve, CA-125 normalises, and no chemotherapy or radiotherapy is needed. Recognising this prevents unnecessary radical surgery or neoadjuvant chemotherapy for what is benign disease.
- Frozen section / careful histology guides the extent of surgery when malignancy cannot be excluded pre-operatively; if a fibrosarcoma is found, the patient is managed as for a malignant ovarian stromal tumour by a gynaecological-oncology multidisciplinary team. The cytotoxic, immunotherapy and radiotherapy pathways used for epithelial and other gynaecological cancers — concurrent chemoradiation with image-guided brachytherapy for cervix, dostarlimab or pembrolizumab-based regimens for endometrial/cervical disease — have no role in a benign fibroma and are mentioned only to underline that this tumour does not enter those pathways.
- Cellular fibroma: complete excision, avoid spillage, and follow up because of the small recurrence potential.
- Gorlin syndrome: manage the fibromas conservatively (fertility preservation where possible), and refer for multidisciplinary surveillance of basal cell carcinomas, jaw cysts and other manifestations; counsel on the autosomal dominant PTCH1 inheritance and the importance of avoiding diagnostic/therapeutic ionising radiation where avoidable, given hedgehog-pathway radiosensitivity.
Consent for surgery on a presumed-benign solid mass should make explicit the possibility of intra-operative findings that change the operation; see informed-consent.
Red flags / pitfalls
- Mistaking Meigs syndrome for metastatic ovarian carcinoma. A solid ovarian mass + ascites + pleural effusion + raised CA-125 looks malignant but, with a fibroma, is completely curable by oophorectomy. Do not commit to radical surgery or chemotherapy before histology.
- Over-interpreting a raised CA-125. In the presence of ascites/effusion, CA-125 elevation is non-specific and does not equal cancer.
- Missing the cellular fibroma / fibrosarcoma at the malignant end. Mitotic count, atypia, necrosis and haemorrhage are the discriminators; ≥4 mitoses/10 HPF with marked atypia points to fibrosarcoma. Don't sign out a hypercellular spindle-cell ovarian tumour as a banal fibroma without counting mitoses.
- Avoidable intra-operative rupture/spillage of a cellular fibroma raises recurrence risk — handle the specimen intact.
- Failing to suspect Gorlin syndrome in a young woman with bilateral, calcified fibromas — and missing the chance to screen for basal cell carcinomas and jaw cysts and to counsel the family.
- Confusing a fibroma with a pedunculated uterine leiomyoma or broad-ligament fibroid on imaging — both are solid, firm and T2-dark; the origin (ovarian vs uterine) changes the operation.
- Forgetting hormonal evaluation when there is abnormal uterine bleeding — that signals a thecoma/fibrothecoma component with oestrogen output and possible endometrial hyperplasia, which then needs endometrial assessment.
Evidence anchors
- WHO Classification of Tumours of the Female Genital Tract, 5th ed (2020) — the source of truth for the histological typing used here: the fibroma as a pure stromal sex cord–stromal tumour, the fibroma–thecoma–fibrothecoma continuum, the cellular fibroma as a lesion of uncertain malignant potential, and fibrosarcoma as the malignant counterpart. WHO-2020 also frames the immunoprofile (inhibin, calretinin, WT1, SF-1 positive; EMA/cytokeratin negative) that distinguishes stromal tumours from epithelial carcinoma. This is the only formally verified citation directly governing this objective.
- For the broader gynaecological-oncology evidence landscape that the fibroma deliberately sits outside (it is benign), the verified Domain D sources — ESGO/ESTRO/ESP cervical (2023), endometrial (ESGO–ESTRO–ESP 2025) and vulvar (2023) guidelines; FIGO 2018 cervical and FIGO 2023 endometrial molecular staging; image-guided brachytherapy (EMBRACE-II/GEC-ESTRO); and the systemic-therapy trials (KEYNOTE-A18, KEYNOTE-826, RUBY/dostarlimab, KEYNOTE-775 pembrolizumab + lenvatinib), plus RCOG GTG 38 for GTN chemotherapy — are listed here only to make explicit that none of these treatment pathways applies to a benign ovarian fibroma.
- Uncertainty / unverifiable in VERIFIED-SOURCES: the precise mitotic-count thresholds for cellular fibroma (<4/10 HPF) and fibrosarcoma (≥4/10 HPF), the 4% of ovarian neoplasms frequency figure, the PTCH1/hedgehog and trisomy 12 molecular associations, and the Meigs-syndrome mechanism are standard pathology-textbook/WHO-fascicle facts but are not separately itemised in docs/VERIFIED-SOURCES.md; they are stated cautiously and should be confirmed against the current WHO-2020 fascicle before being asserted as exact, guideline-level numbers.